Cardiovascular responses to sustained high skin temperature in resting man.

Rowell, L. B.; Brengelmann, G. L.; Murray, JF

doi:10.1152/jappl.1969.27.5.673

Cited by 238 publications

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“…These findings suggest that cardiac output has the potential of changing cerebral blood flow, independent of changes in steady-state perfusion pressure. Although not measured in the present study, cardiac output can more than double during passive heat stress, which is necessary to support heat stressinduced increases in skin blood flow (34). We have observed increases in cardiac output between 2 and 4 l/min during passive heat stress, similar to that in the present study (i.e., ϳ1.1°C increase in internal temperature, unpublished observation).…”

Section: Discussionsupporting

confidence: 85%

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Low

Wingo

Keller

et al. 2008

Journal of Applied Physiology

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CG. Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress. J Appl Physiol 104: 976-981, 2008. First published January 24, 2008 doi:10.1152/japplphysiol.01040.2007.-This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO2 (PETCO 2 ). Nine healthy subjects (4 men and 5 women), each dressed in a water-perfused suit, underwent normoxic hypocapnic hyperventilation (decrease PETCO 2 ϳ20 Torr) and normoxic hypercapnic (increase in PETCO 2 ϳ9 Torr) challenges under normothermic and passive heat stress conditions. The slope of the relationship between calculated cerebrovascular conductance (CBVC; middle cerebral artery blood velocity/mean arterial blood pressure) and PETCO 2 was used to evaluate cerebrovascular CO2 responsiveness. Passive heat stress increased core temperature (1.1 Ϯ 0.2°C, P Ͻ 0.001) and reduced middle cerebral artery blood velocity by 8 Ϯ 8 cm/s (P ϭ 0.01), reduced CBVC by 0.09 Ϯ 0.09 CBVC units (P ϭ 0.02), and decreased PETCO 2 by 3 Ϯ 4 Torr (P ϭ 0.07), while mean arterial blood pressure was well maintained (P ϭ 0.36). The slope of the CBVC-PET CO 2 relationship to the hypocapnic challenge was not different between normothermia and heat stress conditions (0.009 Ϯ 0.006 vs. 0.009 Ϯ 0.004 CBVC units/Torr, P ϭ 0.63). Similarly, in response to the hypercapnic challenge, the slope of the CBVC-PETCO 2 relationship was not different between normothermia and heat stress conditions (0.028 Ϯ 0.020 vs. 0.023 Ϯ 0.008 CBVC units/Torr, P ϭ 0.31). These results indicate that cerebrovascular CO2 responsiveness, to the prescribed steady-state changes in PETCO 2 , is unchanged during passive heat stress. brain blood flow; hyperthermia; hypocapnia; hypercapnia ORTHOSTATIC TOLERANCE IS REDUCED under heat stress, relative to normothermic, conditions (1,8,19,40,41). Although mechanisms responsible for reduced orthostatic tolerance during heat stress are unclear, they are likely associated with factors that directly or indirectly affect cerebral perfusion pressure, cerebral blood flow, and thus cerebral oxygenation (20, 24,38). Cerebral perfusion is very sensitive to changes in arterial carbon dioxide tension (Pa CO 2 ), such that increases in Pa CO 2 increase cerebral perfusion, whereas decreases in Pa CO 2 decrease cerebral perfusion (16, 36). Previously, our laboratory identified decreases in end-tidal carbon dioxide (PET CO 2 ; surrogate of Pa CO 2 ) of ϳ2 Torr in response to whole body passive heat stress, as well as significant reductions in cerebral perfusion and cerebral vascular conductance (40,41). Decreased cerebral perfusion would theoretically reduce the functional reserve by which cerebral blood flow can decrease further, before the onset of syncopal symptoms.It is unlikely that the relatively small decrease in PET CO 2 (i.e., ϳ2 Torr) in response to passive heat stress is the sole mechanism leading to the observed reduction in cerebral perfusion. However, this assumption is based on ca...

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Section: Discussionsupporting

confidence: 85%

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Low

Wingo

Keller

et al. 2008

Journal of Applied Physiology

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“…[7][8][9][10][11] In light of our results, we believe that although victims of heat stroke may have an appreciable total body fluid deficit, it seems that this is mainly at the expense of the intracellular compartment accounting for signs of dehydration while the intravascular compartment manages to keep an adequate circulating volume and avoids significant depletion. The low blood pressure in heat stroke, 12,13 in our experience, is due to low peripheral vascular resistance rather than to significant intravascular depletion or a low cardiac output.…”

Section: Discussionmentioning

confidence: 59%

Hemodynamic Changes and Intravascular Hydration State in Heat Stroke

et al. 1989

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Acute and serial hemodynamic measurements in 13 pilgrims (average age, 55.2 ± SD 9.3 years) suffering from heat stroke (average rectal temperature, 41.3 ± 1.0°C) revealed a hyperdynamic circulation pattern and a low total peripheral resistance. Five patients had pulmonary edema with an average cardiac index of 5.29 ± SD 0.56 L/min/m 2 , which was slightly higher than the average cardiac index in the group of eight patients without pulmonary edema, 4.76 ± SD 0.6 L/min/m 2 . This higher cardiac index was believed to be due to iatrogenic fluid overload which was hard to accommodate intravascularly with the cooling process raising the peripheral vascular resistance, decreasing the venous capacitance, and redistributing the blood from the dilated circulatory bed in the skin to the central circulation. Our data highlight the fact that there is no major intravascular dehydration in heat stroke. The treatment of choice is cooling. The entire process of "supporting the cardiovascular system" should take into consideration avoidance of fluid overload by rapid intravenous fluid administration. Gradual hydration, allowing time for intracellular compartment repletion after cooling, is more appropriate.

