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Cardiovascular Adjustments to Gravitational Stress

C. Gunnar Blomqvist, H. Lowell Stone

10.1002/cphy.cp020328

Source: Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow

Originally published: 1983

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Hydrostatic Pressure
1.1 Models
1.2 Hydrostatic Indifference Point
1.3 Transmural Pressure and Tissue Filtration
2 Immediate Cardiovascular Responses to Posture Changes and Blood Volume Redistribution
2.1 Experimental Conditions
2.2 Blood Volume and Distribution
2.3 Intravascular and Intracardiac Pressures
2.4 Cardiac Dimensions and Pump Performance
2.5 Cardiac Output
2.6 Regional Flow
2.7 Postural Effects on Hemodynamic Responses to Exercise
2.8 Dynamic Responses to Posture Changes
3 Cardiovascular Adaptation to Prolonged Bed Rest, Zero Gravity, and Related Conditions
3.1 Experimental Conditions
3.2 Body Composition
3.3 Blood Volume
3.4 Cardiovascular Function
3.5 Dynamic Responses
4 Hypergravic Conditions
4.1 Experimental Conditions
4.2 Fluid Shifts
4.3 Cardiac Dimensions and Performance
4.4 Cardiac Output and Regional Flow
4.5 Dynamic Responses and Reflex Adjustments
Figure 1. Figure 1.

Hydrostatic pressures (P) in simple fluid‐filled systems of height h. Relationship of hydrostatic pressure and zero in cylinder open to atmosphere (A) and cylinders closed at both ends with rigid membranes (B), with membranes of equal elasticity at both ends (C), and with membrane more elastic at upper end (D).
Figure 2. Figure 2.

Hydrostatic indifference point (HIP) in anesthetized dog is in right ventricle. A: sternal notch; B: xiphoid process. Distance between reference points is 1.00; coordinates of HIP are fractions.

Adapted from Guyton and Greganti 134
Figure 3. Figure 3.

Intrathoracic and venous pressure relationships and hemodynamic responses to changes in body position. Averages of right and left atrial transmural pressures, cardiac output, stroke volume, heart rate, and systemic pressures (left) and average abdominal vena cava, external jugular, pericardial, and right and left atrial pressures (right) in supine, head‐down, and head‐up position in 3 dogs. Adjacent to curves for stroke volume, number of cardiac‐output measurements.

From Avasthey and Wood 11
Figure 4. Figure 4.

Regional pulmonary blood flow at 1 g and 0 g at various lung levels. Measured in volunteer by injecting radioactive tracer during 0 g and in seated position at 1 g. Note flow shifts toward apex of lungs. Similar results in 6 subjects. Zero distance, apex of lung; opposite end of scale, toward base of lung. Top: control measurements; Bottom: 0‐g measurements.
Figure 5. Figure 5.

Responses to graded head‐up and head‐down tilt in 10 humans. LV, left ventricle; PA, pulmonary artery; RA, right atrium. Intravascular pressures in foot (A) and in central circulation (B), and regional and systemic arteriovenous O2 differences (C). Angle of tilt (horizontal axis) plotted as sine function to provide linear scale for primary hydrostatic effects of body‐position changes.

Based on data from Katkov and Chestukhin 177
Figure 6. Figure 6.

Normal individual and group mean values of left ventricular end‐diastolic pressure (LVEDP) in supine and sitting positions at rest and during exercise.

From Thadani and Parker 327
Figure 7. Figure 7.

Left ventricular end‐systolic volume (LVESV; shaded portion), LVEDV (means ± SE; tops of bars), and LV stroke volume (clear portion) at rest (R) and during 3 levels of exercise (SI, SII, PK). Above bars of right panel, P values for corresponding upright and supine measurements of LVEDV at each work load; P values above LVESV data for corresponding supine measurements of LVESV; P values between adjacent bars for change between progressive work loads; P values in small boxes of peak exercise (PK) bars for change from R to PK for LVESV in each position. Between R and PK, LVEDV also increased significantly in both positions (P <0.001 supine, P <0.02 upright). SI, low‐level work (300 kpm/min); SII, intermediate‐level work (600‐750 kpm/min).

From Poliner, Blomqvist, et al. 261, by permission of the American Heart Association, Inc
Figure 8. Figure 8.

Control of central blood volume and cardiac filling pressure by systemic veins. Contracting smooth muscle cells of venous wall, splanchnic veins in particular, actively changes filling of heart. Cutaneous veins mainly react to changes in temperature. Any change in distending pressure, whether due to gravity or changes in arteriolar resistance, passively changes capacity. NE, norepinephrine.

From The Human Cardiovascular System, 1979, by Shepherd and Vanhoutte 297, by permission of Raven Press, NY
Figure 9. Figure 9.

Principal features of human response to progressive lower‐body negative pressure.
Figure 10. Figure 10.

Body‐mass measurement of Skylab‐3 scientist pilot at 0 g with spring‐loaded oscillating system in which frequency of oscillation was proportional to mass.

From Thornton and Ord 335
Figure 11. Figure 11.

Hemodynamic effects of 3‐wk bed rest on cardiac output, stroke volume, heart rate, and mean arterial pressure supine and upright at rest during exercise in 5 normal young men. Control measurements before bed rest = 100%.

Data from Saltin, Blomqvist, et al. 286
Figure 12. Figure 12.

Diagram of early adaptation to simulated 0 g (head‐down tilt, −5°).

From Blomqvist et al. 36
Figure 13. Figure 13.

Standard reference system (direction and nomenclature) for gravitational forces acting on a subject through long axis of body (± Gz), through sternum to backbone (± Gx), and through lateral aspect (± Gy, not shown).
Figure 14. Figure 14.

