scholarly journals Effects of heat stress on dynamic cerebral autoregulation during large fluctuations in arterial blood pressure

2009 ◽  
Vol 107 (6) ◽  
pp. 1722-1729 ◽  
Author(s):  
R. Matthew Brothers ◽  
Rong Zhang ◽  
Jonathan E. Wingo ◽  
Kimberly A. Hubing ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Cerebral Autoregulation ◽  
Lower Body Negative Pressure ◽  
Low Frequency ◽  
Thermal Conditions ◽  
Very Low Frequency ◽  
Arterial Blood ◽  
Dynamic Cerebral Autoregulation

Impaired cerebral autoregulation during marked reductions in arterial blood pressure may contribute to heat stress-induced orthostatic intolerance. This study tested the hypothesis that passive heat stress attenuates dynamic cerebral autoregulation during pronounced swings in arterial blood pressure. Mean arterial blood pressure (MAP) and middle cerebral artery blood velocity were continuously recorded for ∼6 min during normothermia and heat stress (core body temperature = 36.9 ± 0.1°C and 38.0 ± 0.1°C, respectively, P < 0.001) in nine healthy individuals. Swings in MAP were induced by 70-mmHg oscillatory lower body negative pressure (OLBNP) during normothermia and at a sufficient lower body negative pressure to cause similar swings in MAP during heat stress. OLBNP was applied at a very low frequency (∼0.03 Hz, i.e., 15 s on-15 s off) and a low frequency (∼0.1 Hz, i.e., 5 s on-5 s off). For each thermal condition, transfer gain, phase, and coherence function were calculated at both frequencies of OLBNP. During very low-frequency OLBNP, transfer function gain was reduced by heat stress (0.55 ± 0.20 and 0.31 ± 0.07 cm·s−1·mmHg−1 during normothermia and heat stress, respectively, P = 0.02), which is reflective of improved cerebrovascular autoregulation. During low-frequency OLBNP, transfer function gain was similar between thermal conditions (1.19 ± 0.53 and 1.01 ± 0.20 cm·s−1·mmHg−1 during normothermia and heat stress, respectively, P = 0.32). Estimates of phase and coherence were similar between thermal conditions at both frequencies of OLBNP. Contrary to our hypothesis, dynamic cerebral autoregulation during large swings in arterial blood pressure during very low-frequency (i.e., 0.03 Hz) OLBNP is improved during heat stress, but it is unchanged during low-frequency (i.e., 0.1 Hz) OLBNP.

scholarly journals Dynamic cerebral autoregulation during passive heat stress in humans

2009 ◽  
Vol 296 (5) ◽  
pp. R1598-R1605 ◽  
Author(s):  
David A. Low ◽  
Jonathan E. Wingo ◽  
David M. Keller ◽  
Scott L. Davis ◽  
Jian Cui ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Transfer Function ◽  
High Frequency ◽  
Cerebral Autoregulation ◽  
Low Frequency ◽  
Passive Heating ◽  
Frequency Range ◽  
Very Low Frequency ◽  
Dynamic Cerebral Autoregulation

This study tested the hypothesis that passive heating impairs cerebral autoregulation. Transfer function analyses of resting arterial blood pressure and middle cerebral artery blood velocity (MCA Vmean), as well as MCA Vmean and blood pressure responses to rapid deflation of previously inflated thigh cuffs, were examined in nine healthy subjects under normothermic and passive heat stress (increase core temperature 1.1 ± 0.2°C, P < 0.001) conditions. Passive heating reduced MCA Vmean [change (Δ) of 8 ± 8 cm/s, P = 0.01], while blood pressure was maintained (Δ −1 ± 4 mmHg, P = 0.36). Coherence was decreased in the very-low-frequency range during heat stress (0.57 ± 0.13 to 0.26 ± 0.10, P = 0.001), but was >0.5 and similar between normothermia and heat stress in the low- (0.07–0.20 Hz, P = 0.40) and high-frequency (0.20–0.35 Hz, P = 0.12) ranges. Transfer gain was reduced during heat stress in the very-low-frequency (0.88 ± 0.38 to 0.59 ± 0.19 cm·s−1·mmHg−1, P = 0.02) range, but was unaffected in the low- and high-frequency ranges. The magnitude of the decrease in blood pressure (normothermia: 20 ± 4 mmHg, heat stress: 19 ± 6 mmHg, P = 0.88) and MCA Vmean (13 ± 4 to 12 ± 6 cm/s, P = 0.59) in response to cuff deflation was not affected by the thermal condition. Similarly, the rate of regulation of cerebrovascular conductance (CBVC) after cuff release (0.44 ± 0.22 to 0.38 ± 0.13 ΔCBVC units/s, P = 0.16) and the time for MCA Vmean to recover to precuff deflation baseline (10.0 ± 7.9 to 8.7 ± 4.9 s, P = 0.77) were not affected by heat stress. Counter to the proposed hypothesis, similar rate of regulation responses suggests that heat stress does not impair the ability to control cerebral perfusion after a rapid reduction in perfusion pressure, while reduced transfer function gain and coherence in the very-low-frequency range during heat stress suggest that dynamic cerebral autoregulation is improved during spontaneous oscillations in blood pressure within this frequency range.

