Chapters Transcript Video Cardiogenic Shock: A Clinical Framework for the Cardiac Advanced Practice Provider Dr. Anand Krishnan provides an overview of the pathophysiology and etiologies of cardiogenic shock. Uh, good morning, Matt, um, and everyone online. Um, so I think this is a topic that a lot of us kind of see in different types, uh, uh, of the practices that we're in, but I thought Matt felt, uh, it might be a good idea to kind of do this. It's a basic primer, uh, nothing fancy. I'm gonna share kind of four cases that Uh, came up over the past 6 months, and then we'll talk a little bit about, you know, what is cardiogenic shock, what is the, what is the language we use to kind of communicate with each other in terms of severity, etiology, and, uh, what some of the data is in terms of treatment and management. Um, so I have no financial disclosures or conflicts of interest. I did use some AI tools, uh, including cloud and chat GPT for the formatting of this presentation. However, uh, all the data has been verified as authentic from their respective original sources. Alright, so I have 4 cases and I'm just gonna give you guys kind of a snapshot of. The two liner of these cases. So case number one was a 56-year-old female with uh stenia of her left circumflex, had a PCI done, uh, and overnight she had escalating oxygen requirements, requiring BiPAP. She had hypotension, tachycardia with a lactic acid of 3, I got called in on the bedside ultrasound. She had severe MR likely functional due to the infralateral wall not moving. And uh we took her to the cath lab, put in a swan, which showed a right atrial pressure of 8 millimeters of mercury, a pulmonary capillary wedge pressure of 28 with V waves to 40, a cardiac output of 4, an index of 2.2, and an SVR of 1900. Um, the next case was a 72-year-old male with out of hospital cardiac arrest, uh, status post Rosc. Uh, the EKG showed anterolateral ST elevation MI, uh, taking him to the cath lab showed left main trifurcation and an RCA CTO on cath. His blood pressure, when I, when we put the sheath in was 70/30. Uh, case number 3 is a 68-year-old female who presented with syncope. Uh, she was noted to have critical AS due to a unicuspid aortic valve. Her mean gradient was 68 millimeters of mercury across the valve, even with an LVF of 35% with global hyperkinesis. Her blood pressure was 95/60. Her heart rate was 110, and her lactic acid was 3.1. And the last case was an 80-year-old male who presented with VT storm and acute hypoxic respiratory failure. He was emergently intubated, was noted to have incessant monomorphic VT. There was a concern for possible myocarditis, which was permanent, so he got pulse dose steroids. His blood pressure was 80/40, and on echocardiogram he had BV failure on. TTE All right, so each of these 4 cases have 4 differing presentations, um, you know, there's different etiologies, but the final common pathway is that these patients are very sick because they are unable to perfuse their organ systems, as witnessed by the low blood pressure, as well as the rising lactic acid, um. And when you kind of think about, you know, what is cardiogenic shock and the national burden, it's a, it's essentially a cardiac disorder producing sustained clinical and biochemical evidence of tissue hypoperfusion, as witnessed by increasing lactic acid, irrespective of blood pressure, so it doesn't really matter what someone's blood pressure is, uh, and normal intensive patients can still have hypoperfusion, which could be relative. Uh, the two, you know, the two big types of cardiogenic shock that we see are acute MI cardiogenic shock, um, which, but shock from bradyarrhythmias, tachyarrhythmias, advanced heart block, postcardiac arrest, or mechanical complication in the AMI setting are also classified as AMICS. So these are just complications or sequelae of the acute insult. Heart failure cardiogenic shock, um, is another big type. Uh, cartiogenic shock from primary myocardial dysfunction, which can be ischemic or non-ischemic. It can be subclassified as, you know, de novo versus acute and chronic, or based on which ventricle is involved. Uh, there's another shock classification, which kind of talks a little bit about the different types of shock, which includes postcardiotomy, cardiogenic shock, secondary cardiogenic shock, which can be due to arrhythmias, valve or heart disease, or pericardial disease. So kind of think about, you know, those, the other two cases. So the, the last, the case number 3 and 4 would kind of come under this. So when you look at the mortality, just to give you guys some perspective, the mortality of a STEMI patient is about 4%. It's been getting better, but it's about 4%. If that patient were to have cardiogenic shock, that mortality increases approximately 10-fold, right? So it's closer to 40%. Um, on the other hand, if they have a cardiac arrest, that mortality increases further, up to 90%. So which is why it is critical to identify, uh, cardiogenic shock sooner. Um So when you think about the pathophysiology, this is from a paper by Tehrani et al. in uh Jack Heartfielder 2020, and I, I'll show, I'll share the bibliography. Uh, initially, what happens is, in cardiogenic shock, there are progressive cycles of inflammation, ischemia, vasoconstriction, and