Lectures

Cardiac Output – Physiology of the Heart

by Joseph Alpert, MD
(1)

Questions about the lecture
My Notes
  • Required.
Save Cancel
    Learning Material 2
    • PDF
      Slides 02 Cardiology Alpert.pdf
    • PDF
      Download Lecture Overview
    Report mistake
    Transcript

    00:01 So, the two have to be balanced, of course. Now, what determines cardiac output- which is the number of liters of blood that the heart pumps in one minute, is of course, the stroke volume which is put out with each beat times the heart rate. Because stroke volume stays... let’s say the person is resting and not exercising, stroke volume stays about the same with each beat. So, what determines how much blood comes out of the heart then? His heart rate! Because cardiac output is stroke volume times the number of beats per minute. That tells you the number of cubic centimeters or number of, if you want to express it in liters, the number of liters per minute. Usually, the average person puts out about 4 to 5 liters per minute in a resting state and of course, much more, if they are exercising.

    00:47 Now, there is another important point that needs to be remembered about the circulatory system. It has resistance in it as well as blood being pumped into it. It’s just like the famous Ohm’s law in electricity- that the voltage or the pressure in your electrical line is equal to the resistance times the flow in amps. In the cardiovascular system, it’s the blood pressure is equal to the cardiac output times the resistance.

    01:15 In the lung, the resistance is called the pulmonary vascular resistance and in the systemic circuit, it’s called the systemic vascular resistance. So, in the catheterization laboratory, we often calculate, first of all, the cardiac output using a variety of techniques and then we measure the blood pressure and we can then calculate the resistance in the pulmonary circuit and the resistance in the systemic circuit. These two numbers are of great importance because we can often see when there is disease. For example, a patient who is markedly hypertensive will have an elevated systemic vascular resistance. A patient who has disease in the lung may have an elevated pulmonary vascular resistance. And so, with the normal cardiac output you are going to have higher pressures in whichever circuit happens to have the increased vascular resistance. Here we have a very simple diagram of the three factors that determine ventricular function during systole. First of all, there is preload.

    02:18 I’ll tell you what that is in a moment, then there's afterload and then there's contractility. So, let’s look at preload first. Preload is the amount of stretch that the ventricular muscle is under and it directly relates to how well we fill the ventricle.

    02:32 What’s important about preload is that there is an intrinsic law of the heart that was discovered by a physiologist named Starling. It’s called Starling’s Law of the Heart.

    02:41 I like to call it the Rubber Band Law of the Heart. The more you stretch the rubber band, the more it snaps back into place. So, the more you fill the ventricle, the more it’s going to squeeze out in the subsequent beat. This is, therefore, a very important component because if the patient is dehydrated or having a hemorrhage and has decreased blood volume, the ventricle will have decreased filling and it will decrease the amount of stroke volume- the amount of blood that it puts out with each beat. Then there is afterload. Afterload is the resistance that the ventricle experiences when it’s squeezing. So, for example, it could be an increase in peripheral vascular resistance in the systemic circuit due to high blood pressure. In which case, the left ventricle sees a stronger resistance to pushing the blood out through the aortic valve and stroke volume may also decrease. We can manipulate afterload with drugs and we’re going to be talking about that because in patients who have an increased systemic vascular resistance, we can actually make the pumping ability of the left ventricle better by giving drugs that decrease the resistance in these blood vessels and increase the ability of the left ventricle then to pump again. And then the final factor is contractility. This is the intrinsic 'oomph',- the snap of the ventricular muscle when it squeezes and of course, certain diseases rob the ventricle of some of its snap and therefore, stroke volume goes down. So, you see that there is a real integration here - you have to have appropriate preload, you have to have appropriate afterload and appropriate contractility and most normal people have all of these going at the right time when they are well hydrated, when they have their normal blood volume, when they have a normal blood pressure and normal contractility. Now, we have talked already about the Starling Law of the Heart. It says “the more you stretch it, the more it rebounds”. So, that’s really one of the measures of preload. In terms of afterload, of course, the systemic arterial blood pressure or the pulmonary artery pressure determine how much resistance is seen by the ventricles when they contract. On the right side, the diseases, for example, if one has blood clots in the lung, that increases the resistance and will increase the amount of pressure that the right ventricle has to generate to push blood out into the pulmonary arteries. Often on the left side, the patients will have high blood pressure, they will have constriction in the small arteries in the system, and that will resist the left ventricle as it tries to eject blood into the aorta. And there are ways to improve the resistance and therefore, to improve the stroke volume and the cardiac output. It’s again important to remember that the right ventricle, because it’s moving volume at a lower pressure is very preload dependent. And the left ventricle, which is pushing blood out at a high pressure, is more afterload dependent. Now, both of them are affected by preload and afterload.

