Shock | Clinical Medicine

What's up, Ninja Nerds? In this video today, we're going to be talking about shock. This is a part of our clinical medicine section. If you guys like this video, it helps you. It makes sense. Please support us. You guys can do that by hitting that like button, commenting down in the comment section. Please subscribe also. It really goes a long way. Also, highly suggest, go down to the description box below, go to our website. As I said before, we have a lot of great things there. Notes, illustrations. We're developing exam prep programs for those of you taking your step one, step two, your pants, etc.,

Check those out and check out the merchandise that we got there. All right, without further ado, let's talk about shock. There is a couple types of shock that we got to go into a little bit of depth on, and that is hypovolemic, obstructive, distributive, and cardiogenic shock. Out of all of these, one of them has some subtypes that we'll dive into a little bit. We'll actually have separate lectures on all of those into more detail.

So, first one is hypovolemic shock. Hypovolemic shock is super simple. The volume within your vascular system is significantly reduced. Now, when a patient loses volume, you can lose volume in two ways. One is you're losing volume from sources such as the GIT. What would be a way that we could lose some fluid from your GIT? It doesn't take a genius to recognize it. It's coming up from the top tube, vomiting.

If it's coming from the bottom tube, diarrhea. Another thing could also be like excessive NG tube suctioning as well, or very, very poor PO intake from a decent amount of time. This can cause hypovolemia. And the reason why is, is if it's not getting absorbed across the GI tube, you're not absorbing the volume. So this is one particular reason why you drop your blood volume. Second one is excessive skin losses.

That would also lead to it and renal losses. And again, for skin losses, it's again, straightforward. This would be a patient who has usually excessive diaphoresis. In other words, they are sweating up a storm or, and this could be from fevers. So usually that'd be a big thing to think about. So diaphoresis from fevers or burns, like third degree burns. That could be another big one. And then renal losses is usually from things such as like diuretic abuse.

These scenarios will cause the patient not to be able to maintain a good blood volume.

If in these particular scenarios you reduce the blood volume that way, that's going to lead to a problem. You know, generally the systemic circulation, right, you have the venous part and the arterial part. The venous part is supposed to receive this volume, if you will, and take it where? Into the heart and allow for good venous return to offer a good preload, a good stroke volume, cardiac output, etc.,

If you have this problem where you're losing fluid, this will lead to what? A decrease in this particular scenario here, a decrease in the venous return. And if you decrease venous return, you will drop your stroke volume.

and you will drop your cardiac output, right? So these are the underlying effects here because if you don't fill the heart, you don't have enough volume of blood to pump out of the heart in one beat and then in one minute. And that's the problem with this disease is you're losing fluid this way. Another way which is also catastrophic is it could be from blood loss. If a patient has massive blood loss,

What would be some particular scenarios in this? Well, we kind of talked about it a little bit. A AAA rupture would be pretty catastrophic, I would say. Another one would be a GI bleed. These are very, very common. Or like a uterine bleed. And you also can't go wrong with thinking about any type of trauma in that particular situation where it's like an external exsanguination effect. All right, so blood loss.

would be in this particular scenario and it's the same exact concept my friends where you're losing blood, you're having a reduction in venous return. In other words, this process where blood is supposed to be going into the ventricles from the atria is being reduced. If you're reducing this process, you're not having enough filling, your EDV is going down, your stroke volume goes down, cardiac output goes down. Now, if we follow that process, the amount of blood that's coming out of the heart is reduced

And in that particular scenario, that then drops, as we said here, your cardiac output. And then if you drop your cardiac output, what do you do to your blood pressure? You're dropping your blood pressure. And so this will lead to a drop in what's called the mean arterial pressure, which is the perfusion pressure. If that drops, you can't give oxygen to the tissues. And this leads to something called organ malperfusion.

When you have organ malperfusion, then this starts leading to organ dysfunction, if not reversed. In other words, multiple organ systems can start to actually fail.

That is the concept of shock is where in this particular scenario the volume loss or blood loss is leading to reduction of venous return stroke volume cardiac output map and not perfusing the particular tissue and the organs such as liver kidney heart Brain start to fail. That's the concept there. All right. Next one is obstructive shock in obstructive shock It's two particular etiologies here

One is you are massively, massively, massively reducing the preload on the heart or you are massively increasing the afterload on the heart. So it's one of the two. There is a massive drop in the preload or there is a massive increase in the afterload.

