They WILL Ask You About Shock in Your CRNA Interview

(upbeat music) - Hey guys, welcome back to the SierraNate Club podcast. I'm Sachi, practicing SierraNate and founder of the SierraNate Club. Today we're going to be discussing shock. All four types, Hypovolemic, cardiogenic, distributive, and obstructive. At the depths, a SierraNate program expects you to think at. This is going to be a little bit of a longer episode, so hopefully you've got a bit of a commute in front of you. But by the end of this, you'll be able to explain each shock state from the cellular level up, talk through what causes each type, recognize them as they move through the compensated and decompensated phases, and walk an interviewer through your reasoning out loud. This episode is meant to be interview prep for you as well. We'll start with what causes these types of shocks, then move on to the mechanism, and then talk through specific patient signs and symptoms for early and late stages, and we'll finish with how you'd answer if an interviewer put that patient in front of you. But before we get into it real quick, if you're listening to this, you probably are either applying soon or are just starting to think about it, and either way, the SierraNate Club is built for exactly what stage you are at. If you're just starting your school search, you can look at our SierraNate School database where you can save programs, take notes for each one, and check open houses and school events in our event library. If you're applying in the next year or two, this is the perfect time to start working through the lessons in our learning and library. So you actually understand what it takes to be competitive instead of just guessing or reading Reddit. And you start using the tools, the transcript analyzer, the clinical tracker, the shadow day tracker, the event tracker, because the more you track and document, the more our platform learns who you are, and it can give you better personalized recommendations on how to get more competitive. So then when you go to write your resume and your essay, we'll flag what you missed where you're underselling yourself, because this is truly a one of a kind platform we created a smart platform that's meant to guide you through every step. This is totally unique, nothing out there is like this, and I'm pretty proud of it I've been working really hard on it the last two years. So this is not just for the application phase, most people actually join us during the planning phase before they're even quote unquote actively applying. That's the purpose because that's where you get the most out of it and gives yourself the best shot at acceptance. Of course we have interview prep to our mock interview lab, our essay critique tool, our resume review tool, and truthfully the earlier start, the more it works for you. And you can try all this free for seven days at this year on a club dot com. All right, let's go ahead and get into shock. So before any of the four, we need to the framework that sits underneath all of them because shock is really one problem with four different causes, right? Shock is an adequate tissue delivery relative to demand. Oxygen delivery is cardiac output multiplied by arterial oxygen content. Let me see that again. And arterial oxygen content is mostly your hemoglobin multiplied by its saturation with a small dissolved fraction on top. So there are three things that drive oxygen delivery and those are cardiac output, hemoglobin and saturation when any one of them fills delivery falls with it. So now let's think about the demand side of the equation. Under normal conditions, the tissues extract only about a quarter of the oxygen you deliver, which leaves a very large preserve, you know, by design. But when delivery starts to drop, the tissues respond by raising their extraction ratio, meaning they're pulling off a bigger fraction of oxygen. And for a while, oxygen consumption holds steady even as delivery falls. We call that supply independent oxygen consumption. And it's one of the body's earliest compensation mechanisms. But it only works down to a point, right? Once delivery falls far enough, that extraction is maxed out. That's when you hit what's called the critical oxygen delivery threshold. Below that threshold, consumption becomes purely supply dependent, meaning it falls as delivery falls. The cells shift to anaerobic mechanism metabolism and lactate starts to rise. So when you see a rising lactate, that's your signal that delivery has crossed that critical threshold and compensation has failed. And there's one more number that tells you how hard the tissues are working to extract oxygen. And that's the mixed venous oxygen saturation. So that's the saturation of blood coming back to the right heart, which normally runs somewhere around 65 to 75%. So when that number is low, the tissues are extracting more than usual because delivery is low. And that's the case in most shock states. But when it's unexpectedly high in a patient who's clearly sick, it tells you that the tissues aren't extracting oxygen even though they're hypoperfused. And that points you straight to sepsis. So we're gonna talk about that. That's essentially the heart of this entire episode. So there are four ways oxygen delivery breaks down. And I'll keep referring to them as the tank, the pump, the pipes, and the obstruction