volume overload, which kind of sets up a vicious cycle where the, where the heart is no longer able to compensate, uh, for the insult. So there can be a primary cardiac insult, which leads to myocardial dysfunction, which then drops the cardiac output, uh, which can lead to reduced organ perfusion and a drop in blood pressure. This sets off a compensatory mechanism by the body, which increases vasoconstriction, which is called clamping down to kind of keep the blood pressure up, uh, which can further lead and volume overload due to, um, activation of the sympathetic nervous system, the RAS system, uh, and, uh, venal constriction. This further, the organ hyperperfusion can lead to ischemia and inflammation, which then causes hypoxia, microcirculatory dysfunction, pulmonary edema, a systemic inflammatory response syndrome, there can be bacterial translocation from the gut, which can then kind of move over to this vasodilatory sort of picture of cardiogenic shock, uh, which is almost universally fatal, and can lead. To death. And there's different common etiologies of cardiogenic shock, which we kind of touched upon. It can be predominantly LV failure, RV failure, or BV failure. It can be arrhythmias, it can be valvular or mechanical, such as critical AS or severe MR. Uh, it can also be due to pericardial diseases, uh, or it can be toxic metabolic, which is less common, but usually it's one of the four above. So this is the only slide that has math involved, and I think this is critical to understand what is going on. So, you know, we've all kind of spoken a little bit, uh, we've all kind of read a little bit about Ohm's law, which essentially is the relationship between potential difference, flow, and resistance. And when you kind of equate that to a fluid dynamic system, like the heart and the blood vessels, you essentially have the potential difference being the change in the pressures, right? And your flow being cardiac output, which is blood flow, and resistance being either systemic vascular resistance or pulmonary vascular resistance, depending on which kind of circuit you're talking about. And using this equation, you can kind of extrapolate to get cardiac output, uh, and you can get cardiac index, you can get systemic vascular resistance, you can get pulmonary vascular resistance, and we'll talk a little bit about how this kind of ties in. So when you think about it, VO2 is essentially uh the amount of oxygen, uh, your, your tissues are using. And that is nothing but cardiac output, which is multiplied by the difference in the oxygen levels in the arterial system versus the venous system. So if you think about the systemic circulation, it's your aortic 02 saturation minus your pulmonary arterial saturation in the absence of a shunt, because those are the two points, the ends of the circuit. Right, and when you just rearrange this, you can kind of get what cardiac output is if you estimate VO2 and you divide it by uh your. Uh, oxygen carrying capacity in the blood. However, there's a couple of things that go into this, because you have to um. Take into consideration hemoglobin, and you have to take into consideration uh the amount of oxygen that is dissolved in hemoglobin. So, which is why, and when you kind of rearrange this equation, the hemoglobin goes in the denominator, so you have to be careful when you're kind of talking about fake cardiac output, because uh you can get a spuriously or falsely elevated or normal cardiac output if someone were to, were to have a hemoglobin of 5 versus 15. Um, so it's important that you kind of look at the whole picture. Um, in someone with a PA saturation of 40%, right, um, a cardiac output of 5 doesn't, or a cardiac index of over 2.5, there's something else going on there. And uh why do we say that a PA saturation of 65-70% is normal, right? So when you kind of look at the uh molecular level, each hemoglobin molecule attaches to 4 oxygen molecules. So when the blood is fully oxygenated, each hemoglobin molecule has 4 oxygen molecules, so it's 100% saturated. And then when it goes around the body, each of these hemoglobin molecules, ideally in a resting state, only have to give up maybe one oxygen molecule, right, 1 to 1.2, which is why when you kind of summate and look at the PA saturation numbers, it's roughly 65 to 70% because each of those hemoglobin molecules have given off one oxygen molecule. Uh, there, there are some caveats to that, and for that you kind of have to look a little bit at the oxyhemoglobin dissociation curve. This can shift, uh, based on, um, acidosis, it can shift based on, um, if someone is normothermic versus hypothermic versus hyperthermic, uh, but by and large, that's how you kind of get that number of a PASAT of 70%, 65 to 70% considered normal. So for the athletes in the room, especially those who do like marathons, like just think about this, right? So your VO2 is essentially a function of the pump in your, in, in your body. Cardiac output is stroke volume times heart rate, and then you, the other factor that kind of determines how much oxygen your body is getting uh as a function of your cardiac pump is. The, the oxygen carrying capacity or how much oxygen your organs are taking out of, um, each, each, you know, cardiac cycle. So your, you