What's up Ninja Nerds? In this video we're going to be talking about shock. What is shock?
Shock is simple. It's inadequate perfusion to the tissues. When you don't give them an adequate amount of oxygen and nutrients, they start to fail.
If tissues fail, tissues make up organs. So if tissues fail, subsequently the organ will fail. And if organs fail, this will lead to multi-system organ failure that can quickly progress to death.
That's the concept of shock. There's four types, hypovolemic, cardiogenic, obstructive, and distributive. Let's talk about those types of shocks and the causes behind them. Hypovolemic shock is a relatively simple shock. When we talk about it, you're down on volume.
But what's the problem with volume? It's actually blood volume, right? And when you have a decreased blood volume, what that really does is it drops your preload.
That's really the problem with this disease, is that you reduce your total preload. So there is a reduction in preload. And what do we know about preload? What we know about preload is a reduction in preload reduces stroke volume and a reduction in stroke volume reduces cardiac output.
A reduction in cardiac output reduces your blood pressure or your mean arterial pressure and that's the actual perfusion pressure. So that's the overlying pathophysiology behind this. But what actually causes this drop in preload? You're losing blood volume.
When you lose blood volume you can lose it in two ways. One is because you're hemorrhaging. When you're hemorrhaging you can lose lose this from sometimes postpartum hemorrhaging. So massive bleeding from the actual uterus or a massive GI bleed, whether you're bleeding through the GI tract, like an upper GI bleed or lower GI bleed, or sometimes you bleed behind the abdomen, like a retroperitoneal bleed.
The other one is if you're in a massive motor vehicle accident, you can develop so many massive types of injuries where you could bleed internally or externally. And then last one is some type of massive artery that just ruptures or has a massive like So sometimes if you have like an abdominal aortic aneurysm that ruptures, that can quickly and subsequently cause a massive reduction in total blood volume because you're hemorrhaging internally. So those are simple causes.
We go about the non-hemorrhagic losses. It's not blood that we're losing. We're losing like total plasma. So the plasma component within the blood vessels, like water.
In these situations, think about how you can lose lots of actual plasma. If I am In a situation where I end up getting a massive burn, okay, or I have like uncontrollable fevers where I'm constantly sweating. In those situations where I get a massive burn, I'm going to lose a lot of the water from those cells that just got destroyed. Or if I'm having massive constant sweating because I'm diaphoretic and I have terrible fevers, I'm going to lose a lot of fluid from that process.
So massive skin losses from terrible fevers, hyperthermia, or burns. Or you're actually vomiting out. tons of fluids, a massive vomiting, or you're peeing out your butthole, and that end, that can cause a massive volume loss.
The other situation is if you're urinating out large amounts of volume, so people who are on very high doses of diuretics, those could be potential issues as well. The last one that actually can cause a total volume loss, meaning that it's not in the actual vessel, so the total volume of actual blood that's in the vessel is less, because what happens is inflammatory states especially pancreatitis it can cause fluid to leak out of the vessel and into the interstitial spaces this is called third spacing so you're actually losing fluid into the interstitial spaces and it's not in the vessel that reduces your preload so that covers hypovolemic shock pretty straightforward and we talk about the next one that is cardiogenic shock cardiogenic shock in the most basic sense is a true reduction in cardiac out Now cardiac output is dependent upon what? It's dependent upon your heart rate and it's dependent upon your stroke volume.
Your stroke volume is dependent upon preload, contractility, and afterload. So we got to figure out what things are actually affecting the cardiac output. So I think the easiest way is to think about contractility and contractility is dependent upon the myocardium.
So what if you have some myocardial dysfunction or disease? It's really straightforward, right? Think about it.
You damage a the myocardium. So you suffer from a massive MI. You end up having heart failure.
You have myocarditis, inflammation of the myocardium. In these situations, like a massive MI, myocarditis, heart failure, cardiomyopathies, these would be situations where you're actually causing dysfunction and disease of the myocardium. And what's this going to do? It's going to lead to a reduction in the contractility. And if you reduce the contractility, That will reduce your stroke volume and subsequently drop your cardiac output and drop your blood pressure.
Because a drop in cardiac output drops your blood pressure. Straightforward, right? All right. Arrhythmias.
You're probably like, what the heck does this have to do with anything? So if you have, again, think about your... Your formula here, cardiac output is equal to heart rate times stroke volume.
So heart rate also affects cardiac output, right? So you would think in simple, if cardiac output is equal to heart rate times stroke volume, a reduction in heart rate would cause a reduction in cardiac output. That's a straightforward, and it does.
So if somebody has like a third degree heart block, a complete heart block, that's definitely going to drop their cardiac output. Here's the paradoxical end, and it actually, it might be slightly confusing, but I think it'll make sense afterwards. You can also have a drop in cardiac output in very, very fast heart rates, very fast heart rates. So when someone has something like AFib or VTAC or VFib, in those situations where your heart is beating, beating, beating so fast, the ventricles don't have enough time to be able to fill with blood.
So they're contracting, and as they get ready to fill up with blood, they don't even get enough time, they've got to contract again. So there's this nonstop contractility with an inadequate filling time, and that can actually drop your cardiac output. So again, think about these two situations here, where if you have a high heart rate, it reduces diastolic filling, and that can actually reduce your cardiac output.
And in this situation, it just directly does what? Because cardiac output is equal to heart rate times stroke volume. If you drop your heart rate, you will subsequently drop your cardiac output.
It's straightforward. The last one that kind of is a little just bit... different from all of these is that sometimes you can just have a complete valvular dysfunction. So there's a mechanical component of the heart that's having a problem. And this can happen when you have a massive, usually when you want your ventricles to contract, you want to push blood from the actual left ventricle up into the aorta and then out from the aorta to all the vessels.
But what if somebody has like an issue here where their valve in the aorta is not functioning and it's supposed to prevent backflow, but it's not and all the blood or a good chunk of blood that they push onto the aorta just comes right back down. The total volume of blood that we push out of the heart, is it actually going to be low or high or normal? It's going to be a lot lower because our heart was supposed to push it out and keep it out there, but it's just going to come right back down.
So all the blood will trickle back down into the heart and the cardiac output will drop. So in this situation, which we call acute aortic regurgitation, this would be a particular situation that can definitely cause cardiogenic shock. In the same way, you normally don't want blood to back up. from your actual left ventricle into your left atrium. But if you have somebody who has like a terrible like mitral valve that's just regurgitating all the blood, the blood is supposed to go here and out into the systemic circulation.
But if only some of it goes out there and a lot of it goes back into the atrium, then my total volume of blood that I'm pushing out of the heart with one heartbeat or within a minute timeframe is going to drop and that's gonna drop my cardiac output. And so this is what you would see with mitral regurgitation. Okay.
That would cover your cardiogenic and your hypovolemic shocks. Now let's talk about the other two, which is your obstructive and your distributive shock. All right, so the next one is obstructive shock. Now with obstructive shock, this one's a little bit interesting as well. So it's still the same kind of thing, like cardiogenic shock.
Except, okay, so we definitely have a reduction in cardiac output. And again, we know that reduction in cardiac output is dependent upon heart rate and stroke volume. Stroke volume is dependent upon preload, contractility, and afterload.
Now, in these patients with obstructive shock, they have a decreased cardiac output. But it's not due to the heart itself. It's either the vessels outside of the heart or structures around the heart that are actually causing a reduction in cardiac output. Let me explain.
So the way I like to remember this is if you want to think about cardiac output, you think about stroke volume and heart rate. If we think about stroke volume first, we know that stroke volume and afterload are inversely proportional. The higher afterload, the higher amount of work that the ventricles have to do to push blood out, the higher the afterload, the lower the stroke volume, the lower the cardiac output. So let's think about states in which the afterload is high that it's obstructing blood flow out of the heart, thereby reducing cardiac output.
