By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
Study with our TEST PREP SERIES. One test item each post thoroughly explains the correct answer and rationales behind all answer choices. Understand the material, don’t memorize it. Rote memorization isn’t dependable, mastering the material is. This question focuses on the intended side effects of beta agonist medication administration and discusses answer option rationales for both correct and incorrect answers.
SCENARIO
You are a resource nurse in the SICU when a code blue is announced. You were in a patient’s room a few doors away and when you respond to the code, there’s a nurse doing compressions, another is bagging while someone else is sticking defibrillator pads on the patient. The primary nurse, the one doing compressions and running the code until more people responded, yells out to you to crack the cart and pull meds.
You’re looking at the cardiac meds and know the idea behind pushing them in a code is to stimulate the patient’s “fight or flight” response. In other words, stimulate the beta-1 receptors of the patient’s sympathetic nervous system. Remember how to keep them straight? Beta-1, Beta-2, 1-heart, 2-lungs. Beta-1 affects the heart, Beta-2 affects the lungs.
When the beta-1 agonist meds circulate to the heart, you’re anticipating increased automaticity and…
Increased myocardial contractility
For a decreased volume of blood leaving the left ventricle with each beat
For the patient’s heart muscle to use less oxygen
Increase in left ventricular afterload
First, simply thing about the fight or flight response; the body’s coordinated recruitment of its resources to help someone escape from danger. The body’s systems, heart, lungs, skeletal muscles,e tc., would all contribute to keeping this person’s body alive in this situation.
CARDIAC AUTOMATICITY
The question tells us that we are anticipating increased automaticity. Automaticity is a characteristic of heart muscle to be able to generate its own heartbeat. So it would follow that increased automaticity would result in not only the increased likelihood of a heartbeat, but ideally, the increased number of heartbeats. So there, we’ve now established we have a fast beating heart.
THINGS WE KNOW
Increased automaticity
Increased heart rate
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Study with our TEST PREP SERIES. One test item each post thoroughly explains the correct answer and rationales behind all answer choices. Understand the material, don’t memorize it. Rote memorization isn’t dependable, mastering the material is. This question focuses on the intended side effects of beta agonist medication administration and discusses answer option rationales for both correct and incorrect answers.
SCENARIO
You are a resource nurse in the SICU when a code blue is announced. You were in a patient’s room a few doors away and when you respond to the code, there’s a nurse doing compressions, another is bagging while someone else is sticking defibrillator pads on the patient. The primary nurse, the one doing compressions and running the code until more people responded, yells out to you to crack the cart and pull meds.
You’re looking at the cardiac meds and know the idea behind pushing them in a code is to stimulate the patient’s “fight or flight” response. In other words, stimulate the beta-1 receptors of the patient’s sympathetic nervous system. Remember how to keep them straight? Beta-1, Beta-2, 1-heart, 2-lungs. Beta-1 affects the heart, Beta-2 affects the lungs.
When the beta-1 agonist meds circulate to the heart, you’re anticipating increased automaticity and…
Increased myocardial contractility
For a decreased volume of blood leaving the left ventricle with each beat
For the patient’s heart muscle to use less oxygen
Increase in left ventricular afterload
First, simply thing about the fight or flight response; the body’s coordinated recruitment of its resources to help someone escape from danger. The body’s systems, heart, lungs, skeletal muscles,e tc., would all contribute to keeping this person’s body alive in this situation.
CARDIAC AUTOMATICITY
The question tells us that we are anticipating increased automaticity. Automaticity is a characteristic of heart muscle to be able to generate its own heartbeat. So it would follow that increased automaticity would result in not only the increased likelihood of a heartbeat, but ideally, the increased number of heartbeats. So there, we’ve now established we have a fast beating heart.
THINGS WE KNOW
Increased automaticity
Increased heart rate
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Study with our TEST PREP SERIES. One test item each post thoroughly explains the correct answer and rationales behind all answer choices. Understand the material, don’t memorize it. Rote memorization isn’t dependable, mastering the material is. This question focuses on the intended side effects of beta agonist medication administration and discusses answer option rationales for both correct and incorrect answers.
SCENARIO
You are a resource nurse in the SICU when a code blue is announced. You were in a patient’s room a few doors away and when you respond to the code, there’s a nurse doing compressions, another is bagging while someone else is sticking defibrillator pads on the patient. The primary nurse, the one doing compressions and running the code until more people responded, yells out to you to crack the cart and pull meds.
