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This lesson will cover the basics of hemodynamics. Hemodynamics are the measurements we take of various pressures or volumes within the heart and cardiovascular system. These numbers can help us to determine if something is wrong with our patient and if so, what is it and what can we do about it?
When we talk about Hemodynamics it’s important to understand what constitutes a full cardiac cycle, which is a full cycle of relaxation and contraction of the heart muscle. The relaxation period is known as Diastole. During diastolic and the diastolic pause, the mitral and tricuspid valves are open, allowing the ventricles to fill with blood. Systole means contraction. As you’ll see in just a second, the atria contract a split second before the ventricles to help finish filling them completely with blood. This is known as the atrial kick. So you have atrial systole, then ventricular systole a split second later. When the ventricles contract, they force blood out of the aortic and pulmonic valves to the body and the lungs. One great way to visualize what’s happening in the heart during a full cardiac cycle is something called a Wigger’s Diagram.
Now, this isn’t something you need to memorize, but it’s really helpful to see how everything relates. At the bottom, you see the Phonocardiogram, that’s our heart sounds. We’ve talked about these in a previous lesson. But here you can see that the systolic sound (S1) is followed by the diastolic sound (S2) and then there’s a pause...then S1 and S2 again. S1, systole, is the closing of the tricuspid and mitral valves while S2, diastole, is the closing of the aortic and pulmonic valves. You can also see the EKG tracing here showing ventricular systole in your QRS, then the diastolic pause, then atrial systole (the P-wave) a split second before ventricular systole. Now, looking at ventricular pressure and volume, you get a better idea of the filling and contracting that’s happening. When the ventricles contract they push the blood out, the pressure goes up and the volume goes down. Then as the pressure comes down you see them begin to fill back up. Then right here you’ll see during atrial systole there’s a little bump in the volume right before the ventricles contract again - that’s your Atrial Kick - it allows a bit more blood into the ventricles to increase cardiac output. Patients whose atria don’t work correctly (for example Atrial Fibrillation) will lose that atrial kick and their cardiac output can be jeopardized.
So let’s look at some basic terms you need to know and then we’ll talk about how they fit together. The first is just your basic heart rate, that’s how fast your heart is beating - in beats per minute Normal is about 60-100 bpm. Then Stroke Volume is how much volume is pumped out with each beat, we measure that in milliliters Normal is 60-120 mL per beat. Cardiac Output is the total volume of blood pumped out of the heart in one minute. So the way we calculate that is to take the Stroke Volume (or the volume per beat) and multiply it by the number of beats per minute, your heart rate. So CO = HR x SV . It works out to about 4-8 L per minute. Now, for a 90 pound gymnast, 4 L per minute might be plenty, but for a 300 pound wrestler, it might not be enough. So we use a measurement called Cardiac Index. That takes our Cardiac Output and compares it to the patient’s body size. So it’s CI = CO / BSA. Normal should run between 2.5 to 4. This makes it much easier to understand whether a certain Cardiac Output is enough for a patient. Then we have Ejection Fraction. This is the percentage of blood forced out of the Left ventricle with each contraction. So let’s say hypothetically that the ventricle fills with 100 mL of blood. If it squeezes and ejects out 40 mL that would be 40 out of 100 or 40% Ejection Fraction. Normal should be between 55-75%.
The last three measures we look at will be introduced here but discussed in much greater detail in the Preload and Afterload lesson. Preload is a measure of the stretching or filling pressure of the heart. The more it is stretched or filled during diastole, the higher the Preload and vice versa. Think “pre = before” so it’s the blood before the heart coming into it. Afterload is the force that the heart has to pump against in order to eject blood. It has to overcome that pressure to be able to open the valves and push the blood out. Then, finally contractility is the force or strength of contraction of the ventricles.