Think about it on the right side of the heart and the left side of the heart. If someone has a big whopping PE, can you get blood out of the right side of the heart into the actual pulmonary vasculature and eventually into the systemic circulation? No.
So that's going to be one particular cause. That will definitely drop your actual cardiac output because you've got to... big whopping clot there that's blocking blood flow.
What about the left side? Maybe it's not a clot but this valve, the aortic valve, is actually supposed to be working well but it's not and it's so darn stenotic I can't get really any blood out of the left side of the heart. That would also reduce your cardiac output. So you want to think about a massive PE and you also want to think about a critical aortic stenosis as a potential cause here for an obstructive shock.
All right. What if it has nothing to do with the afterload? What if it's a reduction in venous return or diastolic filling?
Either way, a reduction in diastolic filling and a reduction in venous return drops what? Your preload. And if you drop preload, you drop stroke volume, that drops cardiac output. What could do that?
Well, what if you have like a big whopping pneumothorax? See all this space here? And now... Lungs just like pushing and squeezing on the heart and now the heart can't get any blood return from the superior vena cava and inferior vena cava into the right heart.
And all of this is just being squeezed. That's going to have a problem not getting any blood return to the heart. If I drop my preload, I drop my stroke volume and therefore my cardiac output. So a big whopping pneumothorax that is a tension type can actually be a potential cause. The other one is if I have a lot of fluid in this pericardial cavity, and it's squeezing and compressing on the heart and preventing it from filling with blood, am I going to be able to get a good preload into the heart?
No. So I get a reduction in preload, a reduction in stroke volume, and therefore a subsequent drop in cardiac output. And this is something that you would see in cardiac tamponade.
All right, my friends, we talked about all of these for obstructive shock. What about for distributive shock? So for distributive shock, the ultimate problem here is a little bit interesting. It has nothing to do with the actual true, like the cardiac output. It's actually something called systemic vascular resistance, or also known as total peripheral resistance.
It's the same thing. But in these patients, they have a reduction in their systemic vascular resistance. So here's where it's a little bit interesting. Remember there was a formula.
I've been kind of saying a lot of formulas out there. That you have what's called blood pressure is equal to cardiac output times systemic vascular resistance, and then cardiac output is equal to heart rate times stroke volume. So if you have a reduction in your actual systemic vascular resistance, that'll drop your blood pressure.
And so in distributive shocks, these are vasodilatory states. That's one of the words I want you to remember. It's a vasodilatory state.
The vessels are open, relaxed, and that drops your actual blood pressure. So what are the three types? They're septic, that's the most common, anaphylactic, and neurogenic. With septic shock, it's an infectious source.
There's a pathogen that's getting into the bloodstream and how can it get into it? Think about the ways where we have opening or orifices that actual pathogens can get into. Think about your respiratory tract.
So if you have a pneumonia, it can spread into the blood. If you have infective endocarditis, it can spread to the blood. If you have a gastroenteritis or a cholecystitis, that can get into the blood. If you have a pyelonephritis, that can get into the blood. If you have an osteomyelitis, that can get into the blood.
If you have a nasty cellulitis or abscess, that can get into the blood. And once these pathogens get into the bloodstream, what's the problem? The pathogens will interact with your immune system. And when they interact with your immune system, these bad boys will release tons of cytokines.
And these cytokines, like interleukins, will cause our vessels to just massively dilate. And if you massively dilate these vessels, what they do is they leak fluid and they significantly drop your systemic vascular resistance and drop your blood pressure. So you want to think about this and certain types of pathogens, most specifically your gram-negative pathogens.
But this could be other types of pathogens, viruses and fungi and different types of parasites, but most often it's bacteria and it's gram-negative. But that would be your septic shock, okay? The other one is anaphylactic.
Anaphylactic is you're exposed to some type of drug. You're exposed to, you get stung by a little bee, and that bee, you're super allergic to the bee, or you end up eating a peanut. And what happens is some of the molecules from these actual things, the drugs, the bee, or the peanuts, they interact. with these things called mass cells. And mass cells will respond to that allergen and release tons and tons of cytokines like histamines and bradykinins.
And what they'll do is they'll vasodilate and cause these vessels to relax and cause them to leak fluid and that'll drop your systemic vascular resistance. So think about these things. Neurogenic.
In neurogenic shock, there's some type of spinal cord damage or maybe even some type of actual brain damage, injury, whether it be a spinal cord injury, Whether it be from trauma, whether it be because you have some type of hemorrhage within the brain, there's some type of neurological injury. And what happens is, you know your sympathetic nervous system? There's a part of your spinal cord that goes and supplies the heart and supplies the blood vessels.
If you damage your spinal cord or the sympathetic outflow, are you going to be able to have sympathetic effect on the heart? No. What's the sympathetic effect on the heart rate? It's supposed to increase it.
You just lost it, my friend. So now your heart rate drops. Your sympathetic effect on your contractility is supposed to go up, but you just lost it, my friend. So now there's a reduction in contractility, which causes a reduction in stroke volume. What's cardiac output equal to?
Heart rate and stroke volume. You drop both these sons of guns, what do you drop totally? Your cardiac output, and that's going to drop your pressure.
The other thing is because it's supposed to cause constriction of the vessels, but you lose that, my friend. And now they start dilating. And if they dilate, what is that going to do? That's going to cause a drop in the systemic vascular resistance.
And that's going to drop your pressure. Because again, as you increase the diameter, there's less resistance to blood flow. This is the concept of the different types of shock, the pathophysiology, the causes.
Now let's go to the next part, which is what are the big features? What are the complications? What are the vitals that I need to know? Let's talk about that. Let's talk about the features and complications of shocks.
When we talk about these, we're going to get our clinical vignette. You'll see some of the causes that we talked about that may be popping up in the actual case stem. But when we look at their vitals, that's really going to be super important to cue you off to think that they're in shock.
So first thing, what will we see in their vitals? They're probably going to be hypotensive. That's not always the case. Sometimes people can actually have relatively normal systolic and diastolic blood pressures, what looks like it is. but they actually are in shock.
Now when we talk about low blood pressure we really should be careful because sometimes we base it off of like a low systolic blood pressure or a low diastolic blood pressure like oh there's systolic less than 100 the diastolic is less than 60. That's fine but I think what's really determines if a patient is actually in shock is their inadequate perfusion and the pressure that determines perfusion is actually more specifically called your MAP, your mean arterial pressure. That is actually your perfusion pressure. And so when we actually are talking if a person is in shock, we don't really base it completely off of their systolic and diastolic blood pressure, we base it off their MAP. If they have a low MAP, they likely have a low perfusion pressure and that's what we truly go off of.
And the way that you calculate MAP, it's really dependent upon both of these. So it's equal to the diastolic blood pressure plus one third of the pulse pressure, which is the difference between the systolic and the diastolic blood pressure. And usually we say whenever the MAP is less than 65 millimeters of mercury and kind of like a perfect world, this is considered to be low or inadequate to be able to perfuse the tissues. But I think usually in the actual case example, it's just going to be a low blood pressure like 70 over 50 or 80 over dead. So in one of those situations, it'll be pretty obvious.
The other thing is to look at the heart rate. So for the most part, the heart rate tends to be increased except for like a couple scenarios. So.
Sometimes in these patients their heart rate tends to be increased. What's the reason that their heart rate tends to be increased? And we'll talk about the exceptions of why it wouldn't be. Well whenever you have low blood pressure it triggers these different types of pressure receptors, the baroreceptors and the carotids and the aorta. They respond to that and they stimulate your nervous system and say hey the blood pressure is really low we got to try to increase it.
