Coronary arterial perfusion during venoarterial extracorporeal membrane oxygenation,☆☆,,★★,

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Abstract

The effects of venoarterial extracorporeal membrane oxygenation on left ventricular performance have not been studied in detail. Coronary arterial flow obtained by direct measurement with an electromagnetic flowmeter and blood gas analysis from the aortic root were tabulated during venoarterial extracorporeal membrane oxygenation in 14 puppies, and these parameters were evaluated with respect to changes in the venoarterial extracorporeal membrane oxygenation flow. Unique automatic blood pumps generating pulsatile flow were used for the venoarterial extracorporeal membrane oxygenation bypass. Coronary arterial flow decreased as the extracorporeal membrane oxygenation flow increased (106 ± 26 ml/min per 100 gm of left ventricle at 20 ml · min-1 · kg bypass flow to 71 ± 17 ml/min per 100 gm of left ventricle at 100 ml · min-1· kg bypass flow, p < 0.01). There were no significant changes in the mean or diastolic pressures in the ascending aorta despite changes in the extracorporeal membrane oxygenation flow. Arterial oxygen tension in the ascending aorta was not increased even under high-flow venoarterial extracorporeal membrane oxygenation. This result indicates that oxygenated blood from the extracorporeal membrane oxygenation circuit does not pass in a retrograde fashion into the aortic root and thus does not perfuse the coronary arteries. The diastolic aortic pressure did not correlate with the changes in extracorporeal membrane oxygenation flow. The decrease in coronary arterial flow is therefore predominantly caused by increased coronary arterial resistance. Tension-time index, an indicator of myocardial oxygen consumption, did not decrease with venoarterial extracorporeal membrane oxygenation. In conclusion, high-flow venoarterial extracorporeal membrane oxygenation causes undesirable hemodynamic effects on the left ventricle. (J THORAC CARDIOVASC SURG 1996;111:630-6)

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From the Department of Surgery, Branch Hospital, Nagoya University School of Medicine, Nagoya, Japan.

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Supported in part by a grant-in-Aid for Scientific Research (6348039, 2557053) from the Japanese Ministry of Education, Science, and Culture.

Address for reprints: Takahiro Ito, MD, Department of Surgery, Branch Hospital, Nagoya University School of Medicine, Daikohminami 1-1-20, Higashi-ku, Nagoya 461, Japan.

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