You’re looking at the cardiac meds and know the idea behind pushing them in a code is to stimulate the patient’s “fight or flight” response. In other words, stimulate the beta-1 receptors of the patient’s sympathetic nervous system. Remember how to keep them straight? Beta-1, Beta-2, 1-heart, 2-lungs. Beta-1 affects the heart, Beta-2 affects the lungs.
When the beta-1 agonist meds circulate to the heart, you’re anticipating increased automaticity and…
Increased myocardial contractility
For a decreased volume of blood leaving the left ventricle with each beat
For the patient’s heart muscle to use less oxygen
Increase in left ventricular afterload
First, simply thing about the fight or flight response; the body’s coordinated recruitment of its resources to help someone escape from danger. The body’s systems, heart, lungs, skeletal muscles,e tc., would all contribute to keeping this person’s body alive in this situation.
CARDIAC AUTOMATICITY
The question tells us that we are anticipating increased automaticity. Automaticity is a characteristic of heart muscle to be able to generate its own heartbeat. So it would follow that increased automaticity would result in not only the increased likelihood of a heartbeat, but ideally, the increased number of heartbeats. So there, we’ve now established we have a fast beating heart.
THINGS WE KNOW
Increased automaticity
Increased heart rate
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Study with our TEST PREP SERIES. One test item each post thoroughly explains the correct answer and rationales behind all answer choices. Understand the material, don’t memorize it. Rote memorization isn’t dependable, mastering the material is. This question focuses on the intended side effects of beta agonist medication administration and discusses answer option rationales for both correct and incorrect answers.
SCENARIO
You are a resource nurse in the SICU when a code blue is announced. You were in a patient’s room a few doors away and when you respond to the code, there’s a nurse doing compressions, another is bagging while someone else is sticking defibrillator pads on the patient. The primary nurse, the one doing compressions and running the code until more people responded, yells out to you to crack the cart and pull meds.
You’re looking at the cardiac meds and know the idea behind pushing them in a code is to stimulate the patient’s “fight or flight” response. In other words, stimulate the beta-1 receptors of the patient’s sympathetic nervous system. Remember how to keep them straight? Beta-1, Beta-2, 1-heart, 2-lungs. Beta-1 affects the heart, Beta-2 affects the lungs.
When the beta-1 agonist meds circulate to the heart, you’re anticipating increased automaticity and…
Increased myocardial contractility
For a decreased volume of blood leaving the left ventricle with each beat
For the patient’s heart muscle to use less oxygen
Increase in left ventricular afterload
First, simply thing about the fight or flight response; the body’s coordinated recruitment of its resources to help someone escape from danger. The body’s systems, heart, lungs, skeletal muscles,e tc., would all contribute to keeping this person’s body alive in this situation.
CARDIAC AUTOMATICITY
The question tells us that we are anticipating increased automaticity. Automaticity is a characteristic of heart muscle to be able to generate its own heartbeat. So it would follow that increased automaticity would result in not only the increased likelihood of a heartbeat, but ideally, the increased number of heartbeats. So there, we’ve now established we have a fast beating heart.
THINGS WE KNOW
Increased automaticity
Increased heart rate
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Study with our TEST PREP SERIES. One test item each post thoroughly explains the correct answer and rationales behind all answer choices. Understand the material, don’t memorize it. Rote memorization isn’t dependable, mastering the material is. This question focuses on the intended side effects of beta agonist medication administration and discusses answer option rationales for both correct and incorrect answers.
SCENARIO
You are a resource nurse in the SICU when a code blue is announced. You were in a patient’s room a few doors away and when you respond to the code, there’s a nurse doing compressions, another is bagging while someone else is sticking defibrillator pads on the patient. The primary nurse, the one doing compressions and running the code until more people responded, yells out to you to crack the cart and pull meds.
You’re looking at the cardiac meds and know the idea behind pushing them in a code is to stimulate the patient’s “fight or flight” response. In other words, stimulate the beta-1 receptors of the patient’s sympathetic nervous system. Remember how to keep them straight? Beta-1, Beta-2, 1-heart, 2-lungs. Beta-1 affects the heart, Beta-2 affects the lungs.
When the beta-1 agonist meds circulate to the heart, you’re anticipating increased automaticity and…
Increased myocardial contractility
For a decreased volume of blood leaving the left ventricle with each beat
For the patient’s heart muscle to use less oxygen
Increase in left ventricular afterload
First, simply thing about the fight or flight response; the body’s coordinated recruitment of its resources to help someone escape from danger. The body’s systems, heart, lungs, skeletal muscles,e tc., would all contribute to keeping this person’s body alive in this situation.