So it's kind of like similar because if you think about it, preload kind of goes with venous return, right? If you have a reduction of venous return, you have a reduction of preload. So just like you can see that in hypovolemia, you may see that here but it has nothing to do with volume loss. There's something obstructing the heart from filling because in this particular scenario, it was you couldn't fill. Same thing exists here where I can't get blood into the heart. That same concept exists. So there is a reduction of preload, venous return.

Then because of that, if you drop your preload, you drop your stroke volume. And if I drop my stroke volume, I'll also drop my cardiac output and that'll drop my mean arterial pressure. And then the same concept here exists. The difference in this scenario though, is that there's something else reducing the filling. One is you have the pericardium pushing on the heart and it's not allowing good filling of the heart.

or you have a lot of the lung pressing on the heart because the pressure inside of the pleural cavity is crazy high. So it's either pericardial pressures are high or pleural pressures are high. What are the two diseases? This is actually pretty straightforward. One here would be a tension pneumothorax. That would cause the pleural pressures to go high and compress the heart and prevent it from filling. The second one would be tamponade.

And that would be the pericardial pressures are high, compressing the heart, preventing it from filling. And these two scenarios, these will massively drop your preload, drop your perfusion to the tissue, and so subsequently the patient develops organ malperfusion. And again, we'll talk about all the organs that can be malperfused and what that looks like a little bit later. But that's the concept of shock. Now,

Other things actually do happen here that not only does the heart actually get compressed, but it also does like really quickly here cause something called septal shift. So you shift the actual septum into the left ventricle, which impairs its filling process as well. But either way, you're not filling, right? Here's the one with increased afterload. If you increase your afterload, what do you do to your stroke volume and your cardiac output? You reduce it, right?

So the reason why is afterload is the amount of pressure that you have to exert to push blood out of the ventricle, whether it's right or left, into the aorta or into the pulmonary artery. If it's too high, can you get a lot of blood out? So your stroke volume and subsequently your cardiac output will drop and so will your MAP. So in this particular scenario, it's the exact same. It's just a different mechanism.

But the question is coming, what is causing this massive afterload increase? Look at that big chunky clot in the right, right in the pulmonary artery. What is that called? A pulmonary embolism. Now, I can't get blood out of the heart. Why? Because the afterload's high, because something's blocking that flow. And then because of that,

If I can't fill the pulmonary arteries, I won't be able to fill the left atrium and fill the left ventricle. And if I can't fill the left ventricle, I can't get a good stroke volume, cardiac output, MAP drops. I don't perfuse tissues. What in the heck did I just say can cause this? A pulmonary embolism. So a PE is one of the potential etiologies that can really stimulate this. Okay? So we have these etiologies here and these etiologies here.

That's obstructive shock. For distributive shock, it's a little bit different. This one's interesting. So the whole primary pathophysiology here for all of these is the vessels are vasodilated. So let's actually put that right here. You see how these vessels, look at this one, compared to this one, compared to this prior one. These suckers are huge, right? So these patients have massive vasodilation, all right?

When you have massive vasodilation of your vessels, now blood can easily flow through here with very little resistance. What happens to the SVR? I just told you. I done told you. The SVR is going to drop. So, vasodilation occurs intensely. This drops your systemic vascular resistance. When you drop your systemic vascular resistance, what does that do to your blood pressure? We already know.

Cardiac output is equal to heart rate times stroke volume and blood pressure is equal to cardiac output times SVR. So if SVR goes down, blood pressure goes down. So then what happens? The MAP drops, you don't perfuse your tissues, and more organ malperfusion begins to ensue. And that is the problem here. But the question that arises here that we have to try to figure out is what in the stink is causing vasodilation, massive vasodilation? One other thing.

Here's a big thing that's really really important. We'll talk about a little bit more and get into the complications but whenever your SVR, if you'll notice something, and this shock here, this is the only one out of all the shocks where the SVR is really low. In all of these other shocks, the SVR is usually high. The reason why is cardiac output is low, cardiac output is low, and in this one, cardiogenic shock, cardiac output is low. Remember the formula.

