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Human Cardiovascular Responses to Passive Heat Stress

Craig G. Crandall, Thad E. Wilson

10.1002/cphy.c140015

Source: Volume 5, Issue 1, January 2015

Published online: December 2014

Full Article on Wiley Online Library



Abstract

Heat stress increases human morbidity and mortality compared to normothermic conditions. Many occupations, disease states, as well as stages of life are especially vulnerable to the stress imposed on the cardiovascular system during exposure to hot ambient conditions. This review focuses on the cardiovascular responses to heat stress that are necessary for heat dissipation. To accomplish this regulatory feat requires complex autonomic nervous system control of the heart and various vascular beds. For example, during heat stress cardiac output increases up to twofold, by increases in heart rate and an active maintenance of stroke volume via increases in inotropy in the presence of decreases in cardiac preload. Baroreflexes retain the ability to regulate blood pressure in many, but not all, heat stress conditions. Central hypovolemia is another cardiovascular challenge brought about by heat stress, which if added to a subsequent central volumetric stress, such as hemorrhage, can be problematic and potentially dangerous, as syncope and cardiovascular collapse may ensue. These combined stresses can compromise blood flow and oxygenation to important tissues such as the brain. It is notable that this compromised condition can occur at cardiac outputs that are adequate during normothermic conditions but are inadequate in heat because of the increased systemic vascular conductance associated with cutaneous vasodilation. Understanding the mechanisms within this complex regulatory system will allow for the development of treatment recommendations and countermeasures to reduce risks during the ever‐increasing frequency of severe heat events that are predicted to occur. © 2015 American Physiological Society. Compr Physiol 5:17‐43, 2015.

