Episode Transcript
[00:00:07] Hello. Welcome back to another episode of the code 321 podcast. Today's a special episode. We're going to be doing a case review. This is a clinical patient that I had at a critical care level transport post surgical procedure of a coronary artery bypass graft. So we're going to walk through the case a little bit. We'll talk about a couple teaching points, and I'm going to try to make it palatable for a bunch of different levels so we won't get too technical into the biochemistry of how all this went down. But I do think it's important to talk about some of the, some of the teaching points here. So we're going to talk about the case progression. We're going to talk about a little bit about the physiology. We're going to talk about pathophys, some mechanical circulation, and then we're going to talk about some lessons learned, some information that you can take back with you as you see and treat these patients in the field. So this particular patient, 71 year old male patient, he's healthy, he's chopping wood, he's exercising at the gym regularly, likes to go up a steep hill for exercise, doesn't have any sort of exercise intolerance or episodes of hypoxia.
[00:01:12] Had a diagnostic catheterization which identified pretty significant coronary artery disease in three of the vessels in his artery, specifically the lad, the PLV, and the OM. And when they went in, they decided that they wanted to do an elective CABG procedure to try to restore some blood flow to those areas of the hearts and improve some of his circulation. So the plan is, um, they're going to go in there, they're going to give him a coronary artery bypass graft times four. They're going to take care of an aortic valve replacement because he does have some aortic valve stenosis. Um, they're going to take a look at, um, the heart while they're in there. And he has had a couple episodes of atrial fibrillation with rapid ventricular response, one of which needed to be synchronized cardioverted previously, but other than that, doesn't really have any crazy medical history, isn't complaining of anything. So this procedure gets scheduled, and he goes into the. Into the operating room.
[00:02:13] When he gets in the operating room, they open him up, they do the valve replacement of his aortic valve, they do the coronary artery bypass graft. And when they're in there, they identify something called systolic anterior motion of his mitral valve, and they find that he has some septal hypertrophy. So what that means is we'll get more into the systolic anterior motion a little bit later here. But the septal hypertrophy is just what it sounds like. The center of the heart that divides the right ventricle and the left ventricle is extra thick. And that comes into play because when we're looking at these extra thick septums in patients that are having, um, damage to their heart valves, one of the things we can run into is it changes the way that the blood flows out of the heart. So when. And we'll. We'll kind of. We'll talk about that a little bit later. So he goes into surgery. He has this done. There aren't any main complications, with the exception of the identification of this systolic anterior motion, which you might hear me refer to as Sam later on in the talk here. Um, better than that, he gets his chest tubes heads up to the surgical intensive care suite, where he's going to be doing his recovering. His laboratory results immediately post surgery are nothing too crazy. He has a high pressure of arterial oxygen saturation, which you can imagine is probably related to being on bypass during the procedure, as well as the high amounts of oxygen that are being applied when he's intubated during that procedure as well, too.
[00:03:43] No other crazy findings on laboratory results. There does have a elevated lactic, which you can imagine is going to be related to some of the stress of the surgical procedures.
