Distributive Shock

by Carlo Raj, MD

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    00:01 The last step that we'll take a look at, as far as shock, where the cardio and the pulmonary system are affected and, well, with distributive, what's going on here? This is septic shock. Okay, distributive. Good name, actually.

    00:17 So, septic shock means that your individual got exposed to a gram-negative organism, for any type of infection caused sepsis.

    00:25 Now, what is this gram-negative organism going to do? Through its mechanism of lipopolysaccharide and company that you learn from Immunology, you're going to have massive vasodilation caused by cytokines.

    00:37 Now, listen, this vasodilation is going to cause vasodilation of the arteries and also the veins.

    00:46 So, that means that the blood flowing through your circulation is excessively increased.

    00:54 What does that mean? Is it possible that you might have such high flow through your system in which, let's say, that I'm the tissue and, well, let's say that I'm the person who's waiting for the bus to come by, okay? Now, as long as the bus slows down and stops, I can get on the bus and then I can be on my merry way. But, if the bus just goes by and flies, there it goes.

    01:15 How am I going to get on the bus? I'm not. So therefore, I've missed my chance.

    01:19 Well, the bus is the blood flow and I'm waiting for my oxygen.

    01:24 So therefore, if the blood flow, the bus, passes through your capillaries way too quick, which is what happens in sepsis, how are you ever going to get on that bus? How are you ever going to release that oxygen? You can't.

    01:37 The doors don't open. Are we clear? Interesting. So here, you'll notice the following.

    01:42 Cardiac output is going to be increased, but yet, what's the definition of shock? The tissues are starving for oxygen. So, Dr. Raj, you're telling me there's an increase in cardiac output, but yet, the tissue is dying? That is correct.

    01:55 You would go ahead and call this high output cardiac failure.

    01:58 That you've heard of in your medical education and you will continue to.

    02:02 So, let's walk through sepsis now that we've set the foundation.

    02:05 Number 1, you have massive vasodilation. So, would you tell me where you might want to go to first? Let's go to SVR first, systemic vascular resistance. If you have massive vasodilation of the arteriole.

    02:18 What happens to your afterload? Decreased, severely. That's where we begin here. Number 1.

    02:25 So, if you decrease your afterload severely, making it much easier for the left ventricle to then pump its blood into the aorta, then what do you think happens to the cardiac output? Take a look. Increased. Wow. Fascinating.

    02:39 So, now, you have all this blood that's passing through your blood vessels.

    02:42 Wow. What are you going to do now? That's a lot of blood in your blood vessel.

    02:45 Increased or decreased stretch? Increased stretch, okay.

    02:49 The increased stretch then, this is then going to fool who? The medulla.

    02:53 And so, therefore, by fooling the medulla, now the medulla interprets this message as increased blood pressure.

    03:00 It is definitely not going to be sending out the sympathetic. Are we clear? We can definitely say that. So, there's going to be decreased sympathetic outflow.

    03:09 So, who is going to then take control? The parasympathetic.

    03:12 So, what does this mean to you in terms of your diagnosis? Increased blood flow, not cold, but warm. You see that? Next, increased blood flow through your blood vessels, weak or bounding pulses.

    03:28 Next, bounding pulses. Next, we have widening of your pulse pressure.

    03:34 What's your pulse pressure mean to you? It's your systolic blood pressure minus your diastolic blood pressure.

    03:40 If you are excessively vasodilating, what do you think happens to DBP, diastolic blood pressure? Drastically decreased. Now, this I can't help you. It's just simple math.

    03:50 If you decrease your diastolic blood pressure like crazy and systolic blood pressure is maybe increased, what do you think happens to pulse pressure? Oh, there you go, widening.

    04:00 Then, well, what about the sweat? You're going to be dry here.

    04:05 Why? Who controls sweat? Oh, yeah, Dr. Raj, that was one of the exceptions.

    04:10 It was a sympathetic muscarinic. And so, therefore, in septic, you have decreased sympathetic.

    04:17 So, you're going to be warm and dry, widened pulse pressure, bound, you can't miss this.

    04:21 There's no way. Is that clear? So, that's what you have here and then let's just make sure we finish up here.

    04:27 What about preload? Well, all you do, you take a look at cardiac output. It's increased. Okay.

    04:32 So, if there's increased cardiac output, how much blood is left in your heart now? Decreased.

    04:38 So therefore, any test that you're going to use to measure the blood in your heart, you'd expect to be, decreased.

    04:44 Take a look at preload, pulmonary capillary wedge pressure, central venous pressure, it'll be decreased.

    04:50 Understand it. Don't memorize it, when you're dealing with what's known as distributive type of shock.

    04:55 What might you want to do here for treatment? It's still IV fluids because your patient is in a form of shock and obviously pressors.

    05:03 So, it's the combination of the two. So, full table here.

    05:05 Make sure that you are able to walk through the different types of shocks.

    05:10 We put together cardiogenic and obstructive because some of the things that we're looking at in terms of tests and measurements are going to be extremely comparable.

    05:18 Now, the big thing here is in terms of how to distinguish the obstructive and cardiogenic and the diagnoses there and the causes are going to help you do that.

    About the Lecture

    The lecture Distributive Shock by Carlo Raj, MD is from the course Pulmonary Critical Care.

    Included Quiz Questions

    1. Decreased afterload
    2. The magnitude of the decrease in cardiac output
    3. Low cardiac output
    4. Increased pulmonary capillary wedge pressure
    5. Increased afterload
    1. Increased cardiac output
    2. Increased preload
    3. Increased total peripheral resistance
    4. Increased sympathetic output
    5. Decreased baroreceptor stretch
    1. Global and massive vasodilation
    2. Hyperthermia
    3. Increased sympathetic outflow
    4. Fever
    5. Hypothalamic dysfunction

    Author of lecture Distributive Shock

     Carlo Raj, MD

    Carlo Raj, MD

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