    05:55 But for the right ventricle, preload is particularly important; for the left ventricle, afterload is particularly important and we can measure all of these numbers in the catheterization laboratory and we know what normal is. Now, let’s talk a little bit about the measurement of these hemodynamic values. We do that usually in the catheterization laboratory, but it turns out, as I will talk about a little later, sometimes we can use non-invasive tests such as the echocardiogram that will also give us an estimate of cardiac output and an estimate with the blood pressure of the resistance in the lung and the resistance in the body.

    06:35 So, sometimes we don’t have to put a catheter inside the body to make these measurements.

    06:42 Here is an important relationship that I referred to before, just to this graph reiterates that point, and that is the peripheral resistance determines how much stroke volume occurs.

    06:55 You can see in this curve, as the resistance moves to the right, the stroke volume falls and as the resistance moves back to the left, the stroke volume increases. In other words, when we increase the afterload of the ventricle, the resistance to which it’s ejecting will decrease stroke volume. This is an important hemodynamic point that we often use in patients with heart failure where we are trying to decrease the afterload to help a deceased ventricle empty more completely. So, we are just going to say for just a few moments some of things that can increase preload and afterload, I have already mentioned them. Preload is very much determined on the blood volume. Does the patient have appropriate blood volume? Are they dehydrated? Have they lost blood somehow through hemorrhage? On the other hand, in terms of afterload, are the resistances normal in the pulmonary circuit and in the systemic circuit? And those can be changed by disease states, of course, as we have… as we have talked about. Here we note the resistance in the lung, so called pulmonary vascular resistance. We can actually calculate it in… with a parameter of (dyne-second-centimeters ^ -5) and we can also calculate a systemic vascular resistance using similar parameters. This is done in the catheterization laboratory, but as I said, you can get a rough guesstimate of these numbers from the non-invasive studies as well. Now, what happens when we are actually in the catheterization laboratory or sometimes when we have a pulmonary artery balloon catheter in a patient that’s in the Intensive Care Unit, we actually try and correlate the electrocardiogram with the pressure tracing. Here we see a pressure tracing of the pulmonary artery and you can see the rise in the pressure followed by fall to a little notch and then further decline. That little notch represents the closure of the pulmonary valve. The same thing happens in the aorta, there’s a rise in the pressure, then there’s a fall and there’s a little notch as the aortic valve closes and you can see the timing of systole with the QRS above. QRS occurs and then a few seconds later, you have the pressure tracing either in the pulmonary artery or in the aorta. Here it is enlarged, so you can see it a little better. Notice the electrocardiogram above the QRS is the big spike, that’s the electrical activity causing the ventricle to contract and then there’s a little delay because the ventricle mechanical activity doesn’t happen immediately.

    09:32 It takes a few seconds for the mechanical activity to build and then you can see the pressure rising in the aorta or the pulmonary artery. You can see it falls to the notch, the so called dicrotic notch, which is either the pulmonary or the aortic valve closing. And here we see a… a diagram that’s the.. similar. In this case, it’s the aortic pressure.

    09:54 You can see the QRS occurs a little bit before the aortic pressure. The dicrotic notch isn’t quite as clear here, but you can still see the little notch there when the aortic valve closes. Here is a listing of normal values.

    10:12 It’s not necessary that you memorize these. These are all available in tables, but this is a typical set of normal values. The pulmonary artery pressure is generally peak systolic about 25 and diastolic around 12. The peak aortic pressure is generally about 120/80 mmHg, that’s the so called normal blood pressure. Left ventricular diastolic pressure is usually 4-5 mmHg and similarly, right ventricular diastolic pressure is usually 4-5 mmHg.

    10:39 And you can see also the normal resistances that gets calculated from the, if you will, Ohm’s Law of the heart: blood pressure equals heart rate… equals cardiac output times resistance.


    About the Lecture

    The lecture Cardiac Output – Physiology of the Heart by Joseph Alpert, MD is from the course Introduction to the Cardiac System.


    Included Quiz Questions

    1. a wave
    2. x descent
    3. v wave
    4. y descent
    1. 5.6 Liters/min
    2. 4.8 Liters/min
    3. 7.8 Liters/min
    4. 3.5 Liters/min
    1. Heart rate and stroke volume
    2. Stroke volume and systolic blood pressure
    3. Diastolic blood pressure and pulse pressure
    4. Heart rate and mean arterial blood pressure
    5. Pulse pressure and heart rate

    Author of lecture Cardiac Output – Physiology of the Heart

     Joseph Alpert, MD

    Joseph Alpert, MD


    Customer reviews

    (1)
    5,0 of 5 stars
    5 Stars
    5
    4 Stars
    0
    3 Stars
    0
    2 Stars
    0
    1  Star
    0