CARDIAC AUTOMATICITY
The question tells us that we are anticipating increased automaticity. Automaticity is a characteristic of heart muscle to be able to generate its own heartbeat. So it would follow that increased automaticity would result in not only the increased likelihood of a heartbeat, but ideally, the increased number of heartbeats. So there, we’ve now established we have a fast beating heart.
THINGS WE KNOW
Increased automaticity
Increased heart rate
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Study with our TEST PREP SERIES. One test item each post thoroughly explains the correct answer and rationales behind all answer choices. Understand the material, don’t memorize it. Rote memorization isn’t dependable, mastering the material is. This question focuses on the intended side effects of beta agonist medication administration and discusses answer option rationales for both correct and incorrect answers.
SCENARIO
You are a resource nurse in the SICU when a code blue is announced. You were in a patient’s room a few doors away and when you respond to the code, there’s a nurse doing compressions, another is bagging while someone else is sticking defibrillator pads on the patient. The primary nurse, the one doing compressions and running the code until more people responded, yells out to you to crack the cart and pull meds.
You’re looking at the cardiac meds and know the idea behind pushing them in a code is to stimulate the patient’s “fight or flight” response. In other words, stimulate the beta-1 receptors of the patient’s sympathetic nervous system. Remember how to keep them straight? Beta-1, Beta-2, 1-heart, 2-lungs. Beta-1 affects the heart, Beta-2 affects the lungs.
When the beta-1 agonist meds circulate to the heart, you’re anticipating increased automaticity and…
Increased myocardial contractility
For a decreased volume of blood leaving the left ventricle with each beat
For the patient’s heart muscle to use less oxygen
Increase in left ventricular afterload
First, simply thing about the fight or flight response; the body’s coordinated recruitment of its resources to help someone escape from danger. The body’s systems, heart, lungs, skeletal muscles,e tc., would all contribute to keeping this person’s body alive in this situation.
CARDIAC AUTOMATICITY
The question tells us that we are anticipating increased automaticity. Automaticity is a characteristic of heart muscle to be able to generate its own heartbeat. So it would follow that increased automaticity would result in not only the increased likelihood of a heartbeat, but ideally, the increased number of heartbeats. So there, we’ve now established we have a fast beating heart.
THINGS WE KNOW
Increased automaticity
Increased heart rate
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Study with our TEST PREP SERIES. One test item each post thoroughly explains the correct answer and rationales behind all answer choices. Understand the material, don’t memorize it. Rote memorization isn’t dependable, mastering the material is. This question focuses on the intended side effects of beta agonist medication administration and discusses answer option rationales for both correct and incorrect answers.
SCENARIO
You are a resource nurse in the SICU when a code blue is announced. You were in a patient’s room a few doors away and when you respond to the code, there’s a nurse doing compressions, another is bagging while someone else is sticking defibrillator pads on the patient. The primary nurse, the one doing compressions and running the code until more people responded, yells out to you to crack the cart and pull meds.
You’re looking at the cardiac meds and know the idea behind pushing them in a code is to stimulate the patient’s “fight or flight” response. In other words, stimulate the beta-1 receptors of the patient’s sympathetic nervous system. Remember how to keep them straight? Beta-1, Beta-2, 1-heart, 2-lungs. Beta-1 affects the heart, Beta-2 affects the lungs.
When the beta-1 agonist meds circulate to the heart, you’re anticipating increased automaticity and…
Increased myocardial contractility
For a decreased volume of blood leaving the left ventricle with each beat
For the patient’s heart muscle to use less oxygen
Increase in left ventricular afterload
First, simply thing about the fight or flight response; the body’s coordinated recruitment of its resources to help someone escape from danger. The body’s systems, heart, lungs, skeletal muscles,e tc., would all contribute to keeping this person’s body alive in this situation.
CARDIAC AUTOMATICITY
The question tells us that we are anticipating increased automaticity. Automaticity is a characteristic of heart muscle to be able to generate its own heartbeat. So it would follow that increased automaticity would result in not only the increased likelihood of a heartbeat, but ideally, the increased number of heartbeats. So there, we’ve now established we have a fast beating heart.
