Abstract
During development of heart failure there are marked changes in the peripheral circulation. The renal and splanchnic circulations are reduced early. The cerebral circulation is maintained by autoregulation. Skeletal muscle blood flow is reduced in relation to the decrease of cardiac output. There are also important metabolic changes in these muscles with reduced mechanical efficiency. Treatment with arterial vasodilators increase cardiac output. However, most of this increase is usually shunted, probably in the splanchnic circulation. If any, only small increases in muscle blood flow have been reported. ACE-inhibition has been shown to have beneficial acute effects on the renal, cerebral and skeletal muscle blood flow with improved flow in these areas. This treatment seems to be the most beneficial vasodilatory alternative available so far.
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