We said blood pressure is equal to cardiac output times SVR. If cardiac output goes down, what has to happen to the SVR? It has to go up. And if SVR goes down, what has to happen to the cardiac output? It has to go up. So sometimes these patients will exhibit what's called a reflexive increase in cardiac output. In other words, their heart's banging away. It's important to remember what we'll talk about a little bit later. Let's come to the question, what in the heck is causing this vasodilation? One is you're losing your sympathetic tone.

the norepinephrine and epinephrine that are supposed to naturally bind here to your alpha-1 receptors. You know you got alpha-1 receptors here? It's just not happening for some reason. There's some type of disconnect. There is just this disconnect where they aren't being released. So there's like these lower levels of norepinephrine, epinephrine. They're not hitting the alpha-1 receptor. So this is inhibited. Alpha-1 receptors are supposed to cause vasoconstriction. If you don't have them, they'll produce vasodilation. What is the reason why I'm having this disconnect?

Usually the reason is some type of spinal cord injury. It's usually a spinal cord injury, sometimes a spinal anesthetic, and this is called neurogenic shock. Neurogenic shock. And we usually see these, and I'm going to abbreviate this, in spinal cord injuries. Alright? There's a lot of different reasons why these can happen besides spinal cord injuries, but this is the big one. The other thing that's important to remember, just to add in here, is that these epinephrine and norepinephrine also hit the

Just as a little quick note, a little side note, it also has beta receptors on the heart, beta 1 receptors. So this may be the only type of shock, besides maybe cardiogenic shocks, that can also, if there's less norepinephrine, epinephrine hitting these receptors, the heart rate will be a little bit lower. So remember, neurogenic shock is a weird one where they can have hypotension and bradycardia. But look for some type of neurological catastrophe. All right.

Let's come back here. Neurogenic shock is one, probably one of the least common. This is gonna be by far the most common type of distributive shock. And this is called septic shock. And this is usually due to a nasty type of infection. So usually you have some type of bacteria that has reached its way into the bloodstream.

When it gets into the bloodstream, it's called bacteremia. But when the bacteremia starts leading to effects like hypotension, fevers, infectious types of properties, now we're talking about septic shock. So what happens is the bacteria, we're not going to go through the entire mechanism here, we'll do this in the pathology lectures, but these bacteria activate our immune system cells. And these bad boys release bunches of cytokines. And these cytokines, some of the interleukins and tumor necrotic factors, etc.,

What they do is, is they have the capability of precipitating, oh wow, vasodilation. And that's gonna cause this whole downward cascade. Another thing is that they also do cause the vessels to become super leaky. So fluid also leaks out as well. So they get a little bit of volume, hypovolemic too. The last one here is usually anaphylaxis, okay? With anaphylaxis, this is usually an allergic reaction of some sort.

stung by a bee ate something that they're super super allergic to have a contrast allergy they got contrast what happens is that allergic reaction causes them to activate the immune system massive cytokines be released causing vasodilatory shock how do you differentiate these it's usually in the context of some type of spinal cord injury an obvious infection leukocytosis fevers

Whereas, they have some type of angioedema, upper airway obstruction, hives, a recent exposure. But that's some of the big ways of differentiating these from one another as a distributive shock etiology. All right, we come down to the last one. This is preferably one of my favorite ones in comparison to septic shock. Cartogenic shock is really, really interesting in the sense that it can happen in two different ways. One is it can be mechanical or it can be arrhythmogenic. So let me explain here.

Let's say here we have a patient who has cardiogenic shock. They have some type of problem with their myocardium. In other words, they have a poor contractility. That is their disease process, let's say. They have a reduction in the contractility. And what's reasons why you can have a reduction in contractility? One is you have an MI. The second one is you could have heart failure, usually with a reduced EF. So an MI is one heart failure with a reduced EF.

ejection fracture will be another example, right? So this area is damaged and you're losing the ability to get blood out. If contractility drops, I am going to now have a problem getting blood out of the heart. So what is that called? Stroke volume, right? In one kind of beat. And then if that's the case, I may also over a process of a minute drop my cardiac output. And so this is something that you could potentially see is a drop in stroke volume and a drop in cardiac output due to a drop in contractility.

Another thing to think about is, is there a valvular damage? Oftentimes when valves are super, super damaged, and the one that I really would want to point out here is if there is damage to the aortic valve, sometimes the mitral valve as well. In acute, let's say acute aortic regurgitation or mitral regurgitation.