just as a way to keep the category straight. So let's start with the tank. So hypofolimic shock is a loss of circulating volume. The heart is fine and the vasculature is fine. There simply isn't enough volume in circulation to maintain venous return and cardiac output. The causes fall into three groups and grouping them is how you keep them straight when an interviewer puts you on the spot. So the first group is blood loss. And that's trauma, a ruptured aneurysm, a GI bleed, a surgical bleed, or even postpartum hemorrhage. In all of those, the patient is losing volume and oxygen carrying hemoglobin at the same time. Second group is plasma loss, which you see in large burns where plasma leaks out through damaged capillaries or in pancreatitis where fluid third spaces into the retroperitoneum and the gut. The third group is pure water and electrolyte loss. And that's a severe vomiting and diarrhea, high output drainage or diabetic ketoacidosis, which drives big, osmotic dioresis. Different sources, but the end result is always the same, which is an underfilled circulation. Now let's move on to the mechanism of hypofolimic shock. And this is what interviewers are kind of wanting to hear. So when volume drops, the venous return drops, right? And that lowers the preload in both the right and left ventricle. And when we think about the Frank-Storyling relationship, that means less stretch on the cardiac sarcomere at end-diastoleum means a weaker force of contraction. So stroke volume falls and cardiac output falls along with it. The drop in arterial pressure then unloads the baryroreceptors in the carotid sinus and the aortic arch. Those baryroreceptors slow their firing rate, which removes the tonic inhibition. They normally place in the vasomotor center and sympathetic outflow surges. The nor epinephrine acts on cardiac beta-1 receptors to raise the heart rate and contractility. And it acts along with circulating epinephrine on vascular alpha-1 receptors, where it activates the GQ pathway, which raises intracellular calcium and vascular smooth muscle, constricts the arterials and veins. That raises systemic vascular resistance, right, SBR. And it shifts blood out of the venous capacitance vessels back into the central circulation. On top of that, the drop in renal perfusion activates the renin angiotensin aldosterone system. So angiotensin II adds more vasoconstriction, while aldosterone and ADH hold on to sodium and water. Every one of those steps is a compensation. And the reason hypovolemia is dangerous is that these compensations work well right up until they don't, basically. The reason blood loss is distinct from other causes is that you lose two of the three oxygen delivery variables at once, right, the volume and the hemoglobin. So if you replace that loss with crystalloid alone, you, yes, you restore the preload, but you dilute the hemoglobin that's left, which means the patient can normalize their blood pressure and still be oxygen delivery deficient because the carrier is gone. That's the reason hemorrhage needs blood products and not just crystalloid. And if you make that distinction in an interview, you've shown that you understand oxygen delivery and not just blood pressure. Now let's talk about what this patient actually looks like because the early picture and the late picture are completely different and the clearest way to differentiate that is through the graded classes of hemorrhage. So in class one, the patient has lost up to about 15% of their blood volume and the signs are minimal, right? The heart rate is still under 100, the blood pressure is normal, the pulse pressure is normal. They might be slightly anxious. If you weren't told they were bleeding, you could easily miss it. Once they've lost somewhere between 15 and 30% of their volume, you're in class 2 and now the picture is starting to change. a little bit. The heart rate climbs over 100 and their systolic pressure looks still preserved, but the diastolic actually rises because all that construction is squeezing the vessels and that means the pulse pressure narrows. A narrowing pulse pressure is one of the earliest objective signs of hemorrhage and it shows up before the systolic number ever starts to decrease. Alongside that, you'll see cool skin, delayed capillary refill, urine output will be decreasing towards 20 or 30 ml per hour, and of course if they're awake, the arising anxiety. Now, when the patient has lost between 30 and 40% of their volume, they've moved into class 3, and this is where compensation begins to fail. Now, the systolic is finally dropping the tachycardia's market and the pulses go thready, the patient gets confused, that urine output falls below 20 ml an hour and the lactate starts to climb as oxygen delivery crosses that critical threshold we talked about earlier. And then, once they've lost more than 40%, they're in class 4, which is immediately life threatening. At that point, you're looking at profound hypotension and uptended patient, no urine output, and essentially no compensation. So, the single most important takeaway from these classes is that the systolic blood pressure is the last variable to fall, and that's the one we kind of like fixated on the most, right? The heart rate, the narrowing pulse pressure, the cool skin, and the falling urine output all show up before the systolic drop