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Figure 1. Figure 1. Typical cardiovascular responses to whole‐body passive heat stress in humans. Figure modified, with permission, from Rowell (211).
Figure 2. Figure 2. Panel A denotes hypothetical cardiac nodal action potential changes as nodal cell temperatures increases. Note the narrower duration of the action potential waveform and the steeper Phase 4. Panel B depicts redrawn data from rabbit sinus arterial nodal cell action potential durations as a function of nodal cell temperature. Modified, with permission, from Yamagishi & Sano (270).
Figure 3. Figure 3. Regression analysis between central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) at baseline and two lower body negative pressures (LBNP; 15 and 30 mmHg). The strength of relationships and regression equations were r = 0.93, P < 0.001, PCWP = 1.1 × CVP + 2.3 for normothermia and r = 0.81, P < 0.001, PCWP = 1.1 × CVP + 2.1 for whole‐body heating. The black line refers to the line of identity and the grey lines refer to 95% confidence interval. Modified, with permission, from Wilson et al. (266).
Figure 4. Figure 4. Schematic of the effect of thermal stress on the Frank‐Starling relations. (A) Normothermia Frank‐Starling relation with the labeled point being the operating point in the supine position. (B) Heat stress induced changes in the Frank‐Starling relations, as well as the location of the supine operating points on those curves. This figure also highlights slope changes where a similar decrease in pulmonary capillary wedge pressure would cause a relatively large decrease in stroke volume during heat stress compared to normothermia. Figure modified, with permission, from Wilson & Crandall (260).
Figure 5. Figure 5. Peak septal and lateral mitral annular systolic velocities (S′). Individual (left) and group averaged (right) echocardiographic measurements of peak septal mitral annular systolic velocity (A) and peak lateral mitral annular systolic velocity (B) during normothermia (NT) and whole‐body heating (WBH) conditions. Septal annular and lateral annular systolic velocities were increased during heat stress relative to normothermia, indicative of an increase in cardiac systolic function. Group data are means ± SD. Figure, with permission, from Brothers et al. (14).
Figure 6. Figure 6. Effects of heat‐stress on Frank‐Starling curves by expressing the relation between pulmonary capillary wedge pressure and stroke volume during normothermia, heat stress, and heat stress plus volume loading. Data were obtained prior to lower‐body negative pressure (LBNP) and subsequent 15 and 30 mmHg LBNP for each of the indicated conditions. The arrows indicate pre‐LBNP responses (i.e., operating point) for each thermal condition. The operating point is the prevailing pulmonary capillary wedge pressure and stroke volume prior to the onset of LBNP. Lines represent fitted approximations. Figure modified, with permission, from Bundgaard‐Nielsen et al. (21).
Figure 7. Figure 7. Hypothetical model of blood volume distribution as a result of heat stress. Increases in cutaneous blood volume associated with heat stress are partially offset by reductions in splanchnic and renal (not shown) blood volumes secondary to vasoconstriction within these beds. However, the net effect is a reduction in central blood volume (CBV). RV: Right ventricle, LV: Left ventricle, VC: Vasoconstriction. Figure modified, with permission, from Rowell (212).
Figure 8. Figure 8. Representative cross‐sectional Positive Emission Tomography images from mid‐calf during normothermic baseline, local heating, during whole body heating. Note that the water‐perfused suit used to heat the subjects was exposed to only one leg (suit covered calf), and thus the direct and the indirect effects of the applied heat stress were evaluated. Increases in muscle blood flow were only identified from the leg which was covered by the water perfused suit during both the local heating and whole body heating protocols. Figure, with permission, from Heinonen et al. (81).
Figure 9. Figure 9. Effects of whole body heat stress on blood velocity from the middle cerebral artery. Notice the degree of heterogeneity of the response amongst these 25 observations. *Significantly different from normothermia. Figure adapted, with permission, from Wilson et al. (264).
Figure 10. Figure 10. Carotid‐vascular baroreflex responses in normothermia (solid line and circles) and heat stress (dashed lines and squares). The upper panel depicts the averaged baroreflex curves while the lower panel shows the gain of the respective curves in both thermal conditions. Heat stress significantly reduced the gain of the carotid‐vascular baroreflex. Figure adapted, with permission, from Crandall (32).
Figure 11. Figure 11. Blood pressure (BP), heart rate (HR), and mouth pressure responses to a Valsalva maneuver while in normothermic and heat stressed conditions from one subject. The phases of the Valsalva are indicated. Notice the distinctly lower phases IIa and IIb while subjects are heat stressed. Figure adapted, with permission, from Davis et al. (50).
Figure 12. Figure 12. Effects of whole‐body heat stress on changes in mean arterial pressure (MAP) during steady‐state infusions of the α1 agonist phenylephrine. Values are reported relative to a pre‐drug baseline MAP. The magnitude of the elevation in MAP to systemic phenylephrine infusion as attenuated by heat stress. Figure adapted, with permission, from Cui et al. (48).
Figure 13. Figure 13. Tolerance probability curves for lower‐body negative pressure (LBNP) trials while subjects were normothermic (NT day—solid line), whole‐body heat stressed (WBH day—black dashed line), and heat stress with accompanying volume infusion (gray dashed line). Heat stress significantly attenuated the capability to withstand LBNP challenge, whereas this response was preserved when subjects were heat stressed with accompanying rapid volume expansion. Figure adapted, with permission, from Keller et al. (106).
Figure 14. Figure 14. Scintigraphic images from a subject during normothermia, with and without 30 mmHg lower‐body negative pressure (LBNP), and heat stressed, with and without 30 mmHg LBNP. Changes in blood volume to the respective challenges are depicted by changes in the density of the images within particular regions (e.g., the heart), after accounting for isotope decay, attenuation correction, and hematocrit changes associated with the imposed conditions. The magnitude of the reduction in this index of central blood volume to 30 mmHg LBNP was appreciably greater when subjects were heat stressed, relative to normothermic. Figure adapted, with permission, from Crandall et al. (37).
Figure 15. Figure 15. Systemic vascular resistance, cardiac output, and mean arterial pressure responses at normothermia, after internal temperature increased ∼0.7 and 1.2°C via whole‐body heating, an during simulated hemorrhage (via LBNP) to presyncope. Notice the relative absence of a change in systemic vascular resistance during simulated hemorrhage despite profound reductions in arterial blood pressure. Also notice that a cardiac output to maintain arterial blood pressure while normothermic (∼7 L/min) is no longer sufficient when individuals are heat stressed. †Significantly different from heat stress (i.e., 1.2°C elevation in internal temperature); *significantly different from normothermia. Figure is adapted, with permission, from Ganio et al. (72).
Figure 16. Figure 16. Upper panel: Mean arterial blood pressure during normothermia, heat stress just prior to the onset of lower‐body negative pressure (LBNP) or upright tilt, and the final 100 sec of LBNP or upright tilt due to syncopal signs and/or symptoms. Lower Panel: Cutaneous vascular conductance at the same time points as arterial blood pressure. Note that despite profound hypotension leading up to and at presyncope, very little reductions in cutaneous vascular conductance occurred. *Significantly different from normothermia. ¥Significantly different from heat stress just prior to LBNP/upright tilt. Data adapted, with permission, from Crandall et al. (36).
Figure 17. Figure 17. Cerebral blood velocity from the middle cerebral artery (MCAvmean) and calculated cerebrovascular conductance (CBVC) during heat stress and lower‐body negative pressure (LBNP) where subjects inhaled either a hypercapnic gas mixture (solid squares) or room air (open circles—Sham). Notice that at tolerance, both MCAvmean and CBVC were significantly elevated with during the hypercapnic trial relative to the Sham trial. ‡Significantly different from Sham trial; 1Significantly different from 0 mmHg LBNP; 2Significantly different from 20 mmHg LBNP. Figure adapted, with permission, from Lucas et al. (142).


