scholarly journals Validity of auscultatory and Penaz blood pressure measurements during profound heat stress alone and with an orthostatic challenge

2011 ◽  
Vol 301 (5) ◽  
pp. R1510-R1516 ◽  
Author(s):  
Matthew S. Ganio ◽  
R. Matthew Brothers ◽  
Rebekah A. I. Lucas ◽  
Jeffrey L. Hastings ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Heat Stress ◽  
Brachial Artery ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Pressure Measurements ◽  
Lower Body ◽  
Dynamic Changes ◽  
Orthostatic Challenge

Despite frequent reporting of blood pressure (BP) during profound passive heat stress, both with and without a hypotensive challenge, the method by which BP is measured often varies between laboratories. It is unknown whether auscultatory and finger BP measures accurately reflect intra-arterial BP during dynamic changes in cardiac output and peripheral resistance associated with the aforementioned conditions. The purpose of this investigation was to test the hypothesis that auscultatory BP measured at the brachial artery, and finger BP measured by the Penaz method, are valid measures of intra-arterial BP during a passive heat stress and a heat-stressed orthostatic challenge, via lower body negative pressure (LBNP). Absolute (specific aim 1) and the change in (specific aim 2) systolic (SBP), diastolic (DBP), and mean BPs (MBP) were compared at normothermia, after a core temperature increase of 1.47 ± 0.09°C, and during subsequent LBNP. Heat stress did not change auscultatory SBP (6 ± 11 mmHg; P = 0.16), but Penaz SBP (−22 ± 16 mmHg; P < 0.001) and intra-arterial SBP (−11 ± 13 mmHg P = 0.017) decreased. In contrast, DBP and MBP did not differ between methods throughout heat stress. Compared with BP before LBNP, the magnitude of the reduction in BP with all three methods was similar throughout LBNP ( P > 0.05). In conclusion, auscultatory SBP and Penaz SBP failed to track the decrease in intra-arterial SBP that occurred during the profound heat stress, while decreases in arterial BP during an orthostatic challenge are comparable between methodologies.

Hemodynamic Strategies in Blood Pressure Regulation During Orthostatic Challenge in Women

1997 ◽  
Vol 22 (4) ◽  
pp. 351-367
Author(s):  
Tania L. Culham ◽  
Gabrielle K. Savard
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Orthostatic Tolerance ◽  
Lower Body ◽  
Orthostatic Challenge ◽  
Carotid Baroreflex

Several studies indicate that carotid baroreflex responsiveness is a good predictor of orthostatic tolerance. Two groups of healthy women with high (HI) and low (LO) carotid baroreflex responsiveness were studied (a) to determine any differences in the level of orthostatic tolerance of the two groups, and (b) to study the hemodynamic strategies used by HI and LO responders to regulate arterial pressure during the orthostatic challenge of lower body negative pressure (LBNP). Orthostatic tolerance was similar between the two groups, whereas the hemodynamic strategies recruited to maintain blood pressure at −40 mmHg LBNP differed: HI responders exhibited greater LBNP-induced decreases in stroke volume and cardiac output, as well as a greater increase in peripheral resistance compared to LO responders (p < .05). In addition, a significant increase in plasma renin activity during LBNP was found in the HI responders only. No significant between-group differences were found in arterial and cardiopulmonary control of vascular resistance or arterial haroreflex control of heart rate during LBNP. Key words: arterial pressure, carotid baroreceptor, lower body negative pressure, orthostatic tolerance, stroke volume

scholarly journals Forehead versus forearm skin vascular responses at presyncope in humans

2014 ◽  
Vol 307 (7) ◽  
pp. R908-R913 ◽  
Author(s):  
Daniel Gagnon ◽  
R. Matthew Brothers ◽  
Matthew S. Ganio ◽  
Jeffrey L. Hastings ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Heat Stress ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Facial Skin ◽  
Vascular Responses ◽  
Radial Artery Catheterization ◽  
Forearm Skin ◽  
Cutaneous Vasoconstriction