And your sympathetic nervous system increases in activity and tries to increase your actual heart rate. and your contractility if your heart will allow it. And so what will happen is you'll subsequently increase your heart rate. It's a compensatory response to the actual shock state. The times where they actually may not have a tachycardia is if they have neurogenic shock.
So I would think about this if the patient has a neurogenic shock because in neurogenic shock they lose the sympathetic tone to the heart. So that actually may be a cue to think about in these patients is they actually have a low heart rate. The other thing is sometimes patients may be on a beta blocker. That's another particular thing.
So I would actually take that into consideration. Is the patient on a beta blocker? Because sometimes beta blockers can actually reduce your heart rate and reduce your contractility.
And if you have an overdose, it can actually put you into a shock state. So sometimes if they're on some type of heart rate medication, so like a calcium channel blocker or a beta blocker or something of that nature. In those situations, it actually could potentially lower their heart rate. So look for those potentially in the clinical vignette.
But most of the time, low blood pressure and tachycardia. Okay, what about the other components like the respiratory rate and the templates? Come down for that.
All right, for the respiratory rate, it typically can be, it can vary. And what I'm actually, I'm not gonna give you a particular arrow here, but for the most part, the actual respiratory rate can vary from shock to shock. What really kind of may cue you off, and we'll talk about it a little bit later, is whenever you're not perfusing tissues very well, You're not giving them oxygen, so there's a reduction in oxygen delivery to the tissues. When you don't give oxygen to the tissues, they actually make something called lactic acid.
And sometimes we measure this in the form of what's called lactate. And lactic acid is actually a very acidic molecule that it can actually drop your pH. When you drop your pH, your actual body tries to compensate for that by breathing faster. And when you breathe faster, you increase your respiratory rate to try to blow off more CO2.
And so typically when patients get into a really nasty, shocky state, their acidosis can occur, they can increase their respiratory rate. So sometimes what you may see in these patients, especially if they are really, really acidotic from their actual like nasty, shocky state, is they can have an increase in their respiratory rate. Also other times if they have a lot of fluid that's actually accumulating within the lung tissue because fluid's backing up because their heart is failing, that can actually cause a change in the gas exchange process. So sometimes you may see an increase in respiratory rate and the true reason behind that is this acidotic state maybe from lactic acidosis.
Okay, what about the temp? The temp can actually potentially be variable as well, but I think one of the big things to think about for temp when it could be up when could the temp actually be up and actually make you think about the type of shock if the temperature was up you would be thinking about what kind of shock a septic shock my friends so if you think about a septic shock in these situations why because in a septic shock there's some type of pathogen the pathogen is stimulating your immune system your immune system is making all of these different types of cytokines that's telling your central nervous system that there's lots of inflammation and then your hypothalamus will increase the body temperature to be able to make it harder for the pathogen to be able to survive in that temperature. And that can trigger a fever.
So think about a high body temperature or a fever in patients who are septic. Alright, now let's move on to the other things like end-organ dysfunction and some very specific clinical features for each type of shock. Alright, so when we talk about the next part, which is end-organ dysfunction, this is because of inadequate perfusion. You've got a low MAP.
You're not perfusing the tissues. You're not giving oxygen and nutrients to those tissues. What are the organs that can become affected from this?
Well, the first one is the poor old brain. If you're not perfusing this poor old brain, you're not going to give oxygen to it. And if you can't get oxygen to the brain, you're not going to be able to think. If you can't think, you start to become confused.
You start to become delirious. You start to just be super altered. What if I don't deliver enough oxygen to the brain that the actual neurons start actually causing a stroke?
I could actually develop a stroke, potentially. And on top of that, sometimes if there's an abrupt drop in pressure whenever you maybe stand up, oh, I'm just going to syncopize. So these are things to think about if I'm not perfusing the brain. They can be really confused.
They can be altered. They can be delirious and they can potentially even have a stroke or syncopize. If I don't perfuse the liver, if I don't perfuse the poor old liver, it's going to get injured.
And I'm going to have a bump in a lot of my actual liver enzymes that actually can develop potentially a jaundice. I can actually have a lot of increase in AST and ALT and all those nasty liver enzymes can be bumped up. I don't want that, but that's what can happen. What if I don't perfuse the kidneys? Then I can't make urine.
And so I can actually have a drop in my urine output, oliguria, and to the point where maybe I don't even make any urine, anuria. And this can actually cause a massive increase in my BUN, my creatinine, all those waste products that I'm supposed to be getting rid of, my kidneys are supposed to be doing, but that doesn't happen. And then again, going back to the metabolic state, if I don't give oxygen and nutrients to the tissues, they need oxygen to be able to convert pyruvate into an acetyl-CoA. But if you don't have that, what do they start blasting out of the cells then? They start making tons of lactic acid.
And if you have lots of lactic acid, this can lead to a lactic acidosis. And we said that was one of the things that can happen with an increase in respiratory rate. because you're compensating.
All right, cool. So these are the potential organs that can be hit really hard during these situations. The other thing I think is really helpful, especially in the clinical vignette, is looking at the skin.
And the way that we can actually look at the skin is in two different ways. We can look for cold shock, cold extremities, pale, clammy, decreased capillary refill, a lot of those findings. And that could suggest a cold shock. Or they could be well perfused. They could be warm.
They could be pink or red. they could have good cap refill. In those situations it would be a warm shock. You know what's actually nice and easy?
Cold shocks are usually due to a reduction in cardiac output. So that would be all of your hypovolemic, your cardiogenic, and your obstructive shocks. So those types of shock you would see a cold shock.
You want to know why this actually happens? When you have a drop in blood pressure, okay, a drop in blood pressure what happens is you stimulate the actual baroreceptors. The bare receptors tell your sympathetic nervous system that the actual blood pressure is low and what it does it tries to go to the heart to increase the actual heart rate and contractility but in these patients who have hypovolemic or cardiogenic or obstructive shock it doesn't work because the heart's not actually going to pump because they have a problem where they don't have volume or there's some kind of issue with their heart or something squeezing on the heart either way the heart's not going to be working well and so the heart doesn't actually allow for that and so what happens is they end up with a lot of you stimulation to the actual vessels and then the vessels just clamp down like crazy and this tries to increase your systemic vascular resistance to increase your blood pressure because we know that if you increase resistance you increase pressure we got that formula from there and then if I don't actually have a lot of squeeze the vessels near my skin then they get pale they get cold they get clammy if I don't actually perfuse the actual the fingers they actually may have a decreased capillary refill so you get the point you see cold shocks with reduced cardiac output states, hypovolemic, cardiogenic, obstructive shocks.
Warm shocks are due to distributive shocks, anaphylactic shock, septic shock, neurogenic shocks. Now why? And these patients, remember I told you, think about the trigger. There's some type of septic process that's causing inflammation, or there's a lot of allergens that are causing mast cells to release mediators that cause inflammation, or there is a loss of neurogenic tone to the vessels. And all that happens from all those situations is all the vessels start dilating and relaxing.
And all those distributive states, remember it's a vasodilatory state, what does that do to the systemic vascular resistance? Huh? It drops your systemic vascular resistance because now there's like no resistance to blood flow. They're all plump and large and they're going to have a lot of blood flow going to the skin and a lot of blood flow going to the nail bed.
So that's why they have good warm, they have not normal pink or reddish type of huge skin and they have good capillary refill. This is what you would see in a septic and anaphylactic or a neurogenic shock. That covers that part. Now what are some potential features that can cue you off in the question sim to think about? A specific type of shock, let's talk about that.