Random perturbations of arterial blood pressure for the assessment of dynamic cerebral autoregulation

2012 ◽  
Vol 33 (2) ◽  
pp. 103-116 ◽  
Author(s):  
Emmanuel Katsogridakis ◽  
Glen Bush ◽  
Lingke Fan ◽  
Anthony A Birch ◽  
David M Simpson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cerebral Autoregulation ◽  
Random Perturbations ◽  
Arterial Blood ◽  
Dynamic Cerebral Autoregulation

scholarly journals The effect of large fluctuations in arterial blood pressure on cerebral autoregulation during heat stress

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
R. Matthew Brothers ◽  
Rong Zhang ◽  
Jonathan E. Wingo ◽  
Kimberly A. Hubing ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Cerebral Autoregulation ◽  
Arterial Blood ◽  
Large Fluctuations

Vagal cardiac function and arterial blood pressure stability

2001 ◽  
Vol 281 (5) ◽  
pp. H1870-H1880 ◽  
Author(s):  
D. Walter Wray ◽  
Kevin J. Formes ◽  
Martin S. Weiss ◽  
Albert H. O-Yurvati ◽  
Peter B. Raven ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Function ◽  
Arterial Blood Pressure ◽  
Lower Body Negative Pressure ◽  
Low Frequency ◽  
Antimuscarinic Agents ◽  
Cuff Deflation ◽  
Arterial Blood ◽  
Before And After ◽  
The Difference

This study was designed to investigate the importance of vagal cardiac modulation in arterial blood pressure (ABP) stability before and after glycopyrrolate or atropine treatment. Changes in R-R interval (RRI) and ABP were assessed in 10 healthy young (age, 22 ± 1.8 yr) volunteers during graded lower body negative pressure (LBNP) before and after muscarinic cholinergic (MC) blockade. Transient hypertension was induced by phenylephrine (1 μg/kg body wt), whereas systemic hypotension was induced by bilateral thigh cuff deflation after a 3-min suprasystolic occlusion. Power spectral densities of systolic [systolic blood pressure (SBP)] and diastolic ABP variability were examined. Both antimuscarinic agents elicited tachycardia similarly without significantly affecting baseline ABP. The increase in SBP after phenylephrine injection (+14 ± 2 mmHg) was significantly augmented with atropine (+26 ± 2 mmHg) or glycopyrrolate (+27 ± 3 mmHg) and associated with a diminished reflex bradycardia. The decrease in SBP after cuff deflation (−9.2 ± 1.2 mmHg) was significantly greater after atropine (−15 ± 1 mmHg) or glycopyrrolate (−14 ± 1 mmHg), with abolished reflex tachycardia. LBNP significantly decreased both SBP and RRI. However, after antimuscarinic agents, the reduction in SBP was greater ( P < 0.05) and was associated with less tachycardia. Antimuscarinic agents reduced ( P < 0.05) the low-frequency (LF; 0.04–0.12 Hz) power of ABP variability at rest. The LF SBP oscillation was significantly augmented during LBNP, which was accentuated ( P < 0.05) after antimuscarinic agents and was correlated ( r = −0.79) with the decrease in SBP. We conclude that antimuscarinic agents compromised ABP stability by diminishing baroreflex sensitivity, reflecting the importance of vagal cardiac function in hemodynamic homeostasis. The difference between atropine and glycopyrrolate was not significant.

Decreased steady-state cerebral blood flow velocity and altered dynamic cerebral autoregulation during 5-h sustained 15% O2 hypoxia

2010 ◽  
Vol 108 (5) ◽  
pp. 1154-1161 ◽  
Author(s):  
Naoko Nishimura ◽  
Ken-ichi Iwasaki ◽  
Yojiro Ogawa ◽  
Ken Aoki
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Steady State ◽  
Cerebral Circulation ◽  
Cerebral Autoregulation ◽  
Low Frequency ◽  
Very Low Frequency ◽  
Increased Risk ◽  
Dynamic Cerebral Autoregulation ◽  
Mild Hypoxia

