Wanna know how to manage coronavirus patients with ARDS in the ICU? Dr. Herbert Patrick, MD is a pulmonary and critical care specialist in Philadelphia and a master teacher.
The free “Edwards Clinical Education” App may be downloaded at the Apple AppStore, Google Play Store, or the Microsoft Store.
– Hey everyone, it’s Dr. Z. Welcome to the ZDoggMD show. Now, we’ve been talking about COVID for the last, I don’t know how many weeks. It seems like a lifetime that this has been going on, and yet, it’s happened like that. And since it’s happened so fast, many, many, many clinicians on the ground, we’re talking doctors, nurses, respiratory therapist, medical students, residents, everybody, we’re all wondering how do we manage these patients when push comes to shove in the ICU? Now, today’s guest… By the way, this show is brought to you by Edwards Lifesciences. They are the leader in hemodynamic monitoring and this is relevant because our guest today is an ICU critical care physician. He has a history of being a biomedical engineer, he’s an entrepreneur, but right now, he’s a practicing on the ground critical care doc in Philadelphia, Pennsylvania. And he is here to teach us about what his experience is managing COVID patients in the ICU. This is Dr. Herbert Patrick. Welcome to the show, Dr. Patrick, it’s a real thrill.
– Well, thank you, Zubin, and it’s my pleasure to be here. Thank you.
– Listen, I know you were working all week, you were exhausted when we had our prelim call and you’re coming off service now, so I really appreciate your time. But, I think, let’s just jump into it. What is your experience on the ground right now as you’re starting to see COVID-19 patients come into the unit?
– Within the ICU, the patients who are suspected as COVID positive have to be in isolation, the actual type of isolation has been higher than any level of isolation we’ve ever had. This is called enhanced, enhanced isolation, and this enhanced isolation is airborne, airborne. Well, this means that for us to just enter the room, we have to gown, okay, glove, okay, no surprise there, and mask, but wait a minute, the mask now has to be an N95 and we cover the N95 with a paper mask. So that as the paper mask gets soiled, we don’t soil the N95 and we then enter the room. Nurses in the room have to use, what I call the bang on the door technique, to get attention in order to get, I need flushes, I need towels, I need another bag of levophed. This is very time-consuming. Now, myself, as you see, I’m bearded, and with a beard, it means the N95 doesn’t fit. So I wear a PAPR, P-A-P-R, and it is a positive airway pressure resuscitator. It looks like the helmet from NASA up in the space station. Patients are not comfortable looking at me. The first thing I have to tell them is it’s okay, you haven’t died and gone to heaven, this is a special isolation device. So this is taking extra time to just enter enhanced airborne isolation patient’s rooms.
– So every COVID-19 patient in the ICU is under these enhanced precautions? Do you have enough PAPRs and N95s and PPE? Because I’m hearing from around the country, people are saying they don’t.
– Correct, we are looking at a limitation that will occur. The N95s we’re using for, I was gonna say 24 hours, but it’s a shift. We’re being told keep your N95 in a paper bag and use it again. Now, you’ve covered it with a paper mask, so that’s okay with us. It’s not perfect but it’s okay. The rumors are that the N95s will be in short supply, and if you look at the PAPR, the elaborate device I’m wearing, they’re in terrible short supply. I mean, this hood is disposable, but the power source, the fan, the batteries, they have a filter, are all on short supply already.
– Yeah, and that makes perfect sense, in the fact that you’re having to use cloth on top of the N95 to preserve the integrity of the N95. Now, I’m gonna ask a question, I don’t know if you have the answer to. But you know, in the Korean experience, they were finding surgical masks with aggressive hand hygiene, unless you’re doing aerosolizing procedure, were seem to be sufficient, but they had other things going on like aggressive social distancing within the hospital, separate wings and wards for COVID patients. Do you have any thoughts around that? Or do you think that this is an appropriate level of PPE for the risk?
– Zubin, that’s a good question. Because studies with influenza, now influenza, not COVID, have shown exactly as you said, the paper mask properly worn has been as good as an N95. Well, the trouble is those studies went on the COVID-19, so, we don’t know.
– Right, so there’s a lack of knowledge here really. All we have is the experience of some folks that have, I mean, I guess there was an issue where about 40 people were exposed in a procedure in Korea to a patient, most were wearing standard surgical masks and none were converted positive. But again, that’s such limited data, we just don’t know. So, you guys are going into, and they’re negative pressure rooms, each of them?
– Negative pressure rooms and I’m going in gowned, gloved with a hood over my head. Now that allows me to take off my paper mask and allows me not to have the burden of an N95, an N95 is quite a burden. Anybody wants to try an N95, wearing it for even an hour will learn that it’s very hard to breath after an hour through such a dense filter that’s properly protected, but it’s hard to catch your breath through that device. So I go in with my PAPR humming, meaning my motor is humming with the filter and I’m getting fresh air delivered to my headpiece, which is then exhausting through the bottom of this helmet and I am the most refreshed physician, nurse, clinician in the room ’cause I’m not wearing an N95. But these PAPRs are in very short supply.
– Yeah, I mean, I–
– Very short supply.
– Ideally, we’d have them everywhere and everyone would be able to do their job better. Although, again, even doing CPR, say, in a PAPR, is a challenge, I imagine, just because of all the gear you’re wearing.
– Right, but now, as the critical care physician coming in to intubate the patient, we’re recommending that even if you’re not be bearded, not bearded, get that PAPR and go in. ‘Cause during the intubation, you’re faced with the aerosolized material, a highest level. So, of course, that’s what we’re doing. We have the PAPR for the critical care doctor but it is shared by any anesthesia person going into the room to do a intubation or worn by the critical care doc going in to do the intubation.
– Makes sense, and so, now you’re seeing these patients, we talked about the PPE and we’ll circle back by the end to see if we remember to talk about what we’re gonna do when this PPE starts to run short. If it hasn’t already. And I mean, actually, do you have thoughts on that now?
– Well, some of my colleagues have shaved their beards to enable the N95 to be appropriate, others have actually purchased from companies their own PAPRs. They’re going for 1500 to $3000 on outside companies to have a personal PAPR, very impractical, but that’s what some critical care medicine docs have felt they have to do for their own protection.
