Cardiovascular drift in euhydrated prepubertal boys
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"Classic" cardiovascular drift is characterized by findings of decreasing stroke volume and mean arterial pressure, rising heart rate, and stable cardiac output during sustained constant-load exercise. Recent studies in adults indicate that when dehydration is prevented by fluid intake, this pattern is altered, with no change in stroke volume and progressive rise in cardiac output. This study was designed to examine this influence of hydration in prepubertal subjects and assess the relationship between cardiovascular drift and aerobic drift (changes in VO2). Eight boys (Tanner stage 1, mean age 11.7 +/- 0.4 y) cycled at an average of 62.9% +/- 3.9% VO2 peak to exhaustion (41.38 +/- 6.30 min) in a thermoneutral environment. Rectal temperature rose from 37.6 +/- 0.1 degrees C at rest to 38.1 +/- 0.2 degrees C at end exercise. Between 5 min and end exercise, average heart rate rose by 13.2% and cardiac output rose by 14.9%, systemic vascular resistance fell by 10.5%, and stroke volume remained stable. Increases in cardiac output paralleled those of VO2, with no change in arterial venous oxygen difference. These findings are consistent with the conclusion that cardiovascular drift is a reflection of aerobic drift, a relationship obscured by the superimposed physiological effects of dehydration during sustained constant load. This study also suggests that such patterns are no different in prepubertal boys and young adult men.Keywords:
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We suggest a mechanism by which blood volume changes might explain the hypotension that, after space flight, often accompanies the return to normal gravity. Upon entering microgravity, peripheral veins may collapse and, because of volume redistribution, raise the pressure in the central venous compartment. After some time in space, homeostatic mechanisms may cause volume excretion and reduce the pressure in the central venous compartment to normal values. Upon return to normal gravity, peripheral veins may re-expand and distribute a reduced blood volume into an enlarged space, thus lowering pressure in the central venous compartment. This would reduce cardiac preload, output, and arterial pressure. To prevent this sequence of events, leg cuffs might be inflated before the end of the space flight to allow homeostatic mechanisms to increase blood volume to normal levels.
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In anesthetized dogs venous return was drained into a blood reservoir from which blood was pumped to the right atrium at a variable perfusion rate, which was equal to cardiac output in the steady state. When cardiac output was decreased or increased by 25 or 50 percent of the control, the blood volume in the dog's body was changed in the same direction in the intact reflexic state as well as in the areflexic state prepared by hexamethonium and norepinephrine infusion. The volume change in the reflexic state was twice that in the areflexic state when compared 5 min after stepwise changes in cardiac output. When only the flow through the right heart and lungs was changed by-50 percent, with systemic flow unchanged, the decrease in blood volume was about one-fifth of that observed on a 50 percent decrease of cardiac output and not affected by ablation of the reflexes. It is concluded that, on a change in cardiac output, the passive change in blood volume is as large as the active or reflexic change, that the majority of the change in blood volume takes place in the systemic circulation rather than in the pulmonary circulation, and that the receptors for the reflexic change are located in the systemic circulation.
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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.
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The volume of blood in the heart and lungs can be measured, by the Stewart-Hamilton principle, as the product of cardiac output and the mean transit time from right atrium to the aortic root. Although previous investigators have estimated a variety of central blood volumes, measurements of the true cardiopulmonary blood volume in man have not previously been reported. Eighty-one measurements of the total cardiopulmonary blood volume were obtained in 15 normal human subjects. At rest, total cardiopulmonary blood volume ranged from 301 to 546 ml/m 2 , with a mean of 422 ml/m 2 , and it represented 15% of estimated total blood volume. Cardiopulmonary blood volume was significantly larger in the male subjects than in the female. Reproducibility of measurements was good: the mean discrepancy between successive replications was 25 ml/m 2 and the mean coefficient of variation 3.7%. There was no correlation between cardiac output and cardiopulmonary blood volume but a significant correlation (r=0.79, P <0.0001) was evident between cardiopulmonary blood volume and stroke volume. With elevation of the legs to the pedals of a bicycle ergometer, a small but statistically significant increase occurred in cardiopulmonary blood volume, but no significant changes occurred in cardiac output, heart rate, or stroke volume. With exercise, no further significant change in cardiopulmonary blood volume occurred, despite significant increases in output, rate, and stroke volume. Analysis of cardiac output measurements, both at rest and during exercise, indicates that aortic root sampling is characterized by an appreciably higher reproducibility than that reported for peripheral arterial sampling.
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Volume infusions are one of the commonest clinical interventions in critically ill patients yet the relationship of volume to cardiac output is not well understood. Blood volume has a stressed and unstressed component but only the stressed component determines flow. It is usually about 30 % of total volume. Stressed volume is relatively constant under steady state conditions. It creates an elastic recoil pressure that is an important factor in the generation of blood flow. The heart creates circulatory flow by lowering the right atrial pressure and allowing the recoil pressure in veins and venules to drain blood back to the heart. The heart then puts the volume back into the systemic circulation so that stroke return equals stroke volume. The heart cannot pump out more volume than comes back. Changes in cardiac output without changes in stressed volume occur because of changes in arterial and venous resistances which redistribute blood volume and change pressure gradients throughout the vasculature. Stressed volume also can be increased by decreasing vascular capacitance, which means recruiting unstressed volume into stressed volume. This is the equivalent of an auto-transfusion. It is worth noting that during exercise in normal young males, cardiac output can increase five-fold with only small changes in stressed blood volume. The mechanical characteristics of the cardiac chambers and the circulation thus ultimately determine the relationship between volume and cardiac output and are the subject of this review.
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Changes of the venous return of blood to the right heart were studied in respect to changes in the total blood volume. The latters were coarsed by the automatical transfusions of blood, controlled by the feed-back loop. Dynamic components of the dependence under study were treated by the spectral analysis technique. The contribution of them to the mechanism of the shift in systemic circulation can prevail over known static approximations of this dependence.
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Venous blood
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Systemic circulation
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Splanchnic Circulation
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Venous return curve
Oxygen transport
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Venous return curve
Venous pressure
Venous blood
Right heart
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