[00:03:54] When he gets into the surgical intensive care suite, within 24 hours, the patient gets extubated and gets placed on high flow nasal cannula. There really isn't any need to maintain the invasive airway capturing with the tube and the trachea. So they move to that high flow strategy, and that goes pretty well. He isn't having any crazy oxygen demands at this particular moment in time, but one of the things he is having is he's having a pretty common side effect of a coronary artery bypass graft, which is called vasoplegia. So what we talk about with vasoplegia is when the patient gets out of the or after a procedure like this, it's pretty normal for them to be on pacing to control the rate of their heart, and it's pretty normal for them to be on higher amounts of vasopressors to stimulate a higher blood pressure. I think that's pretty normal as the heart transitions from being stopped, being on bypass, and then going back into its own intrinsic rhythm and all of its vascular tone that we're looking for. But what happens in vasoplegia is within that kind of first 24 hours window after coronary artery bypass, you have hypotension. So you have these transient mean arterial pressures that are below 65 mercury and aren't really affected by a fluid challenge. By supplying additional volume to the circulation, you also have a low systemic vascular resistance. So normally what we see with SVR or systemic vascular resistance is we're looking for like, 800 to 1200 dynes is kind of the metric that we use for that. So if you have less than 800 and you have a cardiac index less than 2.2. And just as a quick review, one of the reasons that we like to use cardiac index over cardiac output is because cardiac index is more correlated to the body surface area of the patient. So if you're looking at, you know, a horse racing jockey versus, you know, Kareem Abdul Jabbar, that cardiac index is going to be different, whereas the cardiac output may be the same. So cardiac output is just the stroke volume and the heart rate combined, meaning how much blood is moving around the body through the heart in each minute. So the patient comes to the surgical intensive care suite, gets diagnosed with this, with this vasoplegia, meaning that even though they're giving fluid, even though they're giving some vasopressors, the patient is still not having an appropriate blood pressure. So they need to start addressing that. So one of the things that they start doing here is they start placing him on multiple pressers. So they put him on norepinephrine, they put them on epinephrine, they put them on a trial of phenylephrine, and they're really having a hard time getting these blood pressures up to the point that they want them. So one of the things that they can do, specifically in the patients who are recovering for a coronary artery bypass, is they will actually administer this medication called methylene blue. So, methylene blue, you probably remember this if you took a national registry paramedic exam or if you took like, an IBSc exam. So, flight paramedic or critical care paramedic, they really love to throw this in there because it's the antidote for meth moglobinemia, which is related to the iron on the hemoglobin. It can cause some significant hypoxia. So that's kind of what it's known for. And you can get that from, you know, toxicity of nitrates. So, like nitroglycerin or amyl nitrate. So sometimes you'll see these questions get thrown in there. I know I had, you know, some questions like this in some of the exams that I've taken before, but methylene blue, we kind of always think of it as methymoglobinemia. And a lot of you who are working in emergency care, that's kind of where we see it. But once you get into critical care, we actually will see this medication for patients in the surgical suites post coronary artery bypass. And it's. It's indicated when you have distributive shock. So that low systemic vascular resistance, remember, less than 800 dynes, and it's refractory to epinephrine. So what it does is it basically inhibits the enzymes, the endothelial nitric oxide synthase. And I know that's a big word. You might see it written as enos. Enos. And what that does is it inhibits the smooth muscle relaxation, therefore causing some peripheral and central vasoconstriction.
[00:08:30] So in that setting, the post coronary artery bypass graft administration for vasoplegia, remember, that diagnosis is the low maps, the low cardiac index and the low systemic vascular resistance. Typically, you'll see methylene blue given over about 20 minutes at a dose of two milligrams per kilogram. It's kind of like what you'll see. So I think that's pretty fascinating because a lot of folks think of that methylene blue specifically for methymoglobinemia. But in this case, we're actually giving it almost like a presser because it is having some vasoconstriction effects. Not necessarily that it's squeezing, but it's preventing the dilation through the nitric oxide pathway. So they start him on this medication, they're like, oh, great, perfect. It's indicated, makes sense. And about two thirds of the way in, probably 15 minutes into administering this methylene blue, he starts having really profound diaphoresis, starts having really significant chest pain, and says that he can't breathe, he's having difficulty breathing. So I actually shut that off. So from this point on, it's really listed in his chart that he has an allergy to methylene blue. And I want you to think about, as you listen to this, the methylene blue and the nitric, the nitric oxide pathway and how that's interacting to cause that increase in blood pressure, because we're actually going to flip the script a couple, a couple minutes later here, and they're going to try something different. So just remember that, that the methylene blue is given post coronary artery bypass graft in the setting of vasoplegia. So the unresponsive blood pressures and the way it does that is it inhibits that smooth muscle relaxation of the vasculature.