– And the protection of their families who they are coming home to. How have you handled that yourself?
– With the return home, knowing the PAPR was my safeguard at the facility, we’re also wearing paper masks throughout the entire shift. Without exposure criteria, if you come into a hospital and since no visitors are permitted, you are given a paper mask and you’re gonna wear that the entire eight, 10, 12-hour shift that you’re on, so you then dispose it when you’re done. We hope we are limiting the cross exposure from our own colleagues. And as I come home, what I’m hearing from everyone is we’re throwing our scrubs and clothing into a washer to be immediately washed and dried and taking full showers, and then while at home, using alcohol hand washes extensively as if we might as well be at the hospital. Keeping social distancing at home while also alcohol washing everywhere we go at home.
– I think that’s actually really good advice for people because I get a lot of questions from frontline staff from hospitals and they just don’t really know the best way to keep their own families safe, and I think you pretty much said it. And this is hard, this is difficult, it’s extraordinary, but hopefully it’s not a permanent thing, right? But it’s still very, very difficult and I think talking about is very important. I think the public needs to understand too what our frontline healthcare professionals are going through right now that this is an ordeal. And honestly, the public in general is much safer from this thing statistically than we in the hospitals are and we have to take extraordinary measures, so thanks for describing those so that people really understand. So we’re now in the room and what are you seeing in terms of the pattern of illness when these patients are arriving to you in the ICU?
– Right, now to explain what we see means who gets into the ICU because you could be in enhanced airborne isolation, but not need the ICU. Now some will say, wow, that’s great, while others will say, wow, I’m still infected. Well, true, but if you are not hypoxic low oxygen level in your blood, in need of a ventilator, nor are you in shock with a low blood pressure, you don’t want, you don’t want to be in the ICU, you don’t want to be where other patients are going to be aggregated. So what we see is one of those two. We will admit a patient who has low oxygen level in their blood and we have to admit another patient who has oxygen okay but their blood pressure is low, they’re actually in shock and it’s from the infection. So infectious shock is called septic shock and I like the name even better called vasodilatory shock, vasodilatory. Your blood vessels dilate to bring shock of infectious type and that lowers your blood pressure.
– And are you seeing vasodilatory shock from the pure viral infection? In other words, this is not a bacterial superinfection, this is not necessarily a pure cytokine storm or something like that. This is viral infection causing sepsis? Or what have you experienced?
– I mean, I know this is tough to say, another great question. The fact is we’re seeing vasodilatory septic shock in the COVID-19 patients. However in searching for other causes which you want to do, but yet, you might first think it’s only COVID-19, there’s no reason to search, we have seen endocarditis, infection of the blood stream, from the heart valve being infected, not with COVID, bacteria, straightforward bacteria, a MRSA, MRSA, you know, methicillin-resistant staph aureus. Or we see a patient complaining of a gluteal pain and it turns out, they’ve got a gluteal abcess, they have an abscess that needs draining, but they did show X-ray changes and hypoxia from COVID-19. So, I don’t know, I don’t know what to say, viruses usually don’t pause vasodilatory shock, so we have not let up our search for bacteria in the COVID-19 population.
– So this is an important point I wanna make sure people understand, there can be a true, true unrelated kind of scenario where you have a secondary infection and they could be related, so it could be that your immune system is compromised or there are other predispositions that get you infected with something else. So the idea, if you’re in shock and you have COVID-19, you don’t just attribute the shock to COVID-19, you do need to make sure to rule out secondary causes without, I imagine, without going crazy and bronching and doing stuff that’s gonna put a lot of people at risk. What’s your sort of thinking on the diagnostic workup? Because everything you do could potentially either put the patient or the staff at risk when you’re doing it.
– That’s correct. So let’s look at whether a COVID-19 positive patient has enough of a CT scan X-ray burden to fit the hypoxia or geez, I don’t think they do, I think this could have a component of bacteria and we better search for that bacteria. So in this past week, I did go ahead and do a bronchoscopy to recover an attempted, attempted recovery of an organism ’cause I was not convinced the X-ray itself could explain a septic shock, but it definitely looked like COVID-19 by its appearance, by its appearance which people call ground glass. And in fact, it turned out that it was an aspiration pneumonia, an aspiration pneumonia, and yet, and the COVID was negative.
– The serology was negative. So, this isn’t fair to say we should be bronching everyone, you’re totally right. It’s such a high-risk procedure with patients who might be positive, you’re totally exposed to aerosolized material. But in the atypical cases, I believe we need to look more thoroughly. If that X-ray just doesn’t fit, we ought to look elsewhere.
– Got it. Yeah, that’s really interesting, and I’ve heard that repeatedly that you do not give up the search if your concern is not satisfied by COVID diagnosis or lack thereof too. Because even in a negative, right, if the clinical suspicion is quite high, the false negative rate of the test could come into play, correct? Do you guys have any protocols for that? Or do you manage it clinically?
– No, we do manage clinically. Again, I’m sighing because the nasopharyngeal swab is our, quote, gold standard, but I think we all have to agree, it’s not very gold.
– It’s not very gold. Nurses just are doing their best to get the swab back into the nasopharynx. Oh, come on, it is painful, I like to say slightly painful. I don’t like it if someone pushes a swab all the way back in nasopharynx, so could a negative swab still be a positive patient? Yes.
– Yeah. And that’s the bottom line, so it’s a clinical… This is where the art and science of medicine mingle and that’s why I think experience in training and discussions like this will matter for people to understand that looking at the overall picture. When you look at the overall picture, Dr. Patrick, what are you seeing? Now these patients when they present to you, they’re already quite sick, so they’re hypoxemic, there may be in shock. But what’s the pattern of presentation you’re seeing? Is it mostly dyspnea, cough, fever? Or are there other unusual presentations that you’re seeing? Like the abdominal complaints, diarrhea, those kind of things.