Facial pallor is commonly observed at presyncope in humans, suggestive of reductions in facial skin blood flow (SkBF). Yet, cutaneous vasoconstriction is usually minimal at presyncope when measured at the forearm. We tested the hypothesis that reductions in forehead SkBF at presyncope are greater than in the forearm. Forehead and forearm SkBF (laser-Doppler) and blood pressure (Finometer or radial artery catheterization) were measured during lower body negative pressure (LBNP) to presyncope in 11 normothermic and 13 heat-stressed subjects (intestinal temperature increased ∼1.4°C). LBNP reduced mean arterial pressure from 91 ± 5 to 57 ± 7 mmHg during normothermia ( P ≤ 0.001) and from 82 ± 5 to 57 ± 7 mmHg during heat stress ( P ≤ 0.001). During normothermia, LBNP decreased forehead SkBF 55 ± 14% compared with 24 ± 11% at the forearm ( P = 0.002), while during heat stress LBNP decreased forehead SkBF 39 ± 11% compared with 28 ± 8% in the forearm ( P = 0.007). In both conditions, most (≥68%) of the decreases in SkBF were due to decreases in blood pressure. However, a greater contribution of actively mediated reductions in SkBF was observed at the forehead, relative to the forearm during normothermia (32 ± 13% vs. 11 ± 11%, P = 0.031) and heat stress (30 ± 13% vs. 10 ± 13%, P = 0.004). These data suggest that facial pallor at presyncope is due to a combination of passive decreases in forehead SkBF secondary to reductions in blood pressure and to active decreases in SkBF, the latter of which are relatively greater than in the forearm.

scholarly journals Effect of heat stress on cardiac output and systemic vascular conductance during simulated hemorrhage to presyncope in young men

2012 ◽  
Vol 302 (8) ◽  
pp. H1756-H1761 ◽  
Author(s):  
Matthew S. Ganio ◽  
Morten Overgaard ◽  
Thomas Seifert ◽  
Niels H. Secher ◽  
Pär I. Johansson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Heat Stress ◽  
Blood Pressure Control ◽  
Lower Body Negative Pressure ◽  
Pressure Control ◽  
Vascular Conductance ◽  
Low Cardiac Output ◽  
Primary Mechanism ◽  
Simulated Hemorrhage

During moderate actual or simulated hemorrhage, as cardiac output decreases, reductions in systemic vascular conductance (SVC) maintain mean arterial pressure (MAP). Heat stress, however, compromises the control of MAP during simulated hemorrhage, and it remains unknown whether this response is due to a persistently high SVC and/or a low cardiac output. This study tested the hypothesis that an inadequate decrease in SVC is the primary contributing mechanism by which heat stress compromises blood pressure control during simulated hemorrhage. Simulated hemorrhage was imposed via lower body negative pressure (LBNP) to presyncope in 11 passively heat-stressed subjects (increase core temperature: 1.2 ± 0.2°C; means ± SD). Cardiac output was measured via thermodilution, and SVC was calculated while subjects were normothermic, heat stressed, and throughout subsequent LBNP. MAP was not changed by heat stress but was reduced to 45 ± 12 mmHg at the termination of LBNP. Heat stress increased cardiac output from 7.1 ± 1.1 to 11.7 ± 2.2 l/min ( P < 0.001) and increased SVC from 0.094 ± 0.018 to 0.163 ± 0.032 l·min−1·mmHg−1 ( P < 0.001). Although cardiac output at the onset of syncopal symptoms was 37 ± 16% lower relative to pre-LBNP, presyncope cardiac output (7.3 ± 2.0 l/min) was not different than normothermic values ( P = 0.46). SVC did not change throughout LBNP ( P > 0.05) and at presyncope was 0.168 ± 0.044 l·min−1·mmHg−1. These data indicate that in humans a cardiac output adequate to maintain MAP while normothermic is no longer adequate during a heat-stressed-simulated hemorrhage. The absence of a decrease in SVC at a time of profound reductions in MAP suggests that inadequate control of vascular conductance is a primary mechanism compromising blood pressure control during these conditions.

scholarly journals Insufficient cutaneous vasoconstriction leading up to and during syncopal symptoms in the heat stressed human