Figure 1. Typical cardiovascular responses to whole‐body passive heat stress in humans. Figure modified, with permission, from Rowell (211).


Figure 2. Panel A denotes hypothetical cardiac nodal action potential changes as nodal cell temperatures increases. Note the narrower duration of the action potential waveform and the steeper Phase 4. Panel B depicts redrawn data from rabbit sinus arterial nodal cell action potential durations as a function of nodal cell temperature. Modified, with permission, from Yamagishi & Sano (270).


Figure 3. Regression analysis between central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) at baseline and two lower body negative pressures (LBNP; 15 and 30 mmHg). The strength of relationships and regression equations were r = 0.93, P < 0.001, PCWP = 1.1 × CVP + 2.3 for normothermia and r = 0.81, P < 0.001, PCWP = 1.1 × CVP + 2.1 for whole‐body heating. The black line refers to the line of identity and the grey lines refer to 95% confidence interval. Modified, with permission, from Wilson et al. (266).


Figure 4. Schematic of the effect of thermal stress on the Frank‐Starling relations. (A) Normothermia Frank‐Starling relation with the labeled point being the operating point in the supine position. (B) Heat stress induced changes in the Frank‐Starling relations, as well as the location of the supine operating points on those curves. This figure also highlights slope changes where a similar decrease in pulmonary capillary wedge pressure would cause a relatively large decrease in stroke volume during heat stress compared to normothermia. Figure modified, with permission, from Wilson & Crandall (260).


Figure 5. Peak septal and lateral mitral annular systolic velocities (S′). Individual (left) and group averaged (right) echocardiographic measurements of peak septal mitral annular systolic velocity (A) and peak lateral mitral annular systolic velocity (B) during normothermia (NT) and whole‐body heating (WBH) conditions. Septal annular and lateral annular systolic velocities were increased during heat stress relative to normothermia, indicative of an increase in cardiac systolic function. Group data are means ± SD. Figure, with permission, from Brothers et al. (14).


Figure 6. Effects of heat‐stress on Frank‐Starling curves by expressing the relation between pulmonary capillary wedge pressure and stroke volume during normothermia, heat stress, and heat stress plus volume loading. Data were obtained prior to lower‐body negative pressure (LBNP) and subsequent 15 and 30 mmHg LBNP for each of the indicated conditions. The arrows indicate pre‐LBNP responses (i.e., operating point) for each thermal condition. The operating point is the prevailing pulmonary capillary wedge pressure and stroke volume prior to the onset of LBNP. Lines represent fitted approximations. Figure modified, with permission, from Bundgaard‐Nielsen et al. (21).