– And for us in the ICU, it’s been the typicals, it’s been more typical. Whereas to seeing the patient in the emergency department who’s come in and who is coughing, and who, yes, might have some abdominal complaints, no surprise. But when put on a simple face mask with 100% oxygen, their saturation of oxygen at their fingertip with that little red light that we all joke about, the ET light, turns out to be low. Well, they can’t go to the medical floors if they’re hypoxic, so we are seeing hypoxia with cough and we do have to intubate those patients in order to have them get enough oxygen into their blood and have a chance to survive.
– Now once they’re intubated, what’s your typical pattern or process of lines and monitoring for these patients? Are you doing arterial lines? Are you doing CVP? Are you doing PA cath? Are you doing non-invasive monitoring? What’s your sort of feel for that so far?
– The best answer for that is the one word, dynamic. Dynamic, now dynamic means what? Well, nurses do a great job, but they take blood pressure readings and oxygen readings for their flow sheets only every hour. I’m not satisfied with one hour gaps between data and it’s not me, it’s the concept. So if you put in a central catheter, you have the ability to treat that septic shock and you also have secondary ability to watch a cardiac output, which I can get more into if interested. The art line is needed because you need so many blood gases serially, dynamically, that you don’t wanna continue to just stick the radial artery. Oh, I did the less on the right side, so let me do this one on the left. No, no one wants to get stuck that many times and we don’t want to stick that many times. So putting an arterial line in gives a chance to pull back a blood gas promptly and repetitively without sticking. At the same time, that arterial line does the double duty of heart arterial pressure. We do not want the arterial pressure on these patients to fall below a mean of 65. That will show up only by the hour if you don’t have the art line. So you could be 59 minutes and 59 seconds and all the sudden, you could’ve had your drop for that length of time, but if you have in a art line, you’re not gonna have that drop for any significant length of time. There’s gonna be an attempt made to fix the hypotension. So CDC and art line go together in these patients for proper medical care in our critical care unit.
– And, of course, thank you for that. The dynamics of arterial hypertension in terms of why we care, if you’re gonna keep it above a mean arterial pressure of 65, any drops below that, it can be dicey, particularly for the kidneys, myocardial perfusion and those kind of things, which I’ve heard in these COVID patients now in the ICU, the dynamics of that can change quite rapidly and there is quite a threat or danger of both kidney and cardiac damage. Have you encountered quite a bit of this?
– Yes, yes, when we say cardiac, then we’re working so closely with our cardiology staff where we say kidney, we’re working so closely with our nephrology staff. We’re all concerned about multiple organs and what called multiple organ failure. And that’s going to start with not enough blood flow to the organs and every organ will start to drop out. So, you must keep mean blood pressures about 65 to support all organs. And you do need to know the tricks on how to do that, ’cause it comes down to does the patient need fluid to enhance their blood pressure? Or does the patient have enough fluid? And do they need a presser to increase the bolus?
– And of course you’re gonna have to monitor carefully to do that, whether it’s with arterial line, CVP. Are you putting in a lot of PA caths or have you not seen as much utility there?
– Now, we’re very big on PA catheters for only one group of patients and it’s the pulmonary hypertensive patient, ’cause they’re entering the hospital or the ICUs too, already with a terrible deficit. Their right heart has already failed, it’s failed. I mean, pulmonary hypertension is causing a right heart failure. So now we’ve got a right heart failure that we can’t work with ’cause there’s no test except a PA catheter that will get us those dynamic readings on the right side. So we’ve got a right-sided heart failure palpation and PA pressures are so high, they could be 80 over 40, rivaling the systemic pressures, we do PAC, pulmonary artery catheter for those patients. Luckily, the pulmonary artery does hypertension and pulmonary artery hypertension leading to right ventricular failure is not that common, so we are resting along the CVC and the art line. Now, CVP, I should say it’s CVP in the CVC is not popular because it doesn’t give the actual function of the right heart, or even the left heart, which is way disconnected from the left arm. So you have to come up with a trick to look at volume status and don’t look at the CVT, no good, no good.
– Oh, this is interesting. So now you’re gonna school me hard on this because, you know, in my day, we were down with CVP, you know what I’m sayin’? So that was our proxy measure of volume status, death certainly of right heart overload and that sort of thing. And in COVID patients, what I’ve heard from my ICU colleagues is that volume status is very tricky because they typically wanna run them a little bit dry, given the lung damage that they’re seeing, the diffuse alveolar damage and the ARDS and the fluid and the goo in the lungs. Running them wet is a very difficult thing to do but it’s very difficult to measure. So please teach me and teach our listeners the trick that you are talking about, using your central venous catheter and your… I don’t know if you’re combining with any arterial measurements, but I’d love to hear what you’re doing. Yeah.
– Right. So, CVP is out as a number. Now, I’m careful to say that because I don’t ignore CVP, but as another, I do. So, we just get that off. We’re not gonna say that a CVP that slow means more fluid, or a CVP that’s high means less fluid. But to try to explain CVP tracing changes, that’s not where we should go ’cause there’s a simpler way to do it. The simpler way is to look at that hypotensive patient who the nurse has found has the mean below 65. The nurse tells you, doctor, the patient has dropped their mean, it’s less than 65. You have to challenge that patient with fluid because if that works, by definition, they were fluid deficient.
– This is the way it is, this is the way it is. And if it doesn’t work, they are fluid independent and do not need fluids. You must go to pressers. So now it comes to what’s the trick? The trick has to be a very rapid fluid infusion. If you tell a nurse to bolus a patient with fluid, most nurses turn the IV pump up to setting we joke about, 999. For those who know, I think you know, that means one liter, 999 mLs in an hour. Well, I want 250 in in five minutes. Or I want 500 m in 10 minutes. You’re not gonna get that in a pump. You have to hook that up to a pressure bag, and it’s not hard. That’s not difficult. Meaning you accept the fact that you are gonna get a bag of saline, and let’s make it a 500. And you’re gonna put it in a pressure bag and you’re going to hook it up directly to that CVC. That CVC is not gonna act as a resistor enough to stop 250 from going in in five minutes. And shut off the valve after that ’cause you got another 250 left and you may want a second bullet. You might wanna get this, you know, pull the trigger for a second bullet. Now the issue is what were you watching during the 250 bolus, the bolus? You have to watch the dynamic cardiac number. It’s not blood pressure. Blood pressure may not vary at all during that bolus. But what goes up, telling you it’s a positive response to fluid is either stroke volume by 10% or cardiac output, which is heart rate times stroke line, by 10%. You have to have a device hooked up to the patient that can give your stroke volume and your cardiac output. These devices are non-invasive out there, there are pulse contour devices out there. Sure, we could say PA Cath, but that’s going very, very far into advanced technology. And you then watch that fluid bolus have its effect on stroke volume or cardiac output. You get 10% rise, great. In fact, you do it again, you do it again! ‘Cause you don’t stop until you don’t get the 10% rise, because then you’ve maximized your Frank-Starling curve as using some technical language and you have achieved your optimal fluid loading.
