Non-invasive hemodynamic profile of early COVID-19 infection

Little is known about the systemic and pulmonary macrohemodynamics in early COVID-19 infection. Echocardiography may provide useful insights into COVID-19 physiopathology.

Twenty-three COVID-19 patients were enrolled in a medical ward. Gas exchange, transthoracic echocardiographic, and hemodynamic variables were collected.

Mean 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.

In 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.