Hello, and thank you so much for this opportunity to present at the Society of Critical Care Medicine's Neurocritical Care Board Review Course. I have no relevant disclosures to the content that I'm going to present today. In the next 25 minutes, we're going to cover a very big topic. We're going to review shock subtypes, we're also going to talk a little bit about mechanical circulatory support, as well as hypertensive urgency and emergency. So as you can imagine, we're going to do an overview of some of these topics. Shock is seen in about a third of our critically ill patients. It's a manifestation of the demand-supply mismatch that our patients experience. It's a life-threatening condition, the circulatory failure that causes inadequate oxygen delivery to meet the cellular metabolic needs and oxygen consumption requirements of different tissues leading to cellular and tissue hypoxia. This is then going to lead to clinical manifestations, hemodynamic changes, as well as biochemical changes that help us diagnose shock. This central equation with cardiac output is equal to stroke volume into heart rate is an important equation. And when you think about the right side of the heart and the left side of the heart, and you think about the preload, afterload, what is the source value and how are we going to measure this to understand what is driving shock in our patients? So preload is defined as the myocardial fiber stretch, which is induced by that end-diastolic volume, whether it's the right ventricle or the left ventricle. Afterload is a resistance that the right or the left ventricle must overcome to eject blood. And stroke volume is going to be determined by the contractility of that ventricle preload as well as afterload for that side of the heart. So when you look at the preload of the right side of the heart, central venous blood volume, measurement could be CVP. Preload for the right side of the heart is the pulmonary vascular resistance, and a measurement can be calculated using values that can be derived using a PA catheter. The caveat here, of course, in a lot of our critically ill patients right now, we're not using PA catheters. PA catheters are currently reserved for patients who are in cardiothoracic ICU, CICUs with pre-existing pulmonary hypertension or complex cardiac shock. Preload for the left side of the heart is the pulmonary venous blood volume. And for afterload of the left side of the heart is a systemic vascular resistance. For any word that has index associated with it, whether it's cardiac index, whether it's SVRI, which is systemic vascular resistance index, you divide the value by the body surface area. Does a patient in shock always need to be hypotensive? The simple answer is no, because pressure is not equal to perfusion. Patients in cardiogenic shock may have a normal pressure, but because of their extremely elevated systemic vascular resistance index and drop in their cardiac output, they may be able to maintain a normal MAP, but may not be able to perfuse their end organs. MAP is equal to cardiac output into SVR. So as you can imagine, hypotension is going to occur either if the SVR drops or the cardiac output drops or both drop. A little review of the Frank-Starling curve. For the Frank-Starling curve, we're trying to identify which of our patients are going to respond to fluid administration. So if you plot the preload on the x-axis and stroke volume on the y-axis, there are going to be patients who will respond to fluid administration with an increase in their stroke volume. But after a certain point, they'll become fluid unresponsive. There are patients who may already be fluid unresponsive and may not respond to fluid administration and their stroke volume is not going to go up. There's also another concept that may not be tested on the boards, but understanding fluid intolerance. When does administration of fluid cause actual harm to our patients, whereby there's organ dysfunction, there is organ congestion, leading to a further decrease in organ perfusion. So these are concepts that are difficult to diagnose at the bedside. Who is going to be fluid responsive? Who is fluid unresponsive? And then when can fluid administration actually cause harm? In the next few slides, we'll talk about how we can distinguish between some of these. For shock subtypes, this is really an oversimplification. Oftentimes, there's going to be a spectrum of shock that our patients can suffer from and they can have different types of shock coexisting at the same time. A clinical pearl to manage shock, you identify the primary driver, what type of shock is causing the most amount of decrease in perfusion for our patients, and you begin parallel processing to identify the different types of shock which may coexist, but you begin treatment for that primary driver. So examples of shock include distributive. The most common types of distributive shock are septic shock or neurogenic shock. When you look at the preload, afterload, SVR, and cardiac output, what happens in distributive shock? The preload decreases, afterload decreases, SVR decreases, and cardiac output is going to increase as a compensation to try to maintain the MAP. In cardiogenic shock, preload increases, afterload increases, SVR increases, but your cardiac output drops. In hemorrhagic shock or hypovolemic shock, preload