– Okay, I’m gonna re-package everything you said, which was brilliant, so that I make sure my monkey mind understands this. So, you, okay… You have your central venous catheter, you have a pressure bag, you squeeze in 250 of saline and that’s a rapid over five minutes. So you’re really pushing it into the vasculature, you’re giving a true fluid challenge. And then you’re using your non-invasive device to measure stroke volume, you’re calculating a cardiac output and you’re watching that dynamically, which means you don’t just write the order and go away, you actually follow up right away with the data and go, okay, the stroke volume and the cardiac output went up with my 250. And that tells us that that patient was missing that fluid. In other words, you mentioned the Frank-Starling curve, there wasn’t enough stretch on those ventricles to trigger a aggressive enough contraction, enough filling, enough cardiac output. And so, it is both a diagnostic, so we found out what’s going on, not enough volume, and therapeutic, we fixed the low blood pressure by improving cardiac output, hopefully. And the final thing you said, so that I understand, is keep giving it until you stop getting benefit or you fall off the Starling curve and you actually see cardiac output drop. So, is that correct? So that’s your sort of way of doing this? It’s no longer just, oh, the CVP’s a little low, let’s give fluid. I gave some fluid, the CVP got worse or something, or, you know, it got better but the patient looks worse. And that just says, well, you’re looking at the wrong parameter, you’re look at proxy. That’s not really measuring cardiac output.
– Zubin, you have it perfectly.
– Thank you!
– Dad, I gotta say one thing, dad, I told you I was a doctor, okay? You are just wasting time on YouTube. No, okay? I was trained. I’m sorry, back to you.
– There is a second trick, which is just as good for the 250, but requires a physical positioning of the patient. We can have patients empty their legs, their legs, up 250 mLs of water back into the circulation if you lift their legs up. So it’s called a passive leg raising test, a PLR. Now, that’s even easier, I would say, than the fluid challenge. So why didn’t I use it first? A hospital bed has to be able to straight leg raise the legs 45 degrees while putting the head of the patient down to bed and zero. You won’t believe it or not, that hospital ICU beds don’t usually have that option, it’s crazy, so we can’t do a straight leg raise. And you can’t have someone pick up the ankles of the patient and lift them 45 degrees with the head down against the mattress because they might accidentally stimulate the patient to feel that and vasoconstrict their leg vessels and not get a 40, and not get it 250 bolus back into the vasculature.
– So, it’s interesting point, so maybe from a design standpoint, we oughta look at the engineering of those ICU beds and consider is that another quick way of raising the legs, getting the head down as a fluid infusion from the patient’s own legs? That’s really, really interesting. So these are in… Man, it’s been a long time since I’ve done ICU and I get that thrill of the excitement of connecting physiology to the actual patient’s life, which is right there and that’s the beauty of ICU care. So back to this idea, you’re measuring these parameters in these particular COVID patients, then the other big issue, of course, is the pulmonary management and this ARDS component. Can you describe what you’re seeing and how you’re trying to manage it from a ventilatory standpoint? And how that might affect, we can get to that, how it might affect the cardio dynamics and other issues that you’re measuring and trying to adjust?
– Yeah, and obviously the heart and the lungs work together. So if we now start with how we wanna manage the lungs and assume we’re not touching the heart yet, we’ll get to that, the lung alveoli, the actual sacs in the lung have been invaded by a virus, well, this is different than being invaded by an actual pneumonia bacteria. Bacteria make pus and pus fills the alveoli and makes a block to the oxygen to get into the blood, ’cause the alveoli is the air sac and next to it is the capillary. So if the alveoli is filled with pus then you can’t get blood into the capillary. The virus doesn’t do that as much as it thickens the alveoli wall. It thickens the wall preventing an easy movement of the oxygen into the blood and the exit of CO2 from the blood. So ironically, these patients are not what we call drowning in pus, they’re actually thickened alveoli, which are preventing them from receiving oxygen and having carbon dioxide blown off. However, the treatments of our ventilator mechanics are still the same. We want to help oxygen diffuse, diffuse across that membrane. You do that with pressure and you do it with a high level of oxygen. So the first thing we do is put the patients on a high level of oxygen, actually pure 100% oxygen cold, 1.0 fi2, fraction of inspired option. Number two, we set their volume going into their lungs to hopefully to stand these alveoli properly. But you can’t over distend them in an attempt to help the patient ’cause that backfires. That backfires and leads to alveolar damage by the clinical team. The clinical team injures the lungs with too high a pressure. So it’s accepted that pressures in the lungs should not exceed 30 centimeters of water That’s the centimeters of water, not only is your heart rate. This is a very gentle inhalation that human lungs need to stay healthy. So we set the FiO2 to one, we set your volume going in to not exceed 30 centimeters of water. And then there’s a value of exhalation called PEEP, P-E-E-P, for positive end expiratory pressure and that will keep the alveoli open during exhalation and wait for the next inhalation. So you do want some PEEP, so we set eight as our starting PEEP. FiO2 of one and tidal volume so the pressure does not exceed, it’s actually called plateau pressure, does not exceed 30 centimeters of water.
