COVID-Related ARDS May Not Be So Different After All: An ICU Physician's View of What Works

This transcript has been edited for clarity.

Abraham Verghese, MD: Welcome to another episode of Medicine and the Machine with my co-host, Eric Topol. I am Abraham Verghese. We're excited today to revisit a colleague we spoke with early in the outbreak of SARS-CoV-2, an ICU physician who discussed the stresses and challenges of being in the ICU and planning for the surge — my colleague, Angela Rogers.

Angela is a native of Indiana. She trained at Harvard Medical School and stayed on there for her residency and fellowship. She has a strong research interest in acute respiratory distress syndrome (ARDS) and in biomarkers. We can't imagine a better person with whom to be thinking and talking about COVID. She has done extraordinary research in this area as a basic science investigator, and is a beloved clinician and teacher of our residents here at Stanford.

Welcome back, Angela. It's good to see you after all these many months. How has it been? Reflect on your experience since March 2020.

Angela Rogers, MD: As with every human alive right now, it has been a long haul. I have noticed that in January 2021, meetings started falling off my calendar because I set them to end then. I figured we'd be in a better, not worse, place. Clinically, a lot of things are better about COVID now. I feel much more confident that we're providing good standard of care, and we know that certain things help our patients. Last March, it didn't feel that way at all, and certainly in retrospect, some of our practices, trying the best we could, have changed drastically in the face of new evidence and experience. So clinically, there is a lot that's better.

But on the flip side, the fatigue of it all is very real. I think we all feel that. The politicization of COVID and the feeling of distrust, in addition to the hardship of having so many patients who are sick and dying, and their families not able to be there — that combination was really, really hard. So I would say that some things are better and some things are still hard. Part of it is that it's been a long haul; we thought we'd be in a better place, and we're not yet.

Verghese: I want to stay with that for a moment. From the outside, I witnessed an extraordinary coming together of many different sorts of people to make up the ICU surge team, a lot of great camaraderie and volunteerism. Can you speak about what that was like in the ICU?

Rogers: For me, one of the best parts of COVID has been to actually be the ICU doctor; you're there and you're caring for the 12 patients in front of you, and you feel like you can make a tangible difference for these 12 people. I can't change what's happening nationally, that new drugs are being given emergency use authorization (EUA), and I'm wondering, should we use that based on that evidence? That kind of thing I can't change, but just being a doctor for each patient is great.

As you know, in California, our surge happened many months in. Our biggest surge happened late. One of the most moving aspects has been the number of people who step up and say, "Yes, I'm in, I will be there. I will give up whatever easier thing I was supposed to be doing to help get through this time." That's not just from the physician side; certainly nurses, everyone, is stepping in to ask how they can serve this community and get through this time. This is quite moving.

Improving Survival

Eric J. Topol, MD: If you look back at this year, we've seen many reports that survival and outcomes have improved. How would you rate the things that contributed to that, relative to mechanical ventilation, proning, drugs, all the things in the tool chest?

Rogers: One of the things we were doing early on was intubating patients early. The word from China was that sometimes patients would crash suddenly, and the delays in putting on personal protective equipment (PPE) and getting into the room could lead to harm. So early on, we were intubating patients when they were on only 6 L of oxygen. And I remember, as the ICU attending, having a conversation with a guy who was on 8 L of oxygen, talking on his cell phone, and he was like, "Really? You need to intubate me now?" And I said, "Yes, this is what we need to do." And he ended up on the ventilator.

What we definitely know is that once you are on the ventilator, whether because of thick secretions or de-recruiting or whatever, people tend to have a long haul. So looking at early intubations — and from my knowledge, everyone across the country was doing something similar — in retrospect, a lot of those patients probably would have been okay without it. That patient ended up taking out his own breathing tube a few weeks later, and subsequently he did well.

Now we have many more patients who can bridge on high flow with very high levels of oxygen, even inhaled nitric oxide, just to stave off intubation, and be okay. Their lung compliance is adequate. They hang on sometimes for weeks in the ICU but never need intubation. Those patients, if they never needed intubation, tend to do pretty well.

Whether steroids help or not, clearly our practice was completely changed by the RECOVERY trial. There was a lingering concern at the time that trial came out that our death rate was not 30%, it wasn't as high as in the RECOVERY trial. And we wondered, Are our patients like these patients? This is always a problem in critical care, but even more so when we're clinging to one practice-changing paper.