is going to decrease, afterload will increase, SVR goes up, cardiac output drops, or cardiac output can remain normal. In obstructive shock, preload increases, afterload increases, SVR will also increase, but your cardiac output will drop. As an example, cardiac tamponade or a patient with a massive VE. Now let's talk about a case and think about yourself in this patient's room and what is your approach going to be. 65-year-old male with hypertension, diabetes, coronary artery disease has undergone a left M1 thrombectomy. It was uncomplicated. He's post-op day number one. His post-thrombectomy blood pressure goal was about 100 to 140. And right before you started rounds, your fellow noticed that your patient's blood pressure was in the 90s and gave him a liter of normal saline. When you round on the patient, you notice that the patient's maps are in the 50s. He's in respiratory distress. Heart rate, he's got AFib with RBR. Rate is in the 130s. He's saturating about 90% on two liters. The fellow increases his O2 delivery by nasal cannula and proceeds to perform a POCUS. And POCUS shows poor cardiac contractility, B-lines in bilateral lungs, and a plump IVC. So at the bedside, when we're trying to identify which of our patients are in shock and why, some of those things that can provide us with clues include tissue hyperperfusion and biochemical science. So for tissue hyperperfusion, how is the patient mandating? What is their skin looking like? Is it mottled? Are they warm and perfused? Or are they cold and clamped down? Are they making good urine? Is the urine output greater than 0.5 cc per kg per hour? And with respect to the labs, if you had a baseline lactate and you see an uptrend, or the first lactate you obtain, whether it's arterial or venous, it's more than two, it's suggestive of hyperlactedemia. For abnormal cellular oxygen metabolism, if you had a central venous line or a central venous catheter in place, you could check the central venous O2 sat. In those rare patients in whom there may be a PA catheter, you could certainly get this idea from a mixed venous O2 sat. So most of the times, when do we start suspecting that somebody has shock? We think about this arterial hypotension. With this arterial hypotension, are there any clinical signs of hyperperfusion? With the brain, skin, kidneys, if these are absent, then does the patient have chronic hypotension? Or if these are present signs of hyperperfusion, then they're also going to have some compensatory tachycardia. You may find an elevated blood lactate. So if this is present, tachycardia, that elevated blood lactate, is also suggestive of circulatory shock. When circulatory shock is present, our next step is then to identify what kind of shock is the patient suffering from. And you could certainly use bedside point of care ultrasonography to understand what's going on with the heart and what kind of shock your patient may be suffering from. And the central venous O2 sat, if you have this available, certainly can also help distinguish between different types of shock. When you think about the types of shock, the most common type of shock is distributive shock. And even under distributive shock, about 62% or so patients will be septic. About 4% patients will have non-septic distributive shock. Example, neurogenic shock. 16% patients with cardiogenic, 16% with hypovolemic or hemorrhagic, and about 2% with obstructive. Lots of different ways in which you can monitor patients with shock. You could use semi-invasive devices such as flow-track vigilio, which makes use of an arterial line, a PICO, which uses the pulse contour analysis to get an estimate of the cardiac output, or also has the ability to provide, to give us an estimate of the cardiac output with thermodilution. You could certainly use esophageal Doppler, point of care ultrasonography, the arterial pressure waveform to look at pulse pressure variability, stroke volume variability, so on and so forth. So lots of different ways in which you can monitor your patients with shock to understand whether they're going to be fluid responsive or not. So in terms of a systematic approach, start with the clinical examination, check the extremities, check capillary refill, what are the pulses like, in your hemodynamic assessment, look at the pulse pressure, do a point of care ultrasound to check if the heart is hyperdynamic or hypodynamic, is there poor contractility or not. To estimate whether that cardiac output is high or low, is the heart full or empty? For patients who have a high cardiac output, the pulse pressure will be widened and your heart will appear hyperdynamic. For patients who have a low cardiac output, they will have a narrow pulse pressure, their extremities are going to be cold and clamped down, capillary refill will be more than three seconds, pulses will be thready, and on focus, you'll see poor contractility of the heart. That should suggest that your patient has cardiogenic or obstructive shock. If overall the cardiac output is low but the heart's contractility appears normal and the patient has thready pulses, then you should think about hypovolemic. So for circulatory failure, you could use the central line, point of care ultrasound, A-line, CVP, central venous otosat, the gradient of the venous to arterial CO2 using your central line. For your arterial line, the