THINGS WE KNOW
Increased automaticity
Increased heart rate
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Study with our TEST PREP SERIES. One test item each post thoroughly explains the correct answer and rationales behind all answer choices. Understand the material, don’t memorize it. Rote memorization isn’t dependable, mastering the material is. This question focuses on the intended side effects of beta agonist medication administration and discusses answer option rationales for both correct and incorrect answers.
SCENARIO
You are a resource nurse in the SICU when a code blue is announced. You were in a patient’s room a few doors away and when you respond to the code, there’s a nurse doing compressions, another is bagging while someone else is sticking defibrillator pads on the patient. The primary nurse, the one doing compressions and running the code until more people responded, yells out to you to crack the cart and pull meds.
You’re looking at the cardiac meds and know the idea behind pushing them in a code is to stimulate the patient’s “fight or flight” response. In other words, stimulate the beta-1 receptors of the patient’s sympathetic nervous system. Remember how to keep them straight? Beta-1, Beta-2, 1-heart, 2-lungs. Beta-1 affects the heart, Beta-2 affects the lungs.
When the beta-1 agonist meds circulate to the heart, you’re anticipating increased automaticity and…
Increased myocardial contractility
For a decreased volume of blood leaving the left ventricle with each beat
For the patient’s heart muscle to use less oxygen
Increase in left ventricular afterload
First, simply thing about the fight or flight response; the body’s coordinated recruitment of its resources to help someone escape from danger. The body’s systems, heart, lungs, skeletal muscles,e tc., would all contribute to keeping this person’s body alive in this situation.
CARDIAC AUTOMATICITY
The question tells us that we are anticipating increased automaticity. Automaticity is a characteristic of heart muscle to be able to generate its own heartbeat. So it would follow that increased automaticity would result in not only the increased likelihood of a heartbeat, but ideally, the increased number of heartbeats. So there, we’ve now established we have a fast beating heart.
THINGS WE KNOW
Increased automaticity
Increased heart rate
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Study with our TEST PREP SERIES. One test item each post thoroughly explains the correct answer and rationales behind all answer choices. Understand the material, don’t memorize it. Rote memorization isn’t dependable, mastering the material is. This question focuses on the intended side effects of beta agonist medication administration and discusses answer option rationales for both correct and incorrect answers.
SCENARIO
You are a resource nurse in the SICU when a code blue is announced. You were in a patient’s room a few doors away and when you respond to the code, there’s a nurse doing compressions, another is bagging while someone else is sticking defibrillator pads on the patient. The primary nurse, the one doing compressions and running the code until more people responded, yells out to you to crack the cart and pull meds.
You’re looking at the cardiac meds and know the idea behind pushing them in a code is to stimulate the patient’s “fight or flight” response. In other words, stimulate the beta-1 receptors of the patient’s sympathetic nervous system. Remember how to keep them straight? Beta-1, Beta-2, 1-heart, 2-lungs. Beta-1 affects the heart, Beta-2 affects the lungs.
When the beta-1 agonist meds circulate to the heart, you’re anticipating increased automaticity and…
Increased myocardial contractility
For a decreased volume of blood leaving the left ventricle with each beat
For the patient’s heart muscle to use less oxygen
Increase in left ventricular afterload
First, simply thing about the fight or flight response; the body’s coordinated recruitment of its resources to help someone escape from danger. The body’s systems, heart, lungs, skeletal muscles,e tc., would all contribute to keeping this person’s body alive in this situation.
CARDIAC AUTOMATICITY
The question tells us that we are anticipating increased automaticity. Automaticity is a characteristic of heart muscle to be able to generate its own heartbeat. So it would follow that increased automaticity would result in not only the increased likelihood of a heartbeat, but ideally, the increased number of heartbeats. So there, we’ve now established we have a fast beating heart.
THINGS WE KNOW
Increased automaticity
Increased heart rate
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Study with our TEST PREP SERIES. One test item each post thoroughly explains the correct answer and rationales behind all answer choices. Understand the material, don’t memorize it. Rote memorization isn’t dependable, mastering the material is. This question focuses on the intended side effects of beta agonist medication administration and discusses answer option rationales for both correct and incorrect answers.
SCENARIO
You are a resource nurse in the SICU when a code blue is announced. You were in a patient’s room a few doors away and when you respond to the code, there’s a nurse doing compressions, another is bagging while someone else is sticking defibrillator pads on the patient. The primary nurse, the one doing compressions and running the code until more people responded, yells out to you to crack the cart and pull meds.
