A definition of normovolaemia and consequences for cardiovascular control during orthostatic and environmental stress

Abstract

The Frank-Starling mechanism describes the relationship between stroke volume and preload to the heart, or the volume of blood that is available to the heart--the central blood volume. Understanding the role of the central blood volume for cardiovascular control has been complicated by the fact that a given central blood volume may be associated with markedly different central vascular pressures. The central blood volume varies with posture and, consequently, stroke volume and cardiac output (Q) are affected, but with the increased central blood volume during head-down tilt, stroke volume and Q do not increase further indicating that in the supine resting position the heart operates on the plateau of the Frank-Starling curve which, therefore, may be taken as a functional definition of normovolaemia. Since the capacity of the vascular system surpasses the blood volume, orthostatic and environmental stress including bed rest/microgravity, exercise and training, thermal loading, illness, and trauma/haemorrhage is likely to restrict venous return and Q. Consequently the cardiovascular responses are determined primarily by their effect on the central blood volume. Thus during environmental stress, flow redistribution becomes dependent on sympathetic activation affecting not only skin and splanchnic blood flow, but also flow to skeletal muscles and the brain. This review addresses the hypothesis that deviations from normovolaemia significantly influence these cardiovascular responses.

Fig. 1

Oesophageal Doppler aortic flow velocity during goal-directed fluid treatment with illustration of the Starling curve. Actual volume optimization using oesophageal Doppler technique utilizing flow velocity of blood in the descending aorta to estimate stroke volume in a 79-year-old male undergoing surgery. Panels depict the oesophageal Doppler signal and derived values of stroke volume (Q), cardiac output () and cardiac frequency (f _c) before optimization (a), after 200 ml of colloid (b) and 400 ml of colloid (c) where the top of the Starling curve was considered to be reached since additional colloid administration did not result in >10% increase in Q. Hereafter colloid infusion was discontinued and additional boluses only administered if Q decreased >10%

Fig. 2

Lower cardiac frequency during rowing versus running despite a higher oxygen uptake while rowing. Cardiac frequency rowing versus running (*P < 0.05). Modified from Yoshiga and Higuchi (2002)

Fig. 3

Left ventricular stroke volume and thoracic electrical admittance. Relationship between cardiac output and preload (thoracic admittance) during progressive central hypovolaemia by passive head-up tilt at 60° in 9 healthy humans (1 female) with median age 29 (range 22–39) years, height 183 (170–191) cm, and weight 75 (68–82) kg. The supine and tilt positions are indicated with the duration in the head-up position in minutes. Values are mean ± SE. Modified from Van Lieshout et al. (2005)

Fig. 4

Non-invasive stroke volume tracking during orthostatic variations in central blood volume. Tracking of a thermodilution estimate of stroke volume (Q, solid line) by Modelflow stroke volume (broken line) from non-invasive finger blood pressure (Finapres); averaged values obtained in 10 healthy subjects. Central blood volume was manipulated by passive (tilt) and active (standing) changes in body position. Direction of changes in stroke volume is reciprocal to body position (head-up vs. supine). Modified from Harms et al. (1999)