Hi, my name is Eric Chirula. I'm coming from the Department of Neurology and Neurosurgery at the University of Wisconsin, and today we're going to start with the first part of cardiology review. I have no confidences of interest to disclose. Here are the learning objectives. In brief, we'll look at common arrhythmias and counter-neurocritical care, as well as some core concepts in treatment. We'll learn how to differentiate right-sided MIs from pulmonary embolism and left-sided MIs from stress-induced cardiomyopathy, two very common issues in a neuro-ICU. So we'll start off with the case. Here we have a case 1, a 23-year-old man admitted to a neuro-ICU after sustaining a fall from a ladder, leading to a traumatic C5-6 cord injury. He's basically quadriplegic, and three hours post-admission, you were called to the bedside for hypotension. Phenylephrine has been started. He's afebrile, they're telling you a pulse of 38, respiratory rate of 14, and a blood pressure of 91 over 45, but he has a MAP goal of greater than 85 at the time. The nurse tells you his skin is warm to touch. And here at the bottom, we'll see a rhythm strip, and they're telling you that it's sinus bradycardia. So we'll start with bradyarrhythmias. So in this previous case, it may be tempting to attribute the bradyarrhythmia to medication effect or to his traumatic injury. But in a neuro-ICU, I think we must remain vigilant. We see a lot of traumatic falls, and sometimes these falls are due to intrinsic cardiac disease the other way around. So we'll start off with some basic anatomy. First, you have to be aware of the SA node and AV nodes, since the SA nodes is the pacemaker for the heart. And just for review, the SA node is a conglomerate of cells located in the upper atria next to the superior vena cava, which can be issues sometimes with lines or other things actually mechanically touching these nodes. Some definitions. Sinus pause is when you have a cessation of a sinus rhythm for usually less than three seconds. If it's greater than three seconds, then it's called a sinus arrest. There's usually a junctional AV escape rhythm with sinus arrest, and in the ICU, it's commonly due to vagal stimulation or hypoxemia. And here's an example of someone with just that type of rhythm. We'll look at secondary AV blocks subdivided into MOBIS type 1 and type 2. The type 1 is the progressive PR prolongation, the drop QRS. Commonly due to drug-related ischemia to the heart or infiltrative conditions. The MOBIS type 2 is failure conduction below the AV node. This is usually due to structural disease, and most times you can tell this by the wide QRS. These are more likely to progress and have hemodynamic effects, so these are the ones that you should be more worried about and more attuned to. Going on, third-degree AV blocks are when there's no AV conduction. Here we have an example of that, of the complete dissociation between the SA and AV node. And just for the differential, this is an example of a high AV block. So unlike the third-degree block, there's still some proper P-QRS relationship. Still for these two cases, pacing needs are high. You may also encounter sick sinus syndrome, since these frequently are symptomatic and lead to falls. This is classified as chronic, inappropriate sinus bradycardia, and symptomatic when there's a failed escape rhythm. Usually you can see a variety of things such as sinus pause, sinus arrest, or sinoatrial exit blocks. Most of the times they are caused by intrinsic causes such as ischemic heart disease, but every once in a while you must remain vigilant that it could be from extrinsic, such as drugs, autonomic dysfunction, or hypothyroidism. There is a frequent, sometimes you may come into something called tachybradysyndrome, where there's alternating bradycardia and tachyarrhythmias, and here's an example of that. Again, these patients have a high need for pacing. So we'll talk more about bradycardias and neurologic conditions, since there are many neurologic conditions that can predispose one to sinus bradycardia. First off, space-occupying pathologies, so a large tumor, for instance, can present itself from a cardiology standpoint with sinus bradycardia. Seizures, while most seizures cause a tachyarrhythmia, there are some seizures that predispose one to a bradyarrhythmia. Seizures, strokes, the insula has been, there has been a term coined as the cardunculus, or the CNS representation or control over the cardiac function, mainly from a rhythm standpoint. It has been said that there's the left insula and the right insula can predispose one, if stimulated, to tachyarrhythmias or bradyarrhythmias, but it's not quite clear. But there is plenty of data and case reports that insular strokes, but in particular, posterior insular strokes, can