Understanding Different Types of Shock

All right, Ninge Nerds, in this video we're going to talk about the various types of shock. Now, first off, how would we describe shock just in general? Before we go into each different type of shock, we can say that shock is any situation in which there is an inadequate tissue perfusion. In other words, there's not enough blood flow going to the tissues. And because of that, because there's not enough adequate tissue perfusion, there's not an adequate amount of oxygen delivery to the tissues. So because of that, the tissues start developing a certain type of ischemia. Okay, and ischemia, if it happens over a long period of time, the tissue can start becoming necrotic. In other words, it can die. And then tissues are what make up organs. So if that tissue starts becoming deprived for a long period of time, organs can start failing. So in general, how would we generally classify shock? We can say shock is any situation in which there's inadequate tissue perfusion that can result in ischemia followed by necrosis. and then possibly even organ failure if not reversed. Also shock can progress in various stages. We're not gonna talk about that in this video, but I want you to understand that shock is actually a progressive process. So whenever shock comes about, there's usually the actual beginning compensating stages of shock. So how you're trying to compensate for this significant decrease in blood pressure. The next one is it gets more progressive. You start actually declining, okay? And then after that, it goes into a really, really negative point, which is called the refractory component of shock, where sometimes, even though despite all the efforts of the care, you can't restore the blood pressure. And that's the deadly part. That's the part that can actually lead to death if not reversed. So again, understanding that about shock is very, very crucial. All right, so let's now go ahead and dive into each different type of shock. In general, I want you guys to remember, though, I'm going to write this up here at the top. You guys need to remember, this shock is going to cause low BP. If you guys have not already watched it, I strongly encourage you to go watch our video where we talk about the compensation mechanisms for low blood pressure. Because it's going to make so much sense, okay? So shock can lead to low blood pressure, but the question is, how can it lead to this decrease in blood pressure? There's two ways, and that's where some of these shocks differ. One way is there could be a decrease in the cardiac output. Okay, so if you decrease your cardiac output, you're going to decrease the blood pressure. The other one is a decrease in the systemic vascular resistance, or you might have even heard me write it as total peripheral resistance. Same thing. Okay, so I want you to understand that shock is when there's a low blood pressure, and this low blood pressure could be due to a low cardiac output or a low systemic vascular resistance. Okay. And then remember what cardiac output is dependent upon. It's dependent upon heart rate and stroke volume. Okay? So now that we understand that, this is critical because we're going to go ahead and get started now on hypovolemic. How would we consider hypovolemic shock? Well, decipher the word. Hypo means low or below the normal volume range. So it's a loss of volume. Now, when we're losing blood volume, it can come in two different flavors here. Look at this. One could be due to blood loss. So one could actually be due to blood loss. What are some certain causes of this blood loss? One of them could actually be due to maybe a GI bleed. So a GI bleed is definitely a very, very common cause of this actual blood loss. For example, a very severe peptic ulcer or duodenal ulcer that's perforated and emptying into the actual peritoneal cavity. Another one is an abdominal aortic. aneurysm. If those suckers rupture, they can spill a lot of blood into the abdominal cavity. You can lose a lot of blood very, very fast. Another one could possibly be trauma. Okay, so if I got hit in the back of the head with a 2x4 or if I got shot or something like that, I'm definitely gonna start losing some blood. So certain types of trauma. Other kind of weird ones here is you know postpartum hemorrhage. You've heard of postpartum hemorrhage? It's basically whenever the woman's giving birth after the childbirth. Around 24 hours after the childbirth, if the woman starts losing significant volumes of blood, like about 500 mLs to about 1,000 mLs, they consider that to be postpartum hemorrhage because you're losing a lot of blood. So another one is what's called postpartum hemorrhage. That's another one, okay? So that's another cause. Another situation besides this could even be what's called an ectopic pregnancy. This is another really bad one. This is terrible since we're on this topic of... Getting in this area. Ectopic pregnancy. Normally whenever the... The ovary is ejected from the, whenever the ovum, the oocyte, is ejected from the ovary, it goes into the fallopian tubes, right where the ampulla is, and it waits for the sperm cell to fertilize it. And then when the sperm cell fertilizes it, it gets beaten. by the cilia within the fallopian tubes towards the endometrium where the uterine cavity is, where it implants, okay? But let's say for some terrible reason, the actual cilia didn't beat it towards the uterine cavity and it implanted in the actual fallopian tubes. The fetus will actually be aborted over a certain period of time and it can actually cause a lot of blood loss. It even can lead to another condition called pelvic inflammatory disease. So this could be another one. Another thing is what's called Hemoptysis. This is basically coughing up blood. This could be due to a lot of different things. There's certain situations if a gentleman or a female has what's called esophageal varices and they rupture or if the person has what's called good pasture syndrome which is a collagen connective tissue disorder that could also do it. Even pulmonary embolisms if they're very severe too. So you're losing a lot of blood that way. What's another way? Another one could be due to non- Fluid blood loss. I'm sorry, not blood loss, but fluid other than blood. Okay, so non blood fluid loss So what could be that kind of cause so other causes could be due to non blood fluid loss So this is like common examples of like if someone has a very severe third-degree burn so like third-degree burns That's actually one of the biggest things whenever someone gets a burn First thing you want to take care of is to prevent them from becoming dehydrated. You've got to get them fluids as quickly as possible, right? Another common cause is excessive vomiting or just go out the other hole. You're peeing out your butthole, right? So then you've got diarrhea. That's another situation where you're losing a lot of fluid. Another type of situation could be like a bowel obstruction. If you have a bowel obstruction, it's affecting not only the absorption activities but also food from coming down. So that can initiate vomiting, it can affect the absorption activity, and bowel obstructions can actually pull fluid into the GI tract, which is also pulling fluid from your body. So bowel obstructions, oh, pancreatitis. Acute pancreatitis is also a very terrible one. Many different causes of pancreatitis, we're not going to go over all of them. What I'm going to say though is that whenever there's pancreatitis, the pancreatic proteases which are in the pancreas become undesirably activated, and they start digesting the pancreatic tissue. And there's a lot of pancreatic fluid that starts getting leaked out into the abdominal cavity. Terrible situation. Another one is what's called diabetic ketoacidosis. You know in diabetes you have what's called high glucose levels? What is that called? Hyperglycemia. Well in hyperglycemia, whenever your blood glucose levels get really, really high, remember we talked about in the kidney, there's what's called a transport maximum? Generally it's right around 375 milligrams per minute that can be filtered. It can filter that much glucose and reabsorb it back into the blood. In certain situations when the glucose levels are so, so, so high that it exceeds the transport maximum, we can't reabsorb it and it gets lost into the urine. Why is that a problem? Because when glucose leaves, guess who else leaves? Water. Water leaves also. And when you have that, you have an increased urine output. You're losing a lot of sugar and water. So you get a nice little sugary water. Alright? Now, these are some of the main situations. that are kind of causing this hypovolemic shock. So there's a ton of different causes. The question is, so now we know the causes. Let's write this up here. These are kind of the etiologies of the causes of hypovolemic shock. The next question that we have to ask ourself is, very quickly, how does the body compensate for it? Super quickly. When your blood volume decreases, what are these receptors over here called? Baroreceptors. Remember these baroreceptors that were located within the aortic sinus and the carotid sinus? Again guys, I'm going to fly through this because we should already have talked about this. So these guys are coming to the actual medullary center and doing what? They're stimulating the actual medullary centers to send out action potentials from the actual medulla to do two things. One is to go to the actual smooth muscle within the tunica media, the actual blood vessels. and release chemicals like norepinephrine that try to cause the actual blood vessel to constrict. If this happens, if you try to constrict the blood vessel, what's that going to do to the actual resistance? It increases the resistance. If you increase the systemic vascular resistance, what does that do to the blood pressure? It increases the blood pressure. In hypovolemic shock, the problem is that we're losing blood volume, which is decreasing our blood pressure. Now, if we... increase the actual systemic vascular resistance, we're going to increase our BP. So it's going to try to stabilize it. Here's the problem, though. Another thing it's going to try to do is it's going to try to go to the heart, and it's going to try to increase the contractility of the heart, and it's going to try to go and increase the actual heart rate. Here's the problem, though. In this situation, what is stroke volume dependent upon, if you guys remember? It's dependent upon two big things. We can kind of just say EDV minus the ESV. This is depending upon the filling and this is depending upon how much it pushes out. The problem is that we have a very low EDV. Why? Because we don't have enough blood volume. So even though we're going to try to increase the contractility of the heart and push as much blood out as possible, the blood volume is so low that the EDV is so low that it doesn't matter. It's not going to affect it. So in these individuals who have this hypovolemic shock, they're going to try to increase their cardiac output, but it's not going to help them. And it's not actually going to increase significantly at all. It's actually going to kind of decrease because their blood volume is dropping. So their EDV is dropping. So their stroke volume is dropping. So their cardiac output will drop. So in these people, what are you going to notice so far? What's some clinical manifestations that you'll see? One is you're going to see a decrease in their cardiac output. You're also going to notice that they're going to have an increase in the systemic vascular resistance. That's another thing that you're going to notice. What else will you notice? You'll also notice that these individuals, they're going to try to increase their heart rate. They're going to try to increase the heart rate to try to increase the cardiac output, but it's not going to help. But you will notice that the person is going to have an elevated heart rate. What is that called? Tachycardia. What else would you see here besides these type of situations? If you run a CBC, if you do a CBC on this person, you can notice two different things within the CBC. Within the CBC, you'll notice two different things. They could have a high hematocrit. Or they could have a low hematocrit. If their hematocrit is really, really high, so that means that their red blood cells are kind of, it looks like they might have a lot more red blood cells, but they don't. They're actually losing a lot of plasma. As they