[00:10:12] So he starts to have these declines. So we're starting to see a little bit more increased oxygen demands. We're starting to see a low systemic vascular resistance. We're seeing low mean arterial pressures. And the patient is starting to experience just, like, a general decline after surgery. He also is having these really elevated pulmonary pressures. So we get into this a little bit of a tricky situation because we want to increase the systemic circulation and the mean arterial pressure, because we want that end organ perfusion. But if we increase that pressure with things like inotropic agents like epinephrine, or if we increase it with potent vasodilators, sometimes what can happen is we'll actually increase the pulmonary artery pressures as well, too. So you want to be really cautious about, you know, trying to force too much constriction in the pulmonary arteries. So, normally, what we like to see in terms of the pulmonary artery hemodynamics is something that we call quarters over dimes, meaning that the systolic pressure in your pulmonary artery should be somewhere between, like, 15 and 25 ish, and then your diastolic pressure should be somewhere between, like, eight and 15. So that kind of quarters over dimes is a lot of what people will use to remember that. And this patient has, you know, roughly a pulmonary artery pressure of fifties over 25. So it's almost double what it should be, which is really not great. And so they're trying to balance the need of increasing his maps, but also not pushing his pulmonary artery pressures higher. So you really need to think about how we're going to do that. In addition, if that wasn't enough, this patient also is experiencing some amounts of ectopy, meaning some irregular heartbeats from all these episodes of hypoxia and stress on the heart. So they put him on an amiodarone drip to try to get that under control.
[00:12:07] So his. His pressure seemed to be responding a little bit. When it comes to the vasopressor regiment that they have him on, they're trying to be careful about being judicious with their fluid use, so not giving him too much fluid and overloading him. He is developing some amount of peripheral edema from the right sided heart failure. And he's also having some pulmonary edema from the left side of heart failure. And if you remember from EMT, AEMT, or paramedic class, when we have this high amount of vascular resistance in the lungs, this pulmonary hypertension, which, which is leading to heart failure, that's our definition of core pulmonal. So this patient's really experiencing some amount of core pulmonal, and we really need to get those pulmonary artery pressures down.
[00:12:56] So they take care of him for another day or two, and he starts spiking a fever, his cardiac index starts trending down. The lowest it got was 1.7. And remember, you can always hit that pause button and do a little research on the cardiac index if you want to just kind of see where we're at here. And his systolic pa pressures break 60. So remember, that quarters over dimes. We're looking for, like, 25s on the pulmonary artery pressure for systolic pressure, and here we're looking at 60. The chest x ray looks like some pulmonary congestion, which tracks for the fact that we, we have such high pulmonary hypertension, we can't really get the blood to move through that vasculature.
[00:13:39] And the SVR is coming up a little bit. It's at 1150 right now on the evening of transport, just with the vasopressor regimen. So he's on norepinephrine, and he. He's on, um, he is also on the, uh, vasopressin as well, too. The other thing that starts to worry us is this patient starts having increased oxygen demands, so they have to turn up his high flow oxygen cannula to get him more and more oxygen throughout the shift. Um, they try to diarrhese him, meaning cause him to urinate. So they're giving him, uh, administrations of Lasix, and they're really not getting a lot out. So what they're trying to do is they're trying to take this, this large amount of fluid that's not able to move through the heart because he has cardiogenic shock at this point, um, combined with this vasoplegia, and they're trying to diaries that fluid off, and it's really not working great. So he's having pitting edema. He's having, um, some high amounts of fluid in his lungs, and they're not able to escalate his care to something that has, um, positive end expiratory pressure. So you might think, oh, this makes sense to move him into, like, a biPap or a cPap, um, you know, positive airway pressure.
[00:14:51] The issue is, if we increase any amount of pressure in the intrathoracic cavity, that may cause some constriction specifically on preload, so on the, um, on the vena cava, because that's the soft kind of malleable structure, and that's gonna, that's gonna really cause a problem with this maps, which we already know are kind of an issue.
