Management of acute and chronic RV dysfunction

Abstract

The aim of this article was to outline contemporary treatments of right ventricular (RV) dysfunction and failure. Despite the heterogeneity of disorders underlying RV failure, RV function is a main determinant of long-term prognosis. Therefore, the unique therapeutic goal is to preserve or ameliorate RV function. Although, in advanced stages of RV failure, there is a considerable overlap of pathophysiological mechanisms, the principle targets of treatment are RV contractility, RV pressure overload, and RV volume overload. Apart from surgical strategies such as pulmonary endarterectomy, lung transplantation, closure of shunt lesions, and interventional structural cardiology procedures such as closure of abnormal communications and defects, or graded blade balloon atrial septostomy, targeted pharmacological treatments have become available over the past years. In addition, global strategies such as exercise training, arrhythmia correction, and synchronization treatments may become a new standard of care in the near future. KEYWORDS Right ventricular dysfunction; Right ventricular failure DefinitionRight ventricular (RV) dysfunction has been defined as a state where stroke volume still increases in the presence of increased RV end-diastolic volume. In contrast, RV failure is present when stroke volume cannot increase any further in parallel to increased RV end-diastolic volume. The compromise of the systemic circulation by the septal shift and interventricular dependence causing a severe left ventricular (LV) filling disorder, offsets a vicious cycle. On a molecular basis, it appears that there is a recapitulation of the fetal gene pattern with a decrease in the a-myosin heavy chain gene and an increase in the expression of the fetal b-myosin heavy chain in dysfunctional or failing RV myocardium. Although excessive and longstanding elevation of RV afterload is a major and prevalent cause of RV dysfunction/ failure, evidence accumulates that RV ischemia, 2 excessive sympathetic and renin-angiotensin system stimulation, 3 and volume overload that is accelerated by tricuspid regurgitation 4 contribute. This transition from dysfunction to failure may be ongoing fast or slowly over years, with an unknown genetic component underlying the ability of the RV to resist pressure and volume overload and to maintain stroke volume. RV hypertrophy is a mechanism accounting for preserved RV function. Recent work has demonstrated that in COPD, concentric RV hypertrophy is the earliest sign of RV pressure overload. However, this early structural adaptation of the heart does not yet compromise RV and LV systolic function. 5In practice, the distinction between RV dysfunction and failure can be revealed by a short-time inhalation of NO which, because of its high pulmonary vascular selectivity, 6 will increase RV stroke volume only in the case of a predominantly pulmonary vascular alteration, i.e. in the presence of RV dysfunction.Taken together, pressure, volume, and contractility are main determinants of RV function, and as such, are ...

Non-Coding RNAs as Blood-Based Biomarkers in Cardiovascular Disease

“…Its thin walls and the direct connection with low impedance pulmonary circulation make the RV more sensitive to pressure than to volume overload [91]. Pulmonary hypertension (PH), pulmonary embolism, RV infarction, and cardiomyopathies are among the main causes of RV dysfunction and, consequently, failure [92]. Despite its critical contribution to heart function, the RV has been somewhat neglected, with only a few studies having specifically focused on RV failure.…”

Pulmonary Hypertension in an Oncologic Intensive Care Unit

“…Under excessive volume and pressure, the globular RV eventually pushes the IVS toward and into the LV cavity, compromising LV filling, stroke volume, and cardiac output. The resulting systemic hypotension further reduces coronary flow, RV perfusion, and RV cardiac output [51]. Thus, the cycle propagates, with a failing RV compromising LV function, and a struggling LV increasing the demand on the RV thus leading to worsened RV function followed closely by multi-organ hypoperfusion and failure.…”