does. So if you wait for the blood pressure to start decreasing, you've waited too long. So here's how this might come up in an interview, you know, somebody might ask you, your post-op patients heart rate is climbing into the 130s, and the cuff still reads 98/70. Walk me through what you're thinking. And you'd answer that you're concerned about early high boob early make shock, right? And that the preserved systolic doesn't necessarily reassure you because the tachycardia and the narrowing pulse pressure tell you that the patient is compensating rather than stable. You know, you say you're going to be assessing skin temperature and capillary refill and checking the urine output looking at the surgical site if they have one or drains. You'd name your concern, which is abrupt decomposition once the compensation fails, right? You don't want them going over that end to the cliff. You would tell them you want to establish large bore IV access, make sure there's a type in screen or type in cross, send a lactate, and notice notify the provider. Because if this is volume loss, the treatment is volume. And remember, we said source control. If they're bleeding, you got to stop the bleeding. There's an active hemorrhage. The answer is blood, not always just a pressur. So when you're answering these types of questions, you want to talk through your assessment, what you're thinking, how you're anticipating, what physical signs and symptoms you're looking for, and what the next steps are that you're taking. And real quick, if you want to go deeper on these hemodynamic profiles, the CVP, SVR, the cardiac output patterns, we have all that in our learning library at this urnicclub.com. And in the pathophysiology module, we have a hemodynamic lesson where we go much deeper on all of this. Okay, now let's move on to the pump. So cardiogenic shock is pump failure. The volume is adequate and the vascular chair is intact, but the heart can't generate enough cardiac output to perfuse the tissues. And there are five main causes. The leading one is an acute myocardial infarction that takes out a large mass of the left ventricular muscle. After that, come the mechanical complications of an MI like papillary muscle rupture that causes acute mitral regurgitation or a rupture of the ventricular septum. And then you have end-stage cardiomyopathy and decompensated heart failure. Then the arrhythmias, both the tachy arrhythmias and the brady arrhythmias that are too fast or too slow to maintain output. And finally severe valve disease, like a critically tight erotic valve that the ventricle can't push through. So now let's talk about the mechanism. And this is where we get down to the cellular detail that is important for serenity school and for interviews. When myocardium become ischemic, ATP production drops, right? And the thing that people forget is that both contraction and relaxation depend on ATP. After each contraction, the sercopump, which if you've taken an events physiology course, you'll know what that is. But the sercopump uses ATP to move calcium back into the sercoplasmic reticulum. That's what moves calcium back into its doors. And that's what allows the myocytes to relax. So when ATP runs short, the sercopump fails, calcium is still out there. It's still lingering in the cytosol. And the myocytes can't fully relax between beats. So diastolic stiffness rises and contractility falls. So clinically, this is going to be seen as a result or a drop. It's going to result in a drop in stroke volume. Then the failing output triggers the very same sympathetic composition we saw in hypoverlemia, which is alpha-1 vasoconstriction, raising SVR and beta-1 stimulation, raising heart rate, right? We talked about that. But this compensation actively harms a failing ventricle. And that creates this spiral. Raising SVR raises afterload, which is, of course, the tension that the ventricle has to overcome to eject, right? And a failing ventricle is super afterload sensitive. So a higher afterload reduces stroke volume even further. That's the first loop, the second loop is worse. Cornering profusion to that left ventricle happens mostly during diastole. You need to know that. And it depends on aortic diastolic pressure. So as cardiac output and pressure fall, cornering profusion pressure falls with them. The myocardium gets more ischemic, contractility drops further, and output falls again. You've got two positive feedback loops driving the ventricle down. And talking about that in an interview is the exact kind of reasoning that's going to set you honestly very far apart. It's also why cardiogenic shock carries such a high mortality, and why you have to often offload the ventricle mechanically rather than just chemically. There is a Frank Starling point here too. I know you can't escape the Frank Starling mechanism. And in clinical terms, this is how it goes. So a normal ventricle responds to a fluid bolus with more stroke volume because it's sitting on the steep part of the curve. A failing ventricle is already on that flat portion of the curve, right? So giving it more preload produces absolutely are very little, no increase in output, and instead just raises the filling pressures. And then those pressures transmit backward into the pulmonary circulation as pulmonary edema. That's exactly why we do not bolus, reflexively bolus, a