lose a lot of plasma, there's a lot more red blood cells per plasma composition. So because of that, you're going to notice that they have what's called hemo concentration, which just means that they're actually losing a lot of fluid. Whereas if they have a low hematocrit, all that's telling you is that they actually are losing red blood cells. So if you see here high hematocrit, they might actually be losing fluid, non-blood fluid loss. Their hematocrit's low? They might be hemorrhaging. They might be losing blood in some different type of way. Which way? Maybe it could GI bleed, abdominal aortic aneurysm, rupture, all these different things. It could be a ton of different things. But just understanding that there. Another really important thing, you're going to notice that the person will have what's called cyanosis. So you're also going to notice that the person will have what's called cyanosis. What is cyanosis? It's basically a bluish cast of certain skin areas, like on their fingertips, on their toes, around their lips, certain mucous membranes. So you might notice cyanosis around the lips, maybe even the tongue, maybe even the actual fingertips, fingertips or even the toes. So that's certain things that you'll notice within this person because why? What did we say is the problem with shock? There's a decreased tissue perfusion. In this case, it's due to a decreased blood volume. So the overall problem here is that these people are having a very low blood volume because they're losing blood. Okay? Now because of that, there's decreased tissue perfusion. That means that there's not going to get enough oxygen to the tissues, so this would develop hypoxia also. So another thing that might come up with this individual is they might have some hypoxia. Now... If this continues, if the actual blood volume is not resuscitated, this can cause negative effects where it starts causing ischemia, leads to necrosis, and then it can possibly lead to multisystem organ failure. So it's very, very, very dangerous if not treated quickly. Last thing now is how do you treat them? What do you do for them? First thing that you're going to want to do is you're going to want to put them on fluids. You have to give them, you have to restore their blood volume. So one of the things that they'll do is they'll do actually, they'll start an IV. So they do an IV, whether it be like a central line or they do like a large bore IV line, which is just a bigger gauge needle to get a lot of fluid in there fast. But give them an IV. Definitely got to start giving them an IV and then resuscitating the volume. So you're going to want to put them on fluids right away. So you're probably going to want to put them on crystalloids. And these crystalloids are going to be really important that you put them on like normal saline or a ringer's lactate solution. So these are some really, really important things that you're going to want to do right away. Immediately try to get them on fluids. Sometimes if you need to be able to stabilize their oncotic pressure. Sometimes you can give certain types of plasma volume expanders like you can give albumin, you can give albumin, or you can even give another compound called heta starch. This kind of stabilizes the colloid osmotic pressure. So this is trying to be able to stabilize the colloid osmotic pressure. You want to try to stabilize that because this is controlling the amount of blood, I mean the amount of water that's actually leaving the bloodstream. If we lose a lot of albumin and heta starch, we're going to start losing a lot of water into the tissue spaces. That's bad. that can even make the actual blood volume go down even more. So big thing, make sure you put them on IV, give them a lot of fluids to stabilize them. Another thing you're going to want to watch out for with these individuals is make sure that you prevent them from going into hypothermia because as you start losing blood volume, as you start losing the blood volume and it actually starts decreasing significantly, it affects you being able to regulate your internal body temperature. And so because of that, the person can develop hypothermia, so you want to make sure that you actually watch out for that. And control the hemorrhage. If they start losing too much blood, You might have to do a transfusion. So before we move on to cardiogenic, I want to hit one more thing real quick. Because, like I said, we did cover a lot of this in low blood pressure, but it's going to be the same scheme for the rest of them. But one of the other things that can happen whenever there's low BP, whenever there's hypotension, it can stimulate the kidneys. And the kidneys will start producing a chemical called renin. And then we said eventually renin got converted into angiotensin 1. I'm sorry, we should say renin actually converted angiotensinogen. into angiotensin 1. Angiotensin 1 got converted into angiotensin 2. Angiotensin 2 did two things, if you remember. One is he went over here and binded onto these actual receptors to cause vasoconstriction, to increase the systemic vascular resistance, to increase the BP. Another thing is he went over here to the actual adrenal cortex and caused the production of a hormone called aldosterone. And Aldosterone, if you remember, went to the kidneys and increased the actual reabsorption of sodium and water to try to increase the blood volume. He also came over here to the actual pituitary gland and stimulated the release of another hormone, and this hormone was called the antideretic hormone. The antideretic hormone also went to the kidney and increased the reabsorption of water to increase the blood volume and increase the blood pressure. And at the same time, it's going to try to activate certain centers that are going to trigger thirst. So the person might be a little bit more thirsty to try to consume fluids. So just so that you're aware, the mechanisms are going to be the same as it is whenever there's actually that low blood pressure, as they're trying to compensate for the situation by trying to increase the heart rate and the contractility. It's not going to have any effect, though. The vasomotor center will be activated to constrict the blood vessels. That'll work a little bit. The renin is going to be released, so this renin-angiotensin-aldosterone-ADH system is going to come into play to try to pull a lot of water out of the kidneys into the blood, a lot of sodium out of the water into the blood. And it's going to also try to constrict the blood vessels. Okay, and this is going to be the same for how all these guys are trying to compensate during the shock. Okay, next one. Next one is going to be cardiogenic shock. So you can actually hear what it's actually due to in the actual word. So it's a problem. It's a problem that's actually due to the heart not being able to generate a certain amount of power. So you know the heart is responsible for contracting and propelling blood out into the actual systemic and peripheral. and pulmonary circulation, that's its responsibility. It is the pump of the heart. So this guy is our pump, the ventricles are the pump. And in certain situations, the pump is failing in cardiogenic shock. What type of situations could cardiogenic shock be due to? It could be due to various things. Cardiogenic shock could actually be due to, if we talk about some of the causes, one could actually be due to myocarditis. Myocarditis is an inflammation of the myocardium. The most common cause of this is like a Coxsackie's B virus, which is like an enterovirus. Another one could be due to massive or multiple MIs, myocardial infarctions. So if someone has multiple myocardial infarctions, I'm going to put here MIs, or even really severe MIs, this could also be another cause. Another situation here could be certain types of valve dysfunctions. So you know like aortic valve stenosis or aortic stenosis. So aortic valve stenosis is a big one. Or maybe even mitral valve stenosis. So even mitral valve. Okay? So even the mitral valve stenosis is another situation there too. Because it's, again, putting an increased workload on the heart, and the heart can actually start becoming very weak and not very good at its job. Other causes besides this could even be due to arrhythmias. So arrhythmias is another really, really dangerous one. Because what happens is in arrhythmias, there's two types. There's actually a tachy, and then there's the bradyarrhythmias, right? So what happens in this is in tachyarrhythmia you're trying to increase the heart rate. But you're not giving the heart enough time to fill with blood. As you don't give enough time for the heart to fill with blood, it's not going to be able to contract enough blood out. So it's affecting the filling and the ejection of blood out of the heart. So in tachyarrhythmia, this is also a negative influence. And if your heart rate's really slowing down, it's going to decrease your cardiac output, which is going to decrease the amount of blood that's being pumped out of the heart. So again, it's due to a pump failure. Other common causes could even be due to dilated cardiomyopathy. So dilated cardiomyopathy is another terrible condition here. And what happens is the actual ventricular muscle becomes very weak and actually becomes very flabby. and not very good at being able to pump at all. Or even congenital heart diseases. So other ones could even be due to congenital heart diseases, like ventricular septal defect or truncus arteriosus. There's many of those. But again, they could also contribute to this problem here too, if not completely treated. So congenital heart diseases, or somewhere down the line for these individuals. So that's the overall concept. Now, what's the problem? Because we just said these people are having a hard time being able to pump blood out of the heart. So them trying to pump blood out into the circulation, they're not pumping an adequate volume of blood out into the circulation. So what's happening to the volume of blood that's being circulated? There's a decreased volume circulating. If there's a decreased volume of blood circulating, that means that you're having systemic hypotension. Because if there's a decrease in blood volume, that means that there's a decrease in the blood pressure. So in these people, what are you going to notice right away? They are going to have low blood pressure. They're going to have a low cardiac output. Their heart rate is going to try to go up to compensate for them, right? What else is going to try to compensate for them? What was that other mechanism? The renin, angiotensin, aldosterone, ADH system is also going to try to come into play. And you're going to try to increase the actual vascular resistance. So what's another thing that they're going to try to do? They're going to try to increase the systemic vascular resistance. So you're going to notice that these people are going to have some tachycardia. They're going to have some congestion of blood within the heart. They're going to have a low BP. They're not going to have an adequate volume circulating in the actual bloodstream. Why is this a problem? Because if there's a decreased blood volume coming to the tissues, that means it's not going to deliver enough oxygen. If you don't deliver enough oxygen, that can cause ischemia. Ischemia can lead to necrosis, and necrosis of tissues can lead to organ failure if not treated. You see how it's just a circle constantly. So because of that, if you're not giving oxygen to the tissues, what's the consequence of not getting oxygen to the tissues? So if you're not getting oxygen to the tissues, you know a lot of our metabolic pathways in the body depend upon oxygen to produce ATP. So as ATP levels decrease, two things can happen. I'm sorry, as oxygen levels decrease, two things can happen. You can develop a decrease in ATP. This is really bad. Another thing that can happen is you can develop an increase in what's called lactic acid. So if you're not getting enough oxygen to the tissues, you're not producing enough ATP by cellular respiration. This can decrease a lot of activities within the cell. It can lead to almost complete cellular dysfunction, right? Protein synthesis, transport pumps, muscular contraction, neuron transmissions, all that kind of stuff. Another thing is your body shifts from aerobic cellular respiration, making ATP, to anaerobic cellular respiration, making a lot of lactic acid. Why is lactic acid bad? Because lactic acid... can actually do what? It can