can usually, you know, stroke volume is about 70 mL. You can usually close to triple your heart rate very easily, right? Uh, you can also close to triple your, um, stroke volume. And then in terms of your oxygen carrying capacity, or you can double your stroke volume, and in terms of oxygen carrying capacity, your body can extract more oxygen molecules. So maybe you can extract two or three oxygen molecules instead of just one. So you can close to increase your VO2 by 15 to 18. So that's the, you know, that's the amount of reserve the human body has, which is kind of fascinating. There's not too many pumps that are man-made that have that. Um, so once you use the FIC equation, and this is one way of getting cardiac output, you have thermodilution as well, but if you were to use the FIC equation, a cardiac index is essentially cardiac output divided by your body surface area. Systemic vascular resistance, again, when you plug in this into the Ohms law, is your mean arterial pressure minus your right atrial pressure divided by your cardiac outputs, remember, that's the difference in pressures divided by the flow. You multiply it by 80, it's just a multiplication to get it in dimes, um, PVR is the same equation, but you just switch out the pressures, because the, it's a different parallel circuit, so you look at your mean PA pressure minus your pulmonary capillary wedge pressure. Your PA pulsatility index is essentially an, is, is uh an index of RV function, which kind of takes into consideration pressure as well as the preload, right? So if in any pump the pressure starts falling and the preload starts increasing or backing up, you'd think that the pump is failing. So usually a value of less than 0.9 in an acute MI setting or an acute setting is considered abnormal, and your cardiac power output, we'll talk a little bit more about that, uh, in the, in, uh. In the slides. I'm gonna spend some time kind of going over this, uh, because this is important to understand. There's not a lot of physiology, we're not gonna get into the nitty-gritty of it, but it essentially talks about how we can kind of pull in, uh, our thick cardiac equation into the pressure volume loop. So when you look at the heart function, every cardiac cycle, starting at the lower point here, your mitral valve opens, blood comes into your LD which is diastolic filling. Uh, the pressure doesn't increase a lot because your LV has pretty good capacitance. This is obviously worse off in patients with cardiogenic shock or, you know, heft theft where it increases a lot, uh, but then there is mitral valve closes and systole sets in. There's isovolumetric contraction, at which point the aortic valve opens, there's ejection of blood. When the pressure norm equalizes between the aorta and the LV in the diastolic sense, the aortic valve closes, and then there's isovolumetric relaxation, and as you can see, this curve happens every single time the heart beats. Now, there are certain lines, um, that, and this is, so the, so if you look at, this is your end systolic volume right here, if you were to draw it on the X axis, this is your end diastolic volume. The difference between the same or the width of the curve is going to be the stroke volume. You multiply the stroke volume by the heart rate, you will get your cardiac output. The area under the curve is essentially the stroke work, the work that your heart does each cycle, right? So let's, let's look a little bit closer here. Now, when this is the same curve, right? Now there are a few lines that we've drawn, and these are kind of bordered by each of these points, and this point is different for patients in cardiogenic shock. So the first line, which is the slope of. The curve here is your n-systolic pressure volume relationship, and essentially that is a measure of contractility. So in cardiogenic shock, the slope of that curve is going to drop, all right? Um, here is your end diastolic pressure volume relationship, that is nothing but preload, so if you were to fill this ventricle more, it's gonna go along this line, however, if this end diastolic pressure volume relationship were to be abnormal, like a stiff left ventricle, this is going to be steeper, so even small changes in volume are going to cause massive changes in pressure. So think of your classic Hef-Pf patients, that's what happens in them. And then this line connecting the two points is nothing but your afterloader arterial elastance. So when someone is clamped down and your SVR is elevated, this, the slope of this line increases, right? So when you think about it, so this is nothing but your con this is your. Afterload. So if someone's afterload were to increase, the curve gets steeper. If someone's afterload were to decrease, the curve drops. On the other hand, if someone's preload were to drop, like if they're bleeding, this whole, the, the point on the right is going to shift towards the left. And all of these things, or the contractility drops, the slope of your ESPVR is going to drop, so that's, that's diagram C. So all of these things essentially are going to reduce the area under the curve here, which will then lead to a drop in the cardiac output and the stroke volume, right? So that's what happens at a physiological level, in a very kind of, not