Heart rate and orthostatic stress

Abstract

Orthostatic stress results in decreases in venous return and cardiac output, but, until the point of presyncope, there is little change in mean arterial blood pressure. There is little doubt that vasomotor responses are of fundamental importance in preventing hypotension, but there is also a concomitant increase in heart rate, and the significance of this is much less clear. The article by Convertino and Sather [1] in this issue attempts to clarify the role of the orthostatic tachycardia using healthy volunteer subjects in whom the autonomic nerves were blocked using either atropine (muscarinic block) or propranolol ([3-adrenergic block). In this editorial, I will discuss the physiologic significance of changes in heart rate in the context of orthostatic stress and attempt to interpret the results of Convertino and Sather in the light of existing physiologic knowledge. Orthostatic toleranceOrthostatic stress, including head-up tilting and application of negative pressure to the lower part of the body, reduces venous return by distension of veins and loss of plasma fluid through capillaries [2,3]. Reflexes prevent a decrease in arterial blood pressure despite the continuing effective loss of blood volume until the point is reached when they are no longer adequate and presyncope, or even syncope, ensues. Orthostatic tolerance refers to the degree of orthostatic stress required to cause arterial hypotension. Relatively few studies have succeeded in quantifying orthostatic tolerance. Convertino and Sather applied a progressive negative pressure to the lower part of the body, continued to the point of presyncope, and derived an index based on an integral of pressure and time to cessation of the test. This is comparable to our approach, which combines head-up tilting with negative pressure to the lower part of the body and assesses orthostatic tolerance as the time to presyncope [4,5]. Both these methods allow a quantification of orthostatic tolerance and are sufficiently reproducible to enable the assessment of the effects of various interventions.Orthostatic tolerance is limited by the time or degree of orthostatic stress, which reduces arterial blood pressure at the brain to a level that is insufficient to provide adequate cerebral perfusion. Blood pressure is dependent on both cardiac output (Q) and peripheral vascular resistance (PVR):BPe~ Qx PVR It is agreed that responses of PVR are essential to the maintenance of normal blood pressure during orthostatic challenge [6], and it has been shown that subjects with greater responses of vascular resistance have better orthostatic tolerance [7,8]. However, the mechanisms involved in controlling cardiac output and, in particular, the effect of changes in heart rate are less well-appreciated. Heart rate and cardiac outputwhere SV is stroke volume, This equation is mathematically unarguable, and knowledge of any two of the terms readily allows calculation of the third. However, in relation to understanding the physiologic control, it can be misleading. This is because stro...

Daytime variability in carotid baroreflex function in healthy human subjects

“…In the control of blood pressure it is the magnitude of the vasoconstriction that is of major importance rather than cardiac responses [11] and there have been no previous studies in which controlled stimuli were applied to the carotid regions at different times of the day and responses studied of either blood pressure or VR. The nearest relevant study was that by Hossman et al [12] in which they measured the responses of blood pressure to graded rates of infusion of norepinephrine.…”

Cerebral autoregulation during orthostatic stress in healthy controls and in patients with posturally related syncope

“…As we, and others, have previously reported [15,19,30], control subjects had higher maximal heart rates than the patients, and their heart rates at termination of the test were also higher. This is unlikely to be of direct physiological significance [31], but a rapid heart rate may be associated with a greater degree of peripheral vasoconstriction and this favours a better orthostatic tolerance [15,32,33]. One other observation was that the minimum arterial pressure recorded during the orthostatic stress test was slightly, but significantly, lower in the patients than in the controls.…”

Pathophysiology of syncope

“…The equation Q = HR x SV (where Q is cardiac output and SV is stroke volume) implies that cardiac output is directly proportional to heart rate. The fallacy of this is that heart rate and stroke volume are not independent of each other and in many situations an increase in heart rate is offset by a decrease in stroke volume [21]. The notable exception to this is when venous filling is high, as in exercise where, in absence of tachycardia, cardiac output would be limited by the maximum end-diastolic volume.…”