arterial pressure, the pulse pressure variability, as well as an arterial lactate. And whether your patient has rapid improvement with fluid administration, no improvement or complex cases, you could consider placing a PA catheter, particularly in those patients who are in our cardiothoracic ICUs, CICUs, or who have pre-existing pulmonary hypertension. So for volumes and pressures, is the volume pressure increased or decreased? Other things on the clinical exam that can guide us, is there peripheral edema? What's the JVP like? Does the patient have signs of pulmonary edema? On hemodynamics, pulse pressure variation, CVP, while it has drawbacks, you could certainly look at trends and extremes of values can help you understand whether the volumes and pressures are elevated or not. On point of care ultrasound, in addition to the heart, take a look at the lungs, as well as the IVC, and also two-point compression for the lower extremities to see if there is any clot burden or not. One key thing to keep in mind, as we are trying to ascertain whether our patients are in shock or not, we're trying to measure surrogates in order to understand their fluid status. Are they going to be fluid responsive, fluid unresponsive? Are they fluid tolerant or intolerant? And these continue to remain evolving concepts, and not one single data point should be taken into account, but multiple data points as well. So for the surviving sepsis campaigns from 2004 up till the most recent guidelines in 2021, we see an evolution in how early goal-directed therapy is recommended. In 2004 and 2008, after the MANI reverse trial, early goal-directed therapy was recommended within the first six hours, which included administration of this 30 cc's per kg, and then reassessment and CVP monitoring, blood transfusions, so on and so forth. In 2016, no early goal-directed therapy was recommended, but monitoring for lactate clearance. In 2021, again, no early goal-directed therapy is recommended, and plus minus lactate clearance as a target for resuscitation. And when we look specifically at fluids in 2004, 2008, as well as 2012, aggressive fluids, 2016, there was a strong recommendation for this 30 cc's per kg, and in 2021, this was downgraded to a weak recommendation. And this is very much in line with why we need to be aware of the concepts of fluid tolerance versus fluid responsiveness. So these definitions for sepsis, septic shock, sepsis is now used in place of severe sepsis. The sepsis three guidelines recommend clinical criteria. They do suggest using Quicksofa, but in 2021, there is a recommendation to not use Quicksofa in isolation for diagnosing a patient with sepsis, but as compared to using for sepsis. So the SERS criteria, which include body temperature, heart rate, tachypnea, and white blood cell count, Quicksofa, which includes GCS, systolic blood pressure, respiratory rate, Quicksofa score of two to three, suggestive of high risk of sepsis, and zero to one, not at high risk. But none of these should be used in isolation. Instead, a combination of these different criteria, along with the clinical history, should be used for diagnosing sepsis at high risk. We've got to think of sepsis as a medical emergency. We've got to think about time to fluids, time to antibiotics, time to pressers, time to measuring the effects of our resuscitation, time to source control, as well as time to de-escalation. From the most recent surviving sepsis campaign, we have some good infographics that the campaign has released. So let's talk about antibiotic timing from there. If you think sepsis is definite or probable and shock is present, then administer antibiotics immediately, ideally within one hour of recognition. If sepsis is possible and shock is present, again, administration of antimicrobials immediately is recommended. If sepsis is definite or probable, shock is absent, again, early administration of antibiotics, rapid assessment of what is that underlying etiology of sepsis trying to a certain source control, and administering antimicrobials within three hours if the concern for infection persists in those patients in whom sepsis is possible. Every hour delay of administration of antibiotics in patients with sepsis increases mortality. With respect to vasoactive agents, which presser should you use first? So using norepinephrine as the first line vasopressor is still a class one recommendation. For patients with septic shock on vasopressors, we got a target of MAP of more than 65. All these others are not class one recommendations, but you could consider placing an arterial line, and you could initiate vasopressors peripherally if you do not have central access, and you could consider adding vasopressin. If sepsis associated cardiomyopathy is suspected or a patient has underlying heart failure with reduced ejection fraction, then you could consider switching to epinephrine mortality. Why does lactic acidosis occur in sepsis? So lots of different reasons, catecholamine surge, increased glycolysis, decreased activity of pyruvate dehydrogenase to convert lactate to pyruvate, and mitochondrial dyssepsis. Andromeda shock looked at capillary refill. There was no difference in using lactate versus capillary refill in patients who were being resuscitated with septic shock. For fluid resuscitation, fluids should be used as drugs. We should