Role of heart rate variability in the production of blood pressure variability in man.

Abstract

In both normotensive and hypertensive subjects blood pressure (BP) and heart rate (HR) show concordant changes over 24 h. This may depend on a central factor exerting influences of the same nature on cardiac and vascular targets. An alternative explanation, however, is that a cause-effect relationship links these variabilities, i.e. that HR variations induce BP changes [presumably via variations in cardiac output (CO)]. Blood pressure was recorded intra-arterially in five supine and five exercising (walking) essential hypertensive subjects during a control period of 1 h and during an additional hour in which atropine, 0.04 mg/kg body weight, was injected intravenously (i.v.). The same recordings were performed in seven other subjects, in which saline rather than atropine was employed. One-hour BP and HR variabilities (variation coefficients, VC) were computer analysed. In both the supine and the exercising subjects atropine caused a marked reduction in HR VC (-65.3 and -48.4%, respectively). In the supine subjects this reduction was accompanied by only a modest reduction in BP VC whereas in the exercising subjects the BP VC increased by 30.4%. In the seven subjects in which saline was injected no change in BP and HR VC occurred. Thus a marked reduction in HR variability is not accompanied by a comparable attenuation in BP variability, which rules out a cause-effect link between these two phenomena. Indeed, during physical exercise HR stabilization is followed by an increase rather than a reduction in BP variation, which supports the conclusion that under some circumstances HR plays an anti-oscillatory role.