I'm not sure about those other things. I definitely believe that delaying intubation and going back to our more standard care is better. In general, in every way we were bending standard care before, once we got back to it, things were better. As doctors, we have a tendency to always want to do something. That's our modus operandi. Oh, a new thing? Great. Let me give that to my patient. They're really sick. I should do that new thing.

But we underestimate the importance of really good standard of care that we do in the ICU. Just the basics: lung-protective ventilation, not giving tons of fluid, meticulous observation for superinfections, etc. Doing the check box is important for a reason. We underestimate that. We hear about a new monoclonal antibody (mAb) that could be helpful, but my guess is that getting back to our standard of care is probably what's been most important.

A 'Cleaner' Phenotype of ARDS

Verghese: From your perspective, what is different about the COVID-related ARDS compared with the run-of-the-mill ARDS that you're so used to seeing?

Rogers: It's a good question, Abraham. In part, the people coming through our ICUs with COVID-related ARDS are very different. At academic centers, we tend to see people with ARDS who are very frail. They may have metastatic cancer and are undergoing chemotherapy and then get a pneumonia.

It's rare to see an immunocompetent host who only has a little diabetes and hypertension in the ICU. If that kind of patient gets pneumonia, even bacterial pneumonia, they usually do fine. That patient will be on the wards; it's rare to have that person in our tertiary ICUs. The COVID patients with ARDS are different. They're much healthier.

I don't think that's been discussed enough. We hear in the news that we're overcalling the COVID deaths. But these people who are dying of COVID are rare for us.

Verghese: Mechanically, in terms of the secretions and the complications, should we have a new name for this, other than ARDS? Is this something different?

Rogers: I believe that part of the reason so many clinical trials of treatments are positive in this disease is that this is just ARDS. The patients are not dying of other things and this is not their third trip to the ICU this year. Maybe now we actually have a "cleaner" phenotype of ARDS.

A lot of people are on the vent for a long time. And there is a variance in lung compliance, so this is like better lung compliance ARDS. But when you look in the ARDS clinical trials literature, everyone didn't have super-stiff lungs. On the flip side, some of these COVID patients have very poor lung compliance, too. So I'm not sure that's so different.

Regarding the long-haul aspect, we have a lot of patients who look good, and then you extubate them and they just get worse again. They de-recruit and they have to be re-intubated. So there has been this lingering question about whether there's something different about this. I'm not sure.

Some things are clearly different. The number of young people we see with strokes and pulmonary embolisms is far out of the norm for ARDS. So there's no doubt that parts of this syndrome are different. We have patients on ventilators way longer, in part because these are young, healthy people who you're convinced would want to continue care, want to try an off-the-shelf extra round of steroids, or maybe consider ECMO and lung transplant. But I'm not sure whether that is something we don't offer to many ARDS patients because of who the typical people with ARDS are.

Inflammatory Markers

Topol: I want to get into another topic that you are into — biomarkers — and how you define what would be called a dysregulated immune response or cytokine storm. Do you use any biomarkers? Also, could you respond to the recent data that support IL-6 blockade? Can you help us with the markers and the cytokine storm? It seems chaotic.

Rogers: I would agree. I would say, just as we just talked about ventilators and ARDS, there is emerging evidence, led by Carolyn Calfee's group at UCSF, that there are subphenotypes of ARDS that have these high inflammatory markers. About one third of patients in multiple ARDS clinical trials who were recruited over decades and from multiple centers, and even in cohort studies, have this hyperinflammatory phenotype. And not only do they have a much higher risk for mortality but, interestingly, those hyperinflammatory subsets have a differential benefit of treatment.

Again, this is retrospective. No one has prospectively identified those patients and then targeted them in a prospective way. That's what would need to happen for ARDS. But when you look at IL-6, surprise, surprise, it is one of the key inflammatory markers that defines that subphenotype: high IL-6, high TNF, high IL-8, low bicarb. It's the same markers you'd see in patients with COVID.

Is COVID different? Is it hyperinflammatory? Or do we have immunocompetent hosts who have these phenotypes as well? In regular, non-COVID ARDS, IL-6 levels are high and look a lot like high levels in COVID. The cytokine storm has always bothered me because at least a subset of patients, even the non-hyperinflammatory ARDS patients, have IL-6 levels in the range of those of our sick COVID patients.