understand both the definition of fluid resuscitation, the goal, where does our patient sit on that spectrum, and both the duration of fluid resuscitation as well as deescalating patients appropriately. Hypervolemia has lots of multi-organ, has the ability to induce multi-organ dysfunction, hence volume resuscitation should be avoided. In a systematic review of ARISE process and PROMIS, early goal-directed therapy, so in this forest plot, only the reverse trial from 2001 favored early goal-directed therapy. For all other subsequent trials, there was no difference in those patients who got early goal-directed therapy versus those who used judiciously. What about pressors? So when we look at pressors and their mechanisms of action, Nicole Davis is going to go over all the different pressors. So here's just a table to recap. Phenylephrine, norepinephrine, epinephrine, dopamine, vasopressin, dobutamine, liver cementin. I have not included angiotensin II in this table, but you can see the effects, what is the indication, what types of shock can you use these different agents in, and what are some key considerations. A few words about corticosteroids. Corticosteroids can be used in patients with septic shock to promote the retention of salt and water, improve cardiovascular function, and inhibit inflammatory responses. In this table from Andrea Nee from Current Concepts in Adult Critical Care presented at the Society of Critical Care Medicine, when we look at these different trials, corticus adrenal approaches, the intervention varied between hydrocort plus fludrocortisone, hydrocort plus fludrocortisone in approaches as well. Duration of therapy varied, but mostly seven days. Predicted mortality in all of these cohorts was anywhere between 40% to 60%. Sepsis was present in, medical sepsis and not surgical sepsis, was present in most of these patients, and baseline levodose was about 0.4 to 1 mic per kg per minute. In terms of outcomes, there was mortality benefit seen in the original ANAND study. Shock reversal was seen in all the studies, and length of ICU stay was decreased in a dream. Other causes of distributive shock include hepatic failure, pancreatitis, trauma, thyroid storm, AV fistula, thymine deficiency. Shifting gears to cardiogenic shock, the most common cause of cardiogenic shock is about 2% to 5% will have STEMIs, about 2.5% patients will have NSTEMIs. RV failure due to MI, PE, valvular disease, dysrhythmias, high PE, valvular hypoxia will also contribute to cardiogenic shock. In terms of the spiral that occurs in patients with cardiogenic shock, myocardial infarction will lead to increase in left ventricular end-diastolic pressure, which leads to pulmonary congestion causing hypoxia, ischemia, and progressive myocardial dysfunction. Myocardial infarction and dysfunction, systolic decrease in cardiac output, decrease in stroke volume, leading to decrease in systemic perfusion, and then increase in the systemic vascular resistance, further causing a decrease in cardiac output and progressive myocardial dysfunction and death. How do we fix all of this? By relieving ischemia. Revascularization is one way to break the cycle and spiral of death in cardiogenic shock. Clinical features for the right side and the left side of the heart. For the left side of the heart, pulmonary edema, left-sided heart murmurs. On the right side of the heart, when there's a right heart failure, there'll be limb edema, sacral edema, hepatomegaly, increased JVP, and regurgitant tricuspid area murmur. Shared findings in both suggest about both sides of the heart failing, a cold extremity, cyanosis, orthopnea, and decapillary refill. So when we look at RV dilatation on echo, this is a four-chamber apical view, RV, LV, LA, and RA. It's by atrial enlargement. You can see stasis of blood in the RV. The RV is perhaps as big as the LV here and compared to a normal echo, LV, RV. LA and RA. Here's just an example of different volume and pressure curves to understand cardiac work is equal to pressure into volume. And ventricular work will essentially, when you look at that pressure-volume loop proportional to what the oxygen demand is, and how does IBP impeller, so different kinds of mechanical circulatory devices, help in relieving cardiogenic shock. In IBP, it reduces the systolic aortic pressure, increases stroke volume, and its effect on cardiac work, the stroke volume increase will offset pressure reduction and thereby help maintain MAP. For impeller, it unloads the left ventricle. It reduces diastolic volume. And on cardiac work, the volume reduction reduces the pressure-volume loop area and cardiac work. From cardiogenic shock to hemorrhagic shock, depending upon the amount of blood that's lost, there are different shock classes. And when more than two liters of blood is lost, shock class is identified as four. For shock, just like we were talking about, septic shock, early resuscitation, source control, and reversal of that underlying coagulopathy will help in reversing shock. The principles of damage control resuscitation, while patients are receiving blood-in-blood products, avoiding or correcting hypothermia, making sure that there is mechanical pressure that's applied for preventing further hemorrhage, if that's possible. Fluid administration in these patients should be delayed. Instead, blood-in-blood products should