You’re looking at the cardiac meds and know the idea behind pushing them in a code is to stimulate the patient’s “fight or flight” response. In other words, stimulate the beta-1 receptors of the patient’s sympathetic nervous system. Remember how to keep them straight? Beta-1, Beta-2, 1-heart, 2-lungs. Beta-1 affects the heart, Beta-2 affects the lungs.
When the beta-1 agonist meds circulate to the heart, you’re anticipating increased automaticity and…
Increased myocardial contractility
For a decreased volume of blood leaving the left ventricle with each beat
For the patient’s heart muscle to use less oxygen
Increase in left ventricular afterload
First, simply thing about the fight or flight response; the body’s coordinated recruitment of its resources to help someone escape from danger. The body’s systems, heart, lungs, skeletal muscles,e tc., would all contribute to keeping this person’s body alive in this situation.
CARDIAC AUTOMATICITY
The question tells us that we are anticipating increased automaticity. Automaticity is a characteristic of heart muscle to be able to generate its own heartbeat. So it would follow that increased automaticity would result in not only the increased likelihood of a heartbeat, but ideally, the increased number of heartbeats. So there, we’ve now established we have a fast beating heart.
THINGS WE KNOW
Increased automaticity
Increased heart rate
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
TEST PREP SERIES: What are expected results from beta agonist administration?
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Study with our TEST PREP SERIES. One test item each post thoroughly explains the correct answer and rationales behind all answer choices. Understand the material, don’t memorize it. Rote memorization isn’t dependable, mastering the material is. This question focuses on the intended side effects of beta agonist medication administration and discusses answer option rationales for both correct and incorrect answers.
SCENARIO
You are a resource nurse in the SICU when a code blue is announced. You were in a patient’s room a few doors away and when you respond to the code, there’s a nurse doing compressions, another is bagging while someone else is sticking defibrillator pads on the patient. The primary nurse, the one doing compressions and running the code until more people responded, yells out to you to crack the cart and pull meds.
You’re looking at the cardiac meds and know the idea behind pushing them in a code is to stimulate the patient’s “fight or flight” response. In other words, stimulate the beta-1 receptors of the patient’s sympathetic nervous system. Remember how to keep them straight? Beta-1, Beta-2, 1-heart, 2-lungs. Beta-1 affects the heart, Beta-2 affects the lungs.
When the beta-1 agonist meds circulate to the heart, you’re anticipating increased automaticity and…
Increased myocardial contractility
For a decreased volume of blood leaving the left ventricle with each beat
For the patient’s heart muscle to use less oxygen
Increase in left ventricular afterload
First, simply thing about the fight or flight response; the body’s coordinated recruitment of its resources to help someone escape from danger. The body’s systems, heart, lungs, skeletal muscles,e tc., would all contribute to keeping this person’s body alive in this situation.
CARDIAC AUTOMATICITY
The question tells us that we are anticipating increased automaticity. Automaticity is a characteristic of heart muscle to be able to generate its own heartbeat. So it would follow that increased automaticity would result in not only the increased likelihood of a heartbeat, but ideally, the increased number of heartbeats. So there, we’ve now established we have a fast beating heart.
THINGS WE KNOW
Increased automaticity
Increased heart rate
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
MYOCARDIAL CONTRACTILITY
Hearts are made of muscle and a heart beat is caused by a contraction of the cardiac muscle. If we speed up the heart, that means the cardiac muscle is contracting faster. Now we’ve established that we have increased myocardial contractility, answer choice #1.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
We’re going to continue examining the rest of the answers, since each answer choice on a multiple choice question is a learning opportunity. When you are studying for credentialing exams, always “learn” the other answer options. An important thing to remember is that there are only so many ways to ask a question and as far as credentialing exams go, there are only so many topics to ask about in these questions. If you practice enough quetions, you will immediately recognize what they’re asking and know the answer.
MYOCARDIAL OXYGEN CONSUMPTION
Now, if you are exercising hard, do you use more oxygen? Are you breathing harder? If yes, it stands to reason that your heart tissue would also use more oxygen when it works harder, such as when there’s increased myocardial contractility. So we’ve confirmed that answer choice #3 is wrong.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
The human circulatory system is a closed loop. This means that if you followed one blood cell around the loop, it’d keep going round and round the following path: body, right atrium, right ventricle, lungs, left atrium, left ventricle and body again. These cardiac meds that stimulate cardiac beta-1 receptors, they cause the heart to exhibit a few different effects: pump faster (chronotropic), increases pump squeeze-ness (inotropic) and increases conduction through the pump, essentially, beefier surge of electricity running through its “wiring” (dromotropic).
