Biomechanics of the Right Ventricle in Health and Disease (2013 Grover Conference Series)

Abstract

Right ventricular (RV) function is a major determinant of the symptomatology and outcome in pulmonary hypertension. The normal RV is a thin-walled flow generator able to accommodate large changes in venous return but unable to maintain flow output in the presence of a brisk increase in pulmonary artery pressure. The RV chronically exposed to pulmonary hypertension undergoes hypertrophic changes and an increase in contractility, allowing for preserved flow output in response to peripheral demand. Failure of systolic function adaptation (homeometric adaptation, described by Anrep's law of the heart) results in increased dimensions (heterometric adaptation; Starling's law of the heart), with a negative effect on diastolic ventricular interactions, limitation of exercise capacity, and vascular congestion. Ventricular function is described by pressure-volume relationships. The gold standard of systolic function is maximum elastance (E max ), or the maximal value of the ratio of pressure to volume. This value is not immediately sensitive to changes in loading conditions. The gold standard of afterload is arterial elastance (E a ), defined by the ratio of pressure at E max to stroke volume. The optimal coupling of ventricular function to the arterial circulation occurs at an E max /E a ratio between 1.5 and 2. Patients with severe pulmonary hypertension present with an increased E max , a trend toward decreased E max /E a , and increased RV dimensions, along with progression of the pulmonary vascular disease, systemic factors, and left ventricular function. The molecular mechanisms of RV systolic failure are currently being investigated. It is important to refer biological findings to sound measurements of function. Surrogates for E max and E a are being developed through bedside imaging techniques.Keywords: right ventricle, pulmonary hypertension, preload, afterload, maximum elastance, end-systolic elastance, arterial elastance. One must inquire how increasing pulmonary vascular resistance results in impaired right ventricular function.-J. T. Reeves, 1989 1 In 1988, Jack Reeves and his colleagues noted that pulmonary hypertension is a common complication of cardiac and pulmonary diseases, that associated alterations in right ventricular (RV) function cause symptoms and limit survival, and that, paradoxically, research in this area had been relatively scarce. 1 Accordingly, they called for more studies to improve the understanding of RV failure in health and disease. Twenty-five years later, there has been significant progress, but our present knowledge remains incomplete, and calls for more research have been repeated. 2,3 The right ventricle (RV) in mammals and birds is a thin-walled flow generator, designed to accommodate the entire systemic venous return undergoing gas exchange in the pulmonary circulation, which is a separate high-flow, low-pressure system. 4 The pulmonary vascular pressures at rest and at mild levels of exercise are so low that a mean systemic filling pressure in the range of 10-15 m...

Echocardiographic assessment of right ventricular contractile reserve in healthy subjects

“…Although there is no validated method to estimate RV contractile reserve, exercise or dobutamine stress echocardiography may improve prognostic evaluation by revealing changes in flow output or providing more direct measures of contractile function. In addition, during exercise or inotropic stimulation, RV function is affected by a complex interrelationship involving increased peripheral demand, sympathetic activation, increased PAP, and ventricular interactions . Grunig et al.…”

“…RV functional adaptation to increased afterload is best estimated by the ratio of end‐systolic ventricular to arterial elastance calculated as the slope of end‐systolic pressure–volume relationship . However, these gold standard measurements are difficult to obtain at the bedside, and thus, simplified approaches are being developed . Although echocardiography provides a number of measures of RV function with prognostic significance in PAH, the load dependence of many of these indices does not allow accurate assessment of ventricular–arterial coupling .…”

“…However, these gold standard measurements are difficult to obtain at the bedside, and thus, simplified approaches are being developed . Although echocardiography provides a number of measures of RV function with prognostic significance in PAH, the load dependence of many of these indices does not allow accurate assessment of ventricular–arterial coupling . In addition, resting measurements may not predict RV functional adaptation to increased flow output secondary to peripheral demand during exercise …”

Contemporary management of acute right ventricular failure: a statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the European Society of Cardiology

“…The thin‐walled right ventricle pumps the entire systemic venous return into the pulmonary circulation for gas exchange. Right ventricular function integrates preload, afterload, contractility, pericardial constraint, interaction with the left ventricle, and cardiac rhythm . Venous return depends on the pressure gradient between the peripheral vasculature where the mean systemic filling pressure (although not well characterized in humans) is approximately 7–10 mmHg, and the right atrial (or central venous) pressure, which is usually 0 mmHg at rest .…”

Modern Invasive Hemodynamic Assessment of Pulmonary Hypertension

“…Experimental and clinical studies on right ventriculo-arterial coupling suggest a predominant role of adaptive remodeling of the right ventricle confronted with an increased afterload at least in resting conditions. Maladaptive remodeling will first occur with a too high RV afterload maintained for a prolonged time or in the presence of a systemic disease [55].…”