It's so important for us to get this right. I hope that, as a critical care community that now knows a lot more about ARDS and respiratory failure, we will invest in studying these questions to get it right for our non-COVID patients as well. There also were studies of steroids for ARDS. But they've been small, and sometimes late, and they're not phenotyped for inflammatory levels. But I believe that we have to ask those questions again. Seeing that, with a more homogeneous group of patients with COVID, steroids seem to help, and anecdotally, when patients come off their steroids, sometimes their fevers come back and their C-reactive protein (CRP) level is still 15. Can we study that? Those patients seem to need steroids longer, but it's hard to study them. I'm eager to do that late COVID trial, because we know it takes a long time to get better. Are we doing those patients a favor by hammering away with more anti-inflammatories?

Steroids, Monoclonal Antibodies, and Oxygen

Verghese: These are naive questions, but have you seen a change in the phenotype of patients who come to the ICU, given all the stuff we're doing at the front end for patients with COVID before you see them? Also, I know there's been a push to give steroids much earlier and to continue steroids much later. People are probably doing this off-protocol. Give us a sense of all the ancillary effort that's happening before and after ICU.

Rogers: The RECOVERY trial was amazing — the fact that they did this pragmatic trial so quickly and involved so many hospitals. There was so much that was good about that trial. It would have been great to be able to zero in on the oxygen level of the patients who weren't ventilated. How many were on high flow? How many were on 1 or 2 L? Did they benefit?

To me, an important aspect of the trial was that the people who were not on oxygen had a trend toward harm if they got dexamethasone. We absolutely see patients coming into our hospital whose primary care providers gave them dexamethasone and azithromycin in an outpatient setting. But to me, if you're not on oxygen, for sure you shouldn't get it.

Should you get dexamethasone if you're on 1 or 2 L of oxygen? That is a bit of a line in the sand. What's your trajectory? Here at Stanford, we came to a consensus among ourselves that we would wait until the patient required 4 L, which meant that a lot of people came in and were on the wards for a couple days on a couple liters of oxygen and went home and never got dexamethasone. Our mortality rates have been exceptionally low, as you know, so it felt like a safe thing to do, to not expose them to these anti-inflammatories if they didn't need them. So that's the short answer about the steroids.

For us, you have to be X amount of sick to get to the ICU, so your question about changes in patient phenotypes might be a good one for someone who's more of a hospitalist and seeing the range. In the ICU, we're often seeing people who have been enrolled in clinical trials but still got worse enough to come in. Talking to my colleagues across the United States about the threshold to come to the ICU, we've had a relatively low threshold at Stanford of 6 L of oxygen; in our normal circumstance, we use a much higher threshold of oxygen needs.

In part, this is a recognition that these COVID patients need to be carefully watched, and if they need high flow, they come to the ICU. When ICUs have much more of a surge, sometimes it takes high flow to be admitted, so then you have much sicker patients on the wards. But even with our recent surge, we've been able to keep this low threshold, admitting early, getting close nursing; and if everything goes well, in a day or two, off they go.

So I have not seen a major change in the phenotype. For us at Stanford, it remains overwhelmingly Hispanic patients, people from multifamily homes, and multiple family members being sick at the same time. Those things haven't changed. And people largely with respiratory disease, and then also some devastating strokes.

Topol: I was going to ask you about the early treatment, before patients get to the hospital. We now have mAbs — the Lilly combination with the 70% reduction in hospitalization and death, which is pretty striking. The Regeneron mAb is probably similar, although their phase 3 trial isn't completed. Even though the EUA for the combination isn't yet out — hopefully it will be soon — how are we going to get better organized? Because these antibodies are sitting on shelves when they could actually spare you and your colleagues. It seems dismaying that we don't use these therapies that could make a difference. What do you think?

Rogers: That's a controversial topic. This is one of the cases when I feel that sometimes the really early EUAs, based on a study with just a few patients — like the 6% vs 1% getting admitted, but it's this tiny N — leads people to ask, is that true? I completely understand what the decision-makers are having to weigh. It's a pandemic. If it's true, it's huge, and we've got to get it to the shelf. Compare that with a great study that everyone's behind, like RECOVERY or the Moderna vaccine trial. You just look at that and there is no doubt that we should be doing this. Let me take on one more thing and build a 10-bed space where people can come and get their mAb. One of the hardships is that a lot of great infectious disease doctors who read that paper are thinking, Are we sure that this is enough?

Topol: Actually, there is no paper yet; it's just a press release this week from Lilly.

Rogers: Sorry. I meant the prior study of LY-CoV555.