– Got it, so you’re titrating those parameters to have less pressure, less alveolar damage, high oxygen given the diffusion abnormality in the alveoli and a bit of PEEP to make sure that you’re stenting open those alveoli, at least that’s how I always learned it is it was a kind of a back pressure PEEP. And you can overdo the PEEP too, and I imagine there’s a ladder effect, right? So you might have to really modify these parameters as the patients dynamics change. Have you seen, in your experience, with the COVID patients, that you’re able to ween FiO2 fairly rapidly? Or is it still high? And then do you have to start cranking PEEP to keep things oxygenating?
– The order of events, which is what you’re actually asking, super question, is lower your FiO2 and keep your PEEP where it is. As you lower the FiO2, that means the patient’s improving. If you drop your PEEP, you’re gonna lose this recruitment, you know? This is keeping the ovule open. And it’s better to reduce the FiO2 while you hold your PEEP wherever it was to keep this patient supported. So if the PEEP was 12, if the PEEP was 14, and the FiO2 is one, I’ll drop the FiO2 to .9, 90%, later .8. I’m not gonna stop dropping that FiO2 until I get to .5. At 50% FiO2, I then start lowering the PEEP and get the PEEP down. Once the PEEP reaches eight again, I actually am so pleased we can ween that patient off the ventilator, 50%. And eight a PEEP is weenable territory. Anything above either of those numbers is not, it’s not.
– Yeah. And in a setting of this with your ARDS patients, COVID, are you proning a lot of them? And can you teach us about what proning does and the disadvantages and advantages of it? I imagine when you prone, you’re not gonna be doing a straight leg raise, that’s for sure.
– You’re so right. Now, yeah, proning works on a very, again, simple principle. The idea is if you’re on your back and you’re sick, but even if you’re not sick, your alveoli collapse and get what we call atelectasis when you’re on your back. And where? They do it in the region that’s touching the mattress because you’re not really moving your chest wall very well when you’re laying against the mattress. Meanwhile, let’s say anterior, or toward the ceiling, your alveoli are kind of wide open because that’s where you’re moving your chest, when you’re supine, okay? Now let’s switch to the blood. The blood comes out of the heart and the heart is actually anterior. But wait a minute, you’re on your back? The blood is going down against the mattress. So those alveoli that are open are anterior, but the blood is against the mattress posterior. Wouldn’t it be great to flip the patient into the prone position, have the open alveoli, now, get the gravity blood against the mattress and you’ve got a better match of alveoli air and capillaries blood and it works. Now, after some hours, the alveoli against the mattress will go back into being atelectatic and you have to flip back. Makes sense on a proper type of bed that can prone patients. You just flip, four hours, stomach, four hours, supine. Four hours, prone, four hours, supine. Amazing the effectiveness, but it makes perfect sense. So, ARDS coded patients should be prone if they’re already on FiO2s of one and they’re all on high PEEPs, proning will improve oxygenation.
– That was a beautiful description. You could see my face light up with understanding, right? ‘Cause it’s been a minute since I’ve thought about the physiology of proning. And for the nerds out there, what he’s describing is you’re relieving, you’re improving VQ mismatch, ventilatory perfusion mismatch and why is VQ mismatch bad? And this was my understanding, and correct me and teach me when I’m wrong here, if you’re sending blood to an alveoli that is not getting ventilation, is not having air going through it, you’re not oxygenating, you’re not getting rid of CO2, that blood is returning to the heart as it came, which is basically venous blood. So it’s high in CO2 and low in oxygen and you’re dumping it into your circulation, which is no good. Whereas if you balance that out, you don’t have that problem. Now did I get that physiology wrong? It’s been a minute since I thought about VQ mismatch, or is there another piece of that?
– No, it’s perfect. It’s perfect to say VQ mismatch. Now, there’s even a form of VQ mismatch that’s worse, worse than VQ mismatch and that’s called shunt. A shunt is where the alveolus is gone. It’s so shut off that it is not functioning. And VQ, I teach that as V equals zero, zero. And I’m afraid some of the COVID patients have got to have V units that are gonna be zero functionally because of the viral influence on their alveolar walls. And that means exactly as you said, the blood coming back into the right heart. It is even worse, shunt is worse than VQ. In VQ, you can get an improvement by getting oxygen into the V because V’s not zero. But when V is zero, all the oxygen in the world won’t oxygenate the patient.
– That makes perfect sense. That’s a true… That’s a functional shunt. It’s a functional, it’s not an anatomical shunt. In other words, you’re not shanging the, you know, through a anatomic defect, shunting deoxygenated blood to the left side of the heart. It’s a functional shunt because blood is not getting oxygenated or ventilated and it’s going right back. So that’s an effective shunt. Did I understand that correctly?
– That is correct, it is a non-anotomic shunt. It’s not a hole in the atrium septum, it’s not a hole in the ventricular septum, it is functional, and V must equal zero. When you have a patient on 50% oxygen and look at their hypoxia and raise them to 100% oxygen, and the next flick is, PaO2 didn’t change it all. Wow, that’s shunt, that’s shunt. Because if it does go up, that’s VQ mismatch.
– That’s VQ mismatch.
– That makes sense. So it’s a matter of degrees, a matter of severity, more or less, yeah. So, okay, so proning. Here’s a question from a blood gas acid-base standpoint with these patients. So I’ve heard conflicting things. So some have told me you allow permissive hypercapnia in these patients, some have said no, we can’t because they get so acidotic that it becomes myocardially affecting and so on. What’s your experience with the acid-based status in these patients as related to your interventions?
