Increasing venoarterial extracorporeal membrane oxygenation flow puts higher demands on left ventricular work in a porcine model of chronic heart failure

Abstract

Background: Venoarterial extracorporeal membrane oxygenation (VA ECMO) is widely used in the treatment of circulatory failure, but repeatedly, its negative effects on the left ventricle (LV) have been observed. The purpose of this study is to assess the influence of increasing extracorporeal blood flow (EBF) on LV performance during VA ECMO therapy of decompensated chronic heart failure. Methods: A porcine model of low-output chronic heart failure was developed by long-term fast cardiac pacing. Subsequently, under total anesthesia and artificial ventilation, VA ECMO was introduced to a total of five swine with profound signs of chronic cardiac decompensation. LV performance and organ specific parameters were recorded at different levels of EBF using a pulmonary artery catheter, a pressure-volume loop catheter positioned in the LV, and arterial flow probes on systemic arteries. Results: Tachycardia-induced cardiomyopathy led to decompensated chronic heart failure with mean cardiac output of 2.9 ± 0.4 L/min, severe LV dilation, and systemic hypoperfusion. By increasing the EBF from minimal flow to 5 L/min, we observed a gradual increase of LV peak pressure from 49 ± 15 to 73 ± 11 mmHg (P = 0.001) and an improvement in organ perfusion. On the other hand, cardiac performance parameters revealed higher demands put on LV function: LV end-diastolic pressure increased from 7 ± 2 to 15 ± 3 mmHg, end-diastolic volume increased from 189 ± 26 to 218 ± 30 mL, end-systolic volume increased from 139 ± 17 to 167 ± 15 mL (all P < 0.001), and stroke work increased from 1434 ± 941 to 1892 ± 1036 mmHg*mL (P < 0.05). LV ejection fraction and isovolumetric contractility index did not change significantly. Conclusions: In decompensated chronic heart failure, excessive VA ECMO flow increases demands and has negative effects on the workload of LV. To protect the myocardium from harm, VA ECMO flow should be adjusted with respect to not only systemic perfusion, but also to LV parameters.

New Porcine Model of Arteriovenous Fistula Documents Increased Coronary Blood Flow at the Cost of Brain Perfusion

“…One such example is the reaction to volume overload: in rats, the increase in cardiac output (CO) is accomplished solely by higher stroke volume and not by increased myocardial contractility that is known for humans and pigs at least during weeks and months ( Liu, Hilbelink, and Gerdes 1991 ). This fact together with our previous experience with pig biomodels ( Ostadal et al, 2018 ; Hala et al, 2020 ; Popkova et al, 2020 ), led to the selection of the swine model.…”

“…We presumed that prefabricated tube with a constant orifice area could be used for such AVF. Our lab has considerable experience with the use of the extracorporeal membrane oxygenation (ECMO) in pigs ( Ostadal et al, 2018 ; Hala et al, 2020 ; Popkova et al, 2020 ), thus we have tested several ECMO cannulas and sets for creating an AVF.…”

Left Atrial Decompression in Pediatric Patients Supported With Extracorporeal Membrane Oxygenation for Failure to Wean From Cardiopulmonary Bypass: A Propensity‐Weighted Analysis

“…In some circumstances, it is possible that high ECMO flows may have contributed to increasing the workload of the LV. 24 , 25 , 26 In fact, although venoarterial ECMO can reduce central venous pressure and improve end‐organ perfusion, it can also cause a significant increase in LV afterload because of retrograde perfusion of the aorta, which may inhibit aortic valve opening and suppress LV ejection. 25 , 26 Thus, as ECMO flow increases, the primary hemodynamic effect is an increase in the LV afterload.…”

Effects of varying blood flow rate during peripheral veno-arterial extracorporeal membrane oxygen (V-A ECMO) on left ventricular function measured by two-dimensional strain

“…In the peripheral configuration of V-A ECMO, oxygenated blood from the ECMO circuit returns to the arterial system in a “retrograde” manner from cannulas sited in peripheral vasculature, most commonly the femoral artery. This returning blood flow may increase the left ventricular (LV) afterload, leading to increase in LV wall stress and myocardial oxygen demand, a condition that may be deleterious to the recovery of an acutely-injured heart ( 3 , 4 ). Although this phenomenon has been postulated, the magnitude of changes in LV performance parameters in response to different levels of ECMO blood flow during the immediate period after initiation have not been well-delineated in prospective cohorts, and the lack of such fundamental physiological data regarding the heart-ECMO interaction may be partially accountable for the difficulty in establishing recommendations for target flow rates.…”