Stroke volume of the heart and thoracic fluid content during head‐up and head‐down tilt in humans

Damgaard

Journal of Applied Physiology

et al. 2011

PetersenLG, Damgaard M, Petersen JCG, Norsk P. Mechanisms of increase in cardiac output during acute weightlessness in humans. J Appl Physiol 111: 407-411, 2011. First published June 2, 2011 doi:10.1152/japplphysiol.01188.2010.-Based on previous water immersion results, we tested the hypothesis that the acute 0-Ginduced increase in cardiac output (CO) is primarily caused by redistribution of blood from the vasculature above the legs to the cardiopulmonary circulation. In seated subjects (n ϭ 8), 20 s of 0 G induced by parabolic flight increased CO by 1.7 Ϯ 0.4 l/min (P Ͻ 0.001). This increase was diminished to 0.8 Ϯ 0.4 l/min (P ϭ 0.028), when venous return from the legs was prevented by bilateral venous thigh-cuff inflation (CI) of 60 mmHg. Because the increase in stroke volume during 0 G was unaffected by CI, the lesser increase in CO during 0 G ϩ CI was entirely caused by a lower heart rate (HR). Thus blood from vascular beds above the legs in seated subjects can alone account for some 50% of the increase in CO during acute 0 G. The remaining increase in CO is caused by a higher HR, of which the origin of blood is unresolved. In supine subjects, CO increased from 7.1 Ϯ 0.7 to 7.9 Ϯ 0.8 l/min (P ϭ 0.037) when entering 0 G, which was solely caused by an increase in HR, because stroke volume was unaffected. In conclusion, blood originating from vascular beds above the legs can alone account for one-half of the increase in CO during acute 0 G in seated humans. A Bainbridge-like reflex could be the mechanism for the HR-induced increase in CO during 0 G in particular in supine subjects. regional blood flow; blood pressure; vascular resistance; gravity GRAVITY CONSTANTLY STRESSES the cardiovascular system in upright humans by diminishing venous return. It decreases stroke volume (SV) and thus cardiac output (CO) and, through the baroreflex system, induces arteriolar constriction and an increase in heart rate (HR) to counteract a fall in blood pressure (4,21,30). Compared with the upright 1-G position, sudden entry into weightlessness (0 G) causes a redistribution of blood from the lower vascular beds to the central circulation (4, 29), leading to an increase in venous return, and thus in SV and CO, and, through stimulation of the baroreflexes, to arteriolar vasodilatation and a decrease in HR (18,21,23,29).Our laboratory has previously observed that, in upright seated humans, short-term 0 G created by parabolic airplane flights increases CO by as much as 1.8 l/min, which corresponds to some 0.6 liters over the 20-s period of 0 G (21). Bailliart et al. (2) estimated that, in standing humans, some 165 ml of fluid disappeared from each leg during 20 s of 0 G. These and our observations collectively suggest that the contribution of blood from the legs to the acute 0-G-induced increase in CO amounts to some 50%. In another study from our laboratory, we have, however, observed that water immersion in humans, which is used to simulate the effects of 0 G, increases the diameter of the left atrium to the same degree, whethe...

Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 71%

Mechanisms of increase in cardiac output during acute weightlessness in humans

Damgaard

Journal of Applied Physiology

et al. 2011

“…HDT redistributes blood to the thoracic region, increasing central blood volume and cardiac filling pressures (8,31,32). In the present investigation, early mitral inflow and annular tissue velocities remained unchanged from the supine position with HDT, regardless of thermal condition.…”

Section: Diastolic Functionsupporting

confidence: 49%

Left ventricular systolic and diastolic function during tilt-table positioning and passive heat stress in humans

Nelson

Altamirano-Diaz

American Journal of Physiology-Heart and Circulatory Physiology

et al. 2011

The ventricular response to passive heat stress has predominantly been studied in the supine position. It is presently unclear how acute changes in venous return influence ventricular function during heat stress. To address this question, left ventricular (LV) systolic and diastolic function were studied in 17 healthy men (24.3 Ϯ 4.0 yr; mean Ϯ SD), using two-dimensional transthoracic echocardiography with Doppler ultrasound, during tilt-table positioning (supine, 30°h ead-up tilt, and 30°head-down tilt), under normothermic and passive heat stress (core temperature 0.8 Ϯ 0.1°C above baseline) conditions. The supine heat stress LV volumetric and functional response was consistent with previous reports. Combining head-up tilt with heat stress reduced end-diastolic (25.2 Ϯ 4.1%) and end-systolic (65.4 Ϯ 10.5%) volume from baseline, whereas heart rate (37.7 Ϯ 2.0%), ejection fraction (9.4 Ϯ 2.4%), and LV elastance (37.7 Ϯ 3.6%) increased, and stroke volume (Ϫ28.6 Ϯ 9.4%) and early diastolic inflow (Ϫ17.5 Ϯ 6.5%) and annular tissue (Ϫ35.6 Ϯ 7.0%) velocities were reduced. Combining head-down tilt with heat stress restored end-diastolic volume, whereas LV elastance (16.8 Ϯ 3.2%), ejection fraction (7.2 Ϯ 2.1%), and systolic annular tissue velocities (22.4 Ϯ 5.0%) remained elevated above baseline, and end-systolic volume was reduced (Ϫ15.3 Ϯ 3.9%). Stroke volume and the early and late diastolic inflow and annular tissue velocities were unchanged from baseline. This investigation extends previous work by demonstrating increased LV systolic function with heat stress, under varied levels of venous return, and highlights the preload dependency of early diastolic function during passive heat stress. tilt table; systolic function; left ventricle WHOLE BODY PASSIVE HEAT STRESS results in multiple cardiovascular and neural adjustments, including increases in cardiac output (14,17,29), cutaneous vascular conductance (2, 5), splanchnic and renal sympathetic vasoconstriction (15,26,28), and muscle sympathetic nerve activity (6,19). These responses occur in a coordinated effort to redistribute cardiac output to the cutaneous circulation, limit the reduction in blood pressure, and protect against syncope.In the supine heat-stressed individual, left ventricular (LV) end-diastolic volume is significantly reduced compared with normothermic conditions (17,18,34), along with reductions in central blood volume (5) and cardiac filling pressures (3,27,34,37). Despite this significant reduction in preload, stroke volume (SV) is maintained during passive heating (14,15,17,18,23,37), secondary to increased ventricular contractility (2,5,17,18) and ventricular diastolic suction (17, 18). While supine measures are helpful, an important and understudied issue is what happens when blood pressure control mechanisms are challenged during orthostasis. Likewise, because supine heat stress significantly reduces cardiac preload, an equally important issue is what happens to cardiac function when preload is restored.Passive postural changes by tilt-table...

Int J of Biomed & Adv Res

“…If no compensatory cardiovascular changes occurred, the reduction in cardiac output due to pooling on standing would lead to a reduction of cerebral flow of this magnitude, and consciousness would be lost. In this study we used posture related physiological response to 10,13,14 that the stroke volume and cardiac output decreases on head up tilt by value almost by 40% of its supine value as measured by invasive and other methods. With our noninvasive easy to use method, we found this change as 36%, which is similar to it.…”

Section: Discussionmentioning

confidence: 99%

“…As measured by various other methods directly and indirectly, the cardiac output (CO) decreases 11 on an average by 25% and stroke volume (SV) decreases by 40% during the 70 0 head up tilt (HUT). However, from the supine position to 20 0 head down tilt (HDT), the CO and SV did not change significantly 10 . We have non-invasively measured the CO and SV during postural challenge with indigenous ICG equipment to test its ability to detect these changes on postural challenges.…”

Section: Introductionmentioning

confidence: 99%

Effect of Postural Challenges on Non-invasive Cardiac Output Measurement with Impedance Cardiography in Young Healthy Adults Using New Horizontal Electrode Placement Method.

Barde¹,

Deepak²

2012

Background: Cardiac output is an important hemodynamic parameter of cardiovascular system and a significant indicator of autonomic function status of a person. It can be measured invasively as well as non-invasively. Imepdance cardiography (ICG) is a promising, new, noninvasive technique to measure cardiac output. There are no studies noninvasively measuring cardiac output in healthy subject by impedance cardiography using new horizontal method of electrode placement during postural challenges. Objective: We observed effect of postural challenges on noninvasive cardiac output measurement using ICG by new horizontal electrode placement method. Methods: Cardiac output (CO), stroke volume (SV) and cardiac index (CI), were measured noninvasively, before and after postural challenges namely Head Up Tilt (HUT) of 70 0 and Head Down Tilt (HDT) 20 0 , in 38 healthy male subjects (mean age-28 yrs, range 22-34 yrs). Results: After 70 0 HUT the values of CO, SV and CI decreased by 1.5±0.9 l/min (31%), 25.8±11.4 ml (37%), & 0.8±0.4 l/min/m 2 (27 %), respectively. HDT did not cause significant change in theses hemodynamic parameters. Conclusion: ICG successfully detected physiological changes in cardiac output following postural challenges using new horizontal electrode placement method. The study underscores utility of this simple noninvasive tool for hemodynamic assessment after postural challenge using new horizontal electrode placement method.