Topol: Yes, the data were soft. And especially with one antibody, we've learned that escape is so common, it's got to be a cocktail or combo. Do you have an infusion center in Stanford or Palo Alto? And are you ready for the next phase, when hopefully we can keep people from coming in to the hospital?

Rogers: It's a good question. Based on the prior data of the single mAb, I think that was a limitation. Everyone is working at 130% and has been for a year. Those same people are going to be the people who need to see that data and say, "You know what, it's time. I need to do the things I need to do to get this done."

Definitely our emergency department has been working on this, and I know the infectious disease doctors have a few beds set aside. My sense is that there's a link we can send to physicians, where they can fill out a form and say, "I want this person to get it, and they get it." But the number of patients has been small, and I don't think people were convinced enough by the data to send out a release that says, "You have new COVID; come and do these things."

I believe that a lack of data does influence physician practice in a way that I think is good. So if there are now better data — and it sounds like it's convinced you, Eric, which means something, given your deep knowledge of the field — then I think those things will start to happen much more.

Topol: We want to spare you because we know people staffing the ICUs have been hit as hard. So we're trying to come up with ways to reduce the strain. t

Rogers: I was just going to say the same thing. If we can avoid an ICU stay, that's awesome. If we can avoid mechanical ventilation, that's awesome. Even the data about long-term effects of critical illness, even aside from the mechanical ventilation, even aside from COVID, show that just having sepsis sets people back. Just having a bad infection that leads to hospitalization has a long tail, just like ARDS. I'm not as convinced that COVID is so different. We're focusing on it more because a lot of young, healthy people are complaining of this long-haul syndrome. But it's a real tail. So I agree with you 100%: If people don't need me, I'm thrilled for them.

Lingering Effects

Verghese: Actually, my question was about the tail, because I know there are some vocal colleagues of yours who are keen to keep steroids going in some form on discharge from the ICU, or perhaps even discharge from the hospital. How do you balance experienced clinicians' clinical sense of what the patient needs vs the data that are not yet there? What are we now doing for those patients?

Rogers: I can't comment as much on the steroids at hospital discharge. That I'm not sure about. But as an ICU doctor, I have patients who finish their dexamethasone and then they look worse and their fevers come back. You look everywhere for infection. They're still on the ventilator. Their CRP is sky-high and in fact, it's rising. And you're thinking, It has to be inflammation, right?

At Stanford, we have just developed a plan for what we do with steroids in patients with late ARDS, which includes giving steroids. If you're convinced that the patient doesn't have infection, I would want to give it a try. If there was a clinical trial that we could enroll our patients in to definitively answer the question, I would love to enroll my patients, and I would be willing to do it myself. But in the absence of that, when you have sky-high inflammation and a patient worsening clinically, it feels like the risk/benefit is there for steroids.

So we are doing it. But these are patients where your alternative is essentially death or ECMO, or waiting a little longer and then doing it later. We have data now that patients on autopsy often have cryptogenic organizing pneumonia, and that can be steroid-responsive. For us, that has partly tilted us toward more steroids. The RECOVERY trial, the data from autopsies, our own experience of patients, 40-year-olds rejected for ECMO, you try it and they do get better.

We all know in medicine that an N of 1 is a hard way to practice, but to my knowledge, this isn't being studied, Abraham. It's an important thing that we should be studying. As with convalescent plasma — 40,000 people got it and there was no placebo arm, so we don't know if it was helpful, but we just kind of got it under EUA. It's the same with steroids. Everyone I know is using them sometimes, but the only way to really know is through clinical trials. I think COVID has taught us that as much as any other disease.

Fighting Through Exhaustion

Topol: I'm glad you brought up convalescent plasma because now we're talking about a putative therapy that's been used in hundreds of thousands of Americans, often late, and without assurance that there are high titers of polyclonal antibodies. As you pointed out earlier, an EUA was given in August without sufficient data. There still are not sufficient data.

But it has helped to select out variants. Giving all these antibodies to people who survive and are infectious for some period of time certainly could contribute to the development of variants. Of course, the worst part is that we've not contained the virus here and in many other countries. And also, we have immunocompromised people who have accelerated evolution of the virus inside them.

Last week we got some very depressing news: that the South African variant is resistant to a fair extent to the vaccines. That probably also applies to the Brazil variant because it's very similar. And we also saw the B.1.1.7 UK variant has some, although less, resistance to the Novavax vaccine. So we're looking at a much longer pandemic, unfortunately. Now we have established this kind of fatigue factor that's just extraordinary. How do you see us getting through a longer path to an exit? What are your thoughts about that?