2010 ◽  
Vol 299 (4) ◽  
pp. H1168-H1173 ◽  
Author(s):  
C. G. Crandall ◽  
M. Shibasaki ◽  
T. E. Wilson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Internal Temperature ◽  
Orthostatic Challenge ◽  
Head Up Tilt ◽  
Cutaneous Vasoconstriction

As much as 50% of cardiac output can be distributed to the skin in the hyperthermic human, and therefore the control of cutaneous vascular conductance (CVC) becomes critical for the maintenance of blood pressure. Little is known regarding the magnitude of cutaneous vasoconstriction in profoundly hypotensive individuals while heat stressed. This project investigated the hypothesis that leading up to and during syncopal symptoms associated with combined heat and orthostatic stress, reductions in CVC are inadequate to prevent syncope. Using a retrospective study design, we evaluated data from subjects who experienced syncopal symptoms during lower body negative pressure ( N = 41) and head-up tilt ( N = 5). Subjects were instrumented for measures of internal temperature, forearm skin blood flow, arterial pressure, and heart rate. CVC was calculated as skin blood flow/mean arterial pressure × 100. Data were obtained while subjects were normothermic, immediately before an orthostatic challenge while heat stressed, and at 5-s averages for the 2 min preceding the cessation of the orthostatic challenge due to syncopal symptoms. Whole body heat stress increased internal temperature (1.25 ± 0.3°C; P < 0.001) and CVC (29 ± 20 to 160 ± 58 CVC units; P < 0.001) without altering mean arterial pressure (83 ± 7 to 82 ± 6 mmHg). Mean arterial pressure was reduced to 57 ± 9 mmHg ( P < 0.001) immediately before the termination of the orthostatic challenge. At test termination, CVC decreased to 138 ± 61 CVC units ( P < 0.001) relative to before the orthostatic challenge but remained approximately fourfold greater than when subjects were normothermic. This negligible reduction in CVC during pronounced hypotension likely contributes to reduced orthostatic tolerance in heat-stressed humans. Given that lower body negative pressure and head-up tilt are models of acute hemorrhage, these findings have important implications with respect to mechanisms of compromised blood pressure control in the hemorrhagic individual who is also hyperthermic (e.g., military personnel, firefighters, etc.).

scholarly journals Orthostatic hypotension in aging humans

2000 ◽  
Vol 279 (4) ◽  
pp. H1548-H1554 ◽  
Author(s):  
Xiangrong Shi ◽  
D. Walter Wray ◽  
Kevin J. Formes ◽  
Hong-Wei Wang ◽  
Patrick M. Hayes ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Orthostatic Hypotension ◽  
Parasympathetic Nervous System ◽  
Lower Body Negative Pressure ◽  
The Elderly ◽  
Sympathetic Blockade ◽  
Lower Body ◽  
Younger Adults ◽  
Orthostatic Challenge

We tested the hypothesis that hypotension occurred in older adults at the onset of orthostatic challenge as a result of vagal dysfunction. Responses of heart rate (HR) and mean arterial pressure (MAP) were compared between 10 healthy older and younger adults during onset and sustained lower body negative pressure (LBNP). A younger group was also assessed after blockade of the parasympathetic nervous system with the use of atropine or glycopyrrolate and after blockade of the β1-adrenoceptor by use of metoprolol. Baseline HR (older vs. younger: 59 ± 4 vs. 54 ± 1 beats/min) and MAP (83 ± 2 vs. 89 ± 3 mmHg) were not significantly different between the groups. During −40 Torr, significant tachycardia occurred at the first HR response in the younger subjects without hypotension, whereas significant hypotension [change in MAP (ΔMAP) −7 ± 2 mmHg] was observed in the elderly without tachycardia. After the parasympathetic blockade, tachycardiac responses of younger subjects were diminished and associated with a significant hypotension at the onset of LBNP. However, MAP was not affected after the cardiac sympathetic blockade. We concluded that the elderly experienced orthostatic hypotension at the onset of orthostatic challenge because of a diminished HR response. However, an augmented vasoconstriction helped with the maintenance of their blood pressure during sustained LBNP.