STROKE VOLUME
The heart, by design, pumps blood. If it pumped blood faster and harder, seems like it should also be pumping MORE blood out of the left ventricle. Seems that way, but as we get into arrhythmias later, there CAN be too much of a good thing, but for now, we’ll follow our line of thinking. Another thing happens too and since the cardiac tissue is a muscle and compliant, it can stretch to accommodate more blood. Because of Starling’s Law, the more stretch of the cardiac walls, the more “SLAP BACK” when they finish stretching, which translates to a stronger systolic contraction. This results in an increased stroke volume, meaning that with each beat, the volume of blood that comes out of the left ventricle is more than just a usual beat. Let’s cross answer choice #1 off the list.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
AFTERLOAD
Afterload. Nursing students have a hard time with the concept of afterload. I think it’s the name because preload is a volume coming out of the left ventricle so you think that afterload must be a volume of blood coming out of somewhere as well. Afterload is instead, an amount of WORK the heart has to do. Specifically, afterload is the amount of work the heart has to do to push the blood through the arteries in the body.
VASOCONSTRICTION
Why is it hard to get blood to the body? Sometimes conditions are such that the arteries that deliver blood to the rest of the body, clamp down (the smooth muscle wrapping around the arteries contracts) and get really thin and skinny. This is called vasoconstriction. Examples of things that do this are:
Cold – Vessels clamp down to decrease the amount of blood reaching the surface of the skin. By doing this, these clamped down surface arteries minimize heat loss by keeping the blood in the vessels and tissues deep inside the body, which allows the body to retain the heat and thus maintains its warmth / core temperature.
Blood Loss – If your body loses blood, it tries to be more efficient about getting the blood that it does have, to major organs, so it causes vessels to clamp down, in order to increase blood pressure, to get the blood where it needs to go.
ALPHA ADRENERGICS
Vasopressors – These are the meds we give to increase blood pressure. They deliberately cause the smooth muscle surrounding the vessel to contract, by targeting beta-2 and alpha-1 adrenergic receptors in vascular smooth muscle, thus raising blood pressure. As with all these examples, the larger vessels can only clamp down so far, because they’r so big, so they don’t entirely close off. The tiny arteries shut down completely. This shunts blood away from the tiny vessels and keeps it in the bigger vessels. Typically a class of meds called alpha-1 adrenergic medications does this.
Decongestants like Afrin or Pseudophed – This is why you can breathe better after sniffing Afrin or taking a pseudophed tablet. It causes vessels to shrink down, which in turn causes the tissue causing your stuffy nose to shrink , which helps “make more room” for air to get in and out of your nose, decreasing the stuffiness. Some of these decongestants have a systemic effect, which is why people who have high blood pressure should probably not take them.
Smoking – This is why patients who smoke are at a much greater risk of peripheral vascular disease. Their vessels clamp down and don’t deliver adequate blood flow to the surrounding tissues.
Meth – If a patient under 40 is having a heart attack, the first thing the cath lab team suspects is drug use. Meth causes INTENSE VASOCONSTRICTION to the degree that it clamps down the coronary arterie that feeds blood to the myocardial tissue and causes such a degree of ischemia that it mimics a heart attack caused by a lesion that blocks blood flow in the coronary arteries. Don’t do meth.
By this point, you get the idea that under these conditions, vasoconstriction in the arteries makes it really hard for the heart to push even more blood along these narrowed vascular passageways. This work, what the heart is working against, THAT’s afterload. You’ll eventually learn that sometimes the afterload is so great, that the blood can barely get out of the heart and will back up into the lungs, causing pulmonary congestion. That however is for another day.
THINGS WE KNOW
Increased automaticity
Increased heart rate
Increased myocardial contraction
Increased myocardial oxygen consumption
Increased stroke volume
Beta-1 receptor agonists don’t target tissue that directly increases afterload
All this to teach you that this question is asking you about beta-1 receptors, not alpha receptors, which are the receptors that when targeted, cause vasoconstriction, which in turn causes an increase in afterload. This is why D) Increase in left ventricular afterload, is the wrong answer. Sneaky right?
Bianca Marie Moses, BSN, RN
I decided on a career in nursing after having spent almost 10 years as a molecular biologist designing nucleic acid based diagnostic assays in the biotechnology industry. I was in search of a career path where I could blend my talent for science and problem solving with my intense curiosity and desire to advocate and care for others. After careful research, I found that a career in nursing would be the perfect match for me.