So now we have all these numbers, but how do they even relate to each other?? Well let’s start here looking at Cardiac Output. Like I said before, Cardiac Output is determined as Stroke Volume x Heart Rate - the volume per beat times the beats per minute gives us volume per minute. We can quickly affect Cardiac Output simply by influencing the heart rate. So what kinds of interventions would we do if our heart rate was too slow and we needed to speed it up? We could give anticholinergics like Atropine or Sympathomimetics like Epinephrine that mimic that fight or flight response. What about if it’s too fast, how could we slow it down? Well we would try the vagal maneuver, treat the cause (like anxiety or dehydration) or even electrical cardioversion. The second thing that impacts Cardiac Output is Stroke Volume. Well there are three determinants of Stroke Volume - Preload, Afterload, and Contractility. Remember Afterload is pressure it has to push against, preload is stretch or filling pressure, and contractility is how hard it squeezes. What’s important to note here is that if one of those decreases, the others must increase to compensate in order to maintain the same cardiac output.
How much water squirts out of a water balloon in, let’s say 5 seconds, will be entirely determined by how much you filled it (Preload), how hard you squeeze it (Contractility), and how tight you’re holding the opening of the balloon (Afterload). If you do it again, but this time don’t fill it as much, you will have to squeeze it harder or let go of the opening more to get the same amount out in that 5 seconds. We will look in much more detail at these three things in the Preload and Afterload lesson, but I want you to see where they fit in with this big hemodynamic picture.
So what are the key points here? Well first, a full cardiac cycle involves systole and diastole (or contraction and relaxation) and these things can be visualized on a Wigger’s Diagram. Second, knowing the key hemodynamic terms and what they mean can help us determine what’s wrong with our patient. Think of hemodynamics like the different things a mechanic checks on a car - there’s tire pressure, gas mileage, coolant levels, etc. Depending on which one is out of whack determines how they need to proceed. But ultimately, they all need to be functioning optimally for the car to run safely. We’re just like mechanics for the heart! Finally, understand that all of these things work together in the heart like a well-oiled machine. By influencing one factor, we can directly or indirectly affect another.
We hope this intro to the basics of hemodynamics has been helpful. Enjoy digging in and learning more about what’s going on in your patient’s heart! Go out and be your best self today, and, as always, happy nursing!
When we talk about Hemodynamics it’s important to understand what constitutes a full cardiac cycle, which is a full cycle of relaxation and contraction of the heart muscle. The relaxation period is known as Diastole. During diastolic and the diastolic pause, the mitral and tricuspid valves are open, allowing the ventricles to fill with blood. Systole means contraction. As you’ll see in just a second, the atria contract a split second before the ventricles to help finish filling them completely with blood. This is known as the atrial kick. So you have atrial systole, then ventricular systole a split second later. When the ventricles contract, they force blood out of the aortic and pulmonic valves to the body and the lungs. One great way to visualize what’s happening in the heart during a full cardiac cycle is something called a Wigger’s Diagram.
Now, this isn’t something you need to memorize, but it’s really helpful to see how everything relates. At the bottom, you see the Phonocardiogram, that’s our heart sounds. We’ve talked about these in a previous lesson. But here you can see that the systolic sound (S1) is followed by the diastolic sound (S2) and then there’s a pause...then S1 and S2 again. S1, systole, is the closing of the tricuspid and mitral valves while S2, diastole, is the closing of the aortic and pulmonic valves. You can also see the EKG tracing here showing ventricular systole in your QRS, then the diastolic pause, then atrial systole (the P-wave) a split second before ventricular systole. Now, looking at ventricular pressure and volume, you get a better idea of the filling and contracting that’s happening. When the ventricles contract they push the blood out, the pressure goes up and the volume goes down. Then as the pressure comes down you see them begin to fill back up. Then right here you’ll see during atrial systole there’s a little bump in the volume right before the ventricles contract again - that’s your Atrial Kick - it allows a bit more blood into the ventricles to increase cardiac output. Patients whose atria don’t work correctly (for example Atrial Fibrillation) will lose that atrial kick and their cardiac output can be jeopardized.