predispose one to either brady or tachyarrhythmias. The trigeminal cardiac reflex, this is when the trigeminal nerve causes a bradycardia. This is common in the OR if they're working on a CP angle tumor where the trigeminal nerve is mechanically affected. You can also see this at the bedside. If you're much like me and hate pinching patients to see what their motor response is, sometimes we'll do a nasal tickle, and that will stimulate the trigeminal nerve, and occasionally you may see some slowing of the heart rate or even apnea. AIDP, or otherwise known as Guillain-Barre syndrome, can sometimes predispose one to bradycardias and or tachycardias. Angioplasty and endarterectomy, both of which can damage the carotid body and end up with the bradycardia. Usually these are transient. And then neurogenic shock. So what are the recommendations for pacing in sinus nodal dysfunction? Basically, any sinus nodal dysfunction would document a symptomatic bradycardia. These are the class one recommendations. Basically, in the neuro ICU, if we see someone with a fall, and we think that their fall was from a syncopal event rather than a mechanical fall, those patients should probably be worked up for having a pacemaker placed. I always like to give some pearls throughout my talk. Calcium, I think, is underutilized in bradycardia. It obviously has a good safety profile and has a potentially effective effect for a variety of ideologies. Here are just a list of some calcium-responsive bradycardias. Hyperkalemia, hypermagnesemia, hypocalcemia, calcium channel blockers, and there is some evidence for beta blocker overdose as well. So if you're ever in a pinch and just need more time to think about things, it's always a good idea to think about giving calcium. So in this case, when we were visiting, the patient here suffered a high cervical spine factor with quadriparesis, and they have bradycardia, and their skin is warm to the touch, meaning that they're not vasoconstricting. So this is neurogenic shock. This is when the sympathetic outflow is disrupted, resulting in partially unopposed parasympathetic output, basically anywhere from the T4 level and above. These neurogenic arrhythmias usually occur in the first couple of hours post-trauma and tend to resolve within the first two weeks. So if you have someone that's still bradycardic seven days out, try to ride it out and see where they end up at 14 days. Some of these patients also have asystole, so just to be on the lookout that that may occur. And the choice of impressor should include something with beta stimulation, as opposed to this patient that was put on phenylephrine. Moving on to case two. Here we have a 59-year-old woman with moderate TBI. Day 10, she's on hypertonic saline. Her exam now shows some pitting edema. Vitals, heart rate 80, MAP 85, intracranial pressure of 18, and so millimeters of mercury. She's on midazolam and norepinephrine at 0.45. Her labs include creatinine of 0.8, VUN of 39, potassium 3.7, and MAG 1.4. And also you call to the bedside for suddenly has a MAP of 68 and the heart rate now is in the 150s. And here is the rhythm strip. As you can see, an irregularly irregular rhythm with no discernible P waves. So this is atrial fibrillation. Atrial fibrillation is a two-step process. You have to have an arrhythmogenic atria and a trigger. The arrhythmogenic atria can be from atrial stretch or from inflammation. In this case, we have TBI and hypervolemia. And then you need a trigger. So adrenergic stimulation, ischemia, or electrolyte derangements. In this case, we have the patient on norepi, which causes a beta 1 stimulation, as well as low potassium and low magnesium. So the treatment for this case would be changing the patient from a norepinephrine infusion to a phenylephrine infusion potentially, addressing the volume overload, and then addressing the electrolyte abnormalities. In this case, because of the low cerebral perfusion pressure, you may want to avoid AV nodal blockers or something that would drop their pressures. That's why I have this magnesium question. I think it's an underutilized treatment option when controlling atrial fibrillation. There was at least one study, and there was other smaller studies. In this case, this was a prospective randomized study looking at magnesium infusion versus amiodarone, and they actually found very similar results in terms of rate control. Now, if you have the crashing AFib patient, obviously, you're going to synchronize cardioversion as your primary treatment modality. But occasionally, we have these patients that are resistant to medications or were stuck because of lowering their blood pressure, and in which case, we do consider pharmacologic cardioversion, in this case, amiodarone. There is at least one study out