cardiogenic patient. And it also matters which ventricle is failing. When the left ventricle fails, pressure backs up into the pulmonary circulation. So you get pulmonary edema, crackles, a rising oxygen requirement for all these secretions in a vented patient, and that S3. When the right ventricle fails, as in a large right ventricular infarct, pressure backs up into the systemic venous system instead. So you get JVD distension, hepatic congestion, and peripheral edema with clear lungs. That right-sided patient is the trap because they're hypotensive with clear lungs. And so the reflex is to give them fluid, right? But a failing right ventricle is often preload intolerant and will get worse with a large bolus. So knowing which ventricle failed exactly changes what you do. So when you put the whole picture together, cardiogenic shock shows forward failure and backward congestion at the same time. The forward failure gives you the low output signs, the cool, clammy skin, the modeling, the weak pulses, the oliguria, the altered mentation, narrow pulse pressure, and the rising lactate. The backward congestion gives you pulmonary signs if it's the left ventricle, and systemic venous signs if it's the right. So the classic left-sided patient is cool at the periphery and wet in lungs, which is why people describe cardiogenic shock as cold and wet. So the hemodynamic profile, the way you'd say it in an interview, is high filling pressures, low cardiac output, and a high SVR. And the way that you would distinguish it from hypovolimia is by those filling pressures. Because in cardiogenic shock, the central venous pressure and the wedge are high. Whereas in hypovolimia, they're low, even though both share a low cardiac output and a high SVR. So treatments. Treatment targets contractility and afterload. Dobute mean is a beta-1 agonist, so it raises cyclic AMP, increases calcium influx per beat, and increases contractility with a little beta-2 vasodilation on the side. Milver-known reaches the same endpoint, but a totally different route. Because it inhibits phosphodiesterase-3, which means it preserves cyclic AMP instead of generating it through the receptor. And it inhibits that same enzyme in vascular smooth muscle, so it vasodilates at the same time. We call a drug like that in ionodilator, because it increases contractility and reduces afterload together, which is exactly what a failing afterload sensitive ventricle needs. The catch is that it can drop the blood pressure, so it's often paired with a vasopressor to hold the map up. And the reason we Why you might pick miller-known over dubutamine is that when the beta receptors are down-regulated from days of cataclylumine exposure, phosphodiesterase inhibition works downstream of the receptor, so it still gets its effects through. Beyond the drugs, you break the spiral mechanically by revascularizing BMI, correcting the rhythm, or using mechanical support like an intra-aortic balloon pump and impella, or ECMO to physically unload the ventricle while it recovers. So in an interview, they might say, "Okay, your patient is hypotensive. The lungs are full of crackles and the urine output has dropped. What are you thinking here and what are your next steps?" And you'd answer that you're concerned about cardiogenic shock, right? Because crackles together with oliguria tell you that the heart is failing. It's failing forward and congesting the lungs backward at the same time. You'd talk about how you assess the oxygenation and work of breathing, review the rhythm and the most recent EKG antroponin for ischemia, and listen for an S3 or a new murmur. You'd talk about your concern, of course, as the worsening pulmonary edema continues. You'd talk about forward failure. And you'd say you'd prepare for escalating oxygen support up to positive pressure. You'd anticipate the provider wanting anotropy, rather than a fluid bolus, and you'd be cautious with large volume fluids because more preload just backs into the lungs that are already wet. So that discusses what you're worried about, what you'd assess, and what you'd anticipate. All right, now let's move on to the pipes, distributive shock. Distributive shock is a loss of a vascular tone, so cardiac output is normal or even elevated early on. What collapses is the SVR here. So the causes are worth separating because each one is going to kind of change how we approach to this. The most common is septic shock. We're all familiar with septic shock. That's the one we'll go deep is down here because that's probably what you're going to get asked about in an interview, especially if you work in like a make you. Then there's anaphylaxis, which is IgE mediated. Then there's neurogenic shock, which comes from a spinal cord injury above roughly the T6 level. And then a handful of others, which includes adrenal crisis and certain vasodilatory toxins or overdoses. Now the mechanism of vasodilation in sepsis, bacterial endotoxins and exotoxins trigger the release of inflammatory mediators, including interleukin 1, interleukin 6, and tumor necrosis factor, inducible nitric oxide synthase, thase, or enos, through the vascular endothelium and smooth muscle. Enos then generates large, sustained amounts of nitric oxide. That nitric oxide diffuses into the vascular smooth muscle, which activates Guiana little cyclase, which raises cyclic AMP