Health and medicine
- What is shock?
- Shock - hemodynamics
- Shock - oxygen delivery and metabolism
- Shock - diagnosis and treatment
- Cardiogenic shock
- Sepsis: Systemic inflammatory response syndrome (SIRS) to multiple organ dysfunction syndrome (MODS)
- Septic shock - pathophysiology and symptoms
- Septic shock: Diagnosis and treatment
- Hypovolemic shock
- Neurogenic shock
- Obstructive shock
- Anaphylactic shock
- Dissociative shock
- Differentiating shock
Created by Ian Mannarino.
Want to join the conversation?
- Why would MVO2 be low for dissociative shock? If the tissues are unable to extract oxygen (sure, they get all they can, but still...) wouldn't it be expected to be high? I'm thinking about the whole left shifted curve and wondering if I'm missing something.(6 votes)
MVO2 = Mixed venous oxygen saturation
“it serves as an index of the adequacy of the oxygen delivery system”
dissociative shock = blood has decreased ability to carry oxygen to the tissues
(example causes: CO poisoning, cyanide poisoning, anemia)
if blood can’t carry oxygen = low MVO2 because MVO2 measures the adequacy of the oxygen delivery (low MVO2 = inadequate oxygen delivery)
- Why is heart fluid volume unaffected in septic shock when most of it ends up stagnant in the periphery leading to markedly decreased venous return? Also how does cardiac output increase if this is going on?(1 vote)
- At the beginning, the cardiac output is increased due to do the compensatory mechanisms..the neurohumoral mechanisms mainly the sympathetic sysytem..causes tachycardia and thus increase cardiac output..later on if the increase mediators like nitric oxide reduces the cardiac contractility and worsening the situation which eventually reduces the cardiac output.(2 votes)
- Two questions. one on cardiogenic shock, wouldn't PCWP be dependent on the location and extent of the infarct? would having an MI in that area of the left ventricle or inferior side increase the body's reaction compared to other areas of the heart resulting in cardiogenic shock? my second question (or third now) still on cardiogenic shock wouldn't CO increase or stay the same since CO is SV*HR? i would imagine your HR would increase where SV i guess would decrease?(1 vote)
- Why would PCWP and preload increase with a PE? It seems like there would be less blood on the L side of the heart due to the obstruction in the pulmonary circulation.(0 votes)
- Yes but on the right side it is increased much more than the left is decreased which leads to an overall increase in PCWP and preload.(1 vote)
- So, I want to create one final video on shock, and this is the video to really compare all the different types of shock, and see how you can differentiate between them. Now, this will be an advanced coverage of all the different types of shock, so most of my detail will be very brief, and give you a general gist of the type of shock. But, of all of these, I wanted to look at four different values. The first is cardiac output, and, of course, cardiac output is how much fluid, how much blood, the heart puts out per minute. So, it's usually measured in liters per minute or milliliters per minute. SVR stands for Systemic Vascular Resistance. So, that's resistance of all of the blood vessels in the body. And the two of these, cardiac output and systemic vascular resistance equal blood pressure, so usually, in shock, when one value goes down, the other will go up to try to compensate, unless both of them are shutdown. Cardiac output and systemic vascular resistance also provide information on tissue oxygenation. If they're decreased, tissue oxygenation can be decreased, as well. PCWP stands for Pulmonary Capillary Wedge Pressure, and this is measured with a pulmonary artery catheter. It tells you how well the heart is able to pump fluid forward. If the heart is struggling, or if there's some blockage, or something preventing blood being pushed forward by the heart, then PCWP, Pulmonary Capillary Wedge Pressure, will be elevated. LVEDV stands for Left Ventricular End Diastolic Volume. It's the volume of blood in the left ventricle at the end of relaxation. Basically, it's how much blood is in the left ventricle just before it squeezes out. So, this will also be elevated in a heart that is overloaded with fluid. And last of all, the value MVO2, which stands for Mixed Venous Oxygen Saturation. This will usually be low when the tissues have extracted a lot of oxygen. This is measured in the right atrium, so it's a way to average out the oxygen content in the blood, and so if tissues in the capillaries are able to extract oxygen, the total amount of oxygen going back to the heart will be decreased, so that would be a decreased mixed venous oxygen content. And vice versa, if the tissues are unable to extract oxygen, oxygen will be left in the bloodstream, and this value will be elevated. Okay, so that's the basics, let's go ahead and get started on this. So, cardiogenic shock is an issue with the heart's ability to pump. So, right away, we know that cardiac output is going to be decreased pretty severely, depending on how severely the heart muscle is impaired. With a decreased cardiac output, the blood vessels are going to clamp down, and so you'll have an elevated systemic vascular resistance in an attempt to return blood back to the heart and restore blood pressure. The heart's inability to function leads to back up of fluid, and usually this accumulates in the heart, so you'll see an elevated pulmonary capillary wedge pressure, as well as a left ventricular end diastolic volume. So, these will be increased, because blood is not squeezed out of the heart