In these scenarios, what happens is, is you have a constant backflow of blood, right? So you push blood out, but the blood comes right back in. And that can cause patients to go into an acute heart failure. So it's the same kind of concept. It kind of volume overloads them in the heart, but you can't get blood out. Same concept. So think about a catastrophic mitral or aortic regurgitation or a recent MI, or do they have acute heart failure?

So usually this is heart failure with a reduced ejection fraction, but it's usually acute, not chronic. In other words, they decompensated if they have chronic or they developed acute heart failure or something to that effect. In this particular scenario, if you have a reduction in cardiac output, what do you do to your MAP? You drop your MAP, you don't perfuse the tissues, and what ensues, my friends? Organ malperfusion.

So we're getting the concept here that some problem is there is a reduction of perfusion to the tissue and the tissue start becoming dysfunctional. And all of these reasons just occur based upon the different pathophysiological process. Alright, that's one way cardiogenic shock can ensue. Acute valvular regurgitation or reduction in contractility. And just remember acute aortic regurgitation and mitral regurgitation can be a factor that can cause heart failure, acute heart failure.

Okay, next one here. The other scenario that maybe causes us to get less blood out of the heart, so less stroke volume, and as a response, less cardiac output, and then if there's less cardiac output, there has a lower MAP. This concept here would be it's arrhythmogenic.

So I have an arrhythmia that is preventing me from getting blood out of the heart. There's two types of arrhythmias. It's not too hard, right? One is the heart rate is going way too dang fast or it's going way too dang slow.

And this would be if you have a tachyarrhythmia. This has to be really fast though, guys. I'm talking like a patient who is going like 150 or greater ventricular rate. So we see this particularly in VTAC, maybe V-fib or atrial fibrillation, sometimes SVT, all right, that it can potentially do this. But I'd say it's more these top three. The concept behind this super high heart rate

is that what you do is you impair filling. So what it's supposed to do is this is you're supposed to have blood coming into the heart. This will be inhibited in the situations of tachycardia. So this massive tachycardia will actually do this. Now, bradycardia is really cool because when the heart rate is super, super low, such as in an AV block, right? This is interesting because it directly drags down the cardiac output.

If you increase the heart rate, you'd be like, oh, well, cardiac output is equal to heart rate times stroke volume. So if I increase the heart rate, I would increase my cardiac output. It's like, that doesn't make sense. It's if your cardiac output is so high, it reduces diastolic filling, then it can drop your cardiac output.

But in the other scenario, cardiac output is equal to heart rate times stroke volume. If heart rate drops, so does cardiac output. That is a direct correlation relationship. So these are two particular scenarios here where you can see heart rate driving, a reduction in stroke volume, cardiac output, MAP, and organ malperfusion. So with all of that being said, we've covered the different types of shock. Now what I need us to really kind of understand here is,

How do we really look at the complications and some other differentiating factors for patients with shock? All right, my friends, so now we're going to talk about shock, particularly the complications that can arise from shock, and that is usually multisystem organ failure as the result of organ malperfusion. Regardless of any etiology of shock, this is the problem. So to quickly recap again, and those patients who have cardiogenic shock, obstructive shock, or

hypovolemic shock, all of their problems is a result of their cardiac output being reduced. So the problem is in these particular patients is their cardiac output is reduced. Again, which types of shocks would do this, my friend? This would again be, just as an aside here, this would be cardiogenic, 100% would be cardiogenic. The second one would be obstructive and the last one would be hypovolemic.

All of these via different mechanisms reduce the cardiac output. So that's what we know about these particular shocks here is that these very specifically reduce the cardiac output. Now if we reduce the cardiac output, what that tells me is that I am not getting enough blood out of the heart. So this process here is significantly reduced. So I'm getting a reduction

and cardiac output, which reduces my mean arterial pressure leading to organ malperfusion, right? And that's the concept here. And we'll talk about those organs that get malperfused. One thing that I want to also mention here is when a patient has a low cardiac output, some things happen. You guys remember this formula here, that BP is equal to cardiac output times systemic vascular resistance. The cardiac output in this disease

is doing what? It's dropping, which will drop your blood pressure, right? So the cardiac output is dropping. This will drop your blood pressure. What does your body have to do to compensate here? Increase the systemic vascular resistance. Let's do this in a different color. Let's do the pink. So this will have to increase. Now what that will look like is super, super interesting.