be given and minimizing crystalloid infusions. Otherwise, you can potentiate a dilutional coagulopathy. And massive transfusion protocols with different ratios, the one-to-one-to-one ratio has been studied and been found to be effective in damage control resuscitation. Selectively administering any of these pharmacological anticoagulants may also reversing persistent coagulopathy. For obstructive shock, the primary driver is decrease in venous return. Examples, of course, tension pneumothorax, cardiac tamponade, increased ventricular afterload, for example, patients who have hypertensive crisis or aortic dissection. ECMO. For ECMO, understanding the type of ECMO support for veno-venous ECMO, both the return and both the cannulas are venous cannulas. This is usually used for patients with refractory hypoxemia. Patients who need VA ECMO are patients who are in cardiogenic shock. Patients who have both pulmonary and cardiac needs may need VAB or veno-artic venous ECMO. Indications for VV ECMO, usually refractory hypoxemic respiratory failure, could be used as a bridge to recovery or as a bridge to lung transplantation. The CO2 retention on some of the problems that can occur with VV ECMO, CO2 retention, severe air leak syndromes, and patients may develop cardiac or respiratory lapse if the cannulas get blocked. For VA ECMO as a bridge in patients with cardiogenic shock, lots of different reasons why patients go into cardiogenic shock. Cardiac arrest, or ECPR, is also a VA ECMO bridge. Could be as a bridge to recovery or as a bridge to heart or heart-lung transplantation. Sometimes patients may need to be bridged over to durable mechanical circulatory support, for example, LVAD. ECPR paradigms during cardiac arrest when there's no flow, low flow, or establishing flow around 20 minutes using ECMO. So the suggested transition to ECLS is currently about 21 minutes. Last few slides on hypertensive emergency. For patients with hypertensive emergency, there are lots of different reasons that can be associated with hypertensive emergency. For example, aortic dissection, MI, stroke, pregnancy. And then once we suspect that there is hypertensive emergency, is there an underlying cause? And identifying that underlying etiology and treating and developing specific strategies to treat the underlying condition can help in preventing recurrent episodes. If the patient meets criteria for hypertensive emergency, target the organ, check what kind of target organ damage have they suffered from. If they have severe hypertension and MAP is more than 135, then we don't want to immediately lower their blood pressure. But in the next slide, we'll talk the strategies. About 10% to 20% decrease in MAP in the first few minutes to hours, and about 5% to 15% decrease in the next 24 hours. And then you can normalize the blood pressure over the next several days or weeks. Here's a medication summary. Again, details will be provided by our pharmacy colleagues. But several of these drip-based medications can be used. The onset of action, the purpose of using drips, the onset of action is fairly rapid. Duration is also not long lasting. And here are the common dosages that are used. On aortic dissection, so the problem with aortic dissection is a false lumen is created and there's blood that is going from the true lumen into the false lumen and impeding organ perfusion. In terms of the types of aortic dissection, there are different classifications, Stanford A, Stanford B, or DeBakey classification, DeBakey 1, 2A, 2B, and 3. Ascending, so dissection involving the ascending aorta, dissection involving both the ascending as well as the descending aorta, and dissection that is only limited to the descending aorta. You could remember the Stanford A and B classification, A limited to the ascending aorta, ascending aorta, and descending aorta. And then Stanford B is in the descending aorta alone. Signs and symptoms, chest pain that will mimic an MI, patients can collapse, have vasovagal events, diastolic murmur of aortic insufficiency can be seen particularly in half the cases of patients with the Stanford type A. Pulses paradoxes may be seen due to a concomitant cardiac tamponade. Patients go into cardiogenic shock. They could also have hypovolemic or hemorrhagic shock due to aortic rupture, and due to other arterial territories being involved, for example, hemiplegia or paraplegia with spinal cord hyperperfusion. So here's a good flowchart on how to manage these patients. Patients with chest pain, you get the history and physical, you do your routine testing, you get an EKG. On the chest X-ray, you may end up with a chest X-ray, you may end up with a chest X-ray, you may end up seeing a widened mediastinum. You could do a point-of-care ultrasound or send a patient out for urgent CT. That urgent CT can help you rule out of PE, aortic dissection, as well as acute coronary syndrome. And based on the location of the false lumen or tear, Stanford type A, open surgery, this is a cardiothoracic emergency, Stanford type B, complicated versus uncomplicated. Uncomplicated can be managed medically for complicated endovascular stenosis. Thank you so much for taking the time and looking forward to the Q&A session.

shock subtypes

mechanical circulatory support

hypertensive urgency

cardiac output

preload

distributive shock

fluid resuscitation