Figure 7. Hypothetical model of blood volume distribution as a result of heat stress. Increases in cutaneous blood volume associated with heat stress are partially offset by reductions in splanchnic and renal (not shown) blood volumes secondary to vasoconstriction within these beds. However, the net effect is a reduction in central blood volume (CBV). RV: Right ventricle, LV: Left ventricle, VC: Vasoconstriction. Figure modified, with permission, from Rowell (212).


Figure 8. Representative cross‐sectional Positive Emission Tomography images from mid‐calf during normothermic baseline, local heating, during whole body heating. Note that the water‐perfused suit used to heat the subjects was exposed to only one leg (suit covered calf), and thus the direct and the indirect effects of the applied heat stress were evaluated. Increases in muscle blood flow were only identified from the leg which was covered by the water perfused suit during both the local heating and whole body heating protocols. Figure, with permission, from Heinonen et al. (81).


Figure 9. Effects of whole body heat stress on blood velocity from the middle cerebral artery. Notice the degree of heterogeneity of the response amongst these 25 observations. *Significantly different from normothermia. Figure adapted, with permission, from Wilson et al. (264).


Figure 10. Carotid‐vascular baroreflex responses in normothermia (solid line and circles) and heat stress (dashed lines and squares). The upper panel depicts the averaged baroreflex curves while the lower panel shows the gain of the respective curves in both thermal conditions. Heat stress significantly reduced the gain of the carotid‐vascular baroreflex. Figure adapted, with permission, from Crandall (32).


Figure 11. Blood pressure (BP), heart rate (HR), and mouth pressure responses to a Valsalva maneuver while in normothermic and heat stressed conditions from one subject. The phases of the Valsalva are indicated. Notice the distinctly lower phases IIa and IIb while subjects are heat stressed. Figure adapted, with permission, from Davis et al. (50).


Figure 12. Effects of whole‐body heat stress on changes in mean arterial pressure (MAP) during steady‐state infusions of the α1 agonist phenylephrine. Values are reported relative to a pre‐drug baseline MAP. The magnitude of the elevation in MAP to systemic phenylephrine infusion as attenuated by heat stress. Figure adapted, with permission, from Cui et al. (48).


Figure 13. Tolerance probability curves for lower‐body negative pressure (LBNP) trials while subjects were normothermic (NT day—solid line), whole‐body heat stressed (WBH day—black dashed line), and heat stress with accompanying volume infusion (gray dashed line). Heat stress significantly attenuated the capability to withstand LBNP challenge, whereas this response was preserved when subjects were heat stressed with accompanying rapid volume expansion. Figure adapted, with permission, from Keller et al. (106).


Figure 14. Scintigraphic images from a subject during normothermia, with and without 30 mmHg lower‐body negative pressure (LBNP), and heat stressed, with and without 30 mmHg LBNP. Changes in blood volume to the respective challenges are depicted by changes in the density of the images within particular regions (e.g., the heart), after accounting for isotope decay, attenuation correction, and hematocrit changes associated with the imposed conditions. The magnitude of the reduction in this index of central blood volume to 30 mmHg LBNP was appreciably greater when subjects were heat stressed, relative to normothermic. Figure adapted, with permission, from Crandall et al. (37).


Figure 15. Systemic vascular resistance, cardiac output, and mean arterial pressure responses at normothermia, after internal temperature increased ∼0.7 and 1.2°C via whole‐body heating, an during simulated hemorrhage (via LBNP) to presyncope. Notice the relative absence of a change in systemic vascular resistance during simulated hemorrhage despite profound reductions in arterial blood pressure. Also notice that a cardiac output to maintain arterial blood pressure while normothermic (∼7 L/min) is no longer sufficient when individuals are heat stressed. †Significantly different from heat stress (i.e., 1.2°C elevation in internal temperature); *significantly different from normothermia. Figure is adapted, with permission, from Ganio et al. (72).


Figure 16. Upper panel: Mean arterial blood pressure during normothermia, heat stress just prior to the onset of lower‐body negative pressure (LBNP) or upright tilt, and the final 100 sec of LBNP or upright tilt due to syncopal signs and/or symptoms. Lower Panel: Cutaneous vascular conductance at the same time points as arterial blood pressure. Note that despite profound hypotension leading up to and at presyