The design and use of a simple device for the MRI assessment of changes in cardiovascular function by lower-body negative-pressure-simulated reduction of central blood volume

2021 ◽  
Author(s):  
M.C.K. Hamilton ◽  
S. Neumann ◽  
G. Szantho ◽  
L. Rydon ◽  
C.B. Lawton ◽  
...  
Keyword(s):  
Blood Volume ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Cardiovascular Function ◽  
Simple Device ◽  
Lower Body ◽  
Central Blood Volume

scholarly journals The physiology of blood loss and shock: New insights from a human laboratory model of hemorrhage

2017 ◽  
Vol 242 (8) ◽  
pp. 874-883 ◽  
Author(s):  
Alicia M Schiller ◽  
Jeffrey T Howard ◽  
Victor A Convertino
Keyword(s):  
Blood Loss ◽  
Blood Volume ◽  
Negative Pressure ◽  
Time Course ◽  
Tissue Oxygenation ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Central Blood Volume ◽  
Volume Loss ◽  
Physiological Mechanisms

The ability to quickly diagnose hemorrhagic shock is critical for favorable patient outcomes. Therefore, it is important to understand the time course and involvement of the various physiological mechanisms that are active during volume loss and that have the ability to stave off hemodynamic collapse. This review provides new insights about the physiology that underlies blood loss and shock in humans through the development of a simulated model of hemorrhage using lower body negative pressure. In this review, we present controlled experimental results through utilization of the lower body negative pressure human hemorrhage model that provide novel insights on the integration of physiological mechanisms critical to the compensation for volume loss. We provide data obtained from more than 250 human experiments to classify human subjects into two distinct groups: those who have a high tolerance and can compensate well for reduced central blood volume (e.g. hemorrhage) and those with low tolerance with poor capacity to compensate.We include the conceptual introduction of arterial pressure and cerebral blood flow oscillations, reflex-mediated autonomic and neuroendocrine responses, and respiration that function to protect adequate tissue oxygenation through adjustments in cardiac output and peripheral vascular resistance. Finally, unique time course data are presented that describe mechanistic events associated with the rapid onset of hemodynamic failure (i.e. decompensatory shock). Impact Statement Hemorrhage is the leading cause of death in both civilian and military trauma. The work submitted in this review is important because it advances the understanding of mechanisms that contribute to the total integrated physiological compensations for inadequate tissue oxygenation (i.e. shock) that arise from hemorrhage. Unlike an animal model, we introduce the utilization of lower body negative pressure as a noninvasive model that allows for the study of progressive reductions in central blood volume similar to those reported during actual hemorrhage in conscious humans to the onset of hemodynamic decompensation (i.e. early phase of decompensatory shock), and is repeatable in the same subject. Understanding the fundamental underlying physiology of human hemorrhage helps to test paradigms of critical care medicine, and identify and develop novel clinical practices and technologies for advanced diagnostics and therapeutics in patients with life-threatening blood loss.

scholarly journals Continuous Monitoring of Changes in Blood Volume and Limb Volume During Lower Body Negative Pressure

2007 ◽  
Vol 29 (3) ◽  
pp. 235-245
Author(s):  
Fumio YAMAZAKI ◽  
Keizo SHIRAKI ◽  
Yutaka ENDO ◽  
Sueko SAGAWA
Keyword(s):  
Blood Volume ◽  
Negative Pressure ◽  
Continuous Monitoring ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Limb Volume

scholarly journals Changes in arterial cerebral blood volume during lower body negative pressure measured with MRI

NeuroImage ◽  
2019 ◽  
Vol 187 ◽  
pp. 166-175 ◽  
Author(s):  
Joseph R. Whittaker ◽  
Molly G. Bright ◽  
Ian D. Driver ◽  
Adele Babic ◽  
Sharmila Khot ◽  
...  
Keyword(s):  
Blood Volume ◽  
Negative Pressure ◽  
Cerebral Blood Volume ◽  
Lower Body Negative Pressure ◽  
Lower Body

scholarly journals Hemodynamic response during lower body negative pressure: role of volume status.

1998 ◽  
Vol 9 (1) ◽  
pp. 105-113 ◽  
Author(s):  
G Ligtenberg ◽  
P J Blankestijn ◽  
H A Koomans
Keyword(s):  
Heart Rate ◽  
Cardiac Index ◽  
Blood Volume ◽  
Pulse Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Hemodynamic Response ◽  
Volume Status ◽  
Lower Body