When you increase your systemic vascular resistance, you clamp down on those vessels like you squeeze the living heck out of them. So you have intense vasoconstriction. What that will do is, is that'll reduce the blood flow through the arteries in your extremities. And when you go and look at these patients on exam, what you will know is, is they will have cold,

extremities, pale extremities, and they will have modeling of the extremities. So this is what you will notice. Cold extremities, pale extremities, and modeling of their extremities, all because their vessels are super, super constricted. That's super common. Cold, pale, modeled extremities. Very common in cardiogenic, obstructive, and hypovolemic shocks because of this mechanism here. All right? So this is one thing I want you to understand.

The other thing is that whenever your cardiac output drops, there's another formula that you want to remember. And this is cardiac output is equal to heart rate times the stroke volume. Well, in all of these types of shocks, with the exception of cardiogenic shock, which is the Bradycardia related, if your cardiac output is dropping, what should be the reflexive reaction to your heart rate? It should go up.

And so oftentimes these patients will develop what's called a reflex tachycardia. So we call this a reflex tachycardia. And this is common in all of these shocks. There is an exception. AV blocks would be one particular exception. And anything like a bradycardia, so AV blocks or like a beta blocker overdose. And this will all be related to beta, like a beta bradycardia. All right.

So these are the concepts that I want you guys to understand here. In low cardiac output related shocks, your body increases resistance and increases your heart rate. Super important. The other scenario here is we have the vessels that are jacked up. So the systemic vascular resistance is the problem in the other types of shocks. So whenever we have the systemic vascular resistance is really low,

What does that do to your mean arterial pressure? That also will lower your mean arterial pressure. And what are the shocks that lower your systemic vascular resistance, my friends? You should already know this ones. So again, it's going to be which type of shock here? Oh, son of a gun. This will be distributive shocks. Distributive. And so when a patient has distributive shock, their systemic vascular resistance is massively going to be reduced.

This would be septic shock, this would be neurogenic shock, and this would be anaphylactic shock. Now, what happens here is when the systemic vascular resistance is low, think about the equation. So BP is equal to cardiac output times systemic vascular resistance. If we think about this formula, when the systemic vascular resistance is going to be low, then we know that the blood pressure will be low and so your body will have to increase its cardiac output. So it'll beat harder and beat faster.

But here's the other concept. What's the SVR? It's low. So if you have a low SVR, your vessels are what we call dilated. So that's why we call this a vasodilatory shock or a distributive shock. Are they going to have good blood flow through them? Yeah, because they're going to be pump and plump and leaky. So they should have warm and they should have, it should not be pale.

and it should not be modeled. And in fact, we should actually use this term, this should be warm and pink/red. So warm and well perfused, which means that they're pink and red. So it should be warm, pink and red, and not modeled. This is gonna be your distributive shocks. Okay, the last thing here is whenever your systemic vascular resistance drops, your MAP drops, your cardiac output has to increase. The only other thing to remember here is,

is that whenever the SVR reduces and this happens, it also will try to create a reflex tachycardia. The only exception to this process here is going to be neurogenic shock. Alright, that is the only type of exception. So all of these you should have a reflexive tachycardia, a reflex increase in cardiac output.

That is the big concept that I need you guys to understand. So neurogenic shock will have bradycardia and AV blocks or beta blocker overdose will have bradycardia. All right, now that we have a good understanding of that, when your MAP's low, you stop perfusing organs. So I lead to a lot of problems here. I don't perfuse generalized tissues. When tissues don't get perfused, they produce something called lactic acid. And lactic acid, what it will do is, is it will actually drop your pH. And when it drops your pH,

that is going to create a metabolic acidosis that then does something really interesting. It triggers your lungs to have to breathe faster. And so one of the ways that you can see disease in these patients is their respiratory rate is increased. Look for that in shock. Another one is they don't perfuse the brain and they can actually start to experience things like encephalopathy. They also don't perfuse their coronaries.

