Monitoring of the right ventricular responses to pressure overload: prognostic value and usefulness of echocardiography for clinical decision-making

Abstract

Regardless of whether pulmonary hypertension (PH) results from increased pulmonary venous pressure in left-sided heart diseases or from vascular remodeling and/or obstructions in pre-capillary pulmonary vessels, overload-induced right ventricular (RV) dysfunction and its final transition into right-sided heart failure is a major cause of death in PH patients. Being particularly suited for non-invasive monitoring of the right-sided heart, echocardiography has become a useful tool for optimizing the therapeutic decision-making and evaluation of therapy results in PH. The review provides an updated overview on the pathophysiological insights of heart-lung interactions in PH of different etiology, as well as on the diagnostic and prognostic value of echocardiography for monitoring RV responses to pressure overload. The article focuses particularly on the usefulness of echocardiography for predicting life-threatening aggravation of RV dysfunction in transplant candidates with precapillary PH, as well as for preoperative prediction of post-operative RV failure in patients with primary end-stage left ventricular (LV) failure necessitating heart transplantation or a LV assist device implantation. In transplant candidates with refractory pulmonary arterial hypertension, a timely prediction of impending RV decompensation can contribute to reduce both the mortality risk on the transplant list and the early post-transplant complications caused by severe RV dysfunction, and also to avoid combined heart-lung transplantation. The review also focuses on the usefulness of echocardiography for monitoring the right-sided heart in patients with acute respiratory distress syndrome, particularly in those with refractory respiratory failure requiring extracorporeal membrane oxygenation support. Given the pathophysiologic particularity of severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection to be associated with a high incidence of thrombotic microangiopathy-induced increase in the pulmonary resistance, echocardiography can improve the selection of temporary mechanical cardio-respiratory support strategies and can therefore contribute to the reduction of mortality rates. On the whole, the review aims to provide a theoretical and practical basis for those who are or intend in the future to be engaged in this highly demanding field.

Keywords: Echocardiography; pulmonary hypertension (PH); right heart failure (RHF); right ventricle; right ventricle-pulmonary arterial uncoupling (RV-PA uncoupling).

Figure 1

Major pathophysiological mechanisms involved in the development of high afterload-induced right ventricular failure. The arrows inside the boxes indicate increase (↑) or decrease (↓). Green lettering and green arrows in and outside the box indicate favorable (adaptive) responses. Blue-green lettering in the boxes indicates reversibility of alterations. *, initially a protective mechanism against pulmonary edema. ^‡, Frank-Starling mechanism and adaptive myocardial hypertrophy. PH, pulmonary hypertension; LV, left ventricle; LA, left atrium; HF, heart failure; RV, right ventricle; TV_^Ann, tricuspid valve annulus; TR, tricuspid regurgitation; RVF, RV failure.

Figure 2

Key pathophysiologic steps in the development of non-reversible secondary right ventricular failure in patients with advanced left ventricular failure. The arrows inside the boxes indicate increase (↑) or decrease (↓). LVEDP, left ventricular end-diastolic pressure; VP, venous pressure; PVR, pulmonary vascular resistance; RV, right ventricle; TR, tricuspid regurgitation; PA, pulmonary artery; RVF, RV failure; SV, stroke volume.

Figure 3

Different right ventricular load adaptation in 2 patients with massive pulmonary arterial hypertension and nearly identical pulmonary arterial pressure. Given that in both patients the RV was able to develop a systolic and mean PAP of more than 130 and 74 mmHg, respectively, indicates that their RV systolic function is far better than that of healthy persons. However, the progressive RV dilation in the second patient indicates the existence of an impending risk of RV-pulmonary arterial uncoupling with rapid reduction of cardiac output, which arguments against a delay of the recommended lung transplantation. RV, right ventricle; PAH, pulmonary arterial hypertension; ∆P_^RV-RA, pressure gradient between the RV and right atrium; sPAP, systolic pulmonary arterial pressure.

Figure 4

Key pathophysiological mechanisms involved in the occurrence and progression of severe secondary RV failure during SARS-CoV-2 pulmonary infection associated with widespread thrombotic microangiopathy. Red bold arrows show the major direct damaging effects of the virus on the pulmonary tissue. ↓ and ↑ in the boxes stand for reduced and increased, respectively. *, coexistence of shunt and dead space ventilation. SARS-CoV-2, severe acute respiratory syndrome coronavirus; RV, right ventricle; CO, cardiac output.