Rogers: Our California wave was happening over the holidays, at a time when the hospital didn't want to shut down all elective surgeries because we know that harms patients, too. We were operating at 90% but were asked to just squeeze in the COVID, and it was really hard. But it was so helpful to know that the vaccines were coming. That made a huge emotional difference for us, to think, Okay, this is the last surge. If we can all get through this together... Yes, it's going to be a rough winter, but then spring will come, and people will be vaccinated and we're going to get our lives back.

It's honestly hard to think about. What do you do if April is just as bad or worse? Our trainees want to move on from COVID. I totally get that. I love ARDS, but not everyone does. And it's a harder sell when the trainee is coming back to the ICU for the umpteenth time, and her long-term goal is outpatient medicine.

It's taxing but I'm hopeful. Reading the literature, it sounds like in South Africa, mitigation with people wearing masks and staying socially distanced will help. I am also happy that the idea that "doctors and scientists are lying; this isn't real" seems to have died down.

If we could get around the social aspects of COVID and convey that even a less effective vaccine plus more of a community feel — we're all in this together and we're going to beat this — maybe that will be enough so it won't be as bad this fall as it has been for so many areas of our country. I hope that combination could still work. I've heard 50% efficacy against the South African variant. We were so lucky with the 95%, but I'll take 50% plus a serious investment in masking and at least not undercutting public health efforts.

Topol: If this UK B.1.1.7 variant has at least 50% superspreader potential and it's already here, then we're looking at a grim several weeks ahead. But as you say, if we could all band together and do the things we know work, we could forestall and blunt this. It's hard to watch the lack of unity and the lack of a cohesive response.

Rogers: But I have been encouraged by the new administration's efforts. They have an amazing team and I believe the community is eager for vaccines. Six months ago, we questioned whether people would take it. Watching the frenzy around people wanting the vaccine, at least that tells us that a lot of people will accept it. Those kinds of things are good.

I have a fight with my husband sometimes when we go for walks because he's all, "We're 8 feet from people; what's the data that it matters?" And I say, "But as a community, those people care and they feel cared for by your mask, even if we are outside on a walk. Please just do it as a member of the community." Also, if you see the mask on someone, you don't reflexively go up to them and break the rules.

As a community, if we could all see it as our duty and we could get to 90% masking, then even a 50% effective vaccine could get us there, along with getting back outside when the weather is warmer. Here in the United States, we didn't band together as a community, and I believe that has hampered us.

Verghese: Eric, a couple of days ago, we had the benefit of hearing you at grand rounds at Stanford, and you struck a more optimistic note. As you said, we've had breaking news in the past couple of days. Help us understand where we are now in terms of vaccines, present, past, and future, and what exactly we should be looking for going ahead.

Topol: As of last Wednesday [January 27], we had only in vitro evidence of immune escape for these variants, the South African and the Brazil variant, which is quite similar in its properties for immune escape in the experimental neutralization assays. The UK variant looked like it was not going to be a problem.

But now we have these two large trials showing unequivocal evidence of a drop-off in efficacy. We hoped that wouldn't be the case because we knew that the neutralization antibodies from vaccines reach superhuman, exponential levels, so we figured these variants couldn't be that bad. It turns out, they really are.

The efficacy of the Johnson & Johnson vaccine dropped from the 70% range to the 50% range for the South Africa variant, and the Novavax vaccine dropped from almost 90% to 49% for South Africa. As Angela pointed out, we will still have efficacy. That's good. But we're also going to see further evolution of this virus if we don't get containment.

Look where it has happened. South Africa, Brazil, the United Kingdom, and the United States will be part of that story. We're one of the worst countries in the world in terms of containment. So it's disillusioning. Up until now, we thought we would get out of this with our great vaccines. Now we know these variants are here in the United States. Our colleagues are all pretty burned out now. To think that this could last longer is tough. Even though we have been privileged to have received the first round of our vaccines, it's almost like we're getting loaded up so we can go through a long round of the same.

Verghese: Do you have any evidence that these strains have an increased mortality? Do the trials suggest that as well?

Topol: The UK group called NERVTAG looked at all the data for their variant, which is now quite dominant, and consistently, through various datasets, they found a 30% increase in lethality. That's what led to the press conference with Boris Johnson saying, folks, we don't only have a superspreader variant, but we also have one that, independent of that, is more lethal.

