Warning: This is a Minefield
There seems to be a trend in the management of the COVID-19 patient away from the instant decision to intubate and ventilate, and more towards maximizing the support of these patients with other modalities (depending on access to PPE and safe work environments where things like HFNC and CPAP might be options).
Some errors were made in the initial response to COVID-19 in Italy, in that patients were placed onto ventilators early, based on an SPO2 reading, and not much else. This meant that the number of ventilators available rapidly decreased, and there was some evidence that many of the patients probably didnt require immediate ventilation. Once the patients who really needed ventilators started presenting, there was nothing left with which to treat them. There is a much smarter and more selective way to manage this. Those patients who are placed on ventilators early spend as much time in ICU/on the ventilator as the patient who is not placed on mechanical ventilation. (Weingard, 2020)
COVID seems to be more a diffusion hypoxemia. This is all from observation and not based on actual studies (because they don’t actually exist yet).
Once the diffusion hypoxaemia starts getting worse and we put our patients onto a ventilator, then we start ventilating them with the traditional ARDS approach, which may or may not be causing actual lung injury as well as overdistention and V/Q mismatch (Weingard, 2020).
Often these patients are spontaneously ventilating and able to maintain their own drive, but their rates are high. The lung compliance in these patients seems to be normal, and so our high PEEP and overdistention of the lungs might be causing damage.
There is also the idea that micro-thrombosis may be developing in the smaller vessels, and this leads to massive dead space as alveoli are ventilated (or even over ventilated), and the areas are not perfusing as expected.
We think that there might be two specific types of COVID-19, these are divided into the H and L type. Below is an image that helps to explain the L-type, which is often how the patient initially presents to the ED.
- Low elastance: normal lung compliance
- Low V/Q ratio: the amount of air in the lungs is “normal”, meaning that the low SPO2 readings are likely from a decreased perfusion matching cause and not a ventilation cause. It is postulated that this may be as a result of the loss of hypoxic vasoconstriction in the pulmonary vasculature.
- Low lung weight: on CT scan these patients present with “ground-glass” opacities in certain areas and the density of the lung tissue is not increased too much.
- Low recruitability: these patients have alveoli that are well ventilated, and so are not really able to benefit from recruitments procedures.
(Gatinoni et al. 2020)
The H-type does not seem to be a common presentation to the ED, or really present very much in patients who are not ventilated. There is the idea that this phenotype might be created by the fact that we are ventilating our patients, increasing distention of alveoli and resulting in a certain amount of lung tissue damage.
H-Type present as follows:
- High elastance: Decreased gas volume as oedema occurs in the interstitial and alveolar spaces
- High right to left shunt: Due to the oedema and gravity dependant areas, there is an increase in the amount of blood that is shunted from right to left without any oxygenation.
- High lung weight: CT scans show that there is an increase in the weight and density of the lung tissue in line with “usual” ARDS findings
- High lung recrutability: Volumes of air in the alveoli are decreased and so recruitment in this patient is possible.
(Gattinoni et al. 2020)
The question remains whether the patient would naturally get to the point of H-type without any mechanical invasive positive pressure ventilation, or whether the H-type presents is in fact iatrogenic. There is no answer on this point at the moment.
There is not a lot of proven information about this disease and what the best things are to do for these patients, the information presented here is only POSTULATION of what the possible pathophysiology is.
There is a huge challenge with the COVID-19 patient, where the balance between good SPO2 and ideal compliance (or distention of the lung) will not be where anyone is comfortable. What this means is that the patient will end up with either a safe compliance (and therefore not being overdistended), BUT will likely present with super low SPO2 (less than 90%). The other option is to increase the distention of the alveoli (by increasing the driving pressure) to target higher/”normal” SPO2, but then the risk is damage to the alveoli from over distention, increasing the problem of ventilation/perfusion matching (Weingard, 2020).
There are numerous mentions of the fact that PEEP set too high will increase lung injury for these patients, and the recommendation has been made to maintain PEEP at “normal” levels rather than to ramp up PEEP as we usually do for the traditional ARDS patient. The level recommended in the 2020 paper by Gattinoni et al is 8-10cmH20, watching carefully for hypotension as a result of higher PEEP readings.
Patients who are intubated and ventilated tend to do worse once intubated, it is postulated that this might be as a result of hypovolemia and over-distention of the alveoli. There is a fine line between PEEP that is low enough not to over distend the alveoli, and PEEP high enough to avoid the risk of de-recruitment of the lung.
Bottom line: start ventilation within safe parameters in the emergency setting, and refer onward as soon as possible to better manage the ventilation in a critical care environment (where we access to higher tech vents and monitoring equipment and more time to make decisions about what the patient require).
“Normal SPO2” readings should not be targeted for these patients; it may be a better idea to target the pre-intubation SPO2 and slowly adjust ventilation to achieve safe parameters as outlined below. Don’t get caught up in achieving specific SPO2 reading and call for help/expert advice early rather than later.
The flow diagram below is a possible starting point with some things to think about when starting a COVID-19 patient on ventilation (bearing in mind this wont be the first step and as much should be done as possible to maximize oxygenation before moving to invasive mechanical ventilation).
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Gattinoni, L., Chumello, D. Caironi, P. Busana, M., Romitti, F. Brazzi, L and Camporota, L. 2020. COVID-19 pnuemonia: different respiratiory treatments for different phenotypes. Intensive Care Medicine. Published online: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7154064/pdf/134_2020_Article_6033.pdf [accessed 29 April 2020]
Scott Weingart. EMCrit Wee – COVID Ventilation Round Table Discussion. EMCrit Blog. Published on April 24, 2020. Accessed on April 30th 2020. Available at [https://emcrit.org/emcrit/emcrit-wee-covid-ventilation-round-table-discussion/ ].
Scott Weingart. ThinkingCC COVID Respiratory Management Webinar. EMCrit Blog. Published on April 12, 2020. Accessed on April 30th 2020. Available at [https://emcrit.org/emcrit/covid-respiratory-management/ ].
Salim Rezaie, “REBEL Cast Ep80: A New War Plan for COVID-19 with Richard Levitan”, REBEL EM blog, April 24, 2020. Available at: https://rebelem.com/rebel-cast-ep80-a-new-war-plan-for-covid-19-with-richard-levitan/ [accessed 29 April 2020].
Salim Rezaie, “REBEL Cast Ep79: COVID-19 – Trying Not to Intubate Early & Why ARDSnet may be the Wrong Ventilator Paradigm”, REBEL EM blog, April 5, 2020. Available at: https://rebelem.com/rebel-cast-ep79-covid-19-trying-not-to-intubate-early-why-ardsnet-may-be-the-wrong-ventilator-paradigm/.