European Journal of Cardiovascular Medicine

COVID-19 was declared by the World Health Organization as a “Public Health Emergency of International Concern” [1]. These patients may develop shock due to sepsis or cardiac injury; however, hemodynamic characteristics have not been described. We analyzed the hemodynamic profile of 2 ventilated patients (critical cases), 2 non-ventilated patients with severe pneumonia (severe cases) and 1 patient with pneumonia (moderate cases) admitted to the ICU of the Tropical Medicine Institute “Pedro Kouri”, Havana, Cuba. SARS-CoV-2 infection was confirmed in all cases by reverse-transcriptase-polymerase-chain-reaction at hospital admission. Non-invasive hemodynamic measures (within the first 24 h of ICU admission) were used in order to minimize viral transmission to health-care provider. Arterial and central venous samples were simultaneously collected for testing. Fick method was used to calculate the Cardiac Output (CO) as CO=VO2/Ca-CVO2, where VO2 is the oxygen consumption (using the Bergstra's formula) and Ca-CVO2 is the arterial-to-central venous oxygen content difference. We observed a hyperdynamic profile, characterized by high CO and low systemic vascular resistance, in critical and severe cases; conversely, moderate cases have a normal hemodynamic pattern (Table 1). Of note, hyperdynamic changes were markedly higher for critical cases compared to those for severe cases, suggesting that a poor clinical course is associated with a more severe imbalance in hemodynamic parameters. Despite these finding, impairment in the mean arterial pressure was not observed in severe cases and low-dose norepinephrine was required in critical cases, indicating that tissue perfusion was guaranteed by the increased CO (Table 1). Serum concentrations of inflammation-related biochemical markers were higher in patients with critical disease than those in patients with severe or moderate disease (Table 1), suggesting a close relationship between inflammation and hemodynamic imbalance. Angiotensin II effects are increased in COVID-19 patients because of a reduced activity in the angiotensin-converting enzyme 2, but inflammation-induced vasodilatation may overcome the Angiotensin II - associated vasoconstriction. In fact, Angiotensin II may be an inductor of inflammation and oxidative damage in early phases [2]. All patients had a central venous oxygen saturation >70% and central venous-to-arterial carbon dioxide difference (Pcv-aCO2) <6.0 mmHg, indicating an adequate tissue oxygen supply and CO2 wash-out, respectively; however, biological markers of anaerobic metabolism such as hyperlactatemia and Pcv-aCO2/Ca-cvO2 ratio >1.8 were observed in critical patients (Table 1). These founds suggest microcirculatory or mitochondrial disturbances [3]. In summary, this report highlights that in early phase of COVID-19-assocaited critical illness, patients show a hyperdynamic profile with microcirculatory/mitochondrial disturbances. These abnormalities may contribute to mortality.