there that looked at some retrospective data, looking at the pharmacologic cardioversion with IV amiodarone in neurologically ill patients. At least in a 14-day period, they found that they had no significant issues from this. At least in my institution, we tend to use amiodarone with some caution, but fairly frequent. Moving on to case 3. I'm just going to start off with just a 12-week EKG here, and what you can notice is that this is an irregularly irregular rhythm, a YQRS, and then it has this undulating polymorphic pattern here. If you see this, this is atrial fibrillation with Wolff-Parkinson-White syndrome until proven otherwise. Irregularly irregular, YQRS, polymorphic. The treatment for this should always be synchronized cardioversion. This is not the case that you want to give an AV nodal blockade, such as adenosine. This will throw the person into a cardiac arrest. In general, I will say that adenosine should be avoided in AFib or flutter. If you know that that's the pattern. Unless you're trying to decipher what the underlying rhythm is, try to avoid adenosine. You can consider IV medications such as ibutadolide, procainamide, or amiodarone. Sometimes I think expert consultation with a cardiologist should be done. As a word of caution, since we tend to use amiodarone a lot in the ICUs, the amiodarone can slow down the AV node without affecting the accessory pathway. So again, you may throw someone into an arrest. Just for competition's sake, I'll talk about atrial flutter. That's when you have a reentry circuit that travels around the annulus of the mitral valve and commonly presents in a 2 to 1 ratio. Remember to look at all the leads. Here's an example of a 12 lead, where lead 2 and lead V1 shows you the AFlutter waves. In this case, it's not demonstrated on lead 2. Always get a 12 lead. Sometimes it may be difficult to discern all the P waves. You can use something called the Bix rule. Basically, if the P wave is between two QRSs, then you have the next P wave buried in the QRS. Here's an example of that P wave here. The next P wave is actually buried in this QRS. Sometimes the density may be helpful in these cases to look for the underlying rhythm. Moving on to case 4. Here we have a 61-year-old woman with no prior medical history. She's admitted for a subarachnoid hemorrhage. She's on aspirin and clopidogrel. She had a stent coiling procedure. About two days later, she's noted to have lower blood pressure. Her systolic blood pressure was initially in the 140s, 150s, and now in the 100s. If you get a 12-lead EKG, this is what it shows. Obviously, the thing that jumps out to everybody is this ST elevation in the precordial leads. Does this patient have an MI? I think in the neuro-ICU, you've got to have a reasonable differential diagnosis. In this case, you have to have on differential stress-induced cardiomyopathy. Stress-induced cardiomyopathy versus myocardial infarction. What about the ECG findings? There is no single finding that can differentiate between the both entities. That's the most important thing to remember. But if you are to look for some signals that this can be a stress-induced cardiomyopathy, if you see isolated T-wave inversions, this tends to occur more often in stress-induced cardiomyopathy rather than a myocardial infarction. These isolated T-wave inversions are otherwise known as cerebral T-waves because sometimes they have these deep inverted T-waves. Here's an example of that. At least one study, probably the biggest study that I encountered, I think there was 200 patients in each arm, found that if there was ST depression in the AVR lead without reciprocal changes, that that was the more specific finding for stress-induced cardiomyopathy rather than MI. In this case, they found that 31% in stress-induced rather than 3%. Here's the citation for that study. Stress-induced cardiomyopathy, most people know it as Takotsubo's or octopus trap because that's the way it looks like at least on a catheter study. The pathophysiology of it is thought to be sympathetic activation leading to microvascular spasm. That's the working pathophysiology at the moment. It's most common in postmenopausal women. It's sometimes difficult to differentiate from an acute MI, but what you're looking for, at least in the patient, is are they a postmenopausal woman? Do they have a trigger such as, at least in a neuro-ICU, subarachnoid hemorrhage, a seizure, or a stroke? You will see a modest increase in cardiac troponins, although I've also seen not so modest increases. The wall motion abnormalities extend beyond a single epicardiovascular distribution. That's probably one of the more important things, and just equally as important is that it's transient and reversible. Now, there is a diagnostic scoring tool that you