a super simplified sense, but close enough, this is the easiest way to kind of understand what's going on. So let's talk about what happens, and we have, we, you know, we have a shock team here. So we have uh a level one shock center, we have level twos and a hub and spoke model. So kind of the goal is that. The minute someone in cardiogenic shock comes in, you want to identify them sooner. You want to be able to re-stratify them and and stabilize them as much as you can before you kind of transfer them out, but it's important that you have a common language that you're talking to the surgeons, the AHF providers, to the interventional cardiologists, and you want to be careful about how do you pick which modality of treatment you're going to do. So it's not only knowing the etiology. Of the diagnosis, but also you need to be able to tell the severity of the diagnosis and what the next best step for these patients is. So for the longest time, when you look at all of the cardiogenic shock trials and the working groups, there was a little bit of disconnect between a universal definition for cardiogenic shock. People couldn't really. Um, sort of agree on a universal definition. Now, the, the definition has to be simple, and it needs to be, you know, it needs to be, you need to be, it's like speaking a language, right? So you all need to speak the same language, essentially. So this is from a paper that kind of talks about the contemporary management of care, and the reason why I put this slide is that it kind of gives you a, a, you know, um, kind of a timeline on how quickly you should ideally kind of think about and make the diagnosis. So within 30 minutes, we're off the initial evaluation of the patient, you need to be able to kind of look at some of these basic things, like symptoms and signs, uh, if they have altered mental status, if they have confusion. They have a drop in urine output, are they sustained, uh, hyper hypertension, what is their perfusion levels, is their lactic acid normal, is their liver function test normal? Look at the EKG and the echocardiogram, are they having a stem, are they having an N STEMI, do they have a mechanical complication, is it ByV or LV failure, uh, look for signs of congestion, again, there's both physical exam methods that you can do it, but there's also lung ultrasounds or IVC ultrasounds that you can do. And the goal is that you wanna be able to triage these patients, right? So you wanna know if these patients need to go to a higher level of care, do they need to go to the cardiac cath lab, or do they need to go to the general ICU? And this, within the first hour, this is what needs to be done. And if needed, you have to activate the shock team for potential transfer. If they're in the cath lab, uh, is this someone who needs MCS? Do they need a leave-in swan? Um, do they need uh a PCI? Right? And then within the 1st 24 hours, uh, you need to optimize therapy. You need to have a personalized interventions based on their overall goals of care, what, what are you dealing with, and what is your exit strategy, right? Are they a candidate for advanced support options? Do they need upgradation of MCS? Do they need BV support? And in some patients, if care is futile, oftentimes you need to get palliative care involved sooner. So how do we talk about our language? How do you convey to everyone how sick your patient is? And that's why the, the Society for Coronary Angiography and Interventions called SCI came up with these shock stages. It goes from A to E, and this is usually not a one-way street. Uh, patients can bounce between, so the worst A to E is worse, so, uh, and think of A as a patient who is at risk, right? So these are patients who might have had a STEMI the night before, but they are hemodynamically. Stable, they're not tachycardic. This is your run of the mill, for example, mid-LAD STEMI patient. Most of them are not going to go into cardiogenic shock, so they are, they don't have hypotension, and they don't have hypoperfusion. On the other hand, B is borderline, where they're trying to start showing signs of of hypotension, but usually they do not have hyperperfusion, so their lactic acid is normal, but their heart is kind of trying to compensate. This can be uh from tachycardia, right, sinus tachycardia in a patient with a stemi, with a low EF is oftentimes the most uh the the the the most dangerous rhythm, because some, they're they're borderline risk for deteriorating. And at this point, um, this is when their lactic acid is not rising yet, uh, but you have to be careful about these patients, right? And then if they have a further loss of compensation, they have hypotension with hypoperfusion, and these are patients who not only have hypotension and tachycardia, but now their lactic acid is rising, and these are patients who need vasopressors, ionotropes, one vasopressor or ionotrope, or sometimes they need one MCS, right? If your initial stabilization attempts do not work and they get worse, or they need multiple escalating doses or uh upgradation of their MCS, then they're more in the D stage, which is failure to stabilize or deteriorating stage, where this is when their urine output is getting worse, their lactic acid is going higher, and their LFTs are going up. And then