And if you can't refuse your coronaries enough, guess what? This heart starts to become a little bit sad and becomes a little bit ischemic. And this is called an NSTEMI. This is super common. The other one, and you know what's interesting? Encephalopathy, obviously they'll present with confusion. Lactic acidosis, they can present with a low pH if you check a gas, but they'll also have tachypnea. For NSTEMI, they may present with chest pain, but sometimes the way that this is found is some numbskull checks a troponin.

and these troponins will be elevated. And the other thing is they may have an EKG that gets worked up for because they're in shock. And they can have ST depressions or T wave inversions. They may not present with chest pain, just remember that. The other thing here,

is that they don't perfuse the kidneys and when you don't perfuse the kidneys these poor kidneys they can develop what's called an acute kidney injury and acute kidney injury is usually the way that you'll see this is their urine output will drop off and their creatinine will rise and that is the big things to look for with an acute kidney injury the next thing is if you i mean it is multi-system right my friends is you don't perfuse the git

And if you don't perfuse the GIT, this can lead to what's called acute mesenteric ischemia. And this will precipitate terrible abdominal pain, usually out of proportion to what your exam is. So watch out for this potential finding. And lastly, you may not perfuse the liver. And these patients can develop what's called ischemic hepatitis.

And in these particular scenarios, when I've seen them, these patients usually have LFTs that are through the roof, like into the thousands. And so this is another way that you'll be able to see this is because you just don't perfuse the liver as well. In these scenarios, we see how if a patient develops any shock, cardiogenic, obstructive, hypovolemic shock, distributive shock, they don't perfuse these tissues. These are the complications that ensue.

We also understand that in patients with distributive shock, they're vasodilated. They're warm, pink, red, not mottled. And those with cardiogenic obstructive hypovolemic, they're vasoconstricted. They're cold, they're pale, they're mottled. Both can have reflex tachycardia with the exception. And these, AV block, spade blocker overdose, and here, neurogenic shock. Let's now go into the diagnostics of shock. How do we diagnostically approach shock?

Well, first thing is calculate the shock index. And the way that you can do that is by taking the heart rate and dividing it by the systolic blood pressure. In all shocks, with the exception of a bradycardic shock or neurogenic shock, the heart rate should be high and the systolic blood pressure should decrease. So if you think about that, if that shock index is greater than one, that supports shock. What else supports shock?

Lactate. If lactate is super elevated, that means that you're not perfusing organs potentially, and that could also support shock.

And then ask yourself, okay, are there any features of decreased organ perfusion? In other words, do they have any encephalopathy? Is there any evidence of acute kind of changes in their EKG or troponins? Is there abdominal pain? Is there any features of acute kidney injury, like an increase in creatinine and decrease in their urine output? Is there any bump in their LFTs? If that is the case, that supports shock as well.

Now the question is, is how do we determine which shock it is? We do not do this in every patient, but on your boards, you will have to determine this based upon a swan gans catheter or a right heart cath. You place this catheter into the jugular vein, run it down into the right atrium, right ventricle, pulmonary artery into the pulmonary capillary area and inflate the balloon. And it'll give you some pressures.

What it'll do is it'll give you these different numbers that'll help you to differentiate the type of shock. So the first one is hypovolemic. I want you to remember that this was a cardiac output low. So the way that we look at cardiac output is cardiac index and SVO2. These should both be low.

The next thing is SVR in any shock except for distributive should always be high. What's the only things that aren't kind of like we didn't talk about? CVP and pulmonary capillary wedge pressure. This means that the actual heart is usually in some way, shape, or form having a hard time getting blood out of it.

And so in this, it's usually kind of scenarios of obstructive shock or cardiogenic shock. So we would expect these numbers to be low in patients with hypovolemic shock. So again, low cardiac output based upon these two numbers, high SVR present in all of these other types of shocks generally. Okay? The only difference is CVP and pulmonary capillary wedge pressure should be low. Obstructive shock. CVP should be high because you're not going to have good filling into the right heart.

And the reason why you're not going to have good filling into the right heart is because you have something pushing on it, like a tension or a tamponade, or you have no blood leaving the right heart because they have a pulmonary embolism. So in those scenarios, the CVP should be high. But again, if it's an obstructive, hypovolemic, or cardiogenic,

cardiac output should be low, so that's based upon these two numbers here, their SVR should be high as a compensation, and their CVP will be high. The only thing that is different here is their pulmonary capillary wedge pressure should be low. There's only one exception in obstructive shock where the pulmonary capillary wedge pressure is high, and that is tamponade. Otherwise, that is the big defining difference here between obstructive and hypovolemic is the CVP is high, low here.