and activates protein kinase G, which deactivates miles in light chain kinase and opens potassium channels that hyperpolarize the cell. So essentially the smooth muscle can no longer maintain tone. The vasodilation becomes profound and widespread and resistant to normal vasoconstrictor signaling. The SVR collapses and the arterial pressure falls even though cardiac output is normal or high. So septic shock is not just one shock. It's distributive hypervolumic and cardiogenic kind of all happening at the same time. It's distributive because of that enos driven vasodilation we just walked through. It's hypervolumic in two different ways, right? There's an absolute hypervolumia because of the inflammatory mediators increasing capillary permeability and fluid extravizes out of the vasculature into the interstitium. And then there's a relative hypervolumia because the widespread phenodilation increases venous capacitance. So the same blood volume is now spread across a much larger venous reservoir and the effective venous return to the heart falls even though no fluid has actually been lost. So that's why septic patients are volume responsive and need aggressive fluid resuscitation even when their total body water is high. And on top of that, it's cardiogenic because those same circulating inflammatory mediators directly depress myocardial contractility which we call septic cardiomyopathy. So through the septic pathway, the pump itself starts to fail. So when you see it that way, the staged treatment of sepsis makes complete sense, right? You give antibiotics and control the source to stop the mediator release. You give fluids for the absolute and the relative hypervolumia. You add norepinephrine for the vasoplegium and then you add inotropic support if septic cardiomyopathy develops. That's three physiologic problems treated in layers. Now, let's bring back that mixed venous oxygen saturation we mentioned earlier. So in hypervolumic or cardiogenic shock, that number is low because the tissues are extracting maximally against a low delivery. But in sepsis, it's often normal or even high in a patient who's dying and that's kind of the word part. It happens because micro circulatory shunting routes blood past the tissue beds that need it and mitochondrial dysfunction impairs the cell's ability to actually use the oxygen that's delivered. So in sepsis, the lactate rises from both an impaired delivery and impaired utilization. A high lactate alongside a high mixed venous saturation in a septic patient reflects oxygen that's being delivered but not extracted or used. And that's a graduate level finding that interviewer is really, really like you to talk about. Okay, so let's talk about what this patient looks like because sepsis is the one type that doesn't really resemble the others early on, early septic shock is warm and hyper dynamic. Flush skin, warm skin, bounding pulses, a wide pulse pressure, brisk capillary refill, tachycardia and often a fever, and that's because the high cardiac output and the vasodilation are keeping the periphery well-prefused. That warm phase is exactly what causes people to underestimate how sick the patient is. Then as the septic cardiomyopathy and the capillary leak progress, the picture converts to cold, modeled, oliguric, which is the common end stage appearance of every shock, right? And anaphylaxis layers its own symptoms and findings on top of the vasodilation with ureta-caria, angiodema, broncospasm, you know, you hear those wheezes in the strider and even GI symptoms. And it comes on within minutes of exposure. Neurogenic shock has the most distinctive presentation of all, which is hypotension and bridiocardia together, plus warm dry skin below the level of the injury because the cord injury interrupts sympathetic o-flow so the patient can't mount either a tachycardia or a vasocontrictive response. So the treatment in septic shock follows this mechanism, right? You give early antibiotics and source control, you give fluids while the patient is still volume responsive, you reach for nor epinephrine as your first line vasopressor, and the reason we're reaching for nor epinephrine is because the problem is alpha-1 vasoplegia. And nor epinephrine is a potent alpha-1 agonist that activates GQ, raises smooth muscle calcium and restores vascular tone, with just enough beta-1 supports and maintain the output. And then you add vasopressand, second line as the nor epinephrine climbs. There are two reasons for that. The first is that a relative vasopressant deficiency develops in prolonged sepsis as the bodies and dodging of stores get depleted, so you're actually replacing its efficiency. The second is that vasopressant acts on V1A receptors, which keep working in an acidic patient better than the alpha-1 agonistric receptors do. So it holds when the catacole means it starts to fail. Neuflaxis by contrast is treated with epinephrine rather than nor epinephrine because you also need the beta-2 bronchodilation and the mast cell stabilization alongside the vasoconstriction. And neurogenic shock often needs a coronatropic agent because that Brady cardia is part of the problem. It's not just the hypotension. So now let's get to obstructive. Obstructive shock is a mechanical appearance to cardiac filling or output. And on the numbers, it mimics cardiogenic shock with a high filling pressure, a