in the last stage you have extremists, right? So nothing is working, these patients, and oftentimes out of hospital cardiac arrest automatically means that these patients have had extremists and uh on, on, on the right side of panel, this kind of talks about how you can. Use physical exam, biochemical markers, and hemodynamics if you have them with a SWAN or a PA catheter to kind of help classify each of these patients into each of these stages, right? So, universally, a cardiac index of less than 2.2 is usually considered abnormal. Um, a pulmonary capillary wedge pressure of over 15 is considered abnormal, and hypertension is usually a map less than 65, and then it's, again, it's not, so if the patient is moving from A3, they're getting worse, if the patient is moving from C to A, they're obviously getting better. So what is, why did we pick this language, right? Why do we want to use the sky stage? And there's very good data from multiple papers, which kind of talks about sky stage predicts mortality. It's not only the stage of uh presentation, but it's also the stage at 24 hours and the progression that matters. So when you look at it, in-hospital mortality is, is only 3% for A. So, you know, it's kind of like your STEMI patient, right? 3 to 4% mortality. But if they were to have Sky C, that mortality is immediately 4 times more, and if they have Sky D, which is your worsening cartiogenic shock, that's where that 40% number comes from. Right? And then when you go to E, it's even higher, closer to 70%. So 2 out of 3 patients are going to die if they have Sky E. And the majority of these patients, unfortunately, are going to progress further, and, you know, this 90% number. Um, sky baseline stage B escalating to a higher stage, you know, when you think about it, is it that they're that sick? My suspicion is there's some amount of survival bias because some patients may just die when they're in D and they don't go to E, but on the other hand, I think we, there's also a component of us not diagnosing these patients quick enough, so that is why we're kind of, we're, we're good at picking up patients who are in the C and the D stage, we're not great at picking up patients who are in the B stage, which is why it's important to kind of. Know that this language exists and be kind of cognizant about, you know, hey, this patient had an LAD stemi last night. I need to check a lactic acid within the 1st 6 hours of presentation because it's, I need to know if they have hypoperfusion, right? I need to watch their urine output. I, I need to let the ICU know that they need to call us if their urine output is dropping off or if they have escalating Levofed requirements or dobutamine or epinephrine requirements. So the goal of using this universal language is to be able to find the right patient. At the right time to find them the right place and give them the right treatment because that's how you can lower this mortality. There's, there's, there's a lot of um avenues to improve mortality because this is something that has a very high mortality, but oftentimes it needs a lot of moving parts to kind of fall in. So, you know, if a patient with uh BV failure, left main, uh, uh, you know, stenosis like our case one. Um, who is not doing well with just Levofed and an Impella placement in the cath lab probably needs to be considered for VA ECMO, so we need to kind of initiate the transfer sooner. And when these patients are in the ICU, these are all the things you want to keep an eye on. EKG, look for arrhythmias, the respiratory status, um, an echocardiogram, um, renal markers such as dropping urine output, physical exam, uh, is her JVP up, is her blood pressure dropping, is her heart rate up. Look for lab markers, lactic acid, uh, PH, BUN creatinine, LFT, so renal, liver function, and perfusion markers. Uh, and if you have a SWAN, look at the cardiac index, but also look at the SVR and the PAO2. Remember, the FIC equation has a lot of avenues for incorrect calculations, so you need to be careful about how you calculate it. You look at the big picture, right? Someone with a PA saturation of 30%. And a hemoglobin of 5, your cardiac output is going to be appear normal, but that's not normal, uh, it's just the way how math works, um, so look at the whole patient, not just one number. And to kind of summarize it, it's a standardized pathway. You need to identify and classify. You want to stabilize these. Patients sooner if they need revascularization, you revascularize, so you need timely coronary angiography and revascularization. Look for comprehensive hemodynamics, so if when in doubt, put in a PA catheter, you want to know if it's LV or BV or just RV uh that's gonna help you tailor the therapy, um, you wanna have selective. MCS MCS don't have a universal use, they have selective use, and they have timely use, and both of those things are important. And you always want to have a multidisciplinary CICU care, which includes palliative care. Right, so when you kind of put all of these things together, you kind of get the CICU management of cardiogenic shock. This is from the same paper by Tehrani Atal. It's, I, I'll, I'll give the bibliography at the end. These are some, there are, there are 4 or 5 papers that are, are worth the read. Uh, so your