These should be the same. The only exception is cardiac tamponade. Cardiogenic shock. The problem is getting blood out of the heart. You can't get blood out of the heart. So the CVP, and it's actually hard, again, and these patients, they have problems with being able to get blood out of the heart, and they can't actually get blood out of the heart, and so they kind of call them, become overfilled and congested. So CVP should generally be high in cardiogenic shock.

Pulmonary capillary wedge pressure is a measure of left atrial pressures. Left atrial pressures are usually always high in patients with cardiogenic shock. So you see how that's the big defining feature here between these is pulmonary capillary wedge pressure is high. That's super suggestive of cardiogenic shock. And again, these shocks all have a low cardiac output. So cardiac index should drop and SVO2 should drop.

SVR should always be high in all three of these shocks, but the only defining features between these is CVP is low, CVP is high. Pulmonary capillary wedge pressure is low, pulmonary capillary wedge pressure is high. The only exception here is cardiac tamponade. Last one is distributive. So in this one, we already know that their SVR should be super low. That's the defining feature of the shock. And then what's the compensatory response? An increase in cardiac output. So these should be high.

And then pulmonary capillary wedge pressure and CBP are low because you're having an easy time filling the heart. It's not a problem of filling the heart, okay? So you should be low. And that's the ways that I want you guys to differentiate the types of shock based upon the swan gans catheter.

Okay, now we move into the next step, which is how do we treat shock? It depends upon the type of shock. The type of bulimic, you have to ask, is it fluid loss? Give them fluid. Is it blood loss? Give them blood. How do I do that? Give them IV fluids or if they're losing fluids, give them blood if they're losing blood. Simple as that. Obstructive, treat the cause. If it's tamponade, stick a needle in, pull that fluid off. Pericardiosynthesis. Is it a tension pneumothorax? Chest tube, relieve the air there.

Is it a PE, TPA, or embolectomy if they're hemodynamically unstable? Cardiogenic, you have to treat the cause. It is a reduction in contractility. Due to myocardial infarction, they have to go to the cath lab. Is it an aortic valve that's acutely blown or a mitral valve that's acutely blown? Then you've got to give them a valve replacement. Is it bradycardia, that's second degree MOBAs to a third degree? Okay, then we need to do a pacemaker.

Is it a need potentially because of beta blockers or calcium channel blockers that have caused this patient to go into a bradycardic rhythm? Okay, then we need to reverse that. Beta blockers with glucagon, calcium channel blockers with calcium. And then is it because they're going way too fast? Then we need to give them a cardio version if they're in AFib or if they're in VTAC.

Next concept here is if a patient's in cardiogenic shock and we've tried to treat the underlying cause, but their perfusion is still being reduced. And the examples of that is usually myocardial infarction. And sometimes you may need to initiate inotropes, things like dobutamine or milrinone. And if that doesn't work, sometimes mechanical circulatory support. So things like an aortic balloon pump or VA ECMO. We talked about that again in CHF and we talked about that a little bit in MI.

Distributive shock is another one. So this one is, again, the different types. So anaphylactic shock is the systemic allergic reaction. Usually the best treatment for these patients is epinephrine. Give it to them as soon as you possibly can. Then after that, you can do things like antihistamines and steroids. For septic shock, it's all about antibiotics. You've got to get them on antibiotics. You can give them a 30 cc per kg slug of fluid initially, but it's antibiotics and source control of the infection that's going to prevent them from continuing to be in shock. One thing that's important to remember is

And patients with distributive shock, you want to really support their blood pressure. Any type of shock, you want to support the blood pressure. But distributive most commonly, they need a lot of vasoconstriction.

And so when you vasoconstrict the blood vessels, you increase their SVR, which increases their blood pressure and increases their perfusion. So you want to give drugs that squeeze the heck out of the blood vessels. Things like phenylephrine, things like norepinephrine, things like epinephrine, or things like vasopressin. So this will help to keep their blood pressure up long enough for the primary cause to be treated, which is treating the anaphylaxis, treating the sepsis. Okay?

All right, my friends, in this lecture, we talk about shock. I hope it made sense. I hope that you guys enjoyed it. And as always, until next time.