disassociate and give up protons. As you produce a lot of lactic acid, you produce a lot of protons. What's the problem with protons? They're very acidic. This can lead to metabolic acidosis. So the problem with having a lot of protons is it decreases the pH, and it leads to metabolic acidosis. And this has a negative effect on the heart also. This can actually depress the actual... contractile activity of the heart also, as well as even the heart rate. So that's another negative influence. Now, these are the causes. This is what's leading to this. And it's leading to a decrease in BPA, a decrease in the cardiac output. An increase in the heart rate is a compensating mechanism. So let's actually put this over here. Since the heart rate is trying to increase, it's one of the compensation mechanisms, even though it's not going to be enough. So they're going to try to increase their heart rate, but it's not going to be enough to fix the issue. It's actually going to make it worse in certain situations. If they're not getting an adequate volume of blood delivered to the tissues, this can actually lead to lactic acid buildup, ATP decrease, and if it happens for a long period of time, what do we say? Organ failure. Okay? So this is why it can become so dangerous if it happens for a long period of time. Question is, how do you treat it? What do you do about it? Okay, well the big thing is, is you have to be able to, sometimes you might have to treat the issue. If they've had a myocardial infarction, what would you do about that? How would you treat that? You'd want to definitely, if they have, so sometimes you're going to have to treat the underlying cause. So let's say that one of the underlying causes, just for an example here. Let's say it's an MI. Let's say that you have an MI. What do you do about the MI? You can either do an angioplasty, or they go in and actually kind of remove the actual embolus within the coronary vessels. Or you just put them on thrombolytics. So certain types of things like tissue plasminogen activator, heparin, or things like that that will break up the clot. Okay? So that's kind of some of the big things there. Next thing, how would you treat them in general? Regardless if there's an animal, how would you treat them in general? The big thing that you're going to want to do right away with these people is you're definitely going to want to try to put them on oxygen. So some of the treatment here is you're going to want to put them on oxygen. Give them O2. Okay? This is very, very critical. Give them O2. Maybe give them a little bit of fluids. So very little isotonic fluids. Because the reason why is they're not losing blood volume. They're just not able to circulate enough blood throughout the heart. So it's not a problem of decreased blood volume. It's the problem that the heart can't push enough blood out into the circulation. So you can give them a little bit of isotonic fluids to help the heart out a little bit. But again, main thing is giving them oxygen. Oh, real big one, give them vasopressors. Vasopressors are really important in cardiogenic shock because they have a hard time being able to get the heart to contract very powerfully. So you're probably going to want to give them things like epinephrine. So epinephrine is actually going to be really important here because epinephrine is actually going to be two things. One is it's a positive inotrope, meaning that it can increase the contractility of the heart. The other one is it can increase the systemic vascular resistance by constricting those blood vessels. Other drugs that you could give is like dobutamine. Dobutamine actually acts just like epinephrine, but it actually is primarily a positive inotrope. So it tries to bind on to the beta-1 adrenergic receptors and increase the contractility. Another one that you can use, it's an unfortunate one, it's called amrinone. Remember I told you that there was different stages? This is also going to increase the contractility. It's a positive inotrope. This one is an unfortunate one if you have to use it. Or you can even use atropine also, which is inhibiting the muscarinic receptors. Amrinone is unfortunate if you go into the refractory period. So the refractory period is that point where it can become irreversible, even no matter how hard the doctor or the PA is trying to be able to revive the blood pressure, it's not responding. You can put them on amrinone. Amrinone is really good because it's a phosphodiesterase 3 inhibitor. So it inhibits phosphodiesterases. And if you remember this, we said the phosphodiesterase breaks down cyclic AMP. Cyclic AMP is what controls the protein kinase A levels. If you break down cyclic AMP, you decrease protein kinase A, which decreases the calcium coming into the cell. If calcium isn't coming into the cells fast, it's going to start slowing down the contractility. Okay? So that's another thing that you could do there. Another one that you could actually do in certain situations is you could, if they really need it, you could do what's called an intra-aortic balloon, like pump. And it's a device that you actually kind of... to throw up in the aorta, right in the abdominal aorta. And when you throw it up into the aorta, what it does is whenever your heart contracts, it stays deflated. But whenever the heart relaxes, it inflates and it starts actually expanding. The whole purpose of it is that whenever the person's in cardiogenic shock, their myocardium, their heart isn't getting enough oxygen. So by using that pump, that balloon pump, it actually spreads out whenever the heart's relaxing, which pushes some of the blood into the coronary vessels, which helps to be able to get some blood to the actual myocardium to save the myocardium from irreversible damage. Okay, so that's one of the big things there for cardiogenic. All right, so that's that one. I hope that one made sense. Let's move on to the next one. Let's go into obstructive. All right, guys, so now we're going to move into the last one here that we're going to talk about in this video. In the next video, we'll actually talk about distributive shocks, those different types. Now, obstructive shock is really, really important. The reason why is you can tell what it's due to right in the name. There's either some type of internal obstruction or some type of external obstruction of the heart, the chambers of the heart, or... due to the great vessels that it's supplying. So again, it's due to some type of internal obstruction or external obstruction that is affecting the blood flow out of the heart or into the actual great vessels. And we'll talk about that. So let's go ahead and get started on that. So one of the big ones here is called a tension pneumothorax. I'm sure that you guys have heard this at some point in time. If you watch TV, you probably hear it a lot, like on certain medical shows, right? But a big one here is tension. Pneumothorax. We're not going to go into super detail on this, but just to make it simple, it's some type of situation in which there's, let's say that there's a stab wound. And what happens is, remember we talked about this in the actual respiratory system. We said that there's two types of pressures. We said that there was the called the P-pull, which was the intrapulmonary pressure. And we call it the PIP, which was the intrapleural pressure. We said that the intrapleural pressure is usually negative four. MMHG, and we said the P-Poll is usually 0 MMHG. We also said that you never want the intrapleural pressure to become... equal to or greater than the intrapulmonary pressure. What happens? Let's say that there's some type of situation where there's damage to the actual parietal pleura, maybe due to a stab wound. What happens is air from the atmosphere, atmospheric air is right around 760 millimeters of mercury, whereas in the PIP, it's right around 756 mmHg. And so out here in the atmosphere, it's around 760 mmHg. Whereas what's higher pressure, the PIP or the P of the atmosphere? The atmosphere. And things like to go from areas of high pressure to areas of low pressure. So what happens is the air starts moving into the actual pleural cavity, where it normally is containing fluid. As that happens, the air starts accumulating in this cavity, and what starts happening to the intrapleural pressure? The intrapleural pressure starts increasing, and it starts going from negative 4, possibly to around maybe 0 or plus 1 mmHg. Why is that dangerous? Because now it's becoming greater than the pressure inside of the actual lungs. What that starts trying to do is, is it starts pushing on the lungs. And it starts compressing this way. It starts shifting. So it starts trying to shift the mediastinum to the opposite or contralateral side. So one thing that can happen is as the pneumothorax develops, the air occupies this pleural cavity, pushing on the lungs, and it can shift the mediastinum. Or it could even shift the trachea this way too, to the contralateral side. So what is this person exhibiting? They're exhibiting what's called a mediastinal shift. or a tracheal shift. Okay, now why is that bad? If you shift this, what are you going to be doing? You're going to be compressing the heart and the vessels that are actually bringing blood into it and taking blood out. So as this starts happening, the tension pneumothorax starts pushing on the chambers of the heart and some of the blood vessels that are trying to bring blood up. What's this one vessel right here that brings blood up into the heart right here? Inferior vena cava. If this is pushing, it'll start compressing it. What's the blood vessel that brings blood into the right atrium from the top? The superior vena cava. In certain type of situations where the pneumothorax is really, really pushing and compressing on the heart, it can affect the heart from being able to get filled with blood, and it puts a lot of stress on the heart and restricts the heart from being able to eject the blood out. Okay? So two problems with the tension pneumothorax is it can actually compress the blood coming into the heart and compress the heart so it has a hard time pushing blood out. Okay? That's it. Intention pneumothoraxes though, these are really dangerous. If it becomes really, really bad, what you can actually do is you'll also, they do like a little percussion. They kind of tap on the individual. They'll basically tap and try to listen for sounds. When they tap, they hear this sound. It's like a hyper-resonance. It's a low pitch but kind of like a louder resonance. And it actually is called tympani. And that sound is identifiable that there might be some type of gas or air within that cavity that they're percussing. That is one of the signs that they can actually do during the physical exam to see, oh, maybe this person does have a pneumothorax. Obviously, you'd have to go send them to do certain types of maybe like an x-ray to check that out. But the whole concept is that you might hear what's called hyper-resonance when they do the percussion technique. Also, they might have decreased breath sounds because the lung is collapsing. If that lung is collapsing, they'll have decreased breath sounds on that affected side. Also, since it's compressing the actual superior vena cava and the inferior vena cava, the blood is having a hard time coming back into the heart. So what's another sign that you might see for tension pneumothorax? You might see that the person will have a high jugular venous pressure. You're probably like, okay, well, that's cool. You'll see it because their neck veins will be a little distended too, okay? All right, cool. That covers the tension pneumothorax. Next one is called, you can call it pericardial tamponade or cardiac tamponade. I'm just going to write here pericardial tamponade. Pericardial tamponade is due to some type of situation in which a lot of fluid starts developing with inside of what's called the pericardial cavity. So let's say here's the cavity right here. You have the different parts of the pericardial cavity like the serous layer and then you have the actual outer parietal layer or you call it the visceral layer and the outer parietal layer here. In between those layers of the pericardium, you have this actual serous fluid, this pericardial fluid. In certain situations, it's supposed to be in normal amounts. But... For whatever reason, in these individuals, they start having a lot of fluid accumulation in here. And the fluid starts getting so much in this area that it actually