properly. Last of all, mixed venous oxygen content will be lower, and that's because since blood is not flowing as quickly, because the heart is shutdown, any oxygen that remains in the blood is pulled furiously out by the tissues, and so you'll see a lower content of oxygen when blood returns to the heart. Now, Obstructive I'll rush through really quickly, because it's pretty much identical to cardiogenic shock. Instead of the heart being affected, it's something outside of the heart that's preventing fluid from being squeezed forward. So, of course, blood is left in the heart, meaning PCWP will be elevated, and going back over here, fluid can't be pushed out of the heart, because of some sort of obstruction. Whether this is a pulmonary embolism preventing blood from getting from the right side of the heart to the left side of the heart, or if it's cardiac tamponade, or aortic stenosis, or any of that, and the blood vessels will compensate by trying to increase vascular resistance. And, last of all tissues are trying to pull out oxygen furiously, so we will see a low MVO2. To really differentiate these two, it's important to know a patient's history, as well as the symptoms that they're experiencing, and the onset of the symptoms, as well. For example, if a patient has history of heart attacks, it may be more likely that cardiogenic shock is the cause. So, you'll go through your different diagnostic tools to determine whether it's cardiogenic or obstructive shock. Now, hypovolemic shock, the issue is low blood volume, so because of low blood volume, there is a low amount of blood that can be squeezed forward from the heart. Low fluid return to the heart means low cardiac output, low delivery of oxygen. And because of this low blood volume, blood vessels are trying to clamp down, and so systemic vascular resistance will be very elevated. The fluid accumulation in the heart that's left over will actually be very low, because, right, it's hypovolemic, low volume in the body, and tissues will be extracting oxygen furiously, leaving the MVO2 to be much lower. Next, neurogenic shock causes impaired sympathetic response to the heart and the blood vessels. So, you have very low pressure, because both the heart and the blood vessels are getting low sympathetic tone. And of note in neurogenic shock, you have bradycardia, low heart rate. This is very unique to neurogenic shock as in all the other shocks, heart rate is increased to try to compensate for the low blood pressure. And there should really be no change in ventricular volume, and there will be a decrease in mixed venous oxygen. Essentially, the circulatory system collapses, so blood flow slows way down. And so oxygen is exposed to the tissues longer as blood traverses through the blood vessels, giving more time for oxygen extraction. Next, we have septic shock. Now, the cause for shock in sepsis is the immune system. The immune system responds to infective material and causes systemic vascular dilation, vasodilation. So, vascular resistance drops tremendously. To compensate for this, the heart initially tries to pump faster, but as time goes on, as a patient is exposed to sepsis for a longer period of time, the immune molecules can paralyze the heart and cause damage, which will lead to decreased cardiac output. So, cardiac output can be either elevated initially, or lower in later stages of septic shock. The fluid load on the heart is really not affected, maybe a little bit lowered, and oxygen extraction can either be elevated or decreased. And the reason you might have an elevated MVO2, Mixed Venous Oxygen Saturation, is because the tissues aren't extracting it properly. Septic shock causes a lot of swelling throughout the body, and this can make it difficult for oxygen to be delivered to the tissues. A lot of fluid is accumulating just outside of the blood vessels, and so oxygen has to travel a longer way to get from the blood vessels to the tissues that need the oxygen. And so, that's a perfect segue into anaphylactic shock. There's also increased swelling, and that's one of the major symptoms of anaphylactic shock. So, oxygen cannot be distributed to the tissues properly. And also in anaphylactic shock, you have a large lowering of vascular resistance. The blood vessels throughout the body dilate, which is very similar to septic shock. Now, cardiac output will be elevated in an attempt to counteract the decreased resistance, and the pulmonary capillary wedge pressure will be the same, maybe a little bit decreased. Now, last of all we have dissociative shock, and this is a very interesting shock because both cardiac output and resistance are going to be increased. The tissues are not getting oxygenation because oxygen cannot dissociate off of red blood cells, so, because of that, the body attempts to increase the heart rate and improve cardiac output, as well as clamp blood vessels down to distribute oxygen properly. However, regardless of these changes, red blood cells cannot dissociate from their oxygen, and so that is causing tissue starvation. So, looking over at MVO2, the tissues will pull out any oxygen they can from the blood, so MVO2 will be lowered. Free floating oxygen in the blood plasma will especially be low, since tissues are not getting their oxygen from the red blood cells. And finally, the pulmonary capillary wedge pressure, or the fluid overload of the heart, will be about the same, no real change. So, I encourage you to go back and look over this chart, and attempt to do it on your own, to really reason through each of these types of shock to understand how they cause decreased oxygen profusion.