low cardiac output, and a high SBR. But the difference is the mechanism, right? Because the mild cardium itself is intact. And what's wrong is that an extra cardiac process is physically obstructing either filling or ejection. So three causes dominate here, and for each one, the anatomy itself is actually the diagnosis. So we're going to go over the causes and the signs together. So the first one, massive pulmonary embolism, which obstructs flow through the pulmonary vasculature. You know, a large clot in the main pulmonary artery or in the bilateral branches acutely raises right ventricular afterload. And because the thin walled right ventricle isn't built for high pressure, it dilates and it fails. And ventricular interdependence makes it worse because the right and left ventricle share the intraventricular septum inside a fixed pair of cardiome. So as the right ventricle dilates, the septum bows over into the left ventricle and impairs its filling. Output drops from both ventricles at once. The patient presents with sudden hypotension, tachycardia, and severe hypoxemia that's out of proportion to the lung exam, along with JBD extension from the filling right heart. So the tell here is sudden profound hypoxemia. with a relatively clear chest. The second cause here is attention pneumothorax, where air accumulates under positive pressure in the pleural space, collapsing the lung on that side, and then shifting the media's stynam, which kinks the great vessels at obstructs Venus return. So the patient presents with a sudden hypotension, absent breath sounds on the affected side, hyperresonance to percussion on that side, tracheal deviation away from the affected side, and jugular Venus' distinction. In a ventilated patient, the giveaway is sudden hypotension, along with rising peak and plateau airway pressures, because thoracic compliance is dropping as the pleural pressure builds. So this one is a clinical diagnosis that you need to treat immediately and take action on. You really can't wait for a chest x-ray. The third is cardiac tamponon, where a paracardial fluid under pressure compresses the heart. As the intra-paracardial pressure rises, the thin-walled right atrium and right ventricle get compressed during diastole, so filling is impaired and the out-foot falls. The classic Bex triad, which is hypotension, JVD distension, and muffled heart sounds, shows up in only about a third of cases, so its absence doesn't rule tamponon out. You also want to look for a narrowing pulse pressure, tachycardia, and pulses paradoxes, which is an inspiratory drop in systolic pressure of more than 10 millimeters of mercury. And the context carries the most weight here, because tamponon follows recent cardiac surgery, trauma, malignancy, or procedure near the paracardium. So when the interview panel asks you how to separate obstructive from cardiogenic shock, since they look essentially identical in the numbers, the answer is that you separate them with the history in the exam, right? By looking at the right ventricular strain, the lung exam, the tracheal position, the airway pressures, and by asking what was happening right before the patient decompensated. Now, since your interviewers are serenades, of course, you have to understand the effects of positive pressure ventilation here. So when you put a patient on a ventilator, you raise the intra-thoracic pressure, which reduces videos return, and that's the opposite of normal spontaneous breathing, where negative pressure actually helps draw blood back to the heart. In a patient with normal reserve, that's tolerated without a problem, a patient whose physiology is already dependent on venous return, like a high-bow volumic patient, or anyone in obstructive shock, the moment you put them to sleep and switch them to positive pressure ventilation, the preload can drop precipitous sleep, and patients can rest on the table. That's why a high-bow volumic trauma patient, or a tamponon patient, can code right away as soon as we put them to sleep. And that's why the principal is typically to resuscitate the volume, before we take them to the operating room. All right, the treatment for obstructive shock is mechanical every time. A pulmonary embolism needs anti-collegulation, thrombolytics, catheter-directed therapy, or an embolectomy. Attention pneumothorax needs needle decompression followed by a chest tube. A tamponon needs paracardiocentesis, or surgical drainage. Pressors in fluid will buy you a few minutes, sure, but they don't remove the obstruction, and the patient is not going to recover until you remove the obstructions that's causing their issues. So in an interview, a faculty member might say, "Your ventilated postcardiac surgery patient suddenly drops their pressure. Their neck veins are distended. What are you concerned about, and what do you do?" And you did talk about, okay, your concern about an obstructive process that with recent cardiac surgery, your leading concern might be tamponon with tension pneumothorax goes behind, because the JVD, along with the hypotension, tells you that filling or venous return is being obstructed. You'd say you do a fast and focused assessment checking breast sounds on both sides, the airway pressures on the ventilator, tracheal position, the trend on the chest tube output, and then you'd say you'd call for help, because