Sudden dialysis-related hypotension is characterized by paradoxical vasodilation, suggestive of sympathoinhibition. A similar hypotensive reaction can be evoked by lower body negative pressure (LBNP), which thus allows the study of the numerous factors involved in dialysis hypotension separately. This article examines the influence of changes in volume status on the hemodynamic response to LBNP (45 mmHg up to the iliac crest, maximum 60 min) in 12 healthy subjects. LBNP caused a decrease in cardiac index and pulse pressure, and an increase in heart rate and total peripheral resistance, most of which developed within the first 3 min of LBNP. Six subjects developed sudden hypotension characterized by vasodilation after 9 +/- 4 min of LBNP. After saline expansion (25 ml/kg), which increased blood volume by approximately 8%, five subjects endured LBNP for the full 60 min. However, after 60 min of LBNP, the circulatory parameters suggested a similar critical situation as that observed before presyncope in their first experiment. The other six subjects endured the full 60 min of LBNP. After furosemide-induced volume reduction associated with 1.6 +/- 0.2 kg weight loss and approximately 7% blood volume reduction, five of them developed vasodilatory presyncope after 17 +/- 5 min of LBNP. Comparison of presyncopal and nonpresyncopal experiments within subjects, as well as between subjects, showed that the early (3 min) response to LBNP was different: Despite similar decreases in cardiac index, the values for systolic pressure, pulse pressure, peripheral resistance, and stroke volume were lower, and the heart rate was higher in the experiments ending in presyncope. It is concluded that the volume status is a determinant of the tolerance to LBNP, probably by affecting the vasoconstrictive response. By inference, this study suggests that the vasoconstrictive response to the hemodynamic stress of hemodialysis is also influenced by the volume status.

scholarly journals Differentiating compensatory mechanisms associated with low tolerance to central hypovolemia in women

2019 ◽  
Vol 316 (3) ◽  
pp. H609-H616 ◽  
Author(s):  
Taylor Elyse Schlotman ◽  
Kevin S. Akers ◽  
Shawn C. Nessen ◽  
Victor A. Convertino
Keyword(s):  
Blood Volume ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Reduction Rate ◽  
Lower Body ◽  
Men And Women ◽  
Compensatory Responses ◽  
Arterial Blood ◽  
Compensatory Reserve ◽  
Lower Tolerance

Women generally display lower tolerance to acute central hypovolemia than men. The measurement of compensatory reserve (CRM) is a novel metric that provides information about the sum total of all mechanisms that together work to compensate for the relative blood volume deficit. Hemodynamic decompensation occurs with depletion of the CRM (i.e., 0% CRM). In the present study, we hypothesized that the lower tolerance to progressive central hypovolemia reported in women can be explained by a faster reduction rate in CRM compared with men rather than sex differences in absolute integrated compensatory responses. Continuous, noninvasive measures of CRM were collected from 208 healthy volunteers (107 men and 85 women) who underwent progressive stepwise central hypovolemia induced by lower body negative pressure to the point of presyncope. Comparisons revealed shorter ( P < 0.01) times in female participants compared with male participants to reach 30% and 0% CRM. Similarly, the lower body negative pressure level, represented by the cumulative stress index, was less at 30% and 0% CRM in women compared with men ( P < 0.01). Changes in hemodynamic responses and frequency-domain data (oscillations in cerebral blood flow velocity and mean arterial blood pressure) were similar between men and women at 0% CRM ( P > 0.05). We conclude that compensatory responses to central hypovolemia in women were similar to men but were depleted at a faster rate compared with men. The earlier depletion of the compensatory reserve in women appears to be influenced by failure to maintain adequate cerebral oxygen delivery. NEW & NOTEWORTHY We compared hemodynamic and metabolic responses in men and women to experimentally controlled reductions in central blood volume at physiologically equivalent levels of compensatory reserve. We corroborated previous findings that females have lower tolerance to central hypovolemia than males but demonstrated for the first time that compensatory responses are similar. Our findings suggest lower tolerance to central hypovolemia in women results from reaching critical cerebral delivery of oxygen faster than men.

Central blood volume and blood pressure in conscious primates

1988 ◽  
Vol 254 (4) ◽  
pp. H693-H701 ◽  
Author(s):  
K. G. Cornish ◽  
J. P. Gilmore ◽  
T. McCulloch
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Pulse Pressure ◽  
Left Atrial ◽  
Venous Return ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Central Blood Volume ◽  
Arterial Baroreflex ◽  
Arterial Blood

Conscious intact (I) and sinoaortic-denervated monkeys (SAD) were studied to determine the extent to which high-pressure receptors contribute to the maintenance of arterial blood pressure (BP) when venous return is decreased by hemorrhage (H) or lower body negative pressure (LBNP). In the I animals, mean BP did not decrease significantly until 5% of the estimated blood volume (EBV) was removed, whereas, with sinoaortic denervation, mean BP decreased significantly when less than 2% of EBV was removed. Left atrial pressure (LAP) decreased similarly in both groups of animals. In the I group during LBNP, mean BP did not change significantly, whereas pulse pressure decreased significantly when LBNP was decreased to -5 cmH2O. In the SAD animals, mean BP decreased significantly at an LBNP of -2 cmH2O, and at -5 cmH2O mean BP declined from 134.1 +/- 4 to 102.7 +/- 7 mmHg. LAP decreased similarly in both groups of animals. The data support the view that a nonhypotensive reduction in venous return unloads arterial baroreceptors sufficiently to activate the arterial baroreflex, probably through reductions in pulse pressure. In addition, low-pressure receptors by themselves do not appear to contribute importantly to blood pressure maintenance when venous return is decreased by either LBNP or a nonhypotensive hemorrhage.