treatment objectives essentially are patients, um, for, you want to wean vasopressors and isotropes, you want to improve perfusion, you want to avoid them from getting into refractory shock, and ideally you want to have heart recovery, right? So before we talk about refractory shock. This is what the serial assessments, we kind of went over again, you want to look at the lactic acid, the thick or the thermodilution, and ideally, your cardiac power output and your PAPI, we'll talk a little bit about why those are important, and if they have MCS, you want to look for the position of the MCS, if they're having any complications related to the MCS and you want to do neurovascular assessments, especially if you're putting in large board devices and or if they have a cardiac arrest, um, as well. Uh, and when you talk about when is it that the patient is not getting better, is usually a cardiac power output of less than 0.6 watts, a cardiac index of less than 2.2, or a rising lactic acid. So despite initial stabilization methods, if their lactic acid is getting worse, their cardiac power output. Is dropping or if their cardiac index is low, those patients are not doing well. Uh, but you also need to know that there are certain contraindications to MCS, anoxic brain injury, uh, for example, prolonged cardiac arrest. These are patients who don't, they don't die from a cardiac cause, they die from a neurological cause. If they have irreversible organ failure, prohibitive vascular access or if they're DNR, usually if they have a life expectancy of less than one year before all of this happens, that's also kind of considered a contraindication. And um what is cardiac power output? So cardiac power output is looking at your mean arterial pressure and your cardiac output, and it kind of gives a relationship there. Usually it's about 1, right? So you calculate it for yourself, your cardiac culprits is usually about 5, your mean arterial pressure is about 70, that's 3, you know, it's, in fact, it's usually higher in most patients, um, it's about 90, right? Um, so 90 times 5 is 450, your cardiac power output at least should be 1, but less than 0.6. Bad, uh, PAPI is a measure of your RV failure, so it's, again, it's your change in the pulsativity of the RV divided by the right, uh, the right atrial pressure. So if these patients do not have refractory shock, you try to wean them. On the other hand, if they do have refractory shock, you want to figure out is it BV, is it LV dominant, or is it RV dominant. And then you kind of talk to your shock team and figure out what MCS support would they need, and to make that decision, you kind of see, are they hypoxic or not, because if they're hypoxic, essentially they need an oxygenator that can be, you know, something like a Protect Duo VA ECMO, um. But if they're not hypoxic, you can consider Impela CP, Impela 5.5 for the LV, or an, or a right-sided VAD without an oxygenator for the RV. So that's kind of how this pathway works, but at this point, it's a multidisciplinary meeting which includes AHF, cardiothoracic surgeons, uh, Palmcret, and interventional cardiology. So, uh, why do we need cardiac power output? Because neither the wedge nor the cardiac output give a reflection of the essence of cardiac contractility, meaning the wedge is really a measurement of flow, of pressure, and cardiac output or index are measurements of cardiac flow. They do not really represent the nature of our cardiac system that is composed of an energy source, which is the heart, and its pipes, which are the arteries that conduct this energy through the rest of the body. Which is why you have cardiac power, which is a fundamentally muscular, which is, it kind of assumes the heart is a fundamentally muscular hydraulic pump that can create pressure as well as flow, so cardiac output is the flow through this closed circuit that is influenced by cardiac contractility, and has a multifaceted interaction between vascular resistance, compliance, filling pressures, and overall intravascular volume. And the cardiac power output has the capability of defining this cardiac power out uh this cardiac power, which is a direct correlate of end organ profusion, right? So there's some data from almost 10 years ago now that kind of validates this whole 0.6 number or why cardiac power output is important. So let's, so let's do some math. So the physical rule of fluids is power equals pressure times flow, and when you look at uh pressure, it's your mean arterial pressure and flow is again cardiac output. Your resting cardiac output is uh your uh your CPO is cardiac output times map divided by 451, so that's like a conversion factor, and then you get a a CPO of less than 0.6 is indicative of hemodynamic compromise that is associated with increased risk of mortality. Um, so that's where this 0.6 number comes from and is validated. And cardiac power index is nothing but your CPO divided by your body surface area, right? So again, it's, it's just substituting body, it's like cardiac index is nothing but cardiac output divided by your body surface area. So then once you have your hemodynamics, you have a variety of things to pick. So you can pick pharmacological methods or you can pick MCS methods. So when you look at the iron oppressors, you