a tamponon needs drainage, and attention pneumothorax needs decompression, and a presser only buys you time, right? So answering it this way shows that you've recognized the pattern that you've used surgical contacts to rank your differential, and that you know the definitive fix is mechanical. Now, real patients are not just always going to be one type, right? A lot of the time you'll be looking at mix or undifferentiated shock, where two mechanisms are running at once, where the patient is hypotensive, and you don't know why. Sepsis is the cleanest example, right? Since it's distributive and hypervolemic and cardiogenical together, but it happens everywhere. A trauma patient can be hypervolemic from hemorrhage and obstructive from attention pneumothorax at the same time. A large MI can be cardiogenic from the infarct and distributive from the systemic inflammatory response to all that necrotic muscle. So the question is how are you going to reason when it's not straightforward, right? The way you do that is to go back to the framework. So instead of asking which of the four types of shock, which with the four boxes is it, you interrogate the determinants of perfusion one at a time, which are the preload, the pump function, the vascular tone, and the presence of any mechanical obstruction. And you can assess all four at the bedside. The central vein is pressure, and the JVD tell you about the volume status of the right heart. So flat veins suggest hypervolemia, while distended veins suggest congestion or obstruction. The lung exam and the wedge tell you about the left heart. The skin temperature tells you about vascular tone with warm and vasodilated on one end, and then cool and vasoconstriction on the other. And ultrasound. We use ultrasound a lot in anesthesia. It lets you look at it all directly, you know, with a flat collapsing inferior arena cava, pointing to hypervolemia, a dilated and strained right ventricle, pointing to a PE, a pericardial effusion, pointing to tamponod, and poor contractility, pointing to cardiogenic shock. So you're not pattern matching to a single type of shock, right? You're checking each determinant of oxygen delivery, and treating whatever is deranged, while you keep continuously reassessing, because of course, as you know, shock changes minute by minute. All right, so in summary here, shock. Shock is an adequate oxygen delivery for the tissue demand, and that delivery is cardiac output times hemoglobin times saturation. The tissues compensate by raising their extraction ratio until delivery crosses the critical threshold, and after that, consumption falls and lactate rises. And there are four mechanisms. Hypervolemic shock is volume loss, where preload falls, output falls, and the SBR rises as compensation. And then the systolic is the very last thing to decrease. You fix it with volume and source control, and you give blood when blood is what's been lost, right? Cardiogenic shock is pump failure, where the filling pressures rise, the output falls, and the compensatory rise in SBR, raises afterload on an afterload sensitive ventricle, and which causes a feedback spiral. You support contractility, you reduce afterload, and you break the spiral mechanically. You don't volume overload it. Distributive shock is vasoclesia, and in sepsis, the enosterbin nitric oxide collapses the SBR, while capillary leak and septic cardiomyopathy stack on top of it, so it's three problems at once. You restore the tone, resuscitate the volume, and treat the source. And obstructive shock is an extra cardiac mechanical block that mimics cardiogenic on those numbers, separated by the history and the exam, and fixed only by removing the obstruction. And when it isn't clean, you interrogate the preload, the pump, the tone, and the obstruction, and you treat whatever is deranged. Okay, so three things I really want you to walk away with. Number one, the systolic pressure is the last variable to fall. So the heart rate, the pulse pressure, the capillary refill, the urine output, the lactate, are what you actually monitor. Number two, cardiogenic and obstructive shock are identical on the hemodynamic numbers, so it's the history in the exam that separates them. The context, the lung exam, the airway pressures, and what happened right before the patient decompensated. And number three, treatment always follows the mechanism, and it's never a reflex. So it's volume for volume loss, inotropy for pump failure, vasopressors for vasoplegia, mechanical relief for an obstruction, and a structure differential when it's more than one, right? So that's your shock states, all four of them, we went over the tank, the pumps, the pipes, and the obstruction. If you're preparing for interviews, we have complete interview prep inside our CNN Club platform. We have our AI mock interview lab, where you can take mock interviews as many times as you want, and it will actually give you feedback on each question and a personalized study guide, so you can do quick feedback loops and start learning your weak spots a lot quicker. I'll leave the link below. It's ccRNAclub.com. You can try it seven days for free. This is your all-in-one smart application companion for every single step of the way. We've worked so hard on it, my past year and a half, and I'd love for you to check it out. All right, I'll see you on the next one.