Heart^–COVID-19 Lung Interactions

We read with great interest the paper by Argulian et al. (1), describing the prevalence of right ventricular (RV) dilation among 105 patients with coronavirus disease-2019 (COVID-19). Thirty-one patients were mechanically ventilated, and 32 patients (31%) presented with RV enlargement. The authors (1), however, do not refer on the proportion of mechanically ventilated patients with RV dilation. Mechanical ventilation, vasoactive medication use, and RV enlargement were significantly associated with increased mortality; however, all 3 are interrelated.

Heart–lung interactions may be pronounced in COVID-19 pathophysiology under mechanical ventilation. When lung compliance is relatively normal, as has been reported in COVID-19 lung (2), a substantial amount of the alveolar pressure is transmitted to the pleural pressure. Increased positive end-expiratory pressure (PEEP) levels may induce dead space ventilation and compression of the pulmonary vasculature, leading to increased pulmonary vascular resistance (PVR) and right heart dilation and dysfunction (3). Increased PVRs may be exacerbated in the setting of nonmassive pulmonary embolism (COVID-19 has been related to lung thrombotic events). This could be the case in the 5 patients with confirmed pulmonary embolism (computed tomography angiography) in the study by Argulian et al. (1). Moreover, relatively high PEEP, according to current guidelines (4), in a non-recruitable lung with almost normal compliance (as in COVID-19) may significantly increase pleural pressure and have a detrimental impact on hemodynamics by deteriorating venous return (5). The effects are exaggerated when the patients are relatively hypovolemic in the initial phase after intubation (fever in the preceding days); restricted fluid resuscitation is also indicated in acute respiratory distress syndrome to keep the lung “dry” in an effort to improve oxygenation and avoid intubation (4).

Increased PVRs and a reduction in venous return decrease the cardiac output. The first reaction to correct hypotension, in an intensive care unit setting, is vasopressor initiation. At the tissue level, hypovolemia and vasoconstriction induce hypoperfusion and end-organ damage, which can lead to multiorgan dysfunction syndrome and an unfavorable outcome. Our rationale is that RV dilatation and dysfunction, vasopressors, and mechanical ventilation are interchangeably related in patients with COVID-19. Argulian et al. (1) nicely report that all 3 factors are associated with increased mortality. It would be informative if the authors could provide data on: 1) RV dimensions before and after initiation of mechanical ventilation; 2) PEEP levels in patients with and without RV enlargement; and 3) possible associations between RV dimensions and PEEP levels. Of note, in Figure 1, both patients are mechanically ventilated.

Mechanical ventilation may be a major factor explaining ventricular dilation. Echocardiography can significantly influence decision-making in “adjusting the ventilator settings” in COVID-19.