Abstract
IntroductionLittle is known about the systemic and pulmonary macrohemodynamics in early COVID‐19 infection. Echocardiography may provide useful insights into COVID‐19 physiopathology.MethodsTwenty‐three COVID‐19 patients were enrolled in a medical ward. Gas exchange, transthoracic echocardiographic, and hemodynamic variables were collected.ResultsMean age was 57 ± 17 years. The patients were hypoxemic (PaO2/FiO2 = 273.0 ± 102.6 mmHg) and mildly hypocapnic (PaCO2 = 36.2 ± 6.3 mmHg, pH = 7.45 ± 0.03). Mean arterial pressure was decreased (86.7 [80.0–88.3] mmHg). Cardiac index was elevated (4.32 ± 0.90 L∙min‐1∙m‐2) and the resulting systemic vascular resistance index low (1,458 [1358–1664] dyn∙s∙cm‐5∙m‐2). The right heart was morphologically and functionally normal, with pulmonary artery pressure (PAPm, 18.0 ± 2.9 mmHg) and Total Pulmonary Resistances (TPR, 2.3 [2.1–2.7] mmHg∙l‐1∙min‐1) within normal limits. When stratifying for SVRI, patients with an SVRI value below the cohort median had also more severe oxygenation impairment and lower TPR, despite a similar degree of CXR infiltrates. Oxygen delivery index in this group resulted supranormal.ConclusionsIn the early stages of COVID‐19 infection the hemodynamic profile is characterized by a hyperdynamic circulatory state with high CI and low SVRI, while the right heart is functionally unaffected. Our findings suggest that hypoxemia, viral sepsis or peripheral shunting are possible mechanisms for the vasodilation that dominates at this stage of the disease and may itself worsen the gas exchange.
Highlights
Little is known about the systemic and pulmonary macrohemodynamics in early COVID-19 infection
Our findings suggest that hypoxemia, viral sepsis or peripheral shunting are possible mechanisms for the vasodilation that dominates at this stage of the disease and may itself worsen the gas exchange
This study provides data that could help to understand the interplay between the macrohemodynamics and the mechanisms of the severe hypoxemia in the early stages of COVID-19 infection
Summary
COVID-19 is a new disease and many of its physiopathological features are still unknown. Some observations showed preserved lung mechanics despite high venous admixture (Gattinoni et al, 2020). This supports the hypothesis that the observed oxygenation impairment could, at least in part, depend on severe ventilation-perfusion (VA/Q). Failure of the hypoxic vasoconstriction has been put forward as an alternative or concurrent mechanism for the development of low VA/Q regions (Gattinoni et al, 2020). While this should lead to normal or even decreased pulmonary vascular resistances, widespread microthrombosis should have opposite effects on the pulmonary circulation with possible impairment of the right heart function. This study provides data that could help to understand the interplay between the macrohemodynamics and the mechanisms of the severe hypoxemia in the early stages of COVID-19 infection
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