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.).

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.

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

Direct Cerebral Vasodilatory Effects of Sevoflurane and Isoflurane 

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
End Tidal

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P&lt;0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.

scholarly journals Impact of blood pressure changes in cerebral blood perfusion of patients with ischemic Moyamoya disease evaluated by SPECT

2020 ◽  
pp. 0271678X2096745
Author(s):  
Zhao Liming ◽  
Sun Weiliang ◽  
Jia Jia ◽  
Liang Hao ◽  
Liu Yang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Moyamoya Disease ◽  
Emission Computed Tomography ◽  
Study Cohort ◽  
Pressure Changes ◽  
The Impact

Our aim was to determine the impact of targeted blood pressure modifications on cerebral blood flow in ischemic moyamoya disease patients assessed by single-photon emission computed tomography (SPECT). From March to September 2018, we prospectively collected data of 154 moyamoya disease patients and selected 40 patients with ischemic moyamoya disease. All patients underwent in-hospital blood pressure monitoring to determine the mean arterial pressure baseline values. The study cohort was subdivided into two subgroups: (1) Group A or relative high blood pressure (RHBP) with an induced mean arterial pressure 10–20% higher than baseline and (2) Group B or relative low blood pressure (RLBP) including patients with mean arterial pressure 10–20% lower than baseline. All patients underwent initial SPECT study on admission-day, and on the following day, every subgroup underwent a second SPECT study under their respective targeted blood pressure values. In general, RHBP patients showed an increment in perfusion of 10.13% (SD 2.94%), whereas RLBP patients showed a reduction of perfusion of 12.19% (SD 2.68%). Cerebral blood flow of moyamoya disease patients is susceptible to small blood pressure changes, and cerebral autoregulation might be affected due to short dynamic blood pressure modifications.

Cardiovascular responses to lower body negative pressure in trained and untrained older men

1992 ◽  
Vol 73 (6) ◽  
pp. 2693-2700 ◽  
Author(s):  
S. Fortney ◽  
C. Tankersley ◽  
J. T. Lightfoot ◽  
D. Drinkwater ◽  
J. Clulow ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Older Men ◽  
Volume Index ◽  
Lower Body ◽  
Vo2 Max ◽  
Cardiac Volumes

To determine whether aerobic conditioning alters the orthostatic responses of older subjects, cardiovascular performance was monitored during graded lower body negative pressure in nine highly trained male senior athletes (A) aged 59–73 yr [maximum O2 uptake (VO2 max) = 52.4 +/- 1.7 ml.kg-1 x min-1] and nine age-matched control subjects (C) (VO2 max = 31.0 +/- 2.9 ml.kg-1 x min-1). Cardiac volumes were determined from gated blood pool scintigrams by use of 99mTc-labeled erythrocytes. During lower body negative pressure (0 to -50 mmHg), left ventricular end-diastolic and end-systolic volume indexes and stroke volume index decreased in both groups while heart rate increased. The decreases in cardiac volumes and mean arterial pressure and the increase in heart rate between 0 and -50 mmHg were significantly less in A than in C. For example, end-diastolic volume index decreased by 32 +/- 4 ml in C vs. 14 +/- 2 ml in A (P < 0.01), mean arterial pressure declined 7 +/- 5 mmHg in C and increased by 5 +/- 3 mmHg in A (P < 0.05), and heart rate increased 13 +/- 3 beats/min in C and 7 +/- 1 beats/min in A (P < 0.05). These data suggest that increased VO2 max among older men is associated with improved orthostatic responses.

Blunted autonomic response to standing up and head-up tilt in individuals with intellectual disabilities

2021 ◽  
Author(s):  
Thessa Irena Maria Hilgenkamp ◽  
Elizabeth C. Lefferts ◽  
Daniel W. White ◽  
Tracy Baynard ◽  
Bo Fernhall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Intellectual Disabilities ◽  
Autonomic Response ◽  
Control Group ◽  
Standing Up ◽  
Head Up Tilt ◽  
Individuals With Intellectual Disabilities

Previous research suggests individuals with intellectual disabilities (ID) may experience autonomic dysfunction, however this has not been thoroughly investigated. PURPOSE: To compare the autonomic response to standing up (active orthostasis) and head up tilt (passive orthostasis) in individuals with ID to a control group without ID. METHODS: Eighteen individuals with and 18 individuals without ID were instrumented with an ECG-lead and finger-photoplethysmography for continuous heart rate and blood pressure recordings. The active and passive orthostasis protocol consisted of 10 minutes supine rest, 10 minutes standing, 10 minutes supine recovery, 5 minutes head-up tilt at 70 degrees, followed by 10 minutes supine recovery. The last five minutes of each position was used to calculate hemodynamic and autonomic function (time- and frequency-domain heart rate and blood pressure variability measures and baroreflex sensitivity). RESULTS Individuals with ID had higher heart rate during baseline and recovery (p<0.05), and an attenuated hemodynamic (stroke volume, heart rate) and heart rate variability response to active and passive orthostasis (interaction effect p<0.05) compared to individuals without ID. Mean arterial pressure (MAP) was higher in individuals with ID at all timepoints. CONCLUSION Individuals with ID demonstrated altered hemodynamic and autonomic regulation compared to a sex- and age-matched control group, evidenced by a higher mean arterial pressure and a reduced response in parasympathetic modulation to active and passive orthostasis.

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