COVID appears to cause a form of pseudoARDS (rather than true ARDS). This responds especially well to APRV, often avoiding many forms of iatrogenesis (e.g., proning, paralysis, myopathy, deep sedation, and delirium). Embracing APRV requires a zentensivist perspective on tidal volumes and minute ventilation (they will vary a bit! you won't have total control of them!). This chapter explores the nuts of bolts of performing APRV. Spoiler alert: it's really not rocket science.
The IBCC chapter is located here.
- PulmCrit: “ARDS” is not a real thing - May 27, 2023
- IBCC – ABG, VBG, and pulse oximetry - April 27, 2023
- IBCC – CAR-T cell therapy recipient in the ICU - April 25, 2023
Excuse my ramblings but have been trying to post cogent question thread to frontline clinicians and researchers to mull over. My ramblings condensed below, and work by others; “Is Covid-19 instead a blood based pathogenesis, and attacking the porphyrin binding of heme in red blood cells?” https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173 Please also read the below article, it’s an unscholarly trash of an article. It’s not mine, but there are some cogent and coherent thoughts that are referenced and amalgamated, minus the political references. http://web.archive.org/web/20200405061401/https://medium.com/@agaiziunas/covid-19-had-us-all-fooled-but-now-we-might-have-finally-found-its-secret-91182386efcb Both links above are also supported anecdotally by recent Medscape interview of Dr Cameron Kyle-Siddell – ER Director NYC… Read more »
(Please note I have no medical training.) Dr Paul Marik sent me a press release which is not yet mentioned on his site https://www.evms.edu/covid-19/medical_information_resources/ , where you can get his Marik Protocol guidelines. Google currently doesn’t find a copy anywhere, or any mention of the consortium which supports his work. So I put it on my site: http://aminotheory.com/cv19/icu/ : Front Line COVID-19 Critical Care Consortium Urges Immediate Adoption of Early Intervention Protocol for Any ER or Hospitalized Patient Developing Breathing Difficulty. This concerns the successful early use of methylprednisolone, low molecular weight heparin, IV vitamin C and hydroxychloroquine, before the… Read more »
James Wilson, regarding the hypothesis if viral proteins attacking heme to release the Fe there, two objections come to mind. Firstly, no virus can replicate in an RBC, or even it it gets in, could use its RNA to create its proteins, since there are no ribosomes there. Secondly, it couldn’t get into the RBC, as far as we know, since these have no ACE2 proteins. This leaves the only mechanism being that the proteins escape from infected cells and somehow get into the RBCs. I can’t imagine how this could be possible, and the hypothesis is based only on… Read more »
https://cen.acs.org/biological-chemistry/infectious-disease/know-novel-coronaviruss-29-proteins/98/web/2020/04 29 proteins of Covid to attack the human body. SO far known 29 proteins. I do not yet see an answer to the question regarding bilateral ground glass presentation in the lungs.
How does malaria get into an RBC then? Just because you can conceptualize it does not mean it doesn’t happen. This model actually explains an extensive amount of the poorly understood pathophysiology compared with our “current understanding”. 1. Low sats without dyspnea. Patients with carbon monoxide poisoning do not feel dyspneic either. Covid 19 only attacks the B1 portion (1/4 of hemoglobin) which is why sats drop to around 75% in the sickest of the sick and barely budge with great intervention. 2. COPD and asthma do not appear to be as high risk as hypertension and diabetes. If it… Read more »
Also, Malaria is more likely to be severe in people with type A blood. While those with type O blood are unlikely to suffer severe malaria. Covid is a virus, and Malaria is a bacteria, but could the RBCs of type A blood have some property that renders them vulnerable to both diseases? I’m a healthcare worker, not a scientist, but another thing I have wondered is, genotype vs. phenotype, are people with AA more vulnerable than those who are AO? And does Rh status have any effect on susceptibility? In the 2003 SARS outbreak at a Hong Kong hospital,… Read more »
Malaria is not a bacteria, it is a parasite. A microbiology researcher at Colorado State University said that Corona viruses have never had anything to do with blood cells, this different blood types would not react different to this. They have seen that norovirus can bind to blood antigens but that is a completely different type of virus so what applies to it has nothing to do with Corona viruses.
“How does malaria get into an RBC then?”
The malarial parasite is a single-celled eukaryote, and consequently has mesoscopic infiltration capabilities that are not available to viral particles (basic microbiology).
Malaria is very different from covid 19 though. It is a parasite so it works completely different. What applies to a parasite has nothing to do with a virus, which is what covid is, an rna virus. A parasite is a stand alone living organism that does not use our cells machinery to create progeny. Viruses need our cells machinery to make more virus and they also have limited ways to gain access to a cell such as a RBC, these ways of getting into a cell do not apply to a parasite. If it were true that covid was… Read more »
I perhaps posted under the wrong post below, explaining this post in more detail.. Getting into the RBC is not that difficult. Viruses are known to induce oxidative stress. As part of the oxidative stress cascade, toxic lipid aldehydes are generated, creating holes in the membrane, allowing entry of various molecules as well as providing an exit for lipid aldehydes to neighboring cells, creating a cascade of inflammatory responses. The virus need not replicate in the RBC to continue doing damage via the oxidative stress cascade of events. As far as I am aware, no one is mentioning that blocking… Read more »
Airway Pressure Release Ventilation in Pediatric Acute Respiratory Distress Syndrome. A Randomized Controlled Trial 2,624 Saptharishi Lalgudi Ganesan 1, Muralidharan Jayashree 1, Sunit Chandra Singhi 1,2, and Arun Bansal 1 + Author Affiliations https://doi.org/10.1164/rccm.201705-0989OC PubMed: 29641221 Received: May 19, 2017 Accepted: April 06, 2018 This is a clinical trial of APRV in a pediatric population. It was stopped early due to increased mortality in the treatment group (APRV). The findings were APRV increased pO2 initially but the increased intra-thoracic pressure lead to worsened hemodynamics and death. Since this study came out I have been very cautious with APRV, even though… Read more »
zhou is the best trial on APRV in adults, its showed improved mortality – see discussion here https://emcrit.org/pulmcrit/aprv/
a study that includes months-old infants doesn’t apply to our patients.
Yes, i agree Zhou trial had a different result. It was a small single center trial and the mortality did not reach the .o5 level and the two groups had different care aside from APRV. It was underpowered and undercontrolled. But it think it does show in some circumstances APRV can be used successfully. The peds trial was in a different population but how different is an interesting question. It is my impression that the effects of therapeutic strategies used in adults tend to have exaggerated effects in peds. It is also true both studies were done in a disease… Read more »
I have been intrigued by the possibility that Fe2+ might be released during a COVID-19 infection. Fe2+ would likely contribute to an increase in oxidative stress that generally accompanies a viral infection via the Fenton reaction, the second half of the Haber-Weiss reaction. Viral infections generally induce oxidative stress, although the mechanisms are not completely understood. This induction of oxidative stress is often accompanied by an induction of a zinc deficiency which, in turn, would help the virus replicate. (Zinc is known to block the replication of coronaviruses, at least in cell culture). As most people understand it, oxidative stress… Read more »
I read the “trash” and found it pretty fascinating if not plausible enough to research a bit. Aside from the article by Lui and Li regarding COVID-19 attacking the 1-Beta chain on the heme molecule at the porphyrin ring, I found this article written in 2015 by Janz and Ware in the Journal of Intensive Care titled, “The role of red blood cells and cell-free hemoglobin in the pathogenesis of ARDS” (DOI 10.1186/s40560-015-0086-3). In this article, the observation is the effect of destroyed RBCs (due to sepsis) on lung tissue which consequently leads to ARDS.. Janz and Ware also discuss… Read more »
if its an abnormal hemoglobin causing the hypoxia, clinically there should be a pao2-spo2 gap which has not been reported. spo2 will be low because it measures o2 bound to hemoglobin and pao2 will be high since nothing prevents dissolved in the blood from going up, thus causing a gap.
https://recoverywithoutwalls.com/covidprotocol/ has a press release with COVID Protocol Front Line COVID-19 Critical Care Consortium Urges Immediate Adoption of Early Intervention Protocol for Any ER or Hospitalized Patient Developing Breathing Difficulty and a video from the authors: Drs Umerto Meduri, Pierre Kory, Paul Marik, Jose Iglesias, Joseph Varon, Keith Berkowitz, Howard Kornfeld and Fred Wagshul. This concerns the early use of methylprednisolone, low molecular weight heparin, IV vitamin C and hydroxychloroquine, before to reduce or prevent the development of the cytokine storm which causes the hypercoagulative state which is what harms and kills people. Other elements are nasal cannula oxygen with… Read more »
https://recoverywithoutwalls.com/covidprotocol/ has a press release with COVID Protocol Front Line COVID-19 Critical Care Consortium Urges Immediate Adoption of Early Intervention Protocol for Any ER or Hospitalized Patient Developing Breathing Difficulty and a video from the authors: Drs Umerto Meduri, Pierre Kory, Paul Marik, Jose Iglesias, Joseph Varon, Keith Berkowitz, Howard Kornfeld and Fred Wagshul. This concerns the early use of methylprednisolone, low molecular weight heparin, IV vitamin C and hydroxychloroquine, to reduce or prevent the development of the cytokine storm which causes the hypercoagulative state which is what harms and kills. Other elements are nasal cannula oxygen with prone positioning… Read more »
(Sorry I can’t delete or edit the previous comment.) https://recoverywithoutwalls.com/covidprotocol/ has a press release with COVID Protocol Front Line COVID-19 Critical Care Consortium Urges Immediate Adoption of Early Intervention Protocol for Any ER or Hospitalized Patient Developing Breathing Difficulty and a video from the authors: Drs Umerto Meduri, Pierre Kory, Paul Marik, Jose Iglesias, Joseph Varon, Keith Berkowitz, Howard Kornfeld and Fred Wagshul. This concerns the early use of methylprednisolone, low molecular weight heparin, IV vitamin C and hydroxychloroquine, to reduce or prevent the development of the cytokine storm which causes the hypercoagulative state which is what harms and kills.… Read more »
Great post as always, but this poses me even more questions/considerations.
1. APRV, keeping the lung open, seems to be an excellent strategy in patients where shunt is the primary mechanism of hypoxemia.
2. This approach should not work (and it could be even more harmful decreasing alveolar perfusion in the healthy lung) in patients having dead space due to microthrombosis as the primary mechanism of hypoxemia.
Am I missing something?
Hello! I work in ICU in Moscow, we have just started admitting a lot of people people with Covid pneumonia to our unit. We have started implementing APRV in some patients, however we lack a lot of experience. What we see in moderate-severe ARDS is rapid recruitment on the initial settings (eg Phigh 25, Peep 0, Thigh 5, Tlow 0), however soon we see an increase of expiratory volume (10 cc/kg or so while Tlow is 0,35-0,4 or less). If you start decreasing Phigh derecruitment occurs. Is it a safe strategy to increase PEEP above 5 cm (if pCO2) is… Read more »
You can limit tidal volume by either increasing Plow, or decreasing release time. However, as the lung is recruited, I recommend lowering FIO2 until SpO2 is 88-90%, then lowering Phigh. If Plow is raised sufficiently to get desired tidal volume, compliance can be calculated and used to optimize the Phigh setting. If you use Plow = 0 and use release time to limit tadal volume, compliance can only be estimated. As compliance increases, release time will have to be increased.
Alveolar dead space is ALWAYS increased more with traditional mechanical ventilation than with APRV. If alveolar deadspace is increased by APRV, Phigh is too high and well past the level where recruitment is optimized.
AIRWAY PRESSURE RELEASE VENTILATION PROTOCAL BY DOWNS John B. Downs, M.D. GOALS: -Optimize Gas Exchange (i.e. oxygenation and CO2 elimination) -Optimize Mechanics (i.e. lung compliance and lung-thorax compliance (CLT)) -Optimize Cardiovascular Function (i.e. pulmonary blood flow and V/Q matching) -Minimize Lung Damage -Minimize Cardiovascular Dysfunction (ie. decreased CO and LV dysfunction) -Minimize pleural pressure increase (maximize spontaneous breathing) INITIAL SETTINGS: PHIGH: -30cmH2O (ARF, P/F <300 mmHg, CLT 300 mmHg, CLT > 35 ml/cmH2O) PLOW: -Adjust to VT 6-8 ml/kg (Ideal Body Weight) TRELEASE: -1 sec. (decrease if expiratory flow 0, increase if terminal expiratory flow > 5% of peak expiratory… Read more »
Good day, I can not agree more with Dr.Farcas that APRV should probably be the ventilation mode of choice for Covid 19. With the correct settings it provides better conditions for gas exchange compared to conventional methods,,generally the RR is lower than with the conventional methods hence less ventilator associated damage to the small airways due to their often opening and closing.Also recruitment once achieved can be sustained and derecruitment avoided better compared to the conventional ones. I agree that asthmatic patients may be more difficult to ventilate,but if conventional modes fails even in these patients APRV can be used… Read more »
Hi Josh, what do you think about Dr. Gattinoni’s observations (and many of our observations) regarding the normal compliance, hypoxemic presentation of some of these patients vs the more typical ARDS-like presentation (low compliance etc.)? One of my concerns with early use of APRV in this population is that High transpulmonary pressure-mediated lung injury is particularly likely with spontaneous breathing efforts during Thi (P-SILI). With P-SILI propagating an already robust Virally mediated lung injury. Thanks! Venkat Mangunta, MD Assistant Professor Section of Cardiovascular Anesthesia Section of Critical Care Medicine Mid America Heart Institute University of Missouri – Kansas City School… Read more »
Hi. I hope you are able to see this message. My father had been battling covid for about 2 weeks now and has been in the icu (non-intubated) and been in the prone position for a few days now, about a week. He is unable to move to a different position as his O2 saturation drops in the mid 80s. How long is it safe for to be in this prone position and are there any long term irreversible repercussions to being prone for so long? How/can he slowly get used to moving to a different position or does it… Read more »
Based on my a paper with a limit subset of people (5) all of the people had immediate result and 3 were released after a few days and the other two were stabilized. Not being on a ventilator is good because after 2 weeks on one will cause problems getting off of it or they may have to perform a tracheotomy. The prone position I think is a way to increase pressure in the lungs a mid 80s PO2 level wouldnt be too bad. The issue to watch for is hypoxia. The virus protein appears to bind to hemoglobin and… Read more »
Hello! Does anyone know how to program APRV on GE ventilators? The BiLevel mode is supposed to support it, but it is really confusing (not simple as in Thigh, Tlow, Phigh and Plow).
Hi Josh. Thanks for all your hard work.
How often do you adjust t low if needed? Daily? Every 8 hrs or more often?
Hello, I am a practicing Respiratory Therapist currently working in Texas and I had a question regarding Pressure Support with APRV. Really, what should your PS be set at? I was taught 5 above your PHigh but some others have told me that’s too much. Please, your thoughts?