scholarly journals Factors mediating the pressor response to isometric muscle contraction: An experimental study in healthy volunteers during lower body negative pressure

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0243627
Author(s):  
Niels A. Stens ◽  
Jonny Hisdal ◽  
Espen F. Bakke ◽  
Narinder Kaur ◽  
Archana Sharma ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Isometric Exercise ◽  
Peripheral Resistance ◽  
Relative Importance ◽  
Lower Body ◽  
Arterial Blood

Whilst both cardiac output (CO) and total peripheral resistance (TPR) determine mean arterial blood pressure (MAP), their relative importance in the pressor response to isometric exercise remains unclear. This study aimed to elucidate the relative importance of these two different factors by examining pressor responses during cardiopulmonary unloading leading to step-wise reductions in CO. Hemodynamics were investigated in 11 healthy individuals before, during and after two-minute isometric exercise during lower body negative pressure (LBNP; -20mmHg and -40mmHg). The blood pressure response to isometric exercise was similar during normal and reduced preload, despite a step-wise reduction in CO during LBNP (-20mmHg and -40mmHg). During -20mmHg LBNP, the decreased stroke volume, and consequently CO, was counteracted by an increased TPR, while heart rate (HR) was unaffected. HR was increased during -40 mmHg LBNP, although insufficient to maintain CO; the drop in CO was perfectly compensated by an increased TPR to maintain MAP. Likewise, transient application of LBNP (-20mmHg and -40mmHg) resulted in a short transient drop in MAP, caused by a decrease in CO, which was compensated by an increase in TPR. This study suggests that, in case of reductions of CO, changes in TPR are primarily responsible for maintaining the pressor response during isometric exercise. This highlights the relative importance of TPR compared to CO in mediating the pressor response during isometric exercise.

scholarly journals Face cooling increases blood pressure during central hypovolemia

2017 ◽  
Vol 313 (5) ◽  
pp. R594-R600 ◽  
Author(s):  
Blair D. Johnson ◽  
James R. Sackett ◽  
Suman Sarker ◽  
Zachary J. Schlader
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Plastic Bag ◽  
Ice Water ◽  
Face Cooling ◽  
Healthy Participants ◽  
Cutaneous Vascular Resistance

A reduction in central blood volume can lead to cardiovascular decompensation (i.e., failure to maintain blood pressure). Cooling the forehead and cheeks using ice water raises blood pressure. Therefore, face cooling (FC) could be used to mitigate decreases in blood pressure during central hypovolemia. We tested the hypothesis that FC during central hypovolemia induced by lower-body negative pressure (LBNP) would increase blood pressure. Ten healthy participants (22 ± 2 yr, three women, seven men) completed two randomized LBNP trials on separate days. Trials began with 30 mmHg of LBNP for 6 min. Then, a 2.5-liter plastic bag of ice water (0 ± 0°C) (LBNP+FC) or thermoneutral water (34 ± 1°C) (LBNP+Sham) was placed on the forehead, eyes, and cheeks during 15 min of LBNP at 30 mmHg. Forehead temperature was lower during LBNP+FC than LBNP+Sham, with the greatest difference at 21 min of LBNP (11.1 ± 1.6 vs. 33.9 ± 1.4°C, P < 0.001). Mean arterial pressure was greater during LBNP+FC than LBNP+Sham, with the greatest difference at 8 min of LBNP (98 ± 15 vs. 80 ± 8 mmHg, P < 0.001). Cardiac output was higher during LBNP+FC than LBNP+Sham with the greatest difference at 18 min of LBNP (5.9 ± 1.4 vs. 4.9 ± 1.0 liter/min, P = 0.005). Forearm cutaneous vascular resistance was greater during LBNP+FC than LBNP+Sham, with the greatest difference at 15 min of LBNP (7.2 ± 3.4 vs. 4.9 ± 2.7 mmHg/perfusion units (PU), P < 0.001). Face cooling during LBNP increases blood pressure through increases in cardiac output and vascular resistance.

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