starts compressing on the heart, strangulating the heart, squeezing the heart. So as this starts happening, it starts really, really putting a lot of pressure onto the heart. What do you think that's going to do? Do you think that this heart is going to be able to fill with blood adequately? No, because I'm squeezing it. So I'm decreasing the volume of my heart chambers. So me trying to get blood into the heart is going to be a lot. harder and it's actually squeezing the heart so that the heart is going to have a hard time being able to contract too. Same thing. In this situation, they have a hard time filling the heart with blood and the heart is so restricted because of this actual pericardial tamponade squeezing and strangling the heart that it even has a hard time contracting. Two problems with this person, again, is going to be they're going to have a hard time contracting the heart and filling the heart with blood. Now, a pericardial tamponade, it actually kind of, I don't know, there's some guy, I guess his name was Beck. And he came up with a triad of things that comes about during the pericardial tamponade. So let's say I put a triangle here. So this is called Beck's triad. And this is usually identifiable for someone who's going to have some type of pericardial tamponade. What are these symptoms here? One is because the heart is having a hard time filling with blood, that... that actual superior vena cava and inferior vena cava are probably being compressed. So their jugular vein is going to be actually distended, right? So they're going to have a high jugular venous pressure. Another one is they're going to have a high blood pressure. So they're going to, I'm sorry, not a high blood pressure. They're not being able to pump enough blood onto the tissues. So because of this, they have a low blood pressure because, again, the heart's not filling with blood adequately, and it's not squeezing and pushing enough blood out. So because of that, the amount of blood that's being pumped out of the heart is very, very low, so they can have hypotension. Another one is because if you do what's called oscillation, you're trying to listen to the heart sounds, that fluid is making it a lot thicker. So you trying to hear the sound is not going to be as well. It sounds like it's actually moving from a farther distance. So we call it muffled or distant heart sounds. Okay? So that's some of the things that you'll see within a person with having pericardial tamponade. So again, with this person, there's an obstruction. They're having a hard time getting the blood out. Another super, super terrible one is a massive, massive pulmonary embolism. Let's say that a person develops an unfortunate embolism right here in the pulmonary trunk. You know what that's actually called? That's called a saddle embolism. So let's say that they develop some type of massive PE, okay? So if they have a massive PE, there's a big old embolism. blocking the actual pulmonary artery blood flow. So this person is gonna try to be able to pump blood from the right side of the heart up into the lungs. But what's the problem? They got this big old embolus blocking the way. So the amount of blood flow getting passed through this area is very, very low, which means that very little fluid is coming back to the actual left ventricle. If very little fluid is coming back to the left ventricle, what happens to the EDV? The EDV is going to decrease significantly. As the EDV decreases, what happens to the stroke volume? The stroke volume decreases. As that decreases, what happens to the cardiac output? That decreases. That decreases. Then what happens to the BP? That decreases. So you can see how this can cause hypotension too. You can see how this causes hypotension because the heart can't pump enough out and it can't fill properly. You can see how this one can cause hypotension because the same thing. Heart isn't filling properly. It's not contracting properly. In this situation, there's an embolism blocking blood flow to the left side of the heart, decreasing the BP. Also, think about this. You got a big old embolism. Is there going to be a lot of blood coming out of the right ventricle either? No. It's the same thing. You're not going to get a lot of blood out of the ventricles. That's one problem. But then you got another big problem. What if this embolism is so bad that the pressure starts accumulating in this area so high, the pulmonary capillary wedge pressure? These people have a high pulmonary capillary wedge pressure, which is the pressure that's trying to push blood back to the left atrium. If this pressure is really, really high in this situation, Because the actual, trying to get to that area is really, really being negatively affected here. They aren't able to get this to that area. They aren't able to get the blood to that area. That pulmonary capillary wedge pressure can start getting a little high in this situation. And it can actually rupture some of those capillaries. And as it starts rupturing a lot of those capillaries, it can cause the spitting up of that blood, that hemoptysis. Also, if you don't have a lot of blood flow coming through this area, if you don't have a lot of blood flow coming through this area, what's going to happen to the actual ventilation perfusion process? It's not going to be good. So you guys remember we did this in respiration. We said that there was the VQ ratio and it was equal to normally about 0.8. Well, what is Q? That's the perfusion. In this case, the perfusion is decreasing. If the perfusion is decreasing, what's happening to the overall number then? Then the overall number is going to be greater than 0.8. What do we say happens in this type of situation? In that type of situation, the ventilation has to decrease. So now the ventilation is going to decrease. What does that mean? The bronchioles might start constricting. So you're going to have a lot of, you're going to have a really hard time breathing. So there might be some respiratory distress that could come about in this situation. Also, if there's a VQ mismatch, what happens to the oxygenation of the blood? It doesn't oxygenate properly. And this person can develop what's called hypoxia. Hypoxia. Another negative thing can come about from this, right? And if you develop hypoxia, what does that mean? You're not going to be able to deliver adequate oxygen to the tissues. If you can't give adequate oxygen to the tissues, the tissues become ischemic. If they become ischemic, they become necrotic. If the tissues become necrotic, the organs can start fading. So you can see why this is just a consistent repeat of everything. Other things that you might see within this person is because they have hypoxemic hypoxia, if you do what's called an ABG, an arterial blood gas, if you do an ABG, you're going to... notice that these people have a very low ABG. So they're going to have a partial pressure of oxygen. Their partial pressure of oxygen is actually going to be a lot less than 80 millimeters of mercury. That's one thing that you might notice here. Also you might even notice that they might have some elevated lactic acid levels too. Okay, because again, they're not getting oxygen to the tissues. So their body is shifting from aerobic respiration to anaerobic respiration. And again, if not treated, this can cause the person to go in multiple system organ failure, right? Depending upon the organ, that could be devastating. Another one I'm not going to really include here because it's not one of the serious ones, but it can be, that's very, very close to the heart. So if you get a proximal aortic dissection, A proximal aortic dissection can actually be very, very close to the heart, and if it actually starts dissecting, it can squeeze on some of the vessels supplying the heart, and that can affect the actual filling of the heart, and it can affect the actual ability to eject blood into the aorta as well. So that's another situation. So again, to recap this one, it could be due to a tension pneumothorax, which causes a mediastinal or tracheal shift, which compresses the heart and squeezes the heart, and the heart has a hard time filling with blood. Because it has a hard time filling with blood, it can't contract enough blood into the circulation. So they're not ejecting enough blood out into the peripheral circulation. So their volume that's circulating is decreasing. That's going to cause hypotension. As this happens, they're not able to deliver enough oxygen to the tissues, and this can result in an actual ischemia. Pericardial tamponade is the fluid is accumulating there and strangulating the heart, causing the same situation as this tension in the thorax. And then we said the worst one is a massive pulmonary embolism, like, for example, like a saddle embolism blocking right there at the pulmonary trunk. which is affecting the blood flow towards the actual left side of the heart. Now, the right side of the heart has a hard time getting blood out. That's going to decrease their actual cardiac output, and it's going to decrease the amount of volume coming back to the left side of the heart. So they're going to have a hard time being able to get blood out too. And we shouldn't actually include in this pulmonary capillary wedge pressure. It's not really significant into this one. Really, the important one where the pulmonary capillary wedge pressure can be included is going to be in cardiogenic shock. So we're not going to really talk about... the pulmonary capillary wedge pressure in this one. But seriously, we just need to understand here, if there's a massive PE and it's occluding the blood flow to this area, it can decrease the volume coming back to the left side of the heart, which is decreasing the EDV, decreasing the stroke volume, decreasing the cardiac output, and decreasing the blood pressure. If that volume that's being circulated out to the actual peripheral tissues is decreasing, it can cause ischemia, it can lead to the necrosis, and can cause a serious organ failure. How would you treat these people? it obviously depends upon the actual cause. If they have a tension pneumothorax, do a needle decompression. So insert a needle in there and equalize the pressures that you can get the air out of the actual pleural cavity. If they have a pericardial tamponade, do what's called a pericardiocentesis, where you actually drain the actual fluid out of the pericardial cavity. If they have a massive pulmonary embolism, you might have to give them thrombolytics. You might have to do some type of embolectomy. You might have to give them heparin to be able to prevent that from actually becoming very dangerous, right? It can cause sudden death there. And if they have some type of proximal aortic dissection, you're going to have to go in there and do some type of surgical intervention. But same thing here with these people. Put them on oxygen. What would you do here? So the last thing is the treatment here. We said that if you're going to treat these people, what would you do? Obviously, it's dependent upon each underlying cause. But other ones is you'd want to give oxygen. Give them oxygen. The next thing is you can put them on isotonic fluids. That's another really important one. And same thing with these individuals. You're going to have to give them some vasopressors. So in this situation, give them some vasopressors to increase the inotropic action, the contractility of the heart, and drugs that can actually cause the vascular constriction. And if you start causing vasoconstriction, that's going to increase the resistance and increase the blood pressure. Alright, so what we did in this video is we talked about the types of shock that is usually a result of some type of decrease in the cardiac output, where the heart rate isn't sustaining enough and the stroke volume isn't sustaining enough to increase that. where these people have a high systemic vascular resistance. In the next video, where we talk about distributive shock, we're going to see how this shock is actually more due to actually a decrease in the systemic vascular resistance. So now the blood vessels are excessively dilated and how that can affect tissue perfusion. So Ningeners, I hope to see you there, where we talk about distributive shock in great detail. Thanks for watching this video. I hope that you guys really did enjoy it. If you guys did, please hit the like button, comment down in the comment section, and please subscribe. As always, Ningeners, until next time.