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“…Turkiye Klinikleri J Med Sci 2011;31 (2) 344 Çınar ve ark. Kardiyoloji FIGURE 3: Re la ti ons hip bet we en he art ra te and systo lic blo od pres su re in the arm.…”

Section: Chan Ging Blo Od Pres Su Re and He Art Ra Te With Tem Pe Ra unclassified

“…[1][2][3][4][5][6] In stress of cold en vi ron ment, pe rip he ric re sis tan ce in cre a ses du e to the cons tric ti on of skin ar te ri es and in cre a sed blo od vis co sity. 7 Ho we ver, cold angi na is exp la i ned by in cre a sed myo car di al oxy gen de mand, and cold we at her hyper ven ti la ti on can be used to di ag no se of va sos pas tic an gi na.…”

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confidence: 99%

“…Af ter that, the sub ject was ta ken in to the ex pe ri ment ro om that was cons tantly co o led to 15°C by an air con di ti o ner for one ho ur and af ter that, all the pa ra me ters we re me a su red aga in imme di a tely. Then, the air con di ti o ner was stop ped and the tem pe ra tu re of tho se sub jects was in cre a sed Turkiye Klinikleri J Med Sci 2011;31 (2) with in su la tor and he a ter ef fect of a 100-Watt/h (86.042 kcal/h) tra di ti o nal and stan dard elec tri cal blan ket up to the ir neck for one ho ur. Sub se quently, all the pa ra me ters we re me a su red aga in imme di a tely.…”

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confidence: 99%

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The Effect of Temperature Stress on Hemodynamics: The Mechanisms of Cold Angina, Heat Shock, Tachycardia of Fever and Compensatory Hypertension

Çinar¹,

Demirci²,

Kosku³

2011

Turkiye Klinikleri J Med Sci

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he major discussed effects of increased temperature on the circulatory system are the increased heart rate and vasodilation in the skin that causes heat loss. At rest, high temperature can markedly increTurkiye Klinikleri J Med Sci 2011;31(2) 341 The Effect of Temperature Stress on Hemodynamics: The Mechanisms of Cold Angina, Heat Shock, Tachycardia of Fever and Compensatory HypertensionA AB BS S T TR RA AC CT T O Ob bj je ec ct ti iv ve e: : The aim of the study is to in ves ti ga te the re la ti ons hips bet we en tem pe ra ture, blo od vis co sity and blo od flow ra te, he art ra te, blo od pres su re and pul se pres su re by using tempe ra tu re stress of co o ling and war ming on the blo od cir cu la tory system. M Ma a t te e r ri i a al l a an nd d M Me et t h ho od ds s: : The vo lun te er and he althy 36 ca ses we re se lec ted using the Simp le Ran dom Samp ling Met hod. The study gro up re ma i ned in a co o led ro om (15°C) for one ho ur and then we re al lo wed to warm up with an elec tric blan ked (100-watt) in the next pe ri od of one-ho ur. At the end of the se two pe riods, tem pe ra tu res of arm, leg and axil la, blo od pres su res, he art ra tes and blo od vis co si ti es of the sub jects we re me a su red im me di a tely. R Re e s su ul lt ts s: : The re sults sho wed that the re we re cli ni cally and statis ti cally im por tant re la ti ons hips among blo od pres su re, he art ra te, blo od vis co sity and pul se pressu res du ring tem pe ra tu re stress of co o ling and war ming (p= 0.001). Ho we ver, the pul se pres su res of he althy in di vi du als re ma i ned cons tant des pi te tem pe ra tu re stress re la ted systo lic and di as to lic pres su res chan ged at rest po si ti on, which may re sul ted from cir cu la tory com pen sa ti on. C Co on nc c l lu u s si i --o on n: : The system analy sis of the da ta and re la ti ons hip bet we en the pa ra me ters pro vi ded exp la na ti ons for mec ha nisms of cold an gi na, tach ycar di a of fe ver, he at shock, hyper ten si on and cir cu la tory burden ba sed on tem pe ra tu re stress and blo od vis co sity.K Ke ey y W Wo or rd ds s: : Blood viscosity; angina pectoris; cold temperature; hot temperature; vascular resistance Ö ÖZ ZE ET T A Am ma aç ç: : Ça lış ma nın ama cı, sı cak ve so ğuk or tam lar da ısı stre si uy gu la ya rak, sı cak lık, kan visko si te si ve kan akım hı zı, kalp hı zı, kan ba sın cı ve na bız ba sın cı ara sın da ki iliş ki le ri araş tır mak tır. G Ge e r re eç ç v ve e Y Yö ön n t te em m l le er r: : Sağ lık lı 36 de nek rast ge le ör nek le me yön te miy le se çi le rek ay dın la tıl mış onay la rı alın dı ve bir sa at sü rey le ısı sı 15°C olan or tam da ve da ha son ra bir sa at elek trik li bat ta ni ye (100-watt) al tın da ya ta rak bek le til di ler. Her iki süre nin hemen so nun da de nek le rin kol, ba cak ve ak sil la la rı nın sı cak lık la rı, kan ba sınç la rı, kalp hız la rı ve kan vis ko si te le ri öl çül dü. B Bu ul l g gu u l la ar r: : Be de ni so ğut ma ya ve ısıt ma ya bağ lı stres ler sı r...

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Cardiovascular responses to sustained high skin temperature in resting man.

Cited by 238 publications

References 0 publications

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Hemodynamic Changes and Intravascular Hydration State in Heat Stroke

The Effect of Temperature Stress on Hemodynamics: The Mechanisms of Cold Angina, Heat Shock, Tachycardia of Fever and Compensatory Hypertension

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