A representative average curve for +G, acceleration tolerance in relaxed humans in seated position. Top of graph, reported symptoms at these acceleration levels. Increased tolerance above 10 s is probably circulatory reflex compensating for increased gravitational force.
Figure 15. Figure 15.

Average % change from control in forearm blood flow and resistance (A) and splanchnic flow and resistance (B) in 6 volunteers. Arm suspended at heart level throughout experiments. Arterial pressure was referenced to heart level.

Adapted from Stone et al. 317 and H. L. Stone, unpublished observations


Figure 1.

Hydrostatic pressures (P) in simple fluid‐filled systems of height h. Relationship of hydrostatic pressure and zero in cylinder open to atmosphere (A) and cylinders closed at both ends with rigid membranes (B), with membranes of equal elasticity at both ends (C), and with membrane more elastic at upper end (D).



Figure 2.

Hydrostatic indifference point (HIP) in anesthetized dog is in right ventricle. A: sternal notch; B: xiphoid process. Distance between reference points is 1.00; coordinates of HIP are fractions.

Adapted from Guyton and Greganti 134


Figure 3.

Intrathoracic and venous pressure relationships and hemodynamic responses to changes in body position. Averages of right and left atrial transmural pressures, cardiac output, stroke volume, heart rate, and systemic pressures (left) and average abdominal vena cava, external jugular, pericardial, and right and left atrial pressures (right) in supine, head‐down, and head‐up position in 3 dogs. Adjacent to curves for stroke volume, number of cardiac‐output measurements.

From Avasthey and Wood 11


Figure 4.

Regional pulmonary blood flow at 1 g and 0 g at various lung levels. Measured in volunteer by injecting radioactive tracer during 0 g and in seated position at 1 g. Note flow shifts toward apex of lungs. Similar results in 6 subjects. Zero distance, apex of lung; opposite end of scale, toward base of lung. Top: control measurements; Bottom: 0‐g measurements.



Figure 5.

Responses to graded head‐up and head‐down tilt in 10 humans. LV, left ventricle; PA, pulmonary artery; RA, right atrium. Intravascular pressures in foot (A) and in central circulation (B), and regional and systemic arteriovenous O2 differences (C). Angle of tilt (horizontal axis) plotted as sine function to provide linear scale for primary hydrostatic effects of body‐position changes.

Based on data from Katkov and Chestukhin 177


Figure 6.

Normal individual and group mean values of left ventricular end‐diastolic pressure (LVEDP) in supine and sitting positions at rest and during exercise.

From Thadani and Parker 327


Figure 7.

Left ventricular end‐systolic volume (LVESV; shaded portion), LVEDV (means ± SE; tops of bars), and LV stroke volume (clear portion) at rest (R) and during 3 levels of exercise (SI, SII, PK). Above bars of right panel, P values for corresponding upright and supine measurements of LVEDV at each work load; P values above LVESV data for corresponding supine measurements of LVESV; P values between adjacent bars for change between progressive work loads; P values in small boxes of peak exercise (PK) bars for change from R to PK for LVESV in each position. Between R and PK, LVEDV also increased significantly in both positions (P <0.001 supine, P <0.02 upright). SI, low‐level work (300 kpm/min); SII, intermediate‐level work (600‐750 kpm/min).

From Poliner, Blomqvist, et al. 261, by permission of the American Heart Association, Inc


Figure 8.

Control of central blood volume and cardiac filling pressure by systemic veins. Contracting smooth muscle cells of venous wall, splanchnic veins in particular, actively changes filling of heart. Cutaneous veins mainly react to changes in temperature. Any change in distending pressure, whether due to gravity or changes in arteriolar resistance, passively changes capacity. NE, norepinephrine.

From The Human Cardiovascular System, 1979, by Shepherd and Vanhoutte 297, by permission of Raven Press, NY


Figure 9.

Principal features of human response to progressive lower‐body negative pressure.



Figure 10.

Body‐mass measurement of Skylab‐3 scientist pilot at 0 g with spring‐loaded oscillating system in which frequency of oscillation was proportional to mass.

From Thornton and Ord 335


Figure 11.

Hemodynamic effects of 3‐wk bed rest on cardiac output, stroke volume, heart rate, and mean arterial pressure supine and upright at rest during exercise in 5 normal young men. Control measurements before bed rest = 100%.

Data from Saltin, Blomqvist, et al. 286


Figure 12.

Diagram of early adaptation to simulated 0 g (head‐down tilt, −5°).

From Blomqvist et al. 36


Figure 13.

Standard reference system (direction and nomenclature) for gravitational forces acting on a subject through long axis of body (± Gz), through sternum to backbone (± Gx), and through lateral aspect (± Gy, not shown).



Figure 14.

A representative average curve for +G, acceleration tolerance in relaxed humans in seated position. Top of graph, reported symptoms at these acceleration levels. Increased tolerance above 10 s is probably circulatory reflex compensating for increased gravitational force.



Figure 15.

Average % change from control in forearm blood flow and resistance (A) and splanchnic flow and resistance (B) in 6 volunteers. Arm suspended at heart level throughout experiments. Arterial pressure was referenced to heart level.

Adapted from Stone et al. 317 and H. L. Stone, unpublished observations
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Article Title: Cardiovascular Adjustments to Gravitational Stress
 

How to Cite

C. Gunnar Blomqvist, H. Lowell Stone. Cardiovascular Adjustments to Gravitational Stress. Compr Physiol 2011, Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow: 1025-1063. First published in print 1983. doi: 10.1002/cphy.cp020328