can use for this as well to try to differentiate. Here's an echo of such a case. As you can see here, this is a four-chamber view. You have your right ventricle and your left ventricle. This left ventricle, you can see the apex of this ventricle has some ballooning and hypokinesis, or akinesis really, whereas the base is still functioning. This is the most common pattern. You'll see this apical hypokinesis. The second most common pattern is this mid-ventricular hypokinesis. These ones can sometimes look at people when they see this type of pattern. They tend to think, could this be an MI, specifically if you don't see that posterior wall. There are other patterns, but these are the two most common types. The treatment algorithm for this, if there's just pulmonary congestion without a low cardiac output, you treat it kind of as you would systolic heart failure, so ACEs or ARBs, beta blockers, and diuretics. If there's a low cardiac output or shock, then you have to determine if there is left ventricular outflow tract obstruction. If there is LVL2, then you want to avoid ionotropic agents because this will worsen the obstruction and the subsequent shock or low cardiac output. You can make people much worse with this. I learned that the hard way as a fellow. Without LVL2, then again it goes through supportive care as you would treat systolic heart failure. Just for demonstration, here's an LVL2. This is someone with Takotsubo. You can see the ballooning of that left ventricle. Here you can see the base of this heart pumping still, which is creating a gradient here on this color Doppler. You can see that color Doppler. If you don't happen to have color Doppler on your echo, if you're doing a bedside routine, looking at this posterior leaflet, you can see that posterior leaflet almost hitting this wall right here. If you see that, then you have to start thinking, do they have a gradient here? By definition, a gradient greater than 30 is LVL2. Again, you want to avoid ionotropes. You want to avoid hypovolemia. This is not the patient you want to aggressively diurese as well as avoiding aggressive vasodilators. You want to consider beta blockers in these cases. Moving on to Case 5. Here we have someone with a severe TBI, has a subdural hemorrhage that was evacuated. Then on Day 6, you have a sudden drop in the blood pressure. They were, let's say, in the 130s, 140s, and now it's at 105 or 55. Their heart rate jumps up to 118. Their O2 sets are 90% on room air. I'd say it was better before that. They have a temperature of 99 and a CVP of 11. On exam, they have agitated delirium, no focal deficits. But you notice that their hands and feet are cool to touch, maybe a little clammy. They have a lactate of 3, they have a troponin of 0.8, and a hematocrit at 31%. You do a bedside echo, and they're reporting, let's say someone reports this to you, that their left ventricle is hyperkinetic, they're unable to see the IVC, they see no B lines, and there's a lung sliding present on both sides. You get a 12 EDKG, and this is what it looks like. So maybe a bundle branch block is the only thing that really jumps out, and we'll review this later. So I want to start to introduce shock, in this case as well, for the patient that has shock. Now, there's four main types of shock, distributed, hypovolemic, cardiogenic, and obstructive. As for distributive, well, the patient doesn't have cool extremities, and there's no new drugs that could cause anaphylaxis, and no infectious sources to say. Hypo-hypovolemic, well, the CVP is 11, the hematocrit is 31%, so probably not that. Cardiogenic, you know, you have a hyperdynamic LV. What about obstructive? Well, they have lung sliding, and there's no pericardial fluid. But remember, it's not all about the left ventricle. Take a close look at the right ventricle. Here we see, again, a four-chamber view, and the right ventricle, left ventricle, left ventricle. As you can see, the left ventricle is pumping adequately, but pay attention to the right ventricle. The right ventricle is dilated, ballooned out. There is some flattening of the septum, in fact, even bowing into the left ventricle. And then this little finding, which is called McConnell's sign, at the apex, this little dimple right here, there's some apical sparing, that's still pumping out. That's McConnell's sign, and that's been stated to occur more often in pulmonary embolism. If we look at a parasagittal short view, here we got, again, a dilated right ventricle and a left ventricle. You can see some flattening here of the septum, much kind of as you see this bowing here. That's been termed the D sign. If you see these two things, you want to start thinking of a pulmonary embolism. Pulmonary embolism versus right-sided MI. For right-sided MI, what you're