– Now, I’ll tell you that what colleagues said were both correct. Both correct, neither one is wrong. So what do you want to do? What I do is permissive hypercapnia and I do not let the pH fall that low. So then people say well, what trick are you doing for that? Well, you want to enhance the patient’s bicarb, you want to lead them into permissive hypercapnia, which look, it may already be in it and you don’t have to leave them anywhere because they can exchange their CO2–
– Through the COVID-thickened albuterol. So with that CO2 rise, their pH is gonna fall, but what if we give them bicarb? Now people will say, well, bicarb is sodium bicarb, I don’t wanna give a lot of salt to these patients. Well, I don’t either. There’s other ways to bicarb, but you just have to think about it. One is bicitra. Bicitra is the two salts of citrate that go down an OG tube into these patients. When it hits the stomach and absorbs into the liver circulation, the liver converts to bicarb. This is great, give all the citrate you want and it doesn’t raise the sodium, it doesn’t raise the sodium. And in fact, there are IV riders of a K-citrate or sodium citrate, you can do it that way. And if the patient is, I’m afraid, already on dialysis, if they are on analysis for renal insufficiency, injury, talk to your nephrologist and get the nephrologist to raise the bicarb in a bath. Our nephrology team working with us will raise to 40 milliequivalents per liter, and you can handle these hypercapnic patients using permissive hypercapnia because it is a great way to treat COVID patients, permissive hypercapnia, but nobody wants a pH to fall below 7.2, 715. And then patients I work with with the nephrologist, with the bicitra, we keep the pHs up.
– I’m gonna try to repackage this now so I understand it, and also for like medical students and others who may not fully understand the terminology. So, when we say hypercapnia, we were talking about carbon dioxide, so allowing carbon dioxide to be higher than we would normally physiologically have. Now, remember when your carbon dioxide goes up because of the Henderson-Hasselbalch equation and how carbon–
– Yep, yep, yep. Carbon dioxide. Just a little aside, this kind of nerd stuff, and again, it’s the reason I went to medical school to be honest ’cause I’m a big nerd. And I don’t get it right all the time, but it’s so much fun to think about. So when you have a lot of CO2, you’re actually creating an acidic situation. So your pH drops when your blood becomes more acidic and that can cause lots of problems in multiple organ systems. So the bicarbonate actually that you’re talking about administering buffers that extra acid and allows you then to not worry so much about ventilating off all that CO2. Because in order to do that, you’re gonna have to run your ventilator in a way that A, may be impossible for the patient’s physiology with ARDS, but B, may be an issue of damaging lung because you have to ventilate with higher pressures that’s gonna cause damage. Did I understand that correctly?
– That is perfect. If you add to your thought that no ventilator can enhance O2 and CO2, the settings for each are different and they are separate. It’s like you have to be schizophrenic. If you’re a critical care doctor running a ventilator, take part of your brain and say that’s the oxygen ’cause if you wanna optimize oxygen, you cannot optimize CO2. So permissive hypercapnia is if it’s needed, if it’s needed, go for it, pH should not stop you.
– Got it. So this is a way of saying there’s a trade-off. If you can’t do both, let the CO2 rise to favor better oxygenation.
– That makes sense. And then, so, relating to those trade-offs and the schizophrenia of this, I just have to ask this question, using a single ventilator to ventilate two patients. Is that a feasible thing? And I’ve talked to others on the show about this and everybody has a different kind of idea about this, but have you thought about this at all and how would that work?
– Well, I have thought of it and the connection, let’s set aside the valves and the things, the only way it will work is that that patient needs some positive pressure and a lot of oxygen. While in that setting, you can share a tank, you can share a vent if that’s all you need, but if you’re into permissive hypercapnia, if you’re into high PEEP and adjusted PEEP levels, no, you can’t co-vent, as they call it. COVID.
– COVID, co-vent.
– COVID and co-vent, just great terminology.
– We’re in strange times.
– So it will work, now you gotta hook three, four patients, if all they need is extraction, let’s think of some crazed idea. Let’s seal a room to be airtight and let’s pump in oxygen into that room to make it a hyperbaric room. Look, hyperbaric chambers exist, but you only fit one person into it. Well, let’s make a hyperbaric room and call it the COVID Hotel and you’re in there and you will have all the oxygen you want, and you can share it on a pipe or you can share it in the room with no connections. So co-venting can work if you’re only short of oxygen and a little bit of positive pressure because no one’s gonna, let’s say, get more than 30 centimeters of water and everyone’s gonna share the same FiO2. It will work in that situation. But if you want permissive hypercapnia, if you want to adjust PEEP, if you want to do these individually, no.
– Not gonna happen.
– No, cannot do that.
– So, thank you. So, if we’re talking about, by the way, I gotta compliment you, you have a lovely teaching demeanor and a lot of physicians I’ve met lack that and some have been amazing. And so, to be one of your students would have been a true joy, and right now, it’s a joy to learn from you. So thank you for that before I forget to say that. So this being said, how are these patients dying if they’re dying? How are we finding them spiraling? And what are you seeing? Is this a cardiac issue at that point? Is this a failure to oxygenate? Is it a sepsis and multi-organ failure thing? What are we seeing in the COVID patients in your experience?
– Let’s look at the sequence. So if the sequence toward death has to be hypoxia, we don’t die as humans under almost any circumstance until we’re hypoxic. Now, you’d say, really? But really, think about it. Even if you’re in comfort care and you’re not being stressed in any way, if someone will come in and put a finger oximeter on your finger and you are dying from a terminal disease, an end stage disease, until your finger oximeter falls, you will continue with a heartbeat. Now you may not be awake and you may not be in any way painful, but I am saying you will not have asystole occur until your oxygen falls. Therefore, the trigger that’s happening, the trigger that’s starting the sequence toward death is hypoxia. Now to avoid that, we’ve mentioned a FiO2 of one is as high as you go, we’ve mentioned PEEP and we’ve mentioned tidal volume, if the FiO2 is one, if the tidal volume is getting 30 centimeters of water plateau pressure, you have your PEEP, you have PEEP to work with. You may rescue this patient with PEEP. So, you turn up the PEEP. Of course, the first thing to realize is you have pushed your plateau pressure of 30 centimeters of water higher. By definition, you’ve put more pressure into the lungs, you have to cut down your tidal volume, you have to cut it back to get back to 30 centimeters of water because the PQ added basically one for one. Well, there’s exceptions, has upped the plateau pressure by the same number. So if you were 30, and you added PEEP from 12 to 14, your plateau just went to 32. If your tidal volume was 400, you likely will drop it to 350, maybe even 300, but you’re back at 37 meters for plateau, you’re okay at the high PEEP. So if a team does not respect that need to cut back tidal volume, when PEEP increases, they could end up causing lung injury, which will cycle into more hypoxia, they will go to more PEEP, they will cycle into more damage, they will cycle into more hypoxia, and the patient will be hypoxic and start the trajectory to death.