[00:15:13] So I'm working on the helicopter this night. They give us a ring. We're not able to fly because of poor weather. And we take a look, and we're going to head over there in the ground truck and see if we can move this gentleman down to another ICU about four and a half hours away that is capable of doing extracorporeal membrane oxygenation, or ECMO.
[00:15:34] So he's getting paste. They're trying to make sure that he continues to have an appropriate heart rhythm. One of the fascinating things about cardiogenic shock, and especially, um, shock that involves the heart valves is we really want to prolong the diastolic phase as much as possible to promote a good filling of the ventricle before we squeeze. And that relates a little bit to, um, the starling curve or Frank Starling law, which is the greater the stretch within the physiological possibilities, the, the better the contraction is going to be. So until we reach our physiological maximum, the greater we stretch that ventricle, the harder it's going to contract and the better stroke volume we're going to have in each beat. So we really want to prolong that diastolic phase. There's actually some information for patients who are experiencing shock like this that we want to try to lower the heart rate as low as we can while still maintaining appropriate mean arterial pressures, because that'll promote a good ventricular fill, and that will allow for those good perfusion of the coronary arteries, which happens in diastole as the blood leaves the aorta. The aorta and the valve shut. During the diastolic phase, those valves are actually going to direct, direct blood into the ostia, which is out of the aortic arch and back into the coronary artery. So the higher the heart rate, the worse it actually is for shock when the heart's involved, because the heart is not getting enough oxygen, and we're not having that ventricular fill, which kind of compounds the shock state and then causes their heartbeat to be even faster, which makes everything worse. So higher oxygen demands lower mean arterial pressures. He's having higher pulmonary pressures, so he needs to get to a rescue ECMO center.
[00:17:24] So get over to the bedside. Individuals alert and oriented times four. Um, the blood labs don't look too dramatically different with the exception that the oxygen has gone dramatically down. We have a mixed venous gas, which means that they're taking a sample from the tip of this on Gaines catheter, and that is showing 20 right now. We'd really like to see that closer to, like, 60 or 80. Um, and so, so he's really having a high demand for oxygen. Even though he's on high flow oxygen, he's getting a high saturation of that, um, his, his saturation of oxygen. The thing that's on his finger, um, is showing 98%. So what, what we mean when we're using these different laboratory results is that the saturation of oxygen, the amount of oxygen that is attached to the hemoglobin moving around his body is relatively high. 98% of his, um, of his body is, is getting that. The issue is, we're not getting that into the actual circulation itself. We're not actually using that at the cellular level. So one of the things we talk about is this, like, VQ mismatch. So even though we have high amounts of oxygen available, we may not be able to actually get that oxygen to the cellular membrane and do that internal respiration. So this patient's really sick.
[00:18:38] We have, he's now has a normal temperature after getting packed with some ice and getting some Tylenol and some other medications, and he does still have that pitting edema as well. And that's from that right side of heart failure. Currently, he's on the amiodarone, the vasopressin. He's getting some direl and Lasix, which are both gonna be diuretics. He is getting potassium repletion. For those of you that are nurses or critical care, you know that, um, when we're giving large amounts of Lasix, it's, it's a, um, non potassium, uh, sparing diuretic. So we're going to be urinating out that potassium. So we need to replete it as well, too. And if any rts are listening, um, or any critical care members, the patient's currently on high flow nasal cannon, 40 l a minute at 60% fractured and, uh, aspired oxygen percentage and 40 parts per million of nitric gas. So this patient actually got put on nitric. And one of the fascinating things about the fact that they're on nitric is, remember we talked about methylene blue being a medication that inhibits the nitric oxide pathway specifically to promote the, to, to keep the body from vasodilating. So it's trying to prevent it from vasodilating. So now we're actually giving the medication that does cause vasodilation. And so even though we have these low maps, the nitric gas is being inhaled directly into the pulmonary vasculature. And that pulmonary vasculature is being targeted to try to dilate the vessels inside the lungs. It has a very short half life, and when you inhale it, it's going to be very potent just in the area where it's inhaled. So that's why we're able to give nitric in a patient who has relatively labile maps to try to target that pulmonary hypertension and drop those numbers down. So we want to see those numbers quarters over dimes. We want to try to get that systolic pressure down. Um, and 60 is way too high. So it's kind of a fascinating patient, because you have a patient who is being given methylene blue to try to, um, inhibit the nitric oxide pathway. And then later on, within a day or two, is now getting nitric gas inhaled to stimulate the nitric oxide pathway, both for the same condition. So it's pretty, it's pretty fascinating that these medicines can be used, um, kind of concurrently. That way. The pulmonary pressures are high. The left ventricle needs those higher filling pressures. So we want to promote, um, a high afterload. So this patient isn't a candidate for, um, any medicines that are going to reduce afterload or therapies that are going to reduce afterload. So we want to be careful. Um, this patient is not a candidate for a balloon pump, because, remember, as that balloon deflates in the descending aorta, it's going to cause that vacuum effect to try to cause that assisted diastole, and that's gonna actually reduce afterload. So we can't be using intra aortic balloon pumps in a patient who has this particular diagnosis. The transport goes fine.