So let’s look at some basic terms you need to know and then we’ll talk about how they fit together. The first is just your basic heart rate, that’s how fast your heart is beating - in beats per minute Normal is about 60-100 bpm. Then Stroke Volume is how much volume is pumped out with each beat, we measure that in milliliters Normal is 60-120 mL per beat. Cardiac Output is the total volume of blood pumped out of the heart in one minute. So the way we calculate that is to take the Stroke Volume (or the volume per beat) and multiply it by the number of beats per minute, your heart rate. So CO = HR x SV . It works out to about 4-8 L per minute. Now, for a 90 pound gymnast, 4 L per minute might be plenty, but for a 300 pound wrestler, it might not be enough. So we use a measurement called Cardiac Index. That takes our Cardiac Output and compares it to the patient’s body size. So it’s CI = CO / BSA. Normal should run between 2.5 to 4. This makes it much easier to understand whether a certain Cardiac Output is enough for a patient. Then we have Ejection Fraction. This is the percentage of blood forced out of the Left ventricle with each contraction. So let’s say hypothetically that the ventricle fills with 100 mL of blood. If it squeezes and ejects out 40 mL that would be 40 out of 100 or 40% Ejection Fraction. Normal should be between 55-75%.
The last three measures we look at will be introduced here but discussed in much greater detail in the Preload and Afterload lesson. Preload is a measure of the stretching or filling pressure of the heart. The more it is stretched or filled during diastole, the higher the Preload and vice versa. Think “pre = before” so it’s the blood before the heart coming into it. Afterload is the force that the heart has to pump against in order to eject blood. It has to overcome that pressure to be able to open the valves and push the blood out. Then, finally contractility is the force or strength of contraction of the ventricles.
So now we have all these numbers, but how do they even relate to each other?? Well let’s start here looking at Cardiac Output. Like I said before, Cardiac Output is determined as Stroke Volume x Heart Rate - the volume per beat times the beats per minute gives us volume per minute. We can quickly affect Cardiac Output simply by influencing the heart rate. So what kinds of interventions would we do if our heart rate was too slow and we needed to speed it up? We could give anticholinergics like Atropine or Sympathomimetics like Epinephrine that mimic that fight or flight response. What about if it’s too fast, how could we slow it down? Well we would try the vagal maneuver, treat the cause (like anxiety or dehydration) or even electrical cardioversion. The second thing that impacts Cardiac Output is Stroke Volume. Well there are three determinants of Stroke Volume - Preload, Afterload, and Contractility. Remember Afterload is pressure it has to push against, preload is stretch or filling pressure, and contractility is how hard it squeezes. What’s important to note here is that if one of those decreases, the others must increase to compensate in order to maintain the same cardiac output.
How much water squirts out of a water balloon in, let’s say 5 seconds, will be entirely determined by how much you filled it (Preload), how hard you squeeze it (Contractility), and how tight you’re holding the opening of the balloon (Afterload). If you do it again, but this time don’t fill it as much, you will have to squeeze it harder or let go of the opening more to get the same amount out in that 5 seconds. We will look in much more detail at these three things in the Preload and Afterload lesson, but I want you to see where they fit in with this big hemodynamic picture.
So what are the key points here? Well first, a full cardiac cycle involves systole and diastole (or contraction and relaxation) and these things can be visualized on a Wigger’s Diagram. Second, knowing the key hemodynamic terms and what they mean can help us determine what’s wrong with our patient. Think of hemodynamics like the different things a mechanic checks on a car - there’s tire pressure, gas mileage, coolant levels, etc. Depending on which one is out of whack determines how they need to proceed. But ultimately, they all need to be functioning optimally for the car to run safely. We’re just like mechanics for the heart! Finally, understand that all of these things work together in the heart like a well-oiled machine. By influencing one factor, we can directly or indirectly affect another.
We hope this intro to the basics of hemodynamics has been helpful. Enjoy digging in and learning more about what’s going on in your patient’s heart! Go out and be your best self today, and, as always, happy nursing!
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