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Shock - hemodynamics

Created by Ian Mannarino.

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  • blobby green style avatar for user Mike J Côté
    At this gentleman states that increased SVR equals "greater and better perfusion to the rest of the body". This is incorrect, especially in the context of shock, increased SVR leads to hypoperfusion of all non-essential organs and is part of the cause of MODS. Also, around the gentleman states that SV= preload-afterload, and defines afterload as being the volume remaining after systole, when what he is really talking about is end systolic volume. SV should be states to be "End diastolic volume - End systolic volume". Afterload should be defined as the pressure the ventricle must overcome to eject blood into the systemic or pulmonic circulation.

    (19 votes)
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    • aqualine ultimate style avatar for user Paul Gutekunst
      This happens in medicine. A lot. Words and definitions can and often do become misappropriated or defined differently due to many factors such as where we went to school or the language we speak locally. It is certainly acceptable to stop and ask questions when a possible error in word use is detected - it may have a critical impact in the care we provide to our patients. Even in this presentation by the excellent Mr Mannarino, it stopped me. I looked it up again, refreshing my old lessons and learning more. It's all good :-)
      (1 vote)
  • leaf green style avatar for user Kevin Huynh
    "Afterload can be thought of as the "load" that the heart must eject blood against" cvphysiology.com
    (5 votes)
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    • leafers tree style avatar for user Alott
      He says afterload is the amount of blood that remains in the heart after it squeezes. I don't think that's right though...the afterload is the amount of blood that is causing pressure at the aortic or pulmonary valves, keeping them closed, and against which the heart has to produce force to eject the blood.
      (4 votes)
  • aqualine ultimate style avatar for user Charlotte Imbeau
    At to , he was mentioning that MAP is CO x SVR + CVP. What website is he getting that from? I am more used to MAP being (systolic + 2 diastolic)/3.
    (2 votes)
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  • piceratops sapling style avatar for user Joshthecreator
    A slightly obvious question I am not sure about: Is perfusion similar in any way to diffusion, related in any way, or just similar sounding words?
    (2 votes)
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  • blobby green style avatar for user Timothy J. Calcara Jr.
    Around the two minute mark, you discuss cardiac output. I am wondering about afterload and its impact on stroke volume. Correct me if I am wrong: when afterload increases, stroke volume decreases, and vice versa.
    (1 vote)
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Video transcript