[00:21:41] Just kind of a fascinating case.
[00:21:45] On arrival, the patient, basically, their orders are going to be avoiding inotropes like we talked about. We don't want to stimulate those, the really hard contraction of the heart, because we want to promote appropriate afterloading. We are going to try to lower the rate of the heart as much as possible with supporting the map in order to allow for that ventricular filling.
[00:22:08] And then we really want a map greater than 65. And then the physician who's in taking this patient at this facility is really concerned about possibly needing to go to rescue venous arterial ecMO at some point in the evening. This patient didn't actually need to go to ECMO. Ultimately, what ended up happening to this patient is this patient got a surgical sternectomy, which is basically, um, they went into his heart, and they actually cut out a piece of his, um, septum.
[00:22:41] Sorry, septomyctomy. And so when they went into his heart, the problem with these big, um, septal hypertrophies is it changes the curvature of the left ventricle, which actually causes the blood not only to shoot out the aortic arch and the aortic valve, but it kind of directs it back towards the mitral valve. And when it directs it back towards the mitral valve, it can cause this systolic anterior motion. And what happens with the systolic anterior motion is that, um, sometimes the mitral valve can be pulled anteriorly using kind of the venturi effect. Shout out to my firefighter friends who use that for their foam systems. The mitral valve gets pulled anteriorly and actually kind of folds over on itself, and it shoots the blood back into the lung, which is one of the reasons why we're having these low maps. We're having this cardiogenic shock, and we're having these spikes in pulmonary artery pressure because we're kind of shooting it back towards where we came from, when in reality, we want the blood to go all the way into the left ventricle. We want all the valves to shut, and then we want it to squeeze and push out the aortic valve. We don't want anything coming back the way that we came.
[00:23:48] So, generally, the best practices in a patient like this is inotropes. We want to discontinue those afterload reducing medications like nitrates. We want to avoid those because, remember, we want high afterload to try to support the appropriate movement of those heart valves. The intraortic balloon pump is also not going to be a great idea because it reduces afterload. We do use potent vasoconstrictors. So the phenylephrine makes sense here. Um, you could use norepinephrine. There's been some, some different cases, some different discussions on that. But, um, you might see vasopressin because that's kind of separate from the. From the, um, the alpha and beta pathways. And then you might see beta blockers, if the map can support it, to try to reduce that heart rate to prolong the diastolic phase.
[00:24:36] And this isn't that rare, which is fascinating to me. There's actually a case review that I pulled up, which was from the European Society of Cardiology, and they call it suicide left ventricle, which is pretty wild. And they have done research, and they've shown that when you have a transcatheter aortic valve replacement, the incidence of the suicide left ventricle, this left ventricular outflow tract obstruction is much higher than when it's post surgical, meaning what this gentleman had where they actually cracked his chest open, went in there, and actually did the surgery. And if you have a patient that goes into surgery for an aortic valve replacement comes out, and they're kind of labile to respond to therapies, their label to respond to catecholamines, and their label to respond to fluid challenges. They want you to aggressively do what's called the TTE, and they want you to do a transthoracic echocardiogram to look at the flow of blood to try to see if maybe this systolic anterior motion is at play. And another thing to remember is that the resolution of this left ventricular outflow tract obstruction even after you fix it. So even after that septal myectomy, this patient can also take some time to recover and may still need to be on ECMO.