– And that makes a lot of sense. Is that trajectory manifest by cardiac abnormalities initially? Like if you’re monitoring cardiac output and those kind of things, are you seeing that hypoxemia manifest as cardiac failure first? Is the trajectory of the spiral? And then what do you do at that point? Would you run a code on someone who arrested because of profound unfixable hypoxemia? And how do we think about that?
– The question is perfect because it let’s me discuss PEEP affecting the heart before, before hypoxia affects the heart. What if the uninitiated, unaware team of clinicians ups the PEEP and ups the PEEP and then actually sees a satisfactory response showing up on the oximetry channel and they feel they’ve done the right thing? But here’s where the central venous catheter comes in, or certainly straightforward, the cardiac output. High PEEP will shut down cardiac output. It’s increasing intrathoracic pressure, it’s going to shut down cardiac output, and in doing so, the whole trajectory is going to be accelerated toward death with both pulmonary and now cardiac disarray. So you never want your PEEP to shut off your cardiac output and you have to watch your dynamic displays of cardiac output or a simplistic way again of looking at cardiac output and its drawback blood gas from the central venous catheter as a VBG, not an ABG, a VBG. Now you’re thinking, what does that give you? The oxygen saturation, only that number is all you need of the venous gas, the oxygen saturation should be 60 to 70% on the right heart which is where the tip of your CEC is.
– Venous blood, venous blood, yeah, central venous blood.
– Central venous blood. So with central venous blood, 60 to 70%, you have not shut off cardiac output. If you draw back a venous blood that is dropped from when it was 60 to 70, and it’s now 40 to 50, or terribly 30 to 40 or death is coming in hours if it’s 20 to 30%, you are over PEEPing that patient into a lower cardiac output and the organs will suffer very shortly from lack of perfusion. And you would have had no measure of that unless you were checking with a dynamic cardiac output device or a venous blood gas for saturation, not a PVO2, not the number for millimeters of mercury, don’t get confused. It has to be the SVO2, the venous saturation, not the venous value that’s in millimeters of mercury.
– Mm, mm. Oh, I wanna go into the ICU and see some patients right now. Really because the ICU is the place where all that physiology meets the patient at hand, meets a team-based approach, meets the sickest possible patient you can have who you could save. Like it is a magical sacred place that you work in, seriously, seriously. That’s all of this distilled.
– ‘Cause you have, very nicely, taken us through all this to the final trajectory. If all this is done, when all this is done, and now my back is to the wall, I can’t increase FiO2, I can’t increased PEEP, I can’t increase tidal volume. There’s no pharmacologic treatment that’s being recognized for the virus. So I will use those values in the multi-discipline format to try to support the patient while the virus goes away. But I know I’ve done my best. It was based on the need to have multiple dynamic measures going or it’s not, I can say, not fair. Now, I’m not coming down on the clinicians who don’t use all these tools, but these are the tools that are available to try to save lives.
– That is such an important teaching point. And the thing is we all know in healthcare that knowledge of this stuff, access to this stuff is not equal and we like to believe that it is but it’s not. And so, even talking about this and getting this out there will, I think, help people understand what our armamentarium is, what we need to do to manage these patients. And kind of relating to that, so let’s say a patient’s getting better and I’ve heard some stories, some anecdotes about this, patients getting better or you’re weening FiO2, you’re even starting to ween PEEP, maybe you’ve even extubated them. Suddenly, they have an asystolic event or some other cardiac arrest, and if you throw an echo probe on them, their EF, which was fine is now 10 with no focal wall abnormalities. Have you seen this kind of myopathy, direct cardiac toxicity, we don’t know what it is? But it seems to be reported quite a bit in Washington State and some other places that I’ve heard. Have you seen any of that yourself?
– Yes, I’m afraid that even in the, we say even, the influenza outbreak also showed these viral cardiomyopathy. They exist, they are nearly impossible to deal with because you’re now talking about a mechanical assist device, which will be needed to support the ventricle with the prayer that the viral myocarditis will go through a stage and allow recovery of the heart and being able to come off the mechanical support system. And there are clearly not enough mechanical support centers or devices to keep patients supported.
– Are we talking about ECMO or LVAD or what are we talking about?
– Well, remember that the very first easy one that came out was a intra-aortic balloon pump, the IABP. But that’s been, it’s valuable and many cardiologist like it but a newer device is actually like the propellers on the back of a torpedo and it looks like a tiny catheter. But inside it is the, I’ll say, cutest, cutest little propeller. And so, as you push this into the aortic arch and pat it down into the left ventricle, it is called the Impella, Impella, and it blows blood out its catheter tip supporting a patient with about three liters or up to five liters of cardiac output. So it’s not as complicated as an as IABP, but it’s limited in its availability.
– Right, and I’ve have never used one of those, that’s really interesting, yeah. So, okay, so you are seeing this viral myocarditis type of thing or whether it’s a stress myocarditis or viral myocarditis, are you guys using steroids at all? ‘Cause I’ve heard not to do that unless patients already requiring it for some other reason, COPD, et cetera.
– Correct, personally, I’m not using steroids for this. We all fear that the steroid effect on a virus might be opposite of what we want. That a steroid could allow the virus to proliferate.
– Yeah, and I guess–
– And we’re not convinced that it would stop the viral myocarditis to began with, but that is unfortunately rare, but it’s happening and steroids won’t block it.
– Are you guys doing the chloroquine, azithro, remdesivir, those sort of experimental things?
– And the answer is yes under the guidance of Infectious Disease approval. It cannot be written by me and I can consult ID actually by phone and the Infectious Disease team will judge whether the patient qualifies for that trial, it’s a trial, remember it’s not been shown to be efficacious.
– That makes a lot of sense.