have Levofed, you have epinephrine, or you can have dopamine, but we usually use levorepinephrine, and the mechanism of action based on the receptor bindings, um, uh, are given up here. So there Levofed is, has more alpha one activity than beta one. Epinephrine at more, um, Uh, therapeutic doses has more beta-1 activity than beta-two, so, you know, if you really want something that is going to push the heart or whip the heart, if you think of the of the heart as a horse cart, it's going to be one of these two, right? Uh, so these are going to increase your cardiac output. When you look at Epi, it'll increase your heart rate, uh, but it will also increase SVR because of its alpha one activity. Right, on the other hand, an ionodilator such as Milinone or dobutamine to a certain extent is going to drop your SVR. Which is actually going to improve forward flow, while also increasing your cardiac output. So think of it as unloading the cart of the horse, rather than just whipping the horse up a hill. So if you unload the horse cart, the horse can move forward a little bit more. Uh, or faster, so that's where your iron or dilators come in. So this is why it's important to have a swan, so if your SVR is 1900 with the normal SVR being 800 to 1200, you want, you want to start thinking about putting these patients on something like an iron or dilator or something that drops their afterload, because that can help them, right? On the other hand, in someone in sepsis whose SVR is 600, you don't want to give them mildrinone, because then it, you're kind of, um, they'll die faster. Um, vasopressors, again, like phenylephrine and vasopressin are, are more alpha-1 agonists or vasopressin receptor agonists, so these are pure alpha-1 vasoconstrictors, so they can increase your SVR, increase your blood pressure, they don't have, they don't have a lot of effect on cardiac output or heart rate, but in vasoplegic shock, we use these, or in someone with Hokam, when you want to increase the afterload, you want to use phenylephrine. And then you have some pure vasodilators, which just vasodilate and drop the SVR, so something like nitroprasite, which is an arterial dilator, nitroglycerin is more of a venodilator, um, and then you have your different types of MCS devices. I'm not going to belabor this too much because, um, you have, Uh, your VA ECMO, which is total cardiopulmonary bypass, you have a balloon pump, uh, which essentially works more by dropping your afterload, doesn't give a lot of cardiac output, but increase coronary perfusion pressure. Impela CP, which is a microaxial flow pump, Impela 5.5, which is a larger microaxial flow pump, which is surgically implanted, and then you have your Impela RPFLX, which is a right-sided percutaneous pump. So the last 3 slides that I have are going to kind of show a little bit about what each of these devices do, and I'll see if I'm able to get this to work. So essentially what this is is, so your cardiac contractility is not changing, right? But what is changing is that the slope of the afterload curve. Is, um, is changing. So your slope, which would have been here, is now dropping to here, which in turn increases your stroke volume. So this is what something like a balloon pump or a vasodilator when the SVR is elevated, like in our first patient's case, does. So you're dropping the afterload, which in turn increases stroke volume and cardiac output without really changing contractility or volume status. This is kind of a pictorial representation of what happens. On the other hand, something like this, where this is a patient, and then they have complete, they have aortic LV decoupling, so the aortic valve no longer matters, so instead of it being a um a quadrilateral, it becomes a triangle, and this is what happens when you put in an impella in someone, uh, essentially, um, their cardiac output increases, but that's because the pump is giving them more flow, um. On the other hand, when someone were to go on ECMO, because you're kind of changing the direction of blood flow, their afterload significantly increases, right? The, the pump is kind of pushing oxygenated blood into the femoral artery or the aorta, which is back pressure to the LV, so the already weak LV has a significant increase in afterload, and that is why. In our VT storm patient, even though that patient ended up going on VA ECMO, we put in what we call a LV venting strategy by putting in an impeller CP through the femoral artery to kind of reduce the afterload on the heart, so to promote cardiac, uh, recovery while at the same time allowing for organ perfusion. Right? Um, so that's the end of my slides. Uh, these are some, um, these are the five articles that I used for pre for preparing the presentation. Um, they're all in the last five years, uh, the 2025 concise clinical guideline, uh, there's some data on the sky shock staging classification, phenotyping, criteria for defining the stages of cartiogenic shock, and, um, some of the data from the Tehrani etal paper from Jack heart failure. Um, thank you for listening, and if there's any questions, I'm happy to help with that. Published October 5, 2026 Created by Related Presenters Anand Muthu Krishnan, MD Cardiology View full profile
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