Dynamic Auscultation

by Carlo Raj, MD

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    00:00 Now with dynamic auscultation, things that you want to pay attention to. Altering heart sounds by changing circulatory hemodynamics.

    00:07 We will be spending time with this. You have heard hard grip. You have heard of watch this, I am going to disappear for one second. What did I do? Rapid squat right. So these are some of the changes or these are some of the manuevers that we will be conducting or you will be asked about and depending on the manuever how is that going to affect or influence the heart valves and heart sounds, is that clear? Now this can be separate, but clinical, we are going to use some of these depending on what you are trying to confirm for diagnosis. And once you understand the physiologic alteration, then you've got your diagnosis. Let us continue. Before we even get there though, let us make sure that we understand the difference between preload and afterload please. How do you increase your venous return? We will talk about this manouveres coming up. But if you were to increase your venous return to right atrium, to right ventricle, what have you done to preload? You have increased your preload. What does preload mean to you? Preload means that it is the amount of fluid volume within the heart. So if you increase the venous return for example, if you are to constrict the veins, are you picturing this, not the arteries but the veins, the veins are a major pooling area. If you constrict the veins, you are increasing venous return to the right side. What are you doing to the preload? You are increasing it. It is that simple. Preload is the volume of blood in the ventricle. What if you decrease the venous return? If you decrease the venous return, volume of blood into right atrium, right ventricle such as standing up. If you go from supine position to standing up, then where is my blood? In the dependent areas. It is down in the lower extremity. What happens to venous return? It decrease, didn't it? So you have decreased preload. Now, what is definition of afterload that you want to know here? Because this is important. Afterload is when you have increased resistances that the left ventricle was facing. The left ventricle, when it faces increased resistance. Give me some examples. Aortic stenosis, coarctation of aotra and tell me about the arterials. Take your time. What state are the arterials in, in which it would then provide increased resistance to the left ventricle? Did you listen to my question? What state is my arterials in providing increased resistance to your left ventricle? Constriction. Arterials are the most important component or contributor to resistance as you know especially TPR, total peripheral resistance. If you can split your arterial, what happens with TPR? Increase your TPR. What then happens to afterload? You increase the afterload. Are you seeing this? So afterload is that simple. It is the resistance that the left ventricle is facing period. And I just gave you bunch of differentials. What are they again? Aortic stenosis, coarctation of aorta and arteriolar vasoconstriction. Continue Now let us talk about those actual manuvers and we will go through the pathophysio. Deep inspiration, so what does that mean to you? Let's all take a deep breath. You're with me? Good. But then just happened the diaphragm contracted, which way did it go? Downwards. What happened to abdominal pressure? Increased upon deep inspiration.

    03:29 What happened to the thoracic pressure? It decreased. It literally became a vaccum. It is going to suck up like a straw. It is going to suck up the blood into the heart. What is my topic? Increased venous return upon deep inspiration, is that clear? When you have deep inspiration, increased venous return to the right side, what then may happen to the intensity of the murmurs on the right side? It would obviously increase. Clear? Next. Supine position versus standing up. If you are supine, which I hope that you are not in right now because if you were, there is every possibiity that you are falling asleep. Supine position would be lying flat. So, therefore, you are making it easier or more difficult for blood to return to the heart? You are making it easier. And that is our topic increased venous return, supine position. What if you went from supine to erect position? The blood then drops where? Down to the legs. So decreased in venous return, it is that simple. Passive leg elevation.

    04:30 You pay attention to the same thing here. You are going to raise your legs and when you do so then what happens? You are going to then return the blood to the right side, clear? Increased venous return. Rapid squatting, now this is important. There are two major issues that you want to pay attention with squatting, please. Here you gonna do this quickly, okay? Let's just think of me just rapidly squatting. When I did so, then it increased the venous return. Here comes more blood. That is one example here that you may want to think about clinically.