All right, so for hypovolemic shock, what would be some cues within the question stem? Remember, we already said that we have a lot of ideas of potentially their vitals. We have some of the end organ dysfunction and what's happening with the cold and warm shocks.
With hypovolemic shock, look for really dry, like they're dry. They're going to be intravascularly dry. And so sometimes their mucous membranes, like the eyes, the mouth, a lot of those things, they'll have decreased skin turgor, they'll have drier mucous membranes.
Those are particular things to be looking at. for in these patients. Okay, and pale.
All right, for obstructive shock, what could be some potential things to think about? Well, we talked about if it's like a tension pneumothorax. Well, if they have a tension pneumothorax, you're not going to hear any breath sounds on the one side where the pneumothorax is.
And the trachea will be deviated to the opposite side because the pressure is pushing it to one side. If they have cardiac tamponade, you're listening to their heart, what are you going to have? Very distant or decreased heart sounds that you're actually not going to be able to hear very well because there's all that fluid muffling it up.
And then both of them typically they'll have like a pump, plump jugular vein because all the pressure inside of their actual intrathoracic cavity is high and it's transmitting up into the actual supraveneceva and jugular vein. That's things to think about. For septic shock, in septic shock it's really interesting. So with these nasty little pathogens, you know what they can do?
They stimulate your immune system and your immune system can actually cause lots of inflammatory mediators, lots of different cytokines. And what they can do is they actually can stimulate the activity of different types of... Procoagulants like tissue factor and thromboplastin and cause you to have clots that form.
So then you form a bunch of tiny little clots all over the place and you consume all your clotting factors, you consume all your platelets and then guess what? You end up with a ton of microthrombi but then when you need to be able to clot, you've consumed them and now you start to bleed. This is called DIC. It's a nasty complication that you can see where they bleed a lot and they have tons of microthrombi and sepsis. The other thing is this massive inflammation.
can actually cause the lungs to get so inflamed, bilateral inflammation of the lungs can lead to ARDS. And that's another nasty complication to think about in septic shock. Anaphylactic shock, look for a rash.
So if they have some type of exposure to an allergen, maybe they have like some hives, or they have some wheels, or some type of nasty rash, listen to their lungs. Maybe they have nasty wheezing because you're bronchoconstriction there. Or they have a lot of like stridor of the upper airway because you're inflaming their larynx. Listen for wheezing, listen for bronchospasm, listen for stridor, and look for any obvious rash. For neurogenic, think about this, my friends.
If you have spinal cord injury, when you tap their actual tendons, it's supposed to send signals to their spinal cord and back to the muscles. If you have injury to the spinal cord, will you be able to respond to that? No.
And so the deep tendon reflexes will be decreased or completely absent. That may be a cue in your actual patient there. And lastly for cardiogenic shock, if they just had a massive MI they may have chest pain.
If they have a heart failure they may have jugular venous distension, a lot of lower extremity edema. And if a lot of fluid is backing up into the lungs because they're in heart failure they may have pulmonary edema. You get the point.
Now what we're going to do is, we're going to go ahead and we're going to be crazy and talk about what happens whenever you want to measure these different hemodynamic parameters from utilizing what's called a Swann-Gons catheter. or pulmonary artery catheter, and we get all these different measurements, and this is very, very important for your actual USMLEs. We're going to talk about how you differentiate these, and then a little additional diagnostic test to help you out.
Let's go. All right, so let's talk about the hemodynamic parameters in these different types of shocks. So when we talk about these, we can put in what's called a Swann's-Gans catheter, kind of go through the IJ, you run it down the right atrium, right ventricle, and up into a pulmonary artery and kind of inflate the balloon. And then what can happen is you can utilize this to be able to give you particular types of measurements that may help and aid.
and determining which type of shock you have. So, when we talk about these, let's go over them with the four types of shock. Hypovolemic shock first.
In these patients, let's talk about central venous pressure. This tells you about your right-sided preload. So preload is actually dependent upon volume, right?
In this kind of situation, we would expect that their venous return is a lot lower, so their preload is going to be a lot lower. So we would expect their central venous pressure to be low. Yeah, they're not filling their heart as well, right? So there's a reduction in their central venous pressure. The pulmonary capillary wedge pressure is dependent upon the actual left-sided preload and some of the left-sided pressures.
And these patients, they're not going to be adequately filling their left side of the heart as well because they're having a reduction in their preload because of a bulge. loss. So their pulmonary capillary wedge pressure is going to be lower, which is again, indication of their left side of pressures.
The next thing is their cardiac index. That's dependent upon their cardiac output. So what's their cardiac output? Well, cardiac output's dependent upon heart rate and stroke volume. And patients who have hypovolemic shock, what's their issue?
A preload problem. A reduction in preload leads to reduction in stroke volume, which leads to reduction in cardiac output. So cardiac index should be low. The next thing is the systemic vascular resistance.
Again, we can base that on what's called the actual cold or warm shocks. But think about this, what's the compensatory response in a patient who has hypovolemic shock? They drop their pressure.
When they drop their pressure, stimulates baroreceptors, causes the sympathetic nervous system to try to squeeze the vessels. So what happens to the resistance? It goes up.
And so in these patients, they'll have a high systemic vascular resistance. The next thing is what's called the SVO2 or the mixed venous oxygen saturation. So this is dependent upon two things. It's dependent upon the cardiac output and it's dependent upon the actual state of flow or the oxygen extraction by the...
tissues. So it's dependent upon two things, cardiac output and it's also dependent upon tissue extract, the oxygen extraction from the tissues. So in a patient who has a low cardiac output, their SVO2 will actually be what?
Well think about it. If you have a low cardiac output, it's going to take a longer time for the blood to actually transit across this area from the artery to the venous side where gas exchange occurs. If it takes a longer time because of a low cardiac output That means that these tissues can extract as much oxygen as possible within that slow time period.
And when they take the actual, the oxygen, the blood back to the right side of the heart to sample it and you suck off the oxygen from that area, it's probably going to be pretty stinking low because your cardiac output was so low. So the tissues had an adequate amount of time to be able to yank the oxygen from the blood and utilize that. And so you would see that there is a low SVO2. Okay. Next one, obstructive shock.
In obstructive shock, think about the central venous pressures. So in these situations, there is something that's actually, think about again, a pulmonary embolism, the pressure on the right side of the heart is going to be higher because the afterload is higher. If you think about a patient who has some type of like tension pneumothorax, it's squeezing on the actual right side of the heart, so the pressures are going to be higher.
And if you have like a cardiac tamponade, squeezing on the right side of the heart, and that's going to cause the pressures in those cavities to increase. And so central venous pressure for all of these kinds of situations will be what? Increased.
The next thing is if you move on to pulmonary capillary wedge pressure. This is dependent upon the left-sided pressures. So left-sided preload and just generally left-sided pressures. In these situations for both a tension pneumothorax, for a pulmonary embolism, in those situations the pulmonary capillary wedge pressure tends to be low. So the pulmonary capillary wedge pressure tends to be low.
The only time where I would actually urge you to potentially remember that it could be high in the clinical vignette is in cardiac tamponade. Because cardiac tamponade can squeeze. On the entire heart, especially the left side of the heart, especially the left atrium, it can actually increase the left side of pressures and cause fluid to back up into the heart and cause a little bit of pulmonary edema sometimes. And so we can potentially see an increased pulmonary capillary wedge pressure in cardiac tamponade as a potential exception.
Cardiac index, that's dependent upon cardiac output. In these states, there's either a high afterload or there is a reduction in venous return or preload, okay, in both of them because of a PE, a critical aortic stenosis. tension pneumothorax or a cardiac tamponade.