In other words, there's not enough blood flow going to the tissues. And because of that, because there's not enough adequate tissue perfusion, there's not an adequate amount of oxygen delivery to the tissues. So because of that, the tissues start developing a certain type of ischemia.

Okay, and ischemia, if it happens over a long period of time, the tissue can start becoming necrotic. In other words, it can die. And then tissues are what make up organs. So if that tissue starts becoming deprived for a long period of time, organs can start failing.

So in general, how would we generally classify shock? We can say shock is any situation in which there's inadequate tissue perfusion that can result in ischemia followed by necrosis. and then possibly even organ failure if not reversed. Also shock can progress in various stages. We're not gonna talk about that in this video, but I want you to understand that shock is actually a progressive process.

So whenever shock comes about, there's usually the actual beginning compensating stages of shock. So how you're trying to compensate for this significant decrease in blood pressure. The next one is it gets more progressive. You start actually declining, okay?

And then after that, it goes into a really, really negative point, which is called the refractory component of shock, where sometimes, even though despite all the efforts of the care, you can't restore the blood pressure. And that's the deadly part. That's the part that can actually lead to death if not reversed.

So again, understanding that about shock is very, very crucial. All right, so let's now go ahead and dive into each different type of shock. In general, I want you guys to remember, though, I'm going to write this up here at the top.

You guys need to remember, this shock is going to cause low BP. If you guys have not already watched it, I strongly encourage you to go watch our video where we talk about the compensation mechanisms for low blood pressure. Because it's going to make so much sense, okay? So shock can lead to low blood pressure, but the question is, how can it lead to this decrease in blood pressure? There's two ways, and that's where some of these shocks differ.

One way is there could be a decrease in the cardiac output. Okay, so if you decrease your cardiac output, you're going to decrease the blood pressure. The other one is a decrease in the systemic vascular resistance, or you might have even heard me write it as total peripheral resistance. Same thing. Okay, so I want you to understand that shock is when there's a low blood pressure, and this low blood pressure could be due to a low cardiac output or a low systemic vascular resistance.

Okay. And then remember what cardiac output is dependent upon. It's dependent upon heart rate and stroke volume. Okay? So now that we understand that, this is critical because we're going to go ahead and get started now on hypovolemic.

How would we consider hypovolemic shock? Well, decipher the word. Hypo means low or below the normal volume range. So it's a loss of volume. Now, when we're losing blood volume, it can come in two different flavors here.

Look at this. One could be due to blood loss. So one could actually be due to blood loss. What are some certain causes of this blood loss? One of them could actually be due to maybe a GI bleed.

So a GI bleed is definitely a very, very common cause of this actual blood loss. For example, a very severe peptic ulcer or duodenal ulcer that's perforated and emptying into the actual peritoneal cavity. Another one is an abdominal aortic.

aneurysm. If those suckers rupture, they can spill a lot of blood into the abdominal cavity. You can lose a lot of blood very, very fast.

Another one could possibly be trauma. Okay, so if I got hit in the back of the head with a 2x4 or if I got shot or something like that, I'm definitely gonna start losing some blood. So certain types of trauma. Other kind of weird ones here is you know postpartum hemorrhage. You've heard of postpartum hemorrhage?

It's basically whenever the woman's giving birth after the childbirth. Around 24 hours after the childbirth, if the woman starts losing significant volumes of blood, like about 500 mLs to about 1,000 mLs, they consider that to be postpartum hemorrhage because you're losing a lot of blood. So another one is what's called postpartum hemorrhage. That's another one, okay?

So that's another cause. Another situation besides this could even be what's called an ectopic pregnancy. This is another really bad one.

This is terrible since we're on this topic of... Getting in this area. Ectopic pregnancy.

Normally whenever the... The ovary is ejected from the, whenever the ovum, the oocyte, is ejected from the ovary, it goes into the fallopian tubes, right where the ampulla is, and it waits for the sperm cell to fertilize it. And then when the sperm cell fertilizes it, it gets beaten. by the cilia within the fallopian tubes towards the endometrium where the uterine cavity is, where it implants, okay? But let's say for some terrible reason, the actual cilia didn't beat it towards the uterine cavity and it implanted in the actual fallopian tubes.

The fetus will actually be aborted over a certain period of time and it can actually cause a lot of blood loss. It even can lead to another condition called pelvic inflammatory disease. So this could be another one.

Another thing is what's called Hemoptysis. This is basically coughing up blood. This could be due to a lot of different things.

There's certain situations if a gentleman or a female has what's called esophageal varices and they rupture or if the person has what's called good pasture syndrome which is a collagen connective tissue disorder that could also do it. Even pulmonary embolisms if they're very severe too. So you're losing a lot of blood that way.

What's another way? Another one could be due to non- Fluid blood loss. I'm sorry, not blood loss, but fluid other than blood. Okay, so non blood fluid loss So what could be that kind of cause so other causes could be due to non blood fluid loss So this is like common examples of like if someone has a very severe third-degree burn so like third-degree burns That's actually one of the biggest things whenever someone gets a burn First thing you want to take care of is to prevent them from becoming dehydrated. You've got to get them fluids as quickly as possible, right?

Another common cause is excessive vomiting or just go out the other hole. You're peeing out your butthole, right? So then you've got diarrhea. That's another situation where you're losing a lot of fluid. Another type of situation could be like a bowel obstruction.

If you have a bowel obstruction, it's affecting not only the absorption activities but also food from coming down. So that can initiate vomiting, it can affect the absorption activity, and bowel obstructions can actually pull fluid into the GI tract, which is also pulling fluid from your body. So bowel obstructions, oh, pancreatitis. Acute pancreatitis is also a very terrible one. Many different causes of pancreatitis, we're not going to go over all of them.

What I'm going to say though is that whenever there's pancreatitis, the pancreatic proteases which are in the pancreas become undesirably activated, and they start digesting the pancreatic tissue. And there's a lot of pancreatic fluid that starts getting leaked out into the abdominal cavity. Terrible situation.

Another one is what's called diabetic ketoacidosis. You know in diabetes you have what's called high glucose levels? What is that called? Hyperglycemia.

Well in hyperglycemia, whenever your blood glucose levels get really, really high, remember we talked about in the kidney, there's what's called a transport maximum? Generally it's right around 375 milligrams per minute that can be filtered. It can filter that much glucose and reabsorb it back into the blood. In certain situations when the glucose levels are so, so, so high that it exceeds the transport maximum, we can't reabsorb it and it gets lost into the urine.

Why is that a problem? Because when glucose leaves, guess who else leaves? Water. Water leaves also. And when you have that, you have an increased urine output.

You're losing a lot of sugar and water. So you get a nice little sugary water. Alright? Now, these are some of the main situations. that are kind of causing this hypovolemic shock.

So there's a ton of different causes. The question is, so now we know the causes. Let's write this up here.

These are kind of the etiologies of the causes of hypovolemic shock. The next question that we have to ask ourself is, very quickly, how does the body compensate for it? Super quickly.

When your blood volume decreases, what are these receptors over here called? Baroreceptors. Remember these baroreceptors that were located within the aortic sinus and the carotid sinus? Again guys, I'm going to fly through this because we should already have talked about this. So these guys are coming to the actual medullary center and doing what?

They're stimulating the actual medullary centers to send out action potentials from the actual medulla to do two things. One is to go to the actual smooth muscle within the tunica media, the actual blood vessels. and release chemicals like norepinephrine that try to cause the actual blood vessel to constrict. If this happens, if you try to constrict the blood vessel, what's that going to do to the actual resistance?

It increases the resistance. If you increase the systemic vascular resistance, what does that do to the blood pressure? It increases the blood pressure. In hypovolemic shock, the problem is that we're losing blood volume, which is decreasing our blood pressure. Now, if we...

increase the actual systemic vascular resistance, we're going to increase our BP. So it's going to try to stabilize it. Here's the problem, though.

Another thing it's going to try to do is it's going to try to go to the heart, and it's going to try to increase the contractility of the heart, and it's going to try to go and increase the actual heart rate. Here's the problem, though. In this situation, what is stroke volume dependent upon, if you guys remember?

It's dependent upon two big things. We can kind of just say EDV minus the ESV. This is depending upon the filling and this is depending upon how much it pushes out. The problem is that we have a very low EDV.

Why? Because we don't have enough blood volume. So even though we're going to try to increase the contractility of the heart and push as much blood out as possible, the blood volume is so low that the EDV is so low that it doesn't matter.

It's not going to affect it. So in these individuals who have this hypovolemic shock, they're going to try to increase their cardiac output, but it's not going to help them. And it's not actually going to increase significantly at all.

It's actually going to kind of decrease because their blood volume is dropping. So their EDV is dropping. So their stroke volume is dropping.

So their cardiac output will drop. So in these people, what are you going to notice so far? What's some clinical manifestations that you'll see? One is you're going to see a decrease in their cardiac output. You're also going to notice that they're going to have an increase in the systemic vascular resistance.

That's another thing that you're going to notice. What else will you notice? You'll also notice that these individuals, they're going to try to increase their heart rate.

They're going to try to increase the heart rate to try to increase the cardiac output, but it's not going to help. But you will notice that the person is going to have an elevated heart rate. What is that called? Tachycardia.

What else would you see here besides these type of situations? If you run a CBC, if you do a CBC on this person, you can notice two different things within the CBC. Within the CBC, you'll notice two different things.

They could have a high hematocrit. Or they could have a low hematocrit. If their hematocrit is really, really high, so that means that their red blood cells are kind of, it looks like they might have a lot more red blood cells, but they don't.

They're actually losing a lot of plasma. As they lose a lot of plasma, there's a lot more red blood cells per plasma composition. So because of that, you're going to notice that they have what's called hemo concentration, which just means that they're actually losing a lot of fluid. Whereas if they have a low hematocrit, all that's telling you is that they actually are losing red blood cells.