– I think that what can be mentioned is actually the success and not the trajectory toward death. We see that after you pull… So if a patient begins to improve, the improvement will show through an FiO2 decrease, keeping the same saturation of oxygen at their fingertips. So, they’re getting better, they’re clearing up, the X-ray may not show clearing at all, the CT scan may not show clearing at all. Don’t worry, those are anatomic pictures, they are not physiology. The physiology is in what we call the Pa divided by Fi ratio of O2. So the PaO2 on blood gas divided by the FiO2, that was needed to get that blood gas. So as PaFi goes up, the patient is getting better. When you reach 50%, start dropping your PEEP toward eight or five, whatever your institution uses and place the patient on what’s called a pressure support wean. So we do a pressure support wean. And then at that point, that patient’s breathing on their own, and if they are showing a good gag and a good cough, we will extubate. And they have come through hell but they are alive, and the important thing is while they were supported on high FiO2s, tidal volume is appropriate, adjustments and high PEEPs, they were sedated, they were knocked out, knocked out. They are on high dose of analgesics and high dose of anxiolytic and drugs that are anesthetics and they are out. So they must stay that way during the severe phase of the disease because you can’t have coughing, finding the vent and patients, not synchronous, not synchronous with our ventilators. Like they have those drugs lifted, the drugs get lifted and they are made and they will wake up and they will ween and they will get extubated and that drugs will be off at the time. They need to be explained that they’ve been in a coma, we use the word coma, it’s a drug-induced coma. For as many days as they’ve been in a coma, they have no idea how many days they’ve been out of this world.
– There’s so much, and that’s a whole show in itself because I wanna ask just a couple questions relating to that. So are you having to paralyze patients at all? Or is the sedation sufficient to keep them from being asynchronous on the vent and bucking the vent?
– I find… Now I have to smile and say that I teach, I teach that paralysis is not necessary until you are so unable to synchronize that patient through two mechanisms. Everyone says two, it’s not two mechanisms. It’s only pharmacologic sedation. Ah, no, air is ventilator sedation. There is ventilator knob sedation. If a patient is asynchronous, you may not have worked with the advanced settings of the ventilator with a great respiratory care practitioner who can make that patient calm down by just changing the settings that we’re not talking about, it’s not Fi2, it’s not PEEP, it’s not tidal value, it’s things like flow, it’s things like triggering, it’s advanced settings for inspiratory cut off. I walk those settings to the end, and finally, if pharmacology and those settings cannot control a patient, they have to be paralyzed. But I don’t paralyze till both are exhausted.
– I wanna say something quickly related to that, our respiratory therapists, respiratory care folks are heroes. Like I tell you, they never get enough love, they never get enough appreciation. I’ve done rap song parodies for them and they’re so appreciative because they are ignored and they’re so crucial, and at this time, more crucial than ever. Would you agree?
– Absolutely, absolutely. I can’t think of any other ways to say it. As a past medical director of respiratory care, that’s when I first got to respect them. But we would get nowhere now without the respiratory therapist round the clock, round the clock caring for these patients and knowing those, what I call, hidden buttons. The hidden switches.
– Yeah, yeah.
– The hidden knobs.
– The Easter eggs on that vent that like only they know, right? And oh, man, and so, quick question then as we get ready to wrap up because I’m probably running out of space on my recording device. Are you seeing a lot of, and I know it’s early to say this, are you seeing a lot of ICU delirium and psychosis post-extubation or even during this? Because there have been, you know, it’s such a difficult thing, someone who’s never obviously been in the ICU, maybe never even been in the hospital, and suddenly, they’re in this, like you called it, they’ve been through hell, they’ve come out the other side, they’re a lot of drugs on board. I’m not sure how much sedation holiday you’re doing during this when you’re trying to make sure they’re synchronous on the vent and all that, maybe none. And so, are you seeing this now in the recovery phase now? Obviously, you’re not necessarily directly taking care of them, but I’m just curious if you’ve had any experience with that.
– Yes, and yes, and yes. We are still taking care of the patients, they are in the ICU because they have to be very mobile–
– [Dr. Z] Before going to the floor.
– The PT and O2 to get out of the ICU. And we’ve had patients become 100% delirious after a complete recovery from an ARDS COVID-19 picture. So, yes, it happens and it is happening and it will happen more and we need more than physicians, nurses and respiratory therapist and pharmacists to help these patients. We have stopped all visitors from coming into the hospital.
– No family is allowed into these patient’s rooms. And that means the highest likelihood of calming them down and handling their delirium is being prohibited from coming into the home.
– Yeah, that’s the biggest tragedy of this, and because again, that’s the best way to redirect and recenter and reorient. Otherwise, you’re in a strange place with nurses putting evil snakes in your veins, and you know? And I’ve had young friends who’ve been in ICU and they tell me these harrowing stories of their own delirium, they remember it, and it has left them with the kind of PTSD. They still have a little bit of the paranoia and a little bit of what if some of that was true, that I was imagining it? It’s really something. So we should be cognizant, which you are, and it’s good to talk about. Because another thing I think we’re gonna be dealing with in the aftermath of this kind of rehabbing people cognitively to some degree. Dr. Patrick, wow, I have learned so much, I think the audience will learn a lot. The super pros will be like, yeah, I don’t think I learned anything. But they’re like probably taking notes. This was a fantastic conversation. I would beg you to come back on the show and talk with me more.
– You have a promise. I loved it. This is great. I mean, what can I say? I talk to all my residents, all my fellows, and I do get invitations to talk, but to be in your forum, your forum of reaching so many people is fantastic, fantastic. I do anything I can do to help your ability to teach so widespread.
– What an honor and thank you for all your work on the frontline, please stay safe. And I wanna give a quick shout out to Edwards Lifesciences for making this possible, they are awesome as a sponsor of this because they’re bringing together really great clinicians like Dr. Patrick to help us teach during this crisis. Dr. Patrick, thank you so much. Z-Pack, listen, the call to action is this, share this video. This is especially useful for people who are re-getting back up to speed on how we’re gonna help out our ICU patients in this COVID crisis. Please become a subscriber on YouTube and Facebook, click the little bell on YouTube to make sure that you get notifications for content like this. And if you feel it in your heart to support us by becoming a supporting subscriber on Facebook or YouTube or Patreon, I won’t complain. Thank you to Dr. Patrick, thank you to all of you. Stay safe out there and we out, peace.