There's a reduction in preload or there's an increase in afterload. In both of those situations you drop stroke volume and therefore subsequently drop cardiac output. So cardiac index should be lower. When you drop your blood pressure you compensatorily like respond by vasoconstricting your blood vessels and so if they constrict the resistance should go up. Mixed venous oxygen saturation is dependent upon cardiac output.
In these patients their cardiac output is low. If it's low, that means the transit time from the artery to the venous side where oxygen can actually be extracted is going to be a lot longer time now. So when the blood goes back up to the right side of the heart and you sample off the oxygen, would you expect it to be low or high? It's going to be low because you had plenty of time to be able to extract it. All right, cardiogenic shock.
We think about this one. Think about it simply like this. This is how I like to remember it. Usually your heart is impaired. It's not pumping.
It's not able to get blood out of the heart properly. If it can't get blood out of the heart properly, that means that the pressures in both the right side of the heart and the pressures in both the left side of the heart are going to be high because you can't get blood out of it. And so what would you expect the central venous pressure and the pulmonary capillary wedge pressure to be in these?
You would expect them to be high because you can't get blood out of the heart. Think about the cardiac index. It's dependent upon cardiac output. And these patients who have either too fast of a heart rate, too slow of a heart rate, or their contractility stinks, they're not able to get blood out of the heart.
Their cardiac output is going to drop and therefore their cardiac index will be Low. When you compensatory respond to a drop in blood pressure, what do you do? You cause your vessels to vasoconstrict heavily.
constrict your resistance goes up and this causes that cold type of shock. SVO2 in these patients again SVO2 is dependent upon cardiac output and oxygen extraction time. So in these patients they have a low cardiac output the transit time from the artery to the venous side is going to be prolonged because of that low cardiac output plenty of time to be able to extract oxygen by the time the actual blood gets back to the right side of the heart you sample it what do you think the SVO2 is going to be it's going to be low.
Alright. That would cover this one. Now, distributive shock.
Again, distributive shock is the patient is vasodilatory. Their vasodilatory, their systemic vascular resistance is actually going to be very low. So because of this, think about this very simply for central venous pressure.
If the vessels are vasodilatory, so you have a dilated like inferior, like vessels that are supposed to feed the inferior vena cava. Normally, the venous system is very low pressure. So if you actually have this thing dilate, the pressure is going to even be lower in the venous system.
So the return of blood to the actual right side of the heart is going to be lower because you're so dilated or you know what else happens in a septic shock or distributive shock state? You leak lots of fluid out into the vasculature. So a lot of fluid leaks out into the vasculature in these situations and so there's less actual fluid in the vasculature. So the return of volume back to the right side of the heart is sometimes reduced. So we say that they have a reduction in their preload in these states.
And this will be a low CVP. And same thing, because they have a low volume of blood, like an actual intravascular, because they're leaking a lot of that fluid out into the actual interstitial spaces, especially in septic and anaphylactic shock, the total volume of blood in the right side of the heart and left side of the heart will be low. So their pulmonary capillary wedge pressure will be low.
Good. Now, what did I tell you is a compensatory response? When you have a...
vasodilatory state, okay, your blood pressure drops. When your blood pressure drops, your sympathetic nervous system responds to a drop in blood pressure by doing what? Trying to either squeeze the vessels.
In these situations, their vessels are so dilated they're not going to respond to a try to increase in squeeze. That's not going to work. So what's the other thing that they can actually do, the sympathetic nervous system can do?
So again, whenever you have a drop in BP, what does your actual sympathetic nervous system do? Your sympathetic nervous system can either try to Increase systemic vascular resistance or it can increase heart rate or increase your stroke volume by trying to cause your heart to pound more, contract more, squeeze more blood out of the heart. So what do you think is going to happen to their cardiac index?
It's going to be banging through the roof because they're trying to pump as much blood out of their heart so they can actually increase their blood pressure. That's their response. That's their compensatory response.
But we know that they're vasodilatory. So it's the exact opposite. In all of these states they have a low cardiac output causing their SVR to go up. In these distributive shocks, their SVR is actually going to be what? Low, causing their cardiac output to actually go up and their heart rate to go up.
I hope that makes sense. Now, think about this now. If their cardiac output is high, they are pumping blood.
Their circulation is hyperdynamic. They are pumping blood from the artery to the venous side so fast. that the time that you actually have to be able to release any oxygen to the tissues is reduced. So because of that, this is happening very fast. There's a lot of shunting and movement of blood from the arterial side to the venous side because these vessels are dilated and you're just moving them across.
The oxygen extraction time is going to be a lot lower. What do you think when actually you get blood back to the right side of the heart? What do you think the oxygen concentration is going to be? It's going to be higher. And it's going to be higher because you had a hyperdynamic circulation because your cardiac output's higher.
and you're not having an adequate time during the transit to drop off oxygen. There's one exception I want you to remember for distributive shock, just being a little picky here. When you actually think about these, the best example is usually like your septic shock and your anaphylactic shock for these.
For neurogenic shock, it's a teensy bit different. And what I want you to remember here is in neurogenic shock there's actually a loss of sympathetic flow, right, to the actual heart. So there's a reduction in heart rate and there's a reduction in stroke volume or the cardiac output component.
So because of that, they actually have a total drop in their cardiac output because their sympathetic flow is actually shut down because of a spinal cord injury. If that's the case, then their cardiac index would actually be what? Would it be actually high? No.
In this situation, it would actually be different. It would actually be low. If their cardiac index is low, meaning their cardiac output is actually low, the time between transit, even though they're vasodilated. Because the actual transit time between here is slower because of a lower cardiac output, what's going to happen to the actual oxygen extraction time?
It may be a little bit longer than the usual distributive shock and septic and anaphylactic. So because of that, they're actually going to have a lot less time to be able to pull oxygen off and so the SVO2 when you come back up actually will be... What? It'll be lower because they're going to have more time in comparison to this one where it's just shunting across because they're super hyperdynamic. So that's the big differences here.
The last thing I want you to remember is you don't have to go too crazy on this and remembering this for your exam. I just think it helps you. present these on the exam, whenever you think about the diagnostic test, you can use a CBC to help you determine kind of some of the shocks. If they have a super high white count, you can think about septic shock. Look at your end organ dysfunction.
So if their actual kidneys are injured. they'll have an increase in their bu and creatinine. If their liver's injured, they'll have an increase in their LFTs. If you check an EKG, look to see if they have any ST segment elevation like an MI or an arrhythmia, they're beating an AFib. Look for troponins, evidence of injury.
Look for a chest x-ray for a tension pneumothorax. Look at an echo for any kind of wall motion abnormalities, heart failure, cardiac tamponade. Get your cultures, your urinalysis to look for signs of an infection.
And then a lactate to show you again another sign of potential end organ dysfunction. Alright, let's talk about treatment now. Alright, so when we talk about the treatment of these different types of shock, we got hypovolemic shock. It's simple.
You're either losing plasma volume from those GI, skin, or urinary types of losses. In those situations, give them back the volume. Give them IV fluids. If they can't take PO fluids, it's great.
If they're losing blood from a hemorrhagic blood loss, give them blood back. It's simple as that. That's going to increase their blood volume that way. But ultimately, you got to treat the cause.
Figure out what the cause is and treat that. All right, next thing, cardiogenic shock. It's a simple thing. They have a reduction in their cardiac output, usually because of a what?
A reduction in contractility or their massively high heart rate or a massively slow heart rate. or there's a valvular dysfunction, obviously you got to treat the underlying cause. That's the most important.
If they get an MI, get them to PCI, get a cath. If they're going too fast in their heart rate, you got to cardiovert them. If they're going too slow, then you got to put in a pacemaker.