So if you see here high hematocrit, they might actually be losing fluid, non-blood fluid loss. Their hematocrit's low? They might be hemorrhaging.

They might be losing blood in some different type of way. Which way? Maybe it could GI bleed, abdominal aortic aneurysm, rupture, all these different things. It could be a ton of different things.

But just understanding that there. Another really important thing, you're going to notice that the person will have what's called cyanosis. So you're also going to notice that the person will have what's called cyanosis. What is cyanosis? It's basically a bluish cast of certain skin areas, like on their fingertips, on their toes, around their lips, certain mucous membranes.

So you might notice cyanosis around the lips, maybe even the tongue, maybe even the actual fingertips, fingertips or even the toes. So that's certain things that you'll notice within this person because why? What did we say is the problem with shock? There's a decreased tissue perfusion. In this case, it's due to a decreased blood volume.

So the overall problem here is that these people are having a very low blood volume because they're losing blood. Okay? Now because of that, there's decreased tissue perfusion. That means that there's not going to get enough oxygen to the tissues, so this would develop hypoxia also.

So another thing that might come up with this individual is they might have some hypoxia. Now... If this continues, if the actual blood volume is not resuscitated, this can cause negative effects where it starts causing ischemia, leads to necrosis, and then it can possibly lead to multisystem organ failure. So it's very, very, very dangerous if not treated quickly.

Last thing now is how do you treat them? What do you do for them? First thing that you're going to want to do is you're going to want to put them on fluids. You have to give them, you have to restore their blood volume. So one of the things that they'll do is they'll do actually, they'll start an IV.

So they do an IV, whether it be like a central line or they do like a large bore IV line, which is just a bigger gauge needle to get a lot of fluid in there fast. But give them an IV. Definitely got to start giving them an IV and then resuscitating the volume.

So you're going to want to put them on fluids right away. So you're probably going to want to put them on crystalloids. And these crystalloids are going to be really important that you put them on like normal saline or a ringer's lactate solution. So these are some really, really important things that you're going to want to do right away. Immediately try to get them on fluids.

Sometimes if you need to be able to stabilize their oncotic pressure. Sometimes you can give certain types of plasma volume expanders like you can give albumin, you can give albumin, or you can even give another compound called heta starch. This kind of stabilizes the colloid osmotic pressure.

So this is trying to be able to stabilize the colloid osmotic pressure. You want to try to stabilize that because this is controlling the amount of blood, I mean the amount of water that's actually leaving the bloodstream. If we lose a lot of albumin and heta starch, we're going to start losing a lot of water into the tissue spaces. That's bad. that can even make the actual blood volume go down even more.

So big thing, make sure you put them on IV, give them a lot of fluids to stabilize them. Another thing you're going to want to watch out for with these individuals is make sure that you prevent them from going into hypothermia because as you start losing blood volume, as you start losing the blood volume and it actually starts decreasing significantly, it affects you being able to regulate your internal body temperature. And so because of that, the person can develop hypothermia, so you want to make sure that you actually watch out for that. And control the hemorrhage.

If they start losing too much blood, You might have to do a transfusion. So before we move on to cardiogenic, I want to hit one more thing real quick. Because, like I said, we did cover a lot of this in low blood pressure, but it's going to be the same scheme for the rest of them. But one of the other things that can happen whenever there's low BP, whenever there's hypotension, it can stimulate the kidneys.

And the kidneys will start producing a chemical called renin. And then we said eventually renin got converted into angiotensin 1. I'm sorry, we should say renin actually converted angiotensinogen. into angiotensin 1. Angiotensin 1 got converted into angiotensin 2. Angiotensin 2 did two things, if you remember.

One is he went over here and binded onto these actual receptors to cause vasoconstriction, to increase the systemic vascular resistance, to increase the BP. Another thing is he went over here to the actual adrenal cortex and caused the production of a hormone called aldosterone. And Aldosterone, if you remember, went to the kidneys and increased the actual reabsorption of sodium and water to try to increase the blood volume. He also came over here to the actual pituitary gland and stimulated the release of another hormone, and this hormone was called the antideretic hormone. The antideretic hormone also went to the kidney and increased the reabsorption of water to increase the blood volume and increase the blood pressure.

And at the same time, it's going to try to activate certain centers that are going to trigger thirst. So the person might be a little bit more thirsty to try to consume fluids. So just so that you're aware, the mechanisms are going to be the same as it is whenever there's actually that low blood pressure, as they're trying to compensate for the situation by trying to increase the heart rate and the contractility. It's not going to have any effect, though. The vasomotor center will be activated to constrict the blood vessels.

That'll work a little bit. The renin is going to be released, so this renin-angiotensin-aldosterone-ADH system is going to come into play to try to pull a lot of water out of the kidneys into the blood, a lot of sodium out of the water into the blood. And it's going to also try to constrict the blood vessels. Okay, and this is going to be the same for how all these guys are trying to compensate during the shock. Okay, next one.

Next one is going to be cardiogenic shock. So you can actually hear what it's actually due to in the actual word. So it's a problem.

It's a problem that's actually due to the heart not being able to generate a certain amount of power. So you know the heart is responsible for contracting and propelling blood out into the actual systemic and peripheral. and pulmonary circulation, that's its responsibility.

It is the pump of the heart. So this guy is our pump, the ventricles are the pump. And in certain situations, the pump is failing in cardiogenic shock. What type of situations could cardiogenic shock be due to?

It could be due to various things. Cardiogenic shock could actually be due to, if we talk about some of the causes, one could actually be due to myocarditis. Myocarditis is an inflammation of the myocardium. The most common cause of this is like a Coxsackie's B virus, which is like an enterovirus. Another one could be due to massive or multiple MIs, myocardial infarctions.

So if someone has multiple myocardial infarctions, I'm going to put here MIs, or even really severe MIs, this could also be another cause. Another situation here could be certain types of valve dysfunctions. So you know like aortic valve stenosis or aortic stenosis. So aortic valve stenosis is a big one. Or maybe even mitral valve stenosis.

So even mitral valve. Okay? So even the mitral valve stenosis is another situation there too. Because it's, again, putting an increased workload on the heart, and the heart can actually start becoming very weak and not very good at its job. Other causes besides this could even be due to arrhythmias.

So arrhythmias is another really, really dangerous one. Because what happens is in arrhythmias, there's two types. There's actually a tachy, and then there's the bradyarrhythmias, right? So what happens in this is in tachyarrhythmia you're trying to increase the heart rate. But you're not giving the heart enough time to fill with blood.

As you don't give enough time for the heart to fill with blood, it's not going to be able to contract enough blood out. So it's affecting the filling and the ejection of blood out of the heart. So in tachyarrhythmia, this is also a negative influence.

And if your heart rate's really slowing down, it's going to decrease your cardiac output, which is going to decrease the amount of blood that's being pumped out of the heart. So again, it's due to a pump failure. Other common causes could even be due to dilated cardiomyopathy.

So dilated cardiomyopathy is another terrible condition here. And what happens is the actual ventricular muscle becomes very weak and actually becomes very flabby. and not very good at being able to pump at all.

Or even congenital heart diseases. So other ones could even be due to congenital heart diseases, like ventricular septal defect or truncus arteriosus. There's many of those.

But again, they could also contribute to this problem here too, if not completely treated. So congenital heart diseases, or somewhere down the line for these individuals. So that's the overall concept. Now, what's the problem?

Because we just said these people are having a hard time being able to pump blood out of the heart. So them trying to pump blood out into the circulation, they're not pumping an adequate volume of blood out into the circulation. So what's happening to the volume of blood that's being circulated? There's a decreased volume circulating. If there's a decreased volume of blood circulating, that means that you're having systemic hypotension.

Because if there's a decrease in blood volume, that means that there's a decrease in the blood pressure. So in these people, what are you going to notice right away? They are going to have low blood pressure. They're going to have a low cardiac output. Their heart rate is going to try to go up to compensate for them, right?

What else is going to try to compensate for them? What was that other mechanism? The renin, angiotensin, aldosterone, ADH system is also going to try to come into play.

And you're going to try to increase the actual vascular resistance. So what's another thing that they're going to try to do? They're going to try to increase the systemic vascular resistance. So you're going to notice that these people are going to have some tachycardia.

They're going to have some congestion of blood within the heart. They're going to have a low BP. They're not going to have an adequate volume circulating in the actual bloodstream. Why is this a problem?

Because if there's a decreased blood volume coming to the tissues, that means it's not going to deliver enough oxygen. If you don't deliver enough oxygen, that can cause ischemia. Ischemia can lead to necrosis, and necrosis of tissues can lead to organ failure if not treated. You see how it's just a circle constantly.

So because of that, if you're not giving oxygen to the tissues, what's the consequence of not getting oxygen to the tissues? So if you're not getting oxygen to the tissues, you know a lot of our metabolic pathways in the body depend upon oxygen to produce ATP. So as ATP levels decrease, two things can happen.

I'm sorry, as oxygen levels decrease, two things can happen. You can develop a decrease in ATP. This is really bad.

Another thing that can happen is you can develop an increase in what's called lactic acid. So if you're not getting enough oxygen to the tissues, you're not producing enough ATP by cellular respiration. This can decrease a lot of activities within the cell.

It can lead to almost complete cellular dysfunction, right? Protein synthesis, transport pumps, muscular contraction, neuron transmissions, all that kind of stuff. Another thing is your body shifts from aerobic cellular respiration, making ATP, to anaerobic cellular respiration, making a lot of lactic acid. Why is lactic acid bad? Because lactic acid...

can actually do what? It can disassociate and give up protons. As you produce a lot of lactic acid, you produce a lot of protons.

What's the problem with protons? They're very acidic. This can lead to metabolic acidosis. So the problem with having a lot of protons is it decreases the pH, and it leads to metabolic acidosis.

