Right ventricular failure in left heart disease: from pathophysiology to clinical manifestations and prognosis

Frank L Dini, Nicola Riccardo Pugliese, Pietro Ameri, Umberto Attanasio, Roberto Badagliacca, Michele Correale, Valentina Mercurio, Carlo Gabriele Tocchetti, Piergiuseppe Agostoni, Alberto Palazzuoli, Heart Failure Study Group of the Italian Society of Cardiology, Frank L Dini, Nicola Riccardo Pugliese, Pietro Ameri, Umberto Attanasio, Roberto Badagliacca, Michele Correale, Valentina Mercurio, Carlo Gabriele Tocchetti, Piergiuseppe Agostoni, Alberto Palazzuoli, Heart Failure Study Group of the Italian Society of Cardiology

Abstract

Right heart failure (RHF) is a clinical syndrome in which symptoms and signs are caused by dysfunction and/or overload of the right heart structures, predominantly the right ventricle (RV), resulting in systemic venous hypertension, peripheral oedema and finally, the impaired ability of the right heart to provide tissue perfusion. Pathogenesis of RHF includes the incompetence of the right heart to maintain systemic venous pressure sufficiently low to guarantee an optimal venous return and to preserve renal function. Virtually, all myocardial diseases involving the left heart may be responsible for RHF. This may result from coronary artery disease, hypertension, valvular heart disease, cardiomyopathies and myocarditis. The most prominent clinical signs of RHF comprise swelling of the neck veins with an elevation of jugular venous pressure and ankle oedema. As the situation worsens, fluid accumulation becomes generalised with extensive oedema of the legs, congestive hepatomegaly and eventually ascites. Diagnosis of RHF requires the presence of signs of elevated right atrial and venous pressures, including dilation of neck veins, with at least one of the following criteria: (1) compromised RV function; (2) pulmonary hypertension; (3) peripheral oedema and congestive hepatomegaly. Early recognition of RHF and identifying the underlying aetiology as well as triggering factors are crucial to treating patients and possibly reversing the clinical manifestations effectively and improving prognosis.

Keywords: Heart failure; Oedema; Pulmonary hypertension; Right ventricular dysfunction; Systemic venous pressure.

Conflict of interest statement

The authors declare no competing interests.

© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Figures

Fig. 1
Fig. 1
Modalities of fibre shortening in the right ventricular wall
Fig. 2
Fig. 2
Comparison of the right and left ventricle responses to increased afterload and volume overload
Fig. 3
Fig. 3
Strategies to optimise right ventricular preload, afterload and contractility. IV: intravenous; PAH: pulmonary arterial hypertension

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