"Silent" hypoxemia in COVID-19: Hunt for the shunt!

Dear Editor,

We read with interest the exemplary description of the respiratory and cardiovascular effects of COVID-19 infection by Kapoor, featured recently in the journal.[1] While we appreciate the elaboration upon the multi-faceted spectrum of the novel SARS-Cov-2 pneumonia in the index article, the lack of dyspnea (”silent”or “happy” hypoxemia) and plummeting desaturation in this cohort of patients, continue to bewilder and baffle the fraternity at large.

In this context, we wish to impress upon the very interesting hypothesis recently put forth by Fisher, regarding the role of the unanticipated opening of an underlying patent foramen ovale (PFO) in explaining this mysterious hypoxemia.[2] Nevertheless, a number of factors surrounding this hypothesis merit attention:

(i) Considering the existing literature on the magnitude of intra-thoracic shunt in acute respiratory distress syndrome (ARDS)[2] and given the astonishingly high frequency of a probe-patent PFO (20-25%)[3]; the intra-cardiac right-to-left (R-L) shunt could add significantly to the intrapulmonary shunt in aggravating the systemic hypoxemia ahead of the deterioration in the respiratory mechanics.

(ii) In addition, Gattinoni and colleagues have also adequately highlighted the importance of estimating the shunt fraction in the COVID-related ARDS (as they describe it as a not so “typical” ARDS).[4]

(iii) Moreover, the accompanying pathological elevation of right atrial pressures (RAP) (in background of pulmonary artery hypertension owing to the ongoing inflammatory process) is expected to promote the intra-cardiac R-L shunting (precluded in health by the physiologically higher left atrial pressures compared to RAP) which is unlikely to respond well to oxygenation wherein positive pressure ventilation will only make the matter worse.[15]

While the debate on the mechanisms of “silent” hypoxemia continues to snowball with every passing day of the pandemic, acknowledgement to the shunt patho-physiology and bedside echocardiographic exploration for PFO cannot only provide anatomico-physiological clues to the deteriorating oxygen saturation rather the degree of R-L shunt can also guide the monitoring of the concomitant pulmonary vasodilator therapy with the potential of benefitting a considerable number of critically ill COVID-19 patients.

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Conflicts of interest

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