Pulmonary Circulation in Advanced Heart Failure and Cardiogenic Shock: State-of-the-Art Review

The pulsatile nature of blood flow and the hydrostatic effect of pulmonary capillary wedge pressure are 2 fundamental, yet often overlooked features of right ventricular-pulmonary arterial interactions in advanced heart failure and cardiogenic shock. These 2 features (above all others) define both the mechanical forces experienced by the pulmonary arteries, and in turn, the vascular afterload imposed by the pulmonary circulation on the right ventricular. For over half a century, it has been assumed that the pulsatile components of the pulmonary circulation exist in predictable and constant proportion to resistive afterload. In other words, that the vascular afterload can be estimated from mean pulmonary arterial pressure and pulmonary vascular resistance alone. While this tenet holds true for most forms of pulmonary hypertension, pulmonary hypertension resulting from the passive transmission of elevated left atrial pressure is a notable exception. In these cases, arterial compliance decreases proportionally more than any increase in pulmonary vascular resistance and is highly dependent upon recruitment and distensibility of the pulmonary circulation. As questions regarding the optimal method to predict right ventricular failure resurface, along with a modern armamentarium of techniques to assess pulsatile pressure-flow relations, it serves as a timely reminder that, in those with normal or near-normal pulmonary arterial pressures, the pulsatile component of pulmonary vascular afterload may account for anywhere between one-quarter and half of the total power of the right ventricular. In this State-of-the-Art Review, we address the role of pulmonary circulation in those with advanced heart failure and cardiogenic shock. Unlike previous discussions on this topic, we set aside considerations of established precapillary disease, focusing specifically on the process by which an acute or chronic elevation of pulmonary capillary wedge pressure results in pulmonary hypertension from left-sided heart failure. In doing so, we create a framework to assess pulmonary vascular afterload in an era of advanced therapeutics and device technologies to treat advanced heart failure and cardiogenic shock.