scholarly journals Differential Effects of Lower Body Negative Pressure and Upright Tilt on Splanchnic Blood Volume

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Indu Taneja ◽  
Chistopher Moran ◽  
Marvin Scott Medow ◽  
Julian M. Stewart
Keyword(s):  
Blood Volume ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Differential Effects ◽  
Upright Tilt

Abstract 14436: Nightly Lower Body Negative Pressure Redistributes Blood Volume and Prevents Maladaptive Vascular Remodeling Induced by Microgravity

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Katrin A Dias ◽  
Christopher M Hearon ◽  
Gautam Babu ◽  
John E Marshall ◽  
James P Macnamara ◽  
...  
Keyword(s):  
Blood Volume ◽  
Negative Pressure ◽  
Vascular Remodeling ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Bed Rest ◽  
Lower Body ◽  
Long Duration ◽  
Sustained Reduction ◽  
Area And Volume

Introduction: During space flight and ground based simulations of microgravity, transmural distending pressure increases in resistance vessels above the level of the heart, causing maladaptive vascular remodeling over time. Lower body negative pressure (LBNP) mimics gravity by redistributing blood volume and reinstating hydrostatic gradients, and may preserve vascular structures above the heart while in microgravity. Methods: Ten healthy subjects (5 female, 29 ± 9 years) completed three days of supine (0°) bed rest with and without eight hours of nightly LBNP (-20mmHg) in a randomized, crossover design. Area and volume of the choroid, a highly vascularized layer of the eye sensitive to changes in hydrostatic gradients, were assessed using optical coherence tomography on the first and last day of bed rest. Central venous pressure (CVP) was measured during spontaneous breathing with a peripherally inserted central catheter. Results: CVP increased significantly from the seated to supine position (+9.1 ± 2.4mmHg, P < 0.001), leading to choroid engorgement over three days of supine bed rest (choroid area: +0.09 mm 2 95% CI 0.04 to 0.13, P = 0.0014; choroid volume: +0.37 mm 3 95% CI 0.19 to 0.55, P = 0.0011). Nightly LBNP caused a sustained reduction in supine CVP (5.7 ± 2.2mmHg to 1.2 ± 1.4mmHg, P < 0.001), indicating effective redistribution of blood volume and significantly attenuated the increase in choroid area (3.5% control vs. 0.9% LBNP, P = 0.0164) and volume (3.8% control vs. 1.8% LBNP, P = 0.0040) compared to control (Figure). Conclusions: Nightly LBNP caused caudal redistribution of blood volume that partially reinstated hydrostatic gradients and mitigated the increase in choroid area and volume by 74% and 53%, respectively. These findings illustrate that normalizing transmural distending pressures during simulated microgravity preserves vascularized structures above the level of the heart and may prevent adverse remodeling during long duration spaceflight.

Delayed vasoconstrictor response to venous pooling in the calf is associated with high orthostatic tolerance to LBNP

2010 ◽  
Vol 109 (4) ◽  
pp. 996-1001 ◽  
Author(s):  
T. Hachiya ◽  
M. L. Walsh ◽  
M. Saito ◽  
A. P. Blaber
Keyword(s):  
Blood Volume ◽  
Negative Pressure ◽  
Near Infrared ◽  
Lower Body Negative Pressure ◽  
Orthostatic Stress ◽  
Orthostatic Tolerance ◽  
Lower Body ◽  
High Tolerance ◽  
Venous Pooling ◽  
Vasoconstrictor Response

Central blood volume loss to venous pooling in the lower extremities and vasoconstrictor response are commonly viewed as key factors to distinguish between individuals with high and low tolerance to orthostatic stress. In this study, we analyzed calf vasoconstriction as a function of venous pooling during simulated orthostatic stress. We hypothesized that high orthostatic tolerance (OT) would be associated with greater vasoconstrictor responses to venous pooling compared with low OT. Nineteen participants underwent continuous stepped lower body negative pressure at −10, −20, −30, −40, −50, and −60 mmHg each for 5 min or until exhibiting signs of presyncope. Ten participants completed the lower body negative pressure procedure without presyncope and were categorized with high OT; the remaining nine were categorized as having low OT. Near-infrared spectroscopy measurements of vasoconstriction (Hachiya T, Blaber A, Saito M. Acta Physiologica 193: 117–127, 2008) in calf muscles, along with heart rate (HR) responses for each participant, were evaluated in relation to calf blood volume, estimated by plethysmography. The slopes of this relationship between vasoconstriction and blood volume were not different between the high- and low-tolerance groups. However, the onset of vasoconstriction in the high-tolerance group was delayed. Greater HR increments in the low-tolerance group were also observed as a function of lower limb blood pooling. The delayed vasoconstriction and slower HR increments in the high-tolerance group to similar venous pooling in the low group may suggest a greater vascular reserve and possible delayed reduction in venous return.

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