    05:00 Now, what about if this was a child. What do children like to do? They like to play. They like to go run. "Hey mummy, can I go play?" "Of course you can." Right? Of course the child wants to play. Then all of a sudden the child is playing and cannot breathe or having a hard time breathing, and the child really instinctively is going to do what? Squats.

    05:23 What is the diagnosis in this patient in which after playing for little bit, the child instinctively knows to squat? It is called the tet spell. What is happening there? What I am going to do for you here is make sure that we delineate the two different type of squatting maneuvers and depending as to what you are trying to confirm is going to give you different types of diagnosis. If it is rapid squatting, yes, it does bring about increased venous return but tell me about the patient, the child who just squatted, when the child is feeling a little cyanotic with a little hypoxemia, it is the fact that there might have been what? There might have been pulmonic stenosis, number 1. Number 2, there might have been right ventricular hypertrophy. Number 3, there was what? Ventricular septal defect. Number 4, there was overriding aorta. What am I referring to? Obviously tetralogy of Fallot. Tetra, four. What kind of shunt is this? It is a congenital cyanotic heart disease, a right to left shunt, right from the beginning. Because the right ventricular hypertrophy is then shifting. What kind of blood is in the right ventricle? Tell me. Good, deoxygenated. And that right ventricular hypertrophy is pushing the blood through the VSD into left side. What kind of shunt? Right to left shunt. So what do we have? Cyanosis? Who is feeling it? The child is. What is the child doing instinctively? Squatting. To do what? Not to increase venous return. So why is the child squatting? To increase TPR. How do you do that? You increase TPR by constricting arterials.

    06:57 I just got then telling you what happens when you increase TPR? You increase afterload.

    07:02 When you increase afterload, who is facing increased resistance? The left ventricle. And so therefore what happens to the shunt? It gets reversed, instead of right to left shunt that type of squatting with tetralogy of Fallot will then turn into a right to left shunt. Is this the only time we will see it? Not at all. Talked about this in embryology. We will talk about this further as we are getting to congenital heart disease. Why am I bringing this up? Because you must be very clear about the issues of squatting.

    07:29 Let us talk about valsalva. I have closed my epiglottis phase II, and that's you pay attention to. So when you are expiring against a closed epiglottis, what happens to thoracic pressure? You have increased your thoracic pressure. Initially in phase I, what did you do to your pulmonary capillaries? You close your pulmonary capillaries. Would you tell me as to what is distal to the pulmonary capillaries? I believe it is the left atrium. Correct. And by quickly closing pulmonary capillaries, you increase venous return to left side, but that is not the point. The point here is during phase II. If you continue to squeeze your pulmonary capillaries, there isn't any more blood in there. Look, there is no more blood in there. So what will happen to venous return? It decreases. Are you with me? If you continue to squeeze because of that increased expiration against a closed epiglottis, then at some point you are going to decrease venous return and that you must pay attention to because that becomes important to us as we get into valvular diseases and at that point I will repeat this very point. Well, let us go from supine position to standing up. So you stand or sitting up quickly, then what then happens? The blood then rushes down into your legs. What happens to venous return ladies and gentleman? It is going to decrease. There is your blood down in the feet. It is not in your heart. You take me one step further. What did you learn in physiology already? You've heard about baroreceptor reflex. Where are they located in, these baroreceptors? They are located in your sinuses, aren't they? Which one is more sensitive? The carotid aortic sinus.

    09:16 The carotid sinus because that is not accustomed to large amounts of blood like the aorta is.

