Use of 4% Chlorhexidine Detergent Solution (Hibiscrub) and Other Methods of Skin Disinfection

hypercapnia there is an upper blood pressure limit beyond which autoregulation fails and cerebral blood flow increases (Ekstrdm-Jodal et al., 1971). Such an upper limit of autoregulation was found in four ofour patients but seemed unrelated to their Paco2. No evidence of arteriolar spasm at high pressure was found in any of the patients studied. The 5 to 10 minutes of steady state maximum blood pressure should be ample time for autoregulation to operate, since this mechanism is known to be fully effective within 1 minute after blood pressure changes (Symon et al., 1971). The fact that a similar increase in cerebral blood flow was found in one normotensive patient with a mean arterial blood pressure above 120 mm Hg suggests that the phenomenon is not caused by hypertensive vascular disease per se; it seems more likely that an upper limit of autoregulation is present in all persons and that even this upper limit is raised in hypertension. None of our patients had symptoms during the short period of increased blood pressure. A sustained increase in blood pressure with hyperperfusion of the brain would be expected to cause exudation of plasma through the walls of arterioles and capillaries, this in turn giving rise to focal cerebral oedema, compression of capillaries, a decrease in cerebral blood flow, and the clinical picture of acute hypertensive encephalopathy (Byrom, 1969; Lassen and Agnoli, 1972). The initial event in this pathogenetic chain has been termed a "break-through of autoregulation" (Lassen and Agnoli, 1972). On a smaller scale similar phenomena may occur during sleep hypercapnia, causing the well known morning headache of the hypertensive patient. Further investigations on the pathogenesis of hypertensive encephalopathy probably must rely on animal experiments with repeated measurements of cerebral blood flow with direct methods at very high blood pressure.