Abstract
BackgroundThe aim of this study was to assess the relationship between extracorporeal blood flow (EBF) and left ventricular (LV) performance during venoarterial extracorporeal membrane oxygenation (VA ECMO) therapy.MethodsFive swine (body weight 45 kg) underwent VA ECMO implantation under general anesthesia and artificial ventilation. Subsequently, acute cardiogenic shock with signs of tissue hypoxia was induced. Hemodynamic and cardiac performance parameters were then measured at different levels of EBF (ranging from 1 to 5 L/min) using arterial and venous catheters, a pulmonary artery catheter and a pressure–volume loop catheter introduced into the left ventricle.ResultsMyocardial hypoxia resulted in a decline in mean (±SEM) cardiac output to 2.8 ± 0.3 L/min and systolic blood pressure (SBP) to 60 ± 7 mmHg. With an increase in EBF from 1 to 5 L/min, SBP increased to 97 ± 8 mmHg (P < 0.001); however, increasing EBF from 1 to 5 L/min significantly negatively influences several cardiac performance parameters: cardiac output decreased form 2.8 ± 0.3 L/min to 1.86 ± 0.53 L/min (P < 0.001), LV end-systolic volume increased from 64 ± 11 mL to 83 ± 14 mL (P < 0.001), LV stroke volume decreased from 48 ± 9 mL to 40 ± 8 mL (P = 0.045), LV ejection fraction decreased from 43 ± 3 % to 32 ± 3 % (P < 0.001) and stroke work increased from 2096 ± 342 mmHg mL to 3031 ± 404 mmHg mL (P < 0.001). LV end-diastolic pressure and volume were not significantly affected.ConclusionsThe results of the present study indicate that higher levels of VA ECMO blood flow in cardiogenic shock may negatively affect LV function. Therefore, it appears that to mitigate negative effects on LV function, optimal VA ECMO blood flow should be set as low as possible to allow adequate tissue perfusion.
Highlights
The aim of this study was to assess the relationship between extracorporeal blood flow (EBF) and left ventricular (LV) performance during venoarterial extracorporeal membrane oxygenation (VA Extracorporeal membrane oxygenation (ECMO)) therapy
Myocardial hypoxia alone led to extensive myocardial injury sufficient to cause cardiogenic shock in four of five experimental animals
stroke work (SW) increased from 2096 ± 342 mmHg mL to 2510 ± 335, 2752 ± 346, 3031 ± 404 and 2884 ± 412 mmHg mL, respectively (EBF 1–5 L/min; P < 0.001) (Fig. 3f )
Summary
The aim of this study was to assess the relationship between extracorporeal blood flow (EBF) and left ventricular (LV) performance during venoarterial extracorporeal membrane oxygenation (VA ECMO) therapy. Blood gases are exchanged in the membrane oxygenator and the oxygenated blood is typically returned to the descending aorta through a femoral arterial outflow cannula. This VA ECMO setting offers partial or full circulatory support; it may be associated with specific consequences for the failing heart. The inflow component of the VA ECMO circuit decreases preload and partially or completely unloads the right heart, whereas the outflow component increases left ventricular afterload [7]. In cases of extremely compromised left ventricle systolic function combined with increased afterload and, possibly, persisting (or increasing) bronchial arterial circulation or aortic and mitral regurgitation, the failing left ventricle becomes overloaded, the right ventricle may be fully unloaded [7,8,9]. Progressive distension of the overloaded left ventricle with subsequent severe pulmonary edema is a critical condition that often requires urgent intervention (e.g., left ventricular assist device implantation) [3, 7,8,9,10]
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