    09:21 The aorta is accustomed to large amounts of blood. It is not as sensitive. The carotid has glossopharyngeal. The blood has then gone where? Down into legs. Then what happens? Stretch, decreased stretch. When you have decreased stretch, what happens to pharynx? Decreased pharynx. My blood is then rushed down into legs. What kind of outflow do you want from the autonomic nervous system please? Sympathetic, it is exactly what is happening. It is called the baroreceptor reflex. You're going to be asked about this, guaranteed you will, in many places. Now let us take a look at these other maneuvers that then will help you diagnose your patient. I want you to take your hand and I want you to clench your fist and I want you to come at me right now. Because "Dr. Raj, you're driving me crazy. You are frustrating me. You are giving me all this information. I just want to hit you." Okay, so you clench your fist. You with me? So is that your sympethetic system? Of course, it is. When you do a hand grip, a sympethetic nervous system because you are angry. Calm down, it's okay. If you have a stress probably good time to grab. So here you are, you are squeezing it. And what have you done to your arterials? You have constricted it. What have you done to your TPR? You have increased it. Once again when you increase your TPR, what have your done? Are you affecting your afterload? Yes, you are. Then what have you done to your after load? You have increased it. Why is it important? You shall see and I will keep coming back to this point where you have understood, by increasing that afterload, then where is my blood? In the left ventricle. It is having a hard time getting out of the left ventricle and you shall see and you will understand why an aortic stenosis? When you do a handgrip, what happens intensly as a murmur? Decrease.

    11:06 Don't worry, we will talk about it again. What about exercise? Well exercise, once again, you've talk about this in physiology, what is it going to do to your arterials? It was my question.

    11:17 What is it going to do to your arterials? Vasodilate, it has to. Why in the world would you want to increase your TPR and exercise? That makes no sense. You want to make sure that you have vasodilations so that you properly oxygenate your tissues. Clear? In the meantime, what is happening to your veins in exercise? Venoconstriction. The combination of the two. Well, what do you know about cardiac output? You might go from 5 liters. You might have increased by 100 percent to 10 liters. That is amazing in exercise, but what about blood pressure. It doesn't change much, why? Because the vasodilation and venoconstriction. And so, therefore, the combination of the two will keep your mean arterial pressure approximately normal. Is that clear? It is amazing. Exercise is a beautiful phenomenon and the more that you know about it the more number of questions that you will get right. In this case here, increased flow across your valves.

    About the Lecture

    The lecture Dynamic Auscultation by Carlo Raj, MD is from the course Heart Sounds.

    Included Quiz Questions

    1. Venodilation
    2. Increased venous return
    3. Venoconstriction
    4. Vasoconstriction
    1. Venodilation
    2. Vasoconstriction
    3. Aortic stenosis
    4. Coarctation of the aorta
    5. Increased total peripheral resistance
    1. Phase II Valsava
    2. Decreased thoracic pressure
    3. Increased abdominal pressure
    4. Deep inspiration
    5. Passive leg elevation
    1. Decreased stretch sensed by carotid baroreceptors and transmitted via the glossopharyngeal nerve
    2. Increased stretch sensed by carotid baroreceptors and transmitted via the vagus nerve
    3. Decreased stretch sensed by aortic baroreceptors and transmitted via the glossopharyngeal nerve
    4. Increased stretch sensed by aortic baroreceptors and transmitted via the glossopharyngeal nerve
    5. Decreased stretch sensed by the carotid baroreceptors and transmitted via the vagus nerve
    1. Increased total peripheral resistance permitting a reversal of the right to left shunt
    2. Increased venous return by venoconstriction of lower extremity vessels
    3. Decreasing afterload in order to ease arterial resistance
    4. Decreasing preload in order to assist volume overloaded state
    5. Increasing preload to improve cardiac output
    1. Blood pressure is approximately normal due to a balance between venoconstriction and arterial vasodilation
    2. Blood pressure increases due to a an increase in arterial vasoconstriction and a lesser degree of venodilation
    3. Blood pressure decreases due to global arterial and venous vasodilation
    4. Blood pressure is approximately normal due to a balance between venodilation and arterial vasoconstriction
    5. Blood pressure increases due to arterial and venous vasoconstriction

    Author of lecture Dynamic Auscultation

     Carlo Raj, MD

    Carlo Raj, MD

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