Hemodynamic adaptation of heart failure to percutaneous venoarterial extracorporeal circulatory supports

Abstract

Extracorporeal life support (ECLS) is a treatment modality that provides prolonged blood circulation, gas exchange and can partially support or fully substitute functions of heart and lungs in patients with severe but potentially reversible cardiopulmonary failure refractory to conventional therapy. Due to high-volume bypass, the extracorporeal flow is interacting with native cardiac output. The pathophysiology of circulation and ECLS support reveals significant effects on arterial pressure waveforms, cardiac hemodynamics, and myocardial perfusion. Moreover, it is still subject of research, whether increasing stroke work caused by the extracorporeal flow is accompanied by adequate myocardial oxygen supply. The left ventricular (LV) pressure-volume mechanics are reflecting perfusion and loading conditions and these changes are dependent on the degree of the extracorporeal blood flow. By increasing the afterload, artificial circulation puts higher demands on heart work with increasing myocardial oxygen consumption. Further, this can lead to LV distention, pulmonary edema, and progression of heart failure. Multiple methods of LV decompression (atrial septostomy, active venting, intra-aortic balloon pump, pulsatility of flow) have been suggested to relieve LV overload but the main risk factors still remain unclear. In this context, it has been recommended to keep the rate of circulatory support as low as possible. Also, utilization of detailed hemodynamic monitoring has been suggested in order to avoid possible harm from excessive extracorporeal flow.

Fig. 1

(A) Schematics of cardiac output and venous return interactions. For normal heart (black) and for heart failure with reduced pumping effectivity (red) the cardiac output curves (solid lines) are intersecting with venous return curves (dashed lines) at marked equilibrium points (I and II). Each vascular curve intersects with x-axis at the value of corresponding mean circulatory filling pressure and its slope reflects resistance to venous return. The marked equilibrium points allow to assess the cardiac output (CO), which is equal to the venous return, for normal circulation (point I) and for heart failure with activated adaptation of increased intravascular volume and resistance to venous return (point II). Adapted from Guyton (1955) and Klabunde (2012). (B) Concept of oxygenator “rated flow”. Hyposaturated venous blood with O₂ saturation of about 70 % (blue dotted line) is passed through the gas exchange unit and exits at maximum saturation (blue solid line). Further increasing of the blood flow above certain point limits the maximum outflow saturation. The flow rate at which outlet saturation drops to 95 % is described as “rated flow” (blue arrow), characterizes the capacity of each gas exchange unit, and limits its oxygen delivery (purple line). Adapted from Bartlett and Conrad (2017).

Fig. 2

(A) Normal PV loop (white) and PV loop in cardiogenic shock (dashed and gray); in cardiogenic shock end-systolic elastance is severely reduced (Ees2<Ees1), EDV and EDP are increased, SV reduced. (B) Myocardial oxygen consumption (MVO₂) is linearly correlated with pressure-volume loop area (PVA), which is the sum of the stroke work (SW) and the potential energy (PE). Bottom: Changes of cardiogenic shock PV loop (dashed) by effects of mechanical supports (gray). (C) VA ECMO increases afterload (Ea1<Ea2), reduces SV, and increases EDP and EDV. (D) Intraaortic balloon pump decreases afterload (Ea1>Ea2) and enhances LV ejection with higher stroke volume. Panel B adapted from Burkhoff et al. (2015), panel C adapted from Ostadal et al. (2015) and Hála et al. (2020), and panel D adapted from Rihal et al. (2015).

Fig. 3

Schematic mean PV loop changes by effects of increasing VA ECMO flow. The left ventricular volume, pressure, and work parameters in a porcine model of chronic heart failure reveal a dependence on VA ECMO flow (EBF in l/min). The stepwise increments in VA ECMO blood flow caused increases in both pressure and volume leading to LV dilation and higher energetic demands as the PV loop shifts left- and upward and its area enlarges significantly. Adapted from data by Hála et al. (2020).