Aortic clamping: ischemia mechanism
Last updated: 03/04/2015
Surgery on the descending aorta almost always involves the application of a cross-clamp so the surgeon is able to sew a graft to it. As a general rule, the more proximal the clamp is placed to the heart, the greater amount of stress it places on the heart. This can loosely be defined as “afterload,” meaning the force opposing ventricular ejection. A “high” aortic clamp places a significant amount of afterload on the heart, which can precipitate myocardial ischemia.
A more precise way to think of afterload is systolic wall tension, which is defined as:
Systolic wall tension = Pressure X Radius / wall thickness
A proximal clamp on the descending aorta will increase the peak intraventricular pressure and, particularly if significant aortic regurgitation is present, possibly the left ventriuclar radius. Both of these variables increase wall tension and therefore increase myocardial oxygen consumption. This is the reason vasodilators are typically needed when an aortic cross-clamp is applied. In the case of a clamp on the the thoracic descending aorta, “left heart bypass” may also be used. This involves placement of a cannula into the left atrium, which drains blood and, via a centrifugal pump, puts it into a femoral artery. This diversion of blood effectively decreases systolic wall tension by lowering left ventricular pressure and cavity radius.
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