The increase in transmission was bad enough because that meant more people in the hospital, more deaths. I'm concerned right now because we've seen ICUs and hospitals past the breaking point, and now we've got this strain that's going to become dominant unless we get hyperaggressive right now, when the cases are going down, to get them down as low as we can and do all the right things, including even better masks and home rapid antigen tests. But we're just watching and it's not getting done.

I agree with Angela that we have a great new administration that has assembled a great team. They've only been in charge for 2 weeks — my goodness, how much can we expect from them? If they had been there a year ago, we might not be in this situation.

Rogers: My sense is that, as physicians, we care for the patients in front of us but are not as involved in our society and the inequities in healthcare as we probably should be. But how do we get back to the point where others trust that amazing team too? How do we engage our communities so that people say, "Well, the data aren't clear, but I trust my physicians who say to wear a mask or get the vaccine"? As a physician community, what can we all be doing to help our communities come together?

'We Can't Step Away'

Verghese: As we wind down, perhaps you can reflect on what you, the nurses, and all of the ICU staff have been doing to stay resilient and keep the faith. Have you seen any permanent changes in the way we conduct ICU care, based on our experiences with SARS-CoV-2?

Rogers: Day to-day, being in the COVID ICU, I tell our trainees and anyone who will listen that I think it's one of the most incredible privileges in critical care to be the doctor for these sick patients, who will have an amazing prognosis if we can only get them through. I would say that the day-to-day life of being there is positive. Everyone recognizes that we are all doing our best and working hard for the patients.

One of the hardest things about this whole period has been the politicization of COVID — when you get home after 16 hours at work and log on to Facebook and share a story, and people say doctors are exaggerating or that it's not true. When you're that tired, you just have to step away. But it's hard because, as Eric said, this is the time we can't step away; we have to serve our community. Not only our 10 patients, but looking outward. I would say that the racial injustice focus of last summer, coinciding with seeing that nearly every patient I have in my COVID ICU speaks Spanish, shows me that we have a problem in medicine, that we have not been outward-facing enough.

That is something that must change and has changed. I believe that no one who works in our COVID ICU doesn't see that this isn't fair, this isn't how medicine should be. That's a change.

Topol: Angela, you're a great inspiration to us, and I think you know that more people are applying to medical school now than ever before, and some of these people are tuning in to this podcast, along with medical students. Having been through all you have with your colleagues over the past year, what would you say to them?

Rogers: This year, we have more people applying to pulmonary critical care from our residency than we've ever had before. Obviously, it's a self-selected crowd that comes to my fellowship areas, because they didn't hate COVID or they wouldn't be there. But I think it speaks to our profession, that we want to serve. And you know you're serving when you have a person with mild obesity and hypertension who was so close to dying and they get better. It's amazing to get to be involved in their care.

When I talk to trainees who are applying, I tell them there is no better time to become a doctor than now, to get to serve the community. I believe this outward-facing idea is important. It's so obvious that science matters, right? But we haven't been good enough at being on Twitter and convincing people.

If we could do that, it's an amazing career. I love getting to be an ICU doctor. COVID highlights some things that are wrong with our society for sure, but as doctors, we have a voice for our patients and for the community that's so important. I'm thrilled to hear that there are more people applying than ever. It's an amazing time to become a physician.

Verghese: Wow. Dr Francis Peabody said many years ago that the secret of the care of the patient is caring for the patient. I don't think anyone I know embodies that more than you, Angela. For those of you who don't get to work with her, she's an associate program director and an incredible teacher and physician.

Angela, I hope you will influence many more people with the kind of enthusiasm and optimism you have for medicine, and for waving the flag of the faith of what we do and the importance of this profession. Thank you for taking the time to do this.

Topol: What a great opportunity to talk to Angela. It's always wonderful to have an inspirational force when we need it, and we sure need it right now.

Eric J. Topol, MD, is one of the top 10 most cited researchers in medicine and frequently writes about technology in healthcare, including in his latest book, Deep Medicine: How Artificial Intelligence Can Make Healthcare Human Again.

Abraham Verghese, MD, is a critically acclaimed best-selling author and a physician with an international reputation for his focus on healing in an era when technology often overwhelms the human side of medicine.

Angela Rogers, MD, is a critical care specialist with a particular interest in acute respiratory distress syndrome. She is active in teaching residents and fellows about critical care.

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Cite this: COVID-Related ARDS May Not Be So Different After All: An ICU Physician's View of What Works - Medscape - Feb 03, 2021.