If they have an acute aortic or mitral regurg, you got to fix those and give them valve replacements. But the thing that you can do in the interim when they're hypotensive and near dead is support their blood pressure and their perfusion, right? So how do I do that?
Get the heart to squeeze more. How do I get the heart to squeeze more? I can give them inotropic agents such as dobutamine.
Milrinone, those are really good ones because they squeeze the heart and they actually relax the vessels. Whereas epinephrine and norepinephrine, they actually contract the heart and squeeze the vessels. So those are things to think about. And if these fail in a patient, you can potentially consider an intra-aortic balloon pump to actually support their cardiac output.
That would be for cardiogenic shock. For obstructive shock, we have to figure out the cause. You can support their blood pressure with, you know, giving them norepinephrine or epinephrine if you need to, but I think in the ultimate end game, you have to treat the cause or there's no way that these people will survive. PE, give them something to break up the clot, heparin, TPA, embolectomy.
If they got a big whopping pneumothorax, stick a needle in there, needle decompress them, put in a chest tube and support their hypoxia with oxygen in the anterum. If they have a critical aortic stenosis where literally no blood is getting out, get an aortic valve replacement. And then if they have a big whopping fluid accumulation that's causing tamponade in their pericardium, do a pericardiocentesis.
And if you need to, put a drain in. But that's how we fix that one. For the next one, septic shock. Septic shock, you got to remember what's the end problem here. Their problem is their systemic vascular resistance is super low.
They're vasodilatory. Get their vessels to constrict. Do the opposite. So give them norepinephrine, give them epinephrine to squeeze the vessels and support their blood pressure but treat the cause. It's an infection.
Give them IV antibiotics. And sometimes because their central venous pressures are a little bit low, you can give them fluid to help to be able to increase their actual, their venous return. And if you increase their venous return, their preload, you can increase their cardiac output and maybe their blood pressure.
So I think pressors to squeeze the vessels, fluids to help to fill up the vessels. and then antibiotics to kill the actual bugs or the pathogens. All right, let's come down and talk about anaphylactic and neurogenic. All right, so for anaphylactic shock, again, you got to figure out what the cause is. They're exposed to some type of nasty allergen.
If it's a drug, get rid of the drug. If it's some type of actual like bee sting, obviously try to avoid those. And there's a lot of things that you can do to avoid those particular things.
But in the interim, when there are actual airways like closing up, you need to be able to try to relax those airways. How can I do that? Well, I want to shut down the histamine and inflammatory response. So I can give them things to reduce the histamine response. and shut down the mast cells.
Antihistamines. I can give them steroids. But to actually relax and dilate those airways or actually allow for bronchodilation so you can actually get airflow, give them something like epinephrine.
Typically, it's going to be an IM like injection, but sometimes you can actually give it IV if you absolutely need to. And then because, remember, in these actual situations where there's massive inflammation, the vessels do what? They dilate.
What does that do to the resistance? It drops it. What do you got to do? Do the opposite. Get the resistance to go.
go up so get them to constrict and usually the IM epi will help that but if you need to support blood pressure you can give IV epinephrine and sometimes norepinephrine. Last one is neurogenic shock again in this situation you got to treat the cause so figure out what the actual spinal cord injury is and if you can actually reverse it if not then you have to support them in the ways that you need to which is their systemic vascular resistance is low because they're vasodilatory give them something to squeeze the vessels norepinephrine epinephrine and because their heart rate can actually be low because you take their sympathetic tone away and they have bradycardia, give them something to increase their heart rate, such as atropine or epinephrine. All right, we talked about all the types of shock. You know what we got to do now? We got to put all this stuff to practice, go through some case studies, and really understand shock.
So let's do some practice problems. All right, guys, first case, let's do some practice. All right, so we got a 26-year-old female, massive vomiting diarrhea after eating some old potato salads and baking in the sun.
So what kind of causes do you think that would actually suggest a type of shock here? I see some volume loss. I thought the only thing I see that's super obvious is that there's volume loss, potentially from vomiting and diarrhea. Could be a hypovolemic shock, potentially.
All right, let's move on to the features and the complications. Anything within their vitals that definitely suggests potential signs of like a shock? All right, definitely hypotensive. So 88 over 40 is pretty low blood pressure.
Again, we would actually want to calculate the map, but that would actually potentially correlate with low MAP. So they're hypotensive. Heart rate's 120. They're tachycardic.
Most of the patients are tachycardic because they have a compensatory response. So that's good. Respiratory rate 18. All right.
So they're not super tachypneic. Again, maybe not as acidotic as usual, or there's not like an underlying lung process there. SpO2 98%.
They're not hypoxemic. Again, kind of throwing off a less likely like a lung process or fluid backup. Temp is low grade, not like super rip roaring like fever, but it's a low grade.
Again, can't completely rule out like an early kind of sepsis. All right. But I think it looks like hypovolemic, maybe like a septic picture, tough to determine right away. But when we look at their actual physical exam findings.
Do we see any like end organ dysfunction, cold, warm shock? What do we see there? All right. So for this, I see pallor, potentially like some cold, cool, pale extremities, clammy extremities.
So that makes me think of a cold shock. I also see decreased capillary refill or delayed capillary refill. Again, cold kind of shock.
The next thing I want to look at is any kind of like evidence of like specific characteristics for a type of shock. I see dry mucous membranes and decreased skin turgor and a decreased urine output. Well, the dry mucous membranes and the decreased skin turgor makes me think about like a hypovolemic type of problem, potentially. And the decreased urine output, now it maybe tells me that there's some end organ dysfunction. I'm not perfusing the kidneys very well.
And they may be trailing off on that urine output. All right, cool. So I have a thought process potentially of what kind of shock. But let me go into my actual tests.
When I move on to the tests here, I definitely want to think about a CBC. Is there any elevated white count? Normal. Okay, kind of makes me think less about sepsis, but still can have that potentially.
Buen creatinine, it's elevated. Telling me that that was the end organ dysfunction because I'm not perfusing those kidneys. I got a bump on my actual creatinine.
and BUN. So there's an AKI. EKG, is there anything to suggest a cardiogenic problem here?
When I look here, I see it's fast. So it looks like I'm going a little bit faster. So there's a tachycardia here, definitely. And it looks regular, regular rhythm.
It looks like a narrow QRS complex. So I think about sinus tachycardia potentially. Look in your lead two, upright in lead two, inverted in AVR, and every P for a QRS and a T, this looks like normal sinus rhythm.
So likely a sinus tachycardia, no ST elevation depression. or T-wave inversion. So I don't think that there's any kind of like cardiogenic problem where there's an MI or anything or AFib or anything like that. So I think a sinus tach.
Let's check the tropes to make sure there's not kind of like an underlying like myocardial damage. And there is not. All right.
Chest x-ray. Do we have any tension pneumothorax? No. Good.
All right. Echo. Do we see any evidence of like a decreased heart function, like an EF?
Do we see any kind of like cardiac tamponade or maybe like a wall motion abnormality like from an MI? Nope. Normal.
Okay, good. Urinalysis and any kind of culture to test for any kind of infectious sources? All normal.
Good. Okay. Now unlikely sepsis. So lactate, then we're going to look at that to see if there's any end organ dysfunction.
There is a little bit more end organ dysfunction, not perfusing tissues as well. So there's a little bit of a bump in the lactate. I definitely think this is hypovolemic because I kind of ruled out a cardiogenic and obstructive, a septic, unlikely anaphylactic or neurogenic as well. So from there, I'm going to go ahead and just say, I think this is likely hypovolemic shock.
