The Right Ventricle in COVID-19

Figures

• 

  Figure 1. RV-PA coupling. The pressure volume curve of the RV allows characterization of the end-systolic PV relationship, whose slope corresponds to the RV systolic elastance (Ees), a load-independent measure of RV contractility. The line joining the RV end-systolic volume with its end-diastolic volume is termed the pulmonary arterial elastance (Ea), which is a measure of the afterload as it is seen by the RV. The ratio between Ees and Ea defines the RV-PA coupling, which should always be kept >1 for optimal RV efficiency (black lines). Increased Ea or/and reduced Ees precipitates RV uncoupling (Ees/Ea < 1). The RV must dilate (Frank–Starling mechanism) to maintain its output, at the expense of a marked increase in wall stress, hence myocardial oxygen demand (Red lines).

• 

  Figure 2. Pathophysiological mechanisms of RV dysfunction in COVID-19 ARDS. Upper left panel: Viral infection of lung epithelial cells triggers an intense inflammatory response, promoting the recruitment of inflammatory monocytes and neutrophils, as well as the upregulation of an array of inflammatory cytokines, resulting in endothelial damage and dysfunction, commonly defined as endotheliopathy. Lower left panel: The endotheliopathy is further aggravated by ACE/ACE2 imbalance following ACE2 degradation in endothelial cells (EC) in response to SARS-CoV2 receptor ligation. In turn, ACE2-dependent metabolism of angiotensin II (AT II) into Angiotensin1-7 (AT1-7) is reduced, with decreased signaling through the Mas Receptor (MasR), which normally conveys anti-inflammatory, vasodilatory (NO-dependent), and antithrombotic effects, and increased AT II signaling through the AT II receptor type 1 (AT1R). The latter promotes prothrombotic and pro-inflammatory effects, favoring diffuse pulmonary intravascular coagulation, with both micro and macrothromboses (pulmonary embolism), as well as vasoactive imbalance leading to sustained vasoconstriction. In addition, direct actions on vascular smooth…

• 

  Figure 3. Specific management of RV failure. The figure illustrates the five critical components of the treatment of RV failure, including: (1) The increase of arterial blood pressure (BP) using vasopressors, including norepinephrine (NE, first line) and vasopressin (second line, when NE doses are >0.5 μg/kg/min). (2) The maintenance of sinus rhythm, using anti-arrhythmic drugs or direct current cardioversion in case of atrial fibrillation. (3) The optimization of RV preload, monitored by echocardiography and central venous pressure. The aim is to ensure adequate RV filling (target a CVP of 8–12 mm Hg) and to aggressively treat volume overload, as evidenced by dilated RV and paradoxical septum movement towards the left ventricle (LV) cavity, using diuretics or renal replacement therapy (RRT). (4) The reduction of RV afterload (a) by avoiding elevated plateau pressure (PPlat), driving pressure (DP), and positive end-expiratory pressure (PEEP) in mechanically ventilated patients; (b) by avoiding hypoxemia and hypercapnic acidosis; (c) by prone positioning the patient; (d) by administering inhaled nitric oxide (iNO); (e) by treating thrombo-embolic complications; and (f) in refractory cases,…