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hemodynamics of the veno-arterial extracorporeal membrane oxygenation in cardiogenic shock - function and convalescence of the myocardium

Subject Area Cardiac and Vascular Surgery
Cardiology, Angiology
Term from 2023 to 2025
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 517559015
 
Final Report Year 2024

Final Report Abstract

Cardiogenic shock is a life-threatening circulatory disorder. It results in microcirculatory disturbances and tissue hypoxia. Cardiac diseases that can lead to shock include acute myocardial infarction (MI), cardiac arrhythmia, or myocarditis. Cardiogenic shock is associated with high mortality and hospitalization due to acute lack of oxygen to vital organs. Its severity, according to the expert consensus of the Society of Cardiovascular Angiography and Interventions (SCAI), can be classified into five levels from A (at risk) to E (extremis). Cardiogenic shock is a major focus of research in modern cardiovascular medicine because of its high cost to healthcare systems and fatal consequences for the individual patient. The use of mechanical circulatory support devices, such as veno-arterial extracorporeal membrane oxygenation (VA-ECMO), is a cornerstone of therapy. ECMO is an extracorporeal support system that can be used to alleviate the life-threatening conditions of circulatory failure. The underlying principle is to provide extracorporeal oxygenation of the patient's blood and thus to take over the function of the heart and lungs for a certain period of time until they are able to recover. ECMO is technically similar to a heart-lung machine. It is based on a centrifugal pump connected to a membrane oxygenator. The centrifugal pump creates a pressure gradient that draws deoxygenated blood out of the patient's vein, pumps it through a membrane that is connected to the oxygenator, and extracorporeally enriches it with oxygen before it is returned to the patient. Mechanical circulatory support devices, particularly ECMO, have been increasingly used by clinicians in recent decades. However, they have only partially reduced the high mortality rate of patients in severe cardiogenic shock. Although this system effectively replaces the patient's cardiovascular function, it is also associated with a high rate of complications. These include bleeding, stroke, and vascular complications. In addition, some authors in the past have suggested that VA-ECMO may have a negative impact on cardiac recovery in the medium term. This is thought to be due to increased left ventricular afterload caused by artificial retrograde blood flow from ECMO. This increased afterload is thought to place a greater mechanical demand on the heart, which is already severely compromised, to increase the work of stroke to propel the blood against the increased afterload. Ultimately, by making the native aortic valve less likely to open, this increased afterload is thought to be responsible for LV dilation. If the aortic valve does not open regularly, thereby emptying the left ventricular stroke volume, the left ventricle accumulates blood and becomes distorted, increasing the risk of thrombus formation and other fatal complications. This correlation - increased cardiac workload and left ventricular dilation due to increased afterload caused by VA-ECMO - has become a dogma in cardiovascular medicine without a thorough scientific basis. In order to study these complex physiological relationships, it is necessary to perform invasive measurements on patients undergoing ECMO therapy. We investigated the hemodynamic effects of VA-ECMO in patients with cardiogenic shock using invasive hemodynamic measurements due to the lack of scientific knowledge and published human data. We performed hemodynamic measurements in a total of twenty SCAI D and E shock patients treated with VA-ECMO at the University of Minnesota. We found that ECMO therapy decompressed the LV by decreasing LV preload, contrary to the prevailing belief. This decrease in LV preload may be due to decreased transpulmonary blood flow, left ventricular end-diastolic pressure (LVEDP), left ventricular end-diastolic volume (LVEDV) and endsystolic volume (LVESV), and LV stroke work in the patients studied. This effect was also observed in patients receiving ECMO during ongoing cardiopulmonary resuscitation (ECPR). Therefore, VA-ECMO therapy may promote cardiac recovery by reducing myocardial stroke work based on our findings.

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