[00:26:00] In the european case, the way that they resolve this individual's septal hypertrophy is they actually threaded a catheter in there, and they actually injected a very potent amount of alcohol directly on the septum. So a pure alcohol is injected right on the septum, and that destroys the septum muscle and changes the shape of that ventricle to try to promote the appropriate blood flow back out of the body and not back into the lungs. So, just a review of what this patient actually received over the course of his treatment as they're trying to manage this complicated hemodynamic patient. The patient got norepinephrine, the patient got epi, the patient got vasopressin, methylene blue, milnerone, phenylphrine, and nitric oxide. And I just think it's such a fascinating patient, because you have a patient who is dramatically sick and gets methylene blue to inhibit the nitric oxide pathway, and then later on, gets nitric oxide to lower pulmonary artery pressures. And so there's reasons why this makes sense. Think about the half life and the targeted inhaled nitric oxide versus the systemically intravenous infused methylene blue. Um, and it's just a fascinating case where you're really in between a rock and a hard place. So, on the one hand, you need to increase the systemic vascular resistance, and you need to increase afterload, and you need to increase the overall blood pressure to sustain that end organ perfusion so that map greater than 65. But with every step we take in that direction, by causing vasoconstriction and boosting up that left ventricular pressure, we are also creating a higher pulmonary artery pressure because it's very difficult for us to target, target specific veins and arteries and not other ones when we're treating patients like this. So one of the fascinating things we can do is by using this nitric oxide.
[00:27:58] Another thing to think through as you're treating a patient like this is things like epinephrine are going to make this patient worse. And I know if I arrived on a patient who had labile mean arterial pressures, was receiving norepinephrine and vasopressin, my third presser that I would start to add pretty quickly would be epi. But in this particular case, that's actually going to make this patient worse because it is causing that pulmonary hypertension to get worse. So as you think through these heart failure patients, especially patients who have systolic anterior motion, or if they have some sort of abnormal heart valve, just think about the nuances behind how to care for them and don't be afraid to do a little bit of reading. A great resource would be the Internet book of critical care. You can also use life in the fast lane as a great one. If you use, you know, any other kind of quick reference apps that you can think of, ultimately, what's going to keep you out of the woods with a patient like this or a complicated patient that has a lot of moving parts is going to be good. Team dynamics. Using all your partners to think through a complicated case and having a really strong fundamental understanding of your. Your anatomy, your physiology, and your pathophysiology. I think I've said this for the last ten years, and every class I've been in and every class I've. I've taught is having a good understanding of what the structure is, how it's shaped, how the structure works, or how the system works and what is going wrong, that'll lead you down the right path. Nine times out of ten, to be able to kind of have that x ray vision to see what's going on in your patient and understand what effects you are having on the patient that you're treating. So if you're interested in going into critical care, if you're interested in going into flight, these are the types of patients that you're going to see. These patients have a lot of competing priorities, and every action has an equal and opposite reaction. So it's really important that you think through what changes you're going to make and how you're going to get these things done in a way that's safe for the patient. So hopefully you enjoyed this episode. I know it was a little bit heavy with some terminology, and we talked a lot about hemodynamics. We have to throw a bone out there once in a while for those folks that are really just salivating for more and more information at the critical care level. But don't worry. Next month, we're going to come back. We're going to do something new. And I appreciate all of you for listening, and I hope that you tune in for next month's episode as well. If you have any questions, like always, you can always get a hold of me. The information is in the show notes. And thank you again for listening. Stay safe out there.