And this has a negative effect on the heart also. This can actually depress the actual... contractile activity of the heart also, as well as even the heart rate. So that's another negative influence.

Now, these are the causes. This is what's leading to this. And it's leading to a decrease in BPA, a decrease in the cardiac output. An increase in the heart rate is a compensating mechanism.

So let's actually put this over here. Since the heart rate is trying to increase, it's one of the compensation mechanisms, even though it's not going to be enough. So they're going to try to increase their heart rate, but it's not going to be enough to fix the issue. It's actually going to make it worse in certain situations.

If they're not getting an adequate volume of blood delivered to the tissues, this can actually lead to lactic acid buildup, ATP decrease, and if it happens for a long period of time, what do we say? Organ failure. Okay?

So this is why it can become so dangerous if it happens for a long period of time. Question is, how do you treat it? What do you do about it? Okay, well the big thing is, is you have to be able to, sometimes you might have to treat the issue. If they've had a myocardial infarction, what would you do about that?

How would you treat that? You'd want to definitely, if they have, so sometimes you're going to have to treat the underlying cause. So let's say that one of the underlying causes, just for an example here. Let's say it's an MI.

Let's say that you have an MI. What do you do about the MI? You can either do an angioplasty, or they go in and actually kind of remove the actual embolus within the coronary vessels. Or you just put them on thrombolytics. So certain types of things like tissue plasminogen activator, heparin, or things like that that will break up the clot.

Okay? So that's kind of some of the big things there. Next thing, how would you treat them in general?

Regardless if there's an animal, how would you treat them in general? The big thing that you're going to want to do right away with these people is you're definitely going to want to try to put them on oxygen. So some of the treatment here is you're going to want to put them on oxygen.

Give them O2. Okay? This is very, very critical. Give them O2.

Maybe give them a little bit of fluids. So very little isotonic fluids. Because the reason why is they're not losing blood volume. They're just not able to circulate enough blood throughout the heart.

So it's not a problem of decreased blood volume. It's the problem that the heart can't push enough blood out into the circulation. So you can give them a little bit of isotonic fluids to help the heart out a little bit.

But again, main thing is giving them oxygen. Oh, real big one, give them vasopressors. Vasopressors are really important in cardiogenic shock because they have a hard time being able to get the heart to contract very powerfully. So you're probably going to want to give them things like epinephrine. So epinephrine is actually going to be really important here because epinephrine is actually going to be two things.

One is it's a positive inotrope, meaning that it can increase the contractility of the heart. The other one is it can increase the systemic vascular resistance by constricting those blood vessels. Other drugs that you could give is like dobutamine.

Dobutamine actually acts just like epinephrine, but it actually is primarily a positive inotrope. So it tries to bind on to the beta-1 adrenergic receptors and increase the contractility. Another one that you can use, it's an unfortunate one, it's called amrinone.

Remember I told you that there was different stages? This is also going to increase the contractility. It's a positive inotrope. This one is an unfortunate one if you have to use it. Or you can even use atropine also, which is inhibiting the muscarinic receptors.

Amrinone is unfortunate if you go into the refractory period. So the refractory period is that point where it can become irreversible, even no matter how hard the doctor or the PA is trying to be able to revive the blood pressure, it's not responding. You can put them on amrinone. Amrinone is really good because it's a phosphodiesterase 3 inhibitor.

So it inhibits phosphodiesterases. And if you remember this, we said the phosphodiesterase breaks down cyclic AMP. Cyclic AMP is what controls the protein kinase A levels.

If you break down cyclic AMP, you decrease protein kinase A, which decreases the calcium coming into the cell. If calcium isn't coming into the cells fast, it's going to start slowing down the contractility. Okay?

So that's another thing that you could do there. Another one that you could actually do in certain situations is you could, if they really need it, you could do what's called an intra-aortic balloon, like pump. And it's a device that you actually kind of... to throw up in the aorta, right in the abdominal aorta.

And when you throw it up into the aorta, what it does is whenever your heart contracts, it stays deflated. But whenever the heart relaxes, it inflates and it starts actually expanding. The whole purpose of it is that whenever the person's in cardiogenic shock, their myocardium, their heart isn't getting enough oxygen.

So by using that pump, that balloon pump, it actually spreads out whenever the heart's relaxing, which pushes some of the blood into the coronary vessels, which helps to be able to get some blood to the actual myocardium to save the myocardium from irreversible damage. Okay, so that's one of the big things there for cardiogenic. All right, so that's that one. I hope that one made sense.

Let's move on to the next one. Let's go into obstructive. All right, guys, so now we're going to move into the last one here that we're going to talk about in this video.

In the next video, we'll actually talk about distributive shocks, those different types. Now, obstructive shock is really, really important. The reason why is you can tell what it's due to right in the name.

There's either some type of internal obstruction or some type of external obstruction of the heart, the chambers of the heart, or... due to the great vessels that it's supplying. So again, it's due to some type of internal obstruction or external obstruction that is affecting the blood flow out of the heart or into the actual great vessels.

And we'll talk about that. So let's go ahead and get started on that. So one of the big ones here is called a tension pneumothorax. I'm sure that you guys have heard this at some point in time.

If you watch TV, you probably hear it a lot, like on certain medical shows, right? But a big one here is tension. Pneumothorax.

We're not going to go into super detail on this, but just to make it simple, it's some type of situation in which there's, let's say that there's a stab wound. And what happens is, remember we talked about this in the actual respiratory system. We said that there's two types of pressures. We said that there was the called the P-pull, which was the intrapulmonary pressure. And we call it the PIP, which was the intrapleural pressure.

We said that the intrapleural pressure is usually negative four. MMHG, and we said the P-Poll is usually 0 MMHG. We also said that you never want the intrapleural pressure to become...

equal to or greater than the intrapulmonary pressure. What happens? Let's say that there's some type of situation where there's damage to the actual parietal pleura, maybe due to a stab wound.

What happens is air from the atmosphere, atmospheric air is right around 760 millimeters of mercury, whereas in the PIP, it's right around 756 mmHg. And so out here in the atmosphere, it's around 760 mmHg. Whereas what's higher pressure, the PIP or the P of the atmosphere? The atmosphere.

And things like to go from areas of high pressure to areas of low pressure. So what happens is the air starts moving into the actual pleural cavity, where it normally is containing fluid. As that happens, the air starts accumulating in this cavity, and what starts happening to the intrapleural pressure?

The intrapleural pressure starts increasing, and it starts going from negative 4, possibly to around maybe 0 or plus 1 mmHg. Why is that dangerous? Because now it's becoming greater than the pressure inside of the actual lungs. What that starts trying to do is, is it starts pushing on the lungs. And it starts compressing this way.

It starts shifting. So it starts trying to shift the mediastinum to the opposite or contralateral side. So one thing that can happen is as the pneumothorax develops, the air occupies this pleural cavity, pushing on the lungs, and it can shift the mediastinum.

Or it could even shift the trachea this way too, to the contralateral side. So what is this person exhibiting? They're exhibiting what's called a mediastinal shift. or a tracheal shift. Okay, now why is that bad?

If you shift this, what are you going to be doing? You're going to be compressing the heart and the vessels that are actually bringing blood into it and taking blood out. So as this starts happening, the tension pneumothorax starts pushing on the chambers of the heart and some of the blood vessels that are trying to bring blood up. What's this one vessel right here that brings blood up into the heart right here?

Inferior vena cava. If this is pushing, it'll start compressing it. What's the blood vessel that brings blood into the right atrium from the top?

The superior vena cava. In certain type of situations where the pneumothorax is really, really pushing and compressing on the heart, it can affect the heart from being able to get filled with blood, and it puts a lot of stress on the heart and restricts the heart from being able to eject the blood out. Okay? So two problems with the tension pneumothorax is it can actually compress the blood coming into the heart and compress the heart so it has a hard time pushing blood out. Okay?

That's it. Intention pneumothoraxes though, these are really dangerous. If it becomes really, really bad, what you can actually do is you'll also, they do like a little percussion. They kind of tap on the individual. They'll basically tap and try to listen for sounds.

When they tap, they hear this sound. It's like a hyper-resonance. It's a low pitch but kind of like a louder resonance. And it actually is called tympani. And that sound is identifiable that there might be some type of gas or air within that cavity that they're percussing.

That is one of the signs that they can actually do during the physical exam to see, oh, maybe this person does have a pneumothorax. Obviously, you'd have to go send them to do certain types of maybe like an x-ray to check that out. But the whole concept is that you might hear what's called hyper-resonance when they do the percussion technique. Also, they might have decreased breath sounds because the lung is collapsing.

If that lung is collapsing, they'll have decreased breath sounds on that affected side. Also, since it's compressing the actual superior vena cava and the inferior vena cava, the blood is having a hard time coming back into the heart. So what's another sign that you might see for tension pneumothorax? You might see that the person will have a high jugular venous pressure.

You're probably like, okay, well, that's cool. You'll see it because their neck veins will be a little distended too, okay? All right, cool. That covers the tension pneumothorax. Next one is called, you can call it pericardial tamponade or cardiac tamponade.

I'm just going to write here pericardial tamponade. Pericardial tamponade is due to some type of situation in which a lot of fluid starts developing with inside of what's called the pericardial cavity. So let's say here's the cavity right here.

You have the different parts of the pericardial cavity like the serous layer and then you have the actual outer parietal layer or you call it the visceral layer and the outer parietal layer here. In between those layers of the pericardium, you have this actual serous fluid, this pericardial fluid. In certain situations, it's supposed to be in normal amounts.

But... For whatever reason, in these individuals, they start having a lot of fluid accumulation in here. And the fluid starts getting so much in this area that it actually starts compressing on the heart, strangulating the heart, squeezing the heart. So as this starts happening, it starts really, really putting a lot of pressure onto the heart.