Effects of hypoxia on cerebral circulation are important for occupational, high-altitude, and aviation medicine. Increased risk of fainting might be attributable to altered cerebral circulation by hypoxia. Dynamic cerebral autoregulation is reportedly impaired immediately by mild hypoxia. However, continuous exposure to hypoxia causes hyperventilation, resulting in hypocapnia. This hypocapnia is hypothesized to restore impaired dynamic cerebral autoregulation with reduced steady-state cerebral blood flow (CBF). However, no studies have examined hourly changes in alterations of dynamic cerebral autoregulation and steady-state CBF during sustained hypoxia. We therefore examined cerebral circulation during 5-h exposure to 15% O2 hypoxia and 21% O2 in 13 healthy volunteers in a sitting position. Waveforms of blood pressure and CBF velocity in the middle cerebral artery were measured using finger plethysmography and transcranial Doppler ultrasonography. Dynamic cerebral autoregulation was assessed by spectral and transfer function analysis. As expected, steady-state CBF velocity decreased significantly from 2 to 5 h of hypoxia, accompanying 2- to 3-Torr decreases in end-tidal CO2 (ETCO2). Furthermore, transfer function gain and coherence in the very-low-frequency range increased significantly at the beginning of hypoxia, indicating impaired dynamic cerebral autoregulation. However, contrary to the proposed hypothesis, indexes of dynamic cerebral autoregulation showed no significant restoration despite ETCO2 reductions, resulting in persistent higher values of very-low-frequency power of CBF velocity variability during hypoxia (214 ± 40% at 5 h of hypoxia vs. control) without significant increases in blood pressure variability. These results suggest that sustained mild hypoxia reduces steady-state CBF and continuously impairs dynamic cerebral autoregulation, implying an increased risk of shortage of oxygen supply to the brain.

scholarly journals Heat stress attenuates the increase in arterial blood pressure during the cold pressor test

2010 ◽  
Vol 109 (5) ◽  
pp. 1354-1359 ◽  
Author(s):  
Jian Cui ◽  
Manabu Shibasaki ◽  
David A. Low ◽  
David M. Keller ◽  
Scott L. Davis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
Cold Pressor Test ◽  
Thermal Conditions ◽  
Cold Pressor ◽  
Pressor Test ◽  
Arterial Blood

The mechanisms by which heat stress impairs the control of blood pressure leading to compromised orthostatic tolerance are not thoroughly understood. A possible mechanism may be an attenuated blood pressure response to a given increase in sympathetic activity. This study tested the hypothesis that whole body heating attenuates the blood pressure response to a non-baroreflex-mediated sympathoexcitatory stimulus. Ten healthy subjects were instrumented for the measurement of integrated muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP), heart rate, sweat rate, and forearm skin blood flow. Subjects were exposed to a cold pressor test (CPT) by immersing a hand in an ice water slurry for 3 min while otherwise normothermic and while heat stressed (i.e., increase core temperature ∼0.7°C via water-perfused suit). Mean responses from the final minute of the CPT were evaluated. In both thermal conditions CPT induced significant increases in MSNA and MAP without altering heart rate. Although the increase in MSNA to the CPT was similar between thermal conditions (normothermia: Δ14.0 ± 2.6; heat stress: Δ19.1 ± 2.6 bursts/min; P = 0.09), the accompanying increase in MAP was attenuated when subjects were heat stressed (normothermia: Δ25.6 ± 2.3, heat stress: Δ13.4 ± 3.0 mmHg; P < 0.001). The results demonstrate that heat stress can attenuate the pressor response to a sympathoexcitatory stimulus.

Influence of noninvasive peripheral arterial blood pressure measurements on assessment of dynamic cerebral autoregulation

2007 ◽  
Vol 103 (1) ◽  
pp. 369-375 ◽  
Author(s):  
Emily L. Sammons ◽  
Nilesh J. Samani ◽  
Stephen M. Smith ◽  
Wendy E. Rathbone ◽  
Steve Bentley ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Transfer Function ◽  
Arterial Blood Pressure ◽  
Cerebral Autoregulation ◽  
Aortic Pressure ◽  
Step Response ◽  
Pressure Measurements ◽  
Arterial Blood ◽  
Surface Ecg ◽  
Dynamic Cerebral Autoregulation

Assessment of dynamic cerebral autoregulation (CA) requires continuous recording of arterial blood pressure (ABP). In humans, noninvasive ABP recordings with the Finapres device have often been used for this purpose. We compared estimates of dynamic CA derived from Finapres with those from invasive recordings in the aorta. Measurements of finger noninvasive ABP (Finapres), intra-aortic ABP (Millar catheter), surface ECG, transcutaneous CO2, and bilateral cerebral blood flow velocity (CBFV) in the middle cerebral arteries were simultaneously and continuously recorded in 27 patients scheduled for percutaneous coronary interventions. Phase, gain, coherence, and CBFV step response from both the Finapres and intra-arterial catheter were estimated by transfer function analysis. A dynamic autoregulation index (ARI) was also calculated. For both hemispheres, the ARI index and the CBFV step response recovery at 4 s were significantly greater for the Finapres-derived estimates than for the values obtained from aortic pressure. The transfer function gain for frequencies <0.1 Hz was significantly smaller for the Finapres estimates. The phase frequency response was significantly greater for the Finapres estimates at frequencies >0.1 Hz, but not at lower frequencies. The Finapres gives higher values for the efficiency of dynamic CA compared with values derived from aortic pressure measurements, as indicated by biases in the ARI index, CBFV step response, gain, and phase. Despite the significance of these biases, their relatively small amplitude indicates a good level of agreement between indexes of CA derived from the Finapres compared with corresponding estimates obtained from invasive measurements of aortic ABP.

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