- [Voiceover} Shock is the decrease of perfusion of tissues. Or, in other words, it's the decreased delivery of oxygen to different organs of the body, and perfusion, this delivery of oxygen to the body, is essentially equal to the amount of flow, so the amount of blood flow that gets to the organs, over the amount of tissue that is being delivered to. So, for example, flow could be in measurements of maybe milliliters or liters per minute, so a volume per unit time, and the amount of tissue is measured in mass, so maybe grams of tissue, and this can be really any tissue, maybe 100 grams of kidney. It is the amount of blood that goes to that amount of tissue. However, there is another way to figure out perfusion, oxygen delivery to the tissues. So, perfusion is actually proportional this is a proportional sign, to cardiac output. That's the amount of blood the heart puts out per minute. It's also proportional to the systemic vascular resistance, and this is the resistance of blood vessels, and also the amount of oxygen, O2, content in the blood. So, let's go ahead and dive deeper and take a look at these different factors that can influence the delivery of oxygen and perfusion of the cells. So, cardiac output can be determined by two things. It can be determined by the stroke volume. So, let's take a look at the heart that I have over here. So, stroke volume is the amount of blood that escapes the heart per beat. And the other factor that influences cardiac output is heart rate. So, looking at the units of both of these, stroke volume is measured in liters per beat, so that's how much fluid escapes from the heart with each beat, times the heart rate, which is the number of beats per minute. And, so doing some simple arithmetic, these two cancel out and you see that cardiac output is liters per minute. So this is the measurement of cardiac output. And you can see in our equation up here flow has a similar unit, liters per minute. So, cardiac output really determines the flow of the blood. The more the heart squeezes to push blood out and the faster it does this, leads to increased cardiac output and, therefore, this leads to increased perfusion of the body. So, a better pump leads to better delivery of oxygen to the tissues. Now, heart rate is fairly self-explanatory. This can increase or decrease based off input from the nervous system. But stroke volume, let's break this down a little bit further. Stroke volume can be broken into three different parts, preload, which is the amount of blood that is in the heart at the beginning of a contraction. So, it is blood that is loaded in the heart before, or pre, contraction, before it squeezes. Stroke volume is also determined by afterload, which then, makes sense, is the amount of blood that is remaining in the heart after it squeezes, and contractility, and contractility is a measurement of how well the heart can squeeze. So, increased contractility means the heart can squeeze a little bit better. So, let's look at a quick example of maybe something like hypovolemic shock, where the body has low blood volume. Low blood volume means that blood returning to the heart is decreased. There is actually a lower amount, so less blood getting into the heart, maybe only a little bit makes it in, means less blood can be squeezed out. In the same token, if there is more blood, let's say there is more blood, remaining in the heart afterwards, that means less blood was squeezed out so there was less stroke volume. So, the equation for stroke volume actually makes sense. Stroke volume is the difference between the amount of blood that started in the heart before it contracted and the amount of blood that's left in the heart. So, stroke volume is preload minus afterload. That difference is the amount of blood that escaped the heart with one beat. And, of course, if the heart has greater contractility, it can squeeze harder and force more blood out. Now, resistance of blood vessels, systemic vascular resistance, so that's the total resistance of vessels in the system, also plays a role in perfusion, as I said before. And the way you can think about that is by looking at blood vessels, because blood vessels are like pipes, and that is how blood is delivered to the rest of the body. Now, what is resistance? Well, resistance is the ability for the blood vessel wall to push back against the blood. So, essentially, the blood vessel wall acts like a trampoline, and just like a trampoline, if you're bouncing up and down on the trampoline, if the trampoline material is tighter, you can bounce higher, and so blood behaves similarly in blood vessels. If it bounces against the wall, it can bounce back forward, and this pushes blood forward through the system and allows better oxygen delivery and, therefore, greater perfusion to the cells of the body. Now, there are different factors that can influence resistance, but really the greatest way that our body can change resistance is by changing the diameter of the blood vessels. Having a smaller diameter means more resistance because blood has more opportunity to bump up against the walls and bounce forward. And so, therefore, a smaller diameter blood vessel means increased vascular resistance and, therefore, greater and better perfusion to the rest of the body. So, cardiac output, systemic vascular resistance, and, finally, oxygen content. That is the other big component of perfusion. If there is more oxygen content in the blood, tissues can be perfused better because more oxygen can be delivered to the body. So, keep in my mind these three parameters when are you thinking about shock and perfusion to the tissues because shock is decreased tissue perfusion. Now, there's one final point I want to make, and it is in the equation for blood pressure. Specifically, we look at mean arterial blood pressure. An equation for this is cardiac output times systemic vascular resistance plus central venous pressure. Now, central venous pressure is usually low, so this side of the equation is usually neglected. And you can often just think here that blood pressure is equal to cardiac output times vascular resistance. Now, it is also worth mentioning that blood pressure can also be found by assessing through a sphygmomanometer. That's the little blood pressure cuff that physicians put on the arm of a patient. Whereas in this equation the mean arterial pressure equals cardiac output times systemic vascular resistance is a way to figure out blood pressure hemodynamically, another way to measure blood pressure is using this cuff. Blood pressure is calculated by adding two-thirds of the diastolic blood pressure plus one-third of the systolic blood pressure. So this gives the mean arterial pressure in a different way by using a blood pressure cuff. And note the reason I am going over this is, as you can see, look, cardiac output and systemic vascular resistance are factors that influence perfusion as well as factors that influence pressure, so very often patients in shock will have a lower blood pressure while at the same time they aren't able to adequately oxygenate their tissues. So, again, it is important to consider these different factors when thinking about shock and decreased tissue perfusion.