looking for, at least on the EKG, is SC elevation in lead III greater than lead II. There's a highly specific sign, which is SC elevation in B1 with SC depression in B2. If you see that, that's highly indicative of a right-sided MI. Not very common, but if you see that, it's very specific. And of course, if you're having trouble, you can always get right-sided leads placed. I do that from time to time. Looking at the EKG a little bit closely, for pulmonary embolism, in this case, what you see is an S1, so S wave in lead I, Q wave in lead III, and T wave inversion in lead III. This is a classic S1Q3T3. And this is a study looking at the odds ratio of all these ECG findings in pulmonary embolism. And for this patient, they had this finding, they had bundle bench block, and they were tachycardic, as well as the ultrasound findings. This is the pulmonary embolism. When you're dealing with an acute PE, massive or submassive, you're affecting the right ventricle, and the right ventricle should scare you. Why is that? Here depicted in this is this death spiral. When you get a sudden increase in right ventricle afterload, you increase the right interventricular volume, which decreases its output. You get septal shift. Both these things affect the left ventricle's preload and subsequent cardiac output. Subsequent to that, you have a decrease in your mean arterial pressure, which decreases the right coronary perfusion pressure, leading to more ischemia, increased wall tension, increased afterload, and you keep on going down this spiral. One thing to keep in mind, and it's not commonly known, is that the coronary blood flow to the right ventricle occurs during systole and diastole. This increased volume and pressures, right ventricular wall pressures, can really affect the right ventricular coronary perfusion pressure quite drastically. You should have a plan for these acute PEs, since we tend to see them a lot in our neuro ICUs. First off, you want to be cautious of fluid. The right ventricle is not always fluid dependent. You want to be cautious of intubation. At least in one study, they found that 19% of patients coded on induction. You also want to increase the systolic blood pressure, increase the right ventricular contractility, while decreasing the pulmonary vascular resistance. How do you do this? Your choice suppressor should initially be vasopressin. This will increase the systemic vascular resistance without affecting the pulmonary vascular resistance. Vasopressin should be your first go-to. Obviously, you want to prevent increasing pulmonary vascular resistance by avoiding hypoxemia and acidosis. Putting them on 100% oxygen can sometimes be helpful. For medication rescue therapy, you want to consider inhaled epiprostanol or nitric oxide. There have been people that describe using inhaled nitroglycerin at the bedside. Another option to consider. Most large hospital systems now have a PE response team. In those cases, you want to consider thrombolytics and or catheter-based approach, which I don't have time to discuss at the moment. Here are some other ultrasound findings. This may look like a D sign right here. You see some flattening right here of this left ventricle, but that's happening with inspiration. That's what you see in a restrictive pattern. Here you have septal bounce, also happening in restrictive disease. You see these things, you got to start thinking of restrictive diseases, not a PE. For acute PEs, again, which we sometimes encounter in the neuro-ICUs, you want to think of ECMO. At least in one study, the overall survival in ECMO patients with acute PEs was about 70%. Again, if ECMO is initiated after cardiac arrest, they have a high risk of death. If you're going to consider this, you got to consider this early. For a review on this, I left a paper here. There was one recent study that looked at ECMO in traumatic brain injuries. They found that when indicated and used ECMO, that they had a much higher survival rate than the patients that were not on ECMO. In this case, they actually used non-heparinized systems. You can have that as an option in certain locations. Here's the citation for that. In conclusion, arrhythmia is our common neurocritical care due to underlying cardiac disease or from primary brain injury. I think it's our job to differentiate these two. Right-sided heart failure can be differentiated from an MI, can be differentiated from an acute PE using ECG and ultrasound findings, as well as left-sided MIs from stress-induced cardiomyopathy. I've outlined, and you must have an outline for how to manage acute PEs as well as stress-induced cardiomyopathy. All right. Thank you for your time.

arrhythmias

cardiology review

neurocritical care

bradyarrhythmias

sinus bradycardia

atrial fibrillation