And I think it's from the GI losses. Cause if you go back to your differentials, It was a volume loss or a blood loss, whether it was hemorrhagic or non-hemorrhagic. So GI losses were one, skin losses were another one, and kidney losses were the other one. Or you're losing blood.
In this case, there was no evidence of blood loss. I think it was all from the GI losses that was the cause here. If we were to move to the next step and we put a swan in this patient, and we were to measure these different types of parameters here, what could I tell myself about these?
Well, what I could say is I could guess my hemodynamic parameters. Well, CBP, there's a low preload. It's got to be low.
Pulmonary capillary wedge pressure. There's going to be low preload to the left side. That's going to be low cardiac index. Low preload means low stroke volume, means low cardiac output, means low cardiac index.
And systemic vascular resistance, what's their compensatory response to a low cardiac output? They vasoconstrict, so their systemic vascular resistance should be up. Man, you guys are good.
All right, let's move on to the next thing. Treat these people. What's the problem?
Well, they're losing volume, not blood, so give them IV fluids. And then again, treat the underlying cause. What's the cause? It's the gastroenteritis.
So that's what we're going to do. And we did it. Case two.
An 85-year-old male presents with chest pain, shortness of breath. Past medical history is pertinent. They have a history of AFib. They have hypertension. They have hyperlipidemia.
They did have an MI, and they have a history of underlying coronary artery disease, but they had a stent placed about six months ago for an MI. Okay. There's definitely some potential concerns there for a cardiogenic problem, no doubt about it.
So I definitely have a high degree of cardiogenic cause here in my head, but let's keep moving forward. Look at their vitals. What do we see here? We see potential signs of shock, right? Hypotensive, probably a low MAP, low perfusion pressure.
Look at their heart rate. Holy crap, that's pretty fast. 182, so they're tachycardic. That could be compensatory or that could be the cause of their cardiogenic shock.
Remember, super, super fast heart rates can actually lower diastolic filling. Something to think about. They are tachypneic. They're greater than 20. So it makes me think about, is there anything like edema or lung process going on here? SpO2 is low.
So is there any kind of edema, lung process going on? And then temp's good. So it makes me kind of think less likely about a potential septic source. Then I look at their extremities.
They're cold, cool, clammy. It makes me think about a cold shock. And then they also got some crackles on the lungs.
So there's definitely probably a little bit of fluid in the lungs. Probably from a cardiogenic source. Okay, when we move on to the test, what do we got to do?
Get our CBC. It's normal. Unlikely any kind of elevated white count, so I'm kind of low on the end of sepsis. Buen creatinine, it's bumped.
I'm not perfusing that kidney as well, so there's probably some decrease here in output, or at least beginning that process. EKG, do I have any signs of ischemia or infarction? Oh my gosh, look here. V1, V2, V3, and V4 all have ST segment elevation with hyperacute T waves.
So this is likely a very massive anterior infarct. And if you look at the rhythm, it's irregular, it's narrow complex, and I don't really see any actual P waves. and lead to or an AVR.
So I know that this is not sinus rhythm. It's likely an AFib with RVR and they're having a massive MI. So that's a problematic issue here because that's probably two of the reasons why they're in cardiogenic shock is their heart rate's going too fast.
They're not getting good diastolic filling and they have a massive MI. So their contractility is down. Boom. All right. Troponins.
I probably expect these to be elevated because they had a big MI. Probably an instant thrombosis is probably what happened here. They probably clotted up that stent that they got placed.
Chest x-ray. Do I see any kind of like... Pulmonary edema, any lung process going on here? Looks a little hazy there. So I definitely think that there's probably a little bit of pulmonary edema.
And that's why they probably have a little bit of increased pulmonary capillary wedge pressure, right? So they have a little bit of pulmonary edema, and it's probably from the fluid backing up because their heart's not working as well. Okay, echo. I'd probably see like maybe a decreased EF or potentially like a wall motion abnormality that's not contracting very well. And that's definitely kind of correlates LED territory with V1 to V4.
That's the area supplied by the LED. Urinalysis cultures disembryoled at a septic source. normal, good.
Lactate to see if I'm actually perfusing my tissues very well. Oh, that's bump. So I'm not perfusing the tissues very well.
And there's a bump in the lactate. All right. So inadequate perfusion to the tissues there. All right.
So what do I think that this is? I think it's again, cardiogenic shock. And I think it's due to a massive MI, but I don't think that the AFib with the RVR is helping at all.
And I think that also could be a potential source of their cardiogenic shock. So when you think about the differential of these, again, you got to think, is it a myocardial problem? So cardiomyopathic, do they have a massive MI? Are they in heart failure?
Do they have like a massive inflammation of their... myocardium, or is it a tachycardic or bradycardic cause? And again, they're a mechanical source. So was there a recent trauma or big one?
Was there a valvular dysfunction like a mitral regurgitation or aortic regurgitation here? And I think what fits best is the massive MI and the AFib with RVR for this patient. All right, cool. We get that swan in.
We go ahead and guess their particular hemodynamic parameters. Because the heart stinks, it's not being able to get blood out of the left side of the heart and the right side of the heart. What do you think the CVP and the pulmonary capillary wedge pressure will be? It'll be up.
All right, cardiac index. Their cardiac output probably stinks because they're not getting actually a good cardiac output because their contractility is down or they're having an inadequate diastolic filling. So their cardiac output's dropped.
Cardiac index should drop. What's the compensatory response to a decrease in cardiac output for the cold shocks? They squeeze their vessels. So their resistance is going to go up.
All right, we got cardiogenic shock. How are we going to treat these patients? You have to treat the underlying cause. If they're an AFib and they're hypotensive, they're unstable. You might have to shock them.
So you probably got to cardiovert them for the AFib. Then they also have an MI. So you got to get them to the cath lab to be able to remove that massive cloth that's probably new within that stent that they just had six months ago. But in the interim, before they actually die and become like completely hypotensive that they cardiac arrest, you got to support their blood pressure.
So you got to squeeze that heart. So give them some inotropes like dobutamine, milrinone, maybe even some norepinephrine or epinephrine to actually get them to squeeze the vessels a little bit too so they don't drop their pressure. And then, again, get them to the cath lab so that you can actually remove that clot within that vessel.
All right, man. You guys are good. All right.
Case three, 34-year-old male presents with pleuritic chest pain, severe shortness of breath after falling off a ladder on his left side. No pertinent past medical history. All right, so fell. There's some trauma.
Trauma, it's tough to be able to say. He could potentially have loss. He could be bleeding internally, so it could be like a hypovolemic, like hemorrhagic source, or he could have had like a tension pneumo or a cardiac tamponade, so it could even be like an obstructive shock from this one.
So it's tough to say right off the get-go. Let's look at their vitals. Hypotensive, okay? We see some evidence potentially of shock, probably a low MAP. They're tachycardic, probably a compensatory response here.
Respiratory rate is 28. Makes me think that there's either a lung process or some type of like edema within the lungs. SpO2 is 88%. Makes me think about a lung process or edema within the lungs.
Temp is normal, so it makes me kind of like unlikely to be a septic source. Okay, look at their physical exam. If we added on here that I said that there was cold, cool, clammy extremities, you would think that this is a cold shock.
They're not perfusing their tissues as well. But one of the big things is that you have a big plumping jugular vein. Their trachea is deviated to the actual right, so opposite of where on the side that they fell, which is the left side, and they have absent breath sounds on the left side.
Makes me think about A, obstructive source, potentially A. Tension pneumothorax. I definitely think this is an obstructive shock with likely the secondary to attention pneumothorax But let's go through the lab CBC is normal because again, there's gonna be no infectious source here bu and creatinine It's normal.
We didn't actually have any drop off in the pressure that we haven't perfused the kidneys inadequately just yet over time Maybe EKG look for any evidence here of anything concerning. I think it's a regular rate I had actually I'm sorry a little bit of a fast rate here. Sorry, and I'd say if you look at the rhythm, it's narrow You'd also see that it's a regular rhythm. So I would actually say that this is a narrow QRS complex regular rhythm, so I'd say this is a normal sinus rhythm but I would actually consider it's a normal sinus rhythm because there's an upright P wave in lead 2 and There's an inverted P wave in AVR and then every P wave is followed by QRS by T So it's normal sinus rhythm, but because it's a narrow complex tachycardia. It's likely a sinus tachycardia, but likely compensatory Okay tropes.
Is there any myocardial damage? No Chest x-ray, is there any kind of pneumothorax or pulmonary edema? Oh my gosh, look, there it is.
Tension pneumothorax, likely the cause there. So we've done diagnosis, so we can obviously go on to the next part here. Echo, is there any cardiac tamponade or myocardial dysfunction?
That's normal. Urinalysis cultures in the antiseptic source here. Nope. Lactate, is it bumped?
It's actually normal. We didn't actually have enough end-organ dysfunction yet to cause a massive acidosis. Okay, tension pneumothorax is our diagnosis, so it's definitely an obstructive shock, secondary to a tension pneumothorax.
What's the differentials though for those? Think about, again, pulmonary vasculature. So the right side increased afterload, PE.
Left-sided afterload, if you really, really add this one on, critical aortic stenosis. And then think about, again, your decreased diastolic filling or your significant reduction of venous return, such as attention pneumo or cardiac tamponade. All right, how do we treat?
Oh, actually, sorry, before we go into treatment, get the swan in for these patients. You measure these different parameters. What do you think?
All right, because in these patients, the pressure inside of the heart is actually going to be high because, again, think about you're either Pulmonary embolism, you're having pressure on the right side increase, or because you have a tension pneumo, you're squeezing on the right side of the heart. Cardiac tamponade, you're squeezing on the right side of the heart. The pressures are going to be up on the right side of the heart.
Pulmonary capillary wedge pressure for most of the actual obstructive shocks, except for one, cardiac tamponade. All of them for these situations, usually the pulmonary capillary wedge pressure is low, except for cardiac tamponade, it's elevated. So in this one, it's actually going to be low. Cardiac index, we're reducing venous return in this patient. So we're reducing preload, reducing cardiac output.
Cardiac index should be low. What's your compensatory response to a drop in cardiac output? Squeeze the vessels in cold shock.
It's going to be up. How do we treat them? Stick a needle in there to decompress that air in that area.
Put a chest tube in and give them oxygen to support their hypoxemia in the interim. All right, move on. Next patient, 64-year-old female. Severe fatigue, cough, shortness of breath, sputum production, new onset confusion. Confusion.
That's interesting. What could be a sign of confusion? Confusion or altered mental status, maybe inadequate perfusion to the brain. So there may be actually some end-organ dysfunction.
because we're not perfusing the brain. But again, that's one of the potential features, clinical features, that actually can be important to think about. But then if we look here at this here, severe fatigue, cough, shortness of breath, and sputum production, I'm thinking about potentially an infectious problem here.
And so because I'm thinking about an infectious problem here, that's really important in this situation. I'm kind of leaning towards the septic shock kind of state. All right, let's look at the vitals.
What do we got? BP low, 60 over 32, so they're hypotensive. Tachycardia, 131, all right, compensatory.
Respiratory rate is really high, 34. So they're super tachypneic. So it makes me think that there's either an acidosis, like lactic acidosis, or there's a respiratory process or edema going on here. SpO2, 89%.
So maybe there's a respiratory process going on here as well. And then temp 39.2. So they have a really high temp here, making me definitely think that there's like a septic source here, triggering the hypothalamus to cause an increased body temperature. When I look at their extremities, they're warm. They're well perfused.
They're actually nice and pinkish hue, good cap refill. So it makes me think about a warm shock. So a distributive type of shock definitely kind of fits the septic picture. And then ronchi slash rails on auscultation. So they sound a little bit junky in the lungs.
Makes me think about pneumonia as a potential source for this patient. And then they have septic shock because of the pneumonia. But let's move on. Let's get our CBC.
It's elevated white count. All right. Makes me think about a septic source.
B and creatinine. Are they confusing their kidneys? Do they have end organ dysfunction? They do. Kidneys aren't being perfused well.
EKG, is there any evidence of any cardiogenic problem here? They have a sinus tachycardia. So again, there's no kind of evidence of ST elevation or AFib or anything like that to suggest a cardiogenic problem.
Troponins, do we have any myocardial injury? No. Our chest x-ray, any kind of like pneumothorax, any kind of like potentially a pneumonia here that we see as an obvious problem here.
I don't see a pneumothorax, but I do see a big... whopping kind of pneumonia here on this side and even a little bit on this side, probably like multifocal consolidations in this person. So I definitely got pneumonia and they're probably septic now.
Echo, look for any kind of cardiac tamponade, look for any kind of like decreased ejection fraction or wall motion abnormalities. Their heart's actually just banging away. And what did I tell you was one of the responses when someone has a systemic vascular resistance that actually drops, right?
The vessels dilate, that drops their resistance. What's their compensatory response? Cause their heart.
heart to actually beat faster and their heart to beat harder. So they're more hyperdynamic. So their cardiac output's actually increased.
And that's a response to that. Look at that. We're making sense of stuff.
All right. Look for the cultures. Look at the urinalysis.
Look at the blood. Look at the sputum. And when we do it, it's abnormal.
And their blood culture results actually came back positive with a nasty gram negative pathogen like pseudomonas. So what do we got to check? Lactate as well. Are they having inadequate perfusion to the tissues where there's a lot of anaerobic glycolysis?
There is. This person definitely has septic shock, probably from a pneumonia. And when we look at this and we move forward, what would we say were the differentials for distributive shock?
Distributive shock, there was septic shock, anaphylactic shock, and what else? Neurogenic shock. When we think about this one, it definitely fits septic shock, anaphylactic because they're exposed to some type of life-threatening allergic reaction, or neurogenic shock because they had kind of like spinal cord injury or trauma to the spinal cord or something of that nature where there was actually a hypotension and bradycardia and they wouldn't have like an infectious source here.
So I definitely see that this is likely a septic shock. Well- When we throw that swan catheter in there and we try to measure these things, how do we support their hemodynamic parameter findings? Well, in these patients, they're actually third spacing a lot of fluid because their basals are very dilated, but they're also leaky. So they leak a lot of fluid out. So their preload to the right and left side of the heart is going to drop.
So their CBP for the right heart pressure is going to drop and their PCWP for the left side of the heart pressure is going to drop. Cardiac output, which really we can measure via their cardiac index. Remember, we said that their systemic vascular resistance drops, dropping their pressure, their compensatory response is to increase their heart rate. Okay. and cause the heart to beat harder.
So their cardiac index should actually increase because their cardiac output's gonna increase. And then what do we say is happening to their vessels? Are they dilated or constricted? They're dilated.
So what's that do to the resistance? That drops the resistance. All right, my friends. What do we do to treat pneumonia? We gotta give them antibiotics to treat the underlying cause, and then obviously we give them a little bit of fluids to try to increase their actual blood volume and potentially their blood pressure, but we gotta put them on some type of pressure like norepinephrine or epinephrine to support their actual blood pressure.
And so that's what you would do. And even oxygen in these patients to be able to help with their hypoxemia. All right.
We'd uncovered all the different cases and talked about shock. I hope it made sense. I hope that you guys liked it.
And as always, until next time.