What do you think that's going to do? Do you think that this heart is going to be able to fill with blood adequately? No, because I'm squeezing it. So I'm decreasing the volume of my heart chambers. So me trying to get blood into the heart is going to be a lot.

harder and it's actually squeezing the heart so that the heart is going to have a hard time being able to contract too. Same thing. In this situation, they have a hard time filling the heart with blood and the heart is so restricted because of this actual pericardial tamponade squeezing and strangling the heart that it even has a hard time contracting.

Two problems with this person, again, is going to be they're going to have a hard time contracting the heart and filling the heart with blood. Now, a pericardial tamponade, it actually kind of, I don't know, there's some guy, I guess his name was Beck. And he came up with a triad of things that comes about during the pericardial tamponade. So let's say I put a triangle here. So this is called Beck's triad.

And this is usually identifiable for someone who's going to have some type of pericardial tamponade. What are these symptoms here? One is because the heart is having a hard time filling with blood, that...

that actual superior vena cava and inferior vena cava are probably being compressed. So their jugular vein is going to be actually distended, right? So they're going to have a high jugular venous pressure.

Another one is they're going to have a high blood pressure. So they're going to, I'm sorry, not a high blood pressure. They're not being able to pump enough blood onto the tissues.

So because of this, they have a low blood pressure because, again, the heart's not filling with blood adequately, and it's not squeezing and pushing enough blood out. So because of that, the amount of blood that's being pumped out of the heart is very, very low, so they can have hypotension. Another one is because if you do what's called oscillation, you're trying to listen to the heart sounds, that fluid is making it a lot thicker. So you trying to hear the sound is not going to be as well. It sounds like it's actually moving from a farther distance.

So we call it muffled or distant heart sounds. Okay? So that's some of the things that you'll see within a person with having pericardial tamponade.

So again, with this person, there's an obstruction. They're having a hard time getting the blood out. Another super, super terrible one is a massive, massive pulmonary embolism.

Let's say that a person develops an unfortunate embolism right here in the pulmonary trunk. You know what that's actually called? That's called a saddle embolism.

So let's say that they develop some type of massive PE, okay? So if they have a massive PE, there's a big old embolism. blocking the actual pulmonary artery blood flow. So this person is gonna try to be able to pump blood from the right side of the heart up into the lungs.

But what's the problem? They got this big old embolus blocking the way. So the amount of blood flow getting passed through this area is very, very low, which means that very little fluid is coming back to the actual left ventricle. If very little fluid is coming back to the left ventricle, what happens to the EDV?

The EDV is going to decrease significantly. As the EDV decreases, what happens to the stroke volume? The stroke volume decreases.

As that decreases, what happens to the cardiac output? That decreases. That decreases. Then what happens to the BP?

That decreases. So you can see how this can cause hypotension too. You can see how this causes hypotension because the heart can't pump enough out and it can't fill properly. You can see how this one can cause hypotension because the same thing. Heart isn't filling properly.

It's not contracting properly. In this situation, there's an embolism blocking blood flow to the left side of the heart, decreasing the BP. Also, think about this.

You got a big old embolism. Is there going to be a lot of blood coming out of the right ventricle either? No. It's the same thing.

You're not going to get a lot of blood out of the ventricles. That's one problem. But then you got another big problem. What if this embolism is so bad that the pressure starts accumulating in this area so high, the pulmonary capillary wedge pressure?

These people have a high pulmonary capillary wedge pressure, which is the pressure that's trying to push blood back to the left atrium. If this pressure is really, really high in this situation, Because the actual, trying to get to that area is really, really being negatively affected here. They aren't able to get this to that area. They aren't able to get the blood to that area. That pulmonary capillary wedge pressure can start getting a little high in this situation.

And it can actually rupture some of those capillaries. And as it starts rupturing a lot of those capillaries, it can cause the spitting up of that blood, that hemoptysis. Also, if you don't have a lot of blood flow coming through this area, if you don't have a lot of blood flow coming through this area, what's going to happen to the actual ventilation perfusion process? It's not going to be good.

So you guys remember we did this in respiration. We said that there was the VQ ratio and it was equal to normally about 0.8. Well, what is Q? That's the perfusion. In this case, the perfusion is decreasing.

If the perfusion is decreasing, what's happening to the overall number then? Then the overall number is going to be greater than 0.8. What do we say happens in this type of situation? In that type of situation, the ventilation has to decrease.

So now the ventilation is going to decrease. What does that mean? The bronchioles might start constricting. So you're going to have a lot of, you're going to have a really hard time breathing.

So there might be some respiratory distress that could come about in this situation. Also, if there's a VQ mismatch, what happens to the oxygenation of the blood? It doesn't oxygenate properly. And this person can develop what's called hypoxia. Hypoxia.

Another negative thing can come about from this, right? And if you develop hypoxia, what does that mean? You're not going to be able to deliver adequate oxygen to the tissues.

If you can't give adequate oxygen to the tissues, the tissues become ischemic. If they become ischemic, they become necrotic. If the tissues become necrotic, the organs can start fading. So you can see why this is just a consistent repeat of everything. Other things that you might see within this person is because they have hypoxemic hypoxia, if you do what's called an ABG, an arterial blood gas, if you do an ABG, you're going to...

notice that these people have a very low ABG. So they're going to have a partial pressure of oxygen. Their partial pressure of oxygen is actually going to be a lot less than 80 millimeters of mercury. That's one thing that you might notice here. Also you might even notice that they might have some elevated lactic acid levels too.

Okay, because again, they're not getting oxygen to the tissues. So their body is shifting from aerobic respiration to anaerobic respiration. And again, if not treated, this can cause the person to go in multiple system organ failure, right? Depending upon the organ, that could be devastating.

Another one I'm not going to really include here because it's not one of the serious ones, but it can be, that's very, very close to the heart. So if you get a proximal aortic dissection, A proximal aortic dissection can actually be very, very close to the heart, and if it actually starts dissecting, it can squeeze on some of the vessels supplying the heart, and that can affect the actual filling of the heart, and it can affect the actual ability to eject blood into the aorta as well. So that's another situation.

So again, to recap this one, it could be due to a tension pneumothorax, which causes a mediastinal or tracheal shift, which compresses the heart and squeezes the heart, and the heart has a hard time filling with blood. Because it has a hard time filling with blood, it can't contract enough blood into the circulation. So they're not ejecting enough blood out into the peripheral circulation.

So their volume that's circulating is decreasing. That's going to cause hypotension. As this happens, they're not able to deliver enough oxygen to the tissues, and this can result in an actual ischemia. Pericardial tamponade is the fluid is accumulating there and strangulating the heart, causing the same situation as this tension in the thorax.

And then we said the worst one is a massive pulmonary embolism, like, for example, like a saddle embolism blocking right there at the pulmonary trunk. which is affecting the blood flow towards the actual left side of the heart. Now, the right side of the heart has a hard time getting blood out.

That's going to decrease their actual cardiac output, and it's going to decrease the amount of volume coming back to the left side of the heart. So they're going to have a hard time being able to get blood out too. And we shouldn't actually include in this pulmonary capillary wedge pressure.

It's not really significant into this one. Really, the important one where the pulmonary capillary wedge pressure can be included is going to be in cardiogenic shock. So we're not going to really talk about... the pulmonary capillary wedge pressure in this one.

But seriously, we just need to understand here, if there's a massive PE and it's occluding the blood flow to this area, it can decrease the volume coming back to the left side of the heart, which is decreasing the EDV, decreasing the stroke volume, decreasing the cardiac output, and decreasing the blood pressure. If that volume that's being circulated out to the actual peripheral tissues is decreasing, it can cause ischemia, it can lead to the necrosis, and can cause a serious organ failure. How would you treat these people?

it obviously depends upon the actual cause. If they have a tension pneumothorax, do a needle decompression. So insert a needle in there and equalize the pressures that you can get the air out of the actual pleural cavity.

If they have a pericardial tamponade, do what's called a pericardiocentesis, where you actually drain the actual fluid out of the pericardial cavity. If they have a massive pulmonary embolism, you might have to give them thrombolytics. You might have to do some type of embolectomy. You might have to give them heparin to be able to prevent that from actually becoming very dangerous, right?

It can cause sudden death there. And if they have some type of proximal aortic dissection, you're going to have to go in there and do some type of surgical intervention. But same thing here with these people. Put them on oxygen.

What would you do here? So the last thing is the treatment here. We said that if you're going to treat these people, what would you do? Obviously, it's dependent upon each underlying cause. But other ones is you'd want to give oxygen.

Give them oxygen. The next thing is you can put them on isotonic fluids. That's another really important one. And same thing with these individuals. You're going to have to give them some vasopressors.

So in this situation, give them some vasopressors to increase the inotropic action, the contractility of the heart, and drugs that can actually cause the vascular constriction. And if you start causing vasoconstriction, that's going to increase the resistance and increase the blood pressure. Alright, so what we did in this video is we talked about the types of shock that is usually a result of some type of decrease in the cardiac output, where the heart rate isn't sustaining enough and the stroke volume isn't sustaining enough to increase that.

where these people have a high systemic vascular resistance. In the next video, where we talk about distributive shock, we're going to see how this shock is actually more due to actually a decrease in the systemic vascular resistance. So now the blood vessels are excessively dilated and how that can affect tissue perfusion. So Ningeners, I hope to see you there, where we talk about distributive shock in great detail.

Thanks for watching this video. I hope that you guys really did enjoy it. If you guys did, please hit the like button, comment down in the comment section, and please subscribe.

As always, Ningeners, until next time.

Transcript for:Understanding Different Types of Shock

Transcript for:
Understanding Different Types of Shock