Wednesday, April 8, 2020

Two phenotypes for Respiratory Failure

Conventional ARDS treatment is not cool anymore, or is it? Gattinoni, one of the authors of this paper, has really made a name for himself during this pandemic as we have learned much from his experience and that of his team. They start off by pointing out that the Surviving Sepsis Campaign guidelines need adjusting. Shots fired! Kidding... ish... Please download the paper for yourself and don't trust me.

In this editorial which has yet to be published in the Intensive Care Medicine journal discusses two phenotypes: L and H. There could be a transition from L to H, by the way. The virus can't make this too easy for us. The type could be identified via CT scan but also looking at the respiratory system elastance and recruitability. The rationales as to why someone would fit into one category or another is dependent on many factors (gray area yet to be determined).

Type L (more than 50% of patients, what they come in with)

- Low elastance (i.e. high compliance)


- Low ventilation to perfusion ratio (loss of regulation of perfusion and loss of hypoxic vasoconstriction/vasoplegia) *I have mixed feelings about this one. 

- Low lung weight (not much generalized infiltrate nor edema)

- Low recruitability (since there's not much infiltrate nor edema)

Tx: Reverse hypoxemia. Try non-invasive options. Try higher tidal volumes (8-9cc/kg) if hypercapnic and intubated. Keep PEEP from 8-10. Prone positioning doesn't really work.

This is where we see the tachypnic patients before they crash. They may improve on their own or worsen. They describe patient-self inflicted lung injury (P-SILI). Perhaps decreasing their work of breathing could buy the patient time to recover before transitioning to type H.

Type H (20-30% of patients)

High elastance (lots of edema in there)

High right-to-left-shunt

High lung weight

High recruitability

Tx: treat like severe ARDS, high PEEP, prone positioning, ECMO if needed.


My take is that this paper is missing some components on the microthrombi and leading to some of the shunt physiology we are seeing leading to the refractory hypoxia. I feel that rather than vasoplegia we are seeing the effects of micro thrombi creating shunts. I could be totally wrong.

Gattinoni L. et al. COVID-19 pneumonia: different respiratory treatment for different phenotypes? (2020) Intensive Care Medicine; DOI: 10.1007/s00134-020-06033-2

Link to PDF




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