Postoperative Right Ventricular Failure

This chapter examines postoperative right ventricular (RV) failure. RV failure is not uncommon following cardiac surgery and often portends a worse clinical outcome. After establishing the diagnosis of RV failure, the central goal of treatment is to increase RV function in order to achieve adequate left ventricular preload and cardiac output. Key management points include decreasing RV volume and preload, increasing RV contractility, reducing RV afterload, maintaining normal rate and rhythm, and supporting RV and systemic perfusion. Diuresis, inodilators and inopressors, and inhaled direct pulmonary vasodilators are mainstays of treatment. Meanwhile, serial transthoracic echocardiogram and central venous pressure measurements, as well as markers of cardiac output and systemic perfusion, are critical for guiding RV failure management.

Cardiovascular–Pulmonary Interactions

Intramural pressures within a tube or circuit determine the rate and direction of flow, whereas the transmural pressure of an elastic structure determines its volume. In Chapter 1, we applied these principles when talking about the pressure needed to overcome viscous forces and elastic recoil during ventilation. In this chapter, we use them to explain changes in blood flow between two portions of the circulatory system and changes in the volume and size of the heart chambers. Cardio–Pulmonary Interactions provides an overview of essential cardiovascular physiology as well as an in-depth discussion of how and why changes in pleural, alveolar, lung transmural, and intra-abdominal pressure during spontaneous and mechanical ventilation can alter right and left ventricular preload, afterload, and stroke volume, cardiac output, and blood pressure. The chapter also reviews the beneficial and detrimental effects of positive end-expiratory pressure (PEEP) on cardiovascular function.

Additional mechanism for left ventricular dysfunction: chronic pulmonary regurgitation decreases left ventricular preload in patients with tetralogy of Fallot

BackgroundRight ventricular dysfunction in patients with tetralogy of Fallot and significant pulmonary regurgitation may lead to systolic dysfunction of the left ventricle due to altered ventricular interaction. We were interested in determining whether chronic pulmonary regurgitation affects the preload of the left ventricle. In addition, we wanted to study whether severe chronic pulmonary regurgitation would alter the preload of the left ventricle when compared with patients having preserved pulmonary valve annulus.MethodsThe study group comprised 38 patients with tetralogy of Fallot who underwent surgical repair between 1990 and 2003. Transannular patching was required in 21 patients to reconstruct the right ventricular outflow tract. Altogether, 48 age- and gender-matched healthy volunteers were recruited. Cardiac MRI was performed on all study patients to assess the atrial and ventricular volumes and function.ResultsSevere pulmonary regurgitation (>30 ml/m2) was present in 13 patients, of whom 11 had a transannular patch, but only two had a preserved pulmonary valve annulus. The ventricular preload volumes from both atria were significantly reduced in patients with severe pulmonary regurgitation, and left ventricular stroke volumes (44.1±4.7 versus 58.9±10.7 ml/m2; p<0.0001) were smaller compared with that in patients with pulmonary regurgitation <30 ml/m2or in controls.ConclusionsIn patients with tetralogy of Fallot, severe pulmonary regurgitation has a significant effect on volume flow through the left atrium. Reduction in left ventricular preload volume may be an additional factor contributing to left ventricular dysfunction.