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2020 ; 143
(ä): 110022
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Hypoxemia in COVID-19 patients: An hypothesis
#MMPMID32634734
Fisher HK
Med Hypotheses
2020[Oct]; 143
(ä): 110022
PMID32634734
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The current SARS-Cov-2 virus pandemic challenges critical care physicians and
other caregivers to find effective treatment for desperately ill patients -
especially those with sudden and extreme hypoxemia. Unlike patients with other
forms of Acute Respiratory Distress Syndrome, these patients do not exhibit
increased lung stiffness or dramatic dyspnea., even in the presence of arterial
blood oxygen levels lower than that seen normally in mixed venous blood. Urgent
intubation and mechanical ventilation with high inflation pressures and raised
inhaled oxygen concentration have proved unhelpful or worse, but why? Our
Hypothesis is that sudden opening of a previously undetected probe-patent foramen
ovale (PPFO) may explain this mystery. As hypoxemia without acidosis is a rather
weak stimulus of dyspnea or increased ventilation, and opening of such an
intracardiac shunt would not worsen lung mechanical properties, the absence of
dramatic symptom changes would not be surprising. We point out the high frequency
of PFO both in life and at autopsy, and the physiological evidence of large shunt
fractions found in Covid-19 patients. Published evidence of hypercoagulability
and abundant evidence of pulmonary emboli found at autopsy are in accord with our
hypothesis, as they would contribute to raised pressure in the pulmonary arteries
and right heart chambers, potentially causing a shunt to open. We review the
interaction between viral corona spike protein and ACE-2 receptors present on the
surface of alveolar lining cells, and contribution to hypercoagulabilty caused by
the spike protein. Search for an open PFO after a large drop in arterial oxygen
saturation can be performed at the bedside with a variety of well-established
techniques including bedside echocardiography, nitrogen washout test, and imaging
studies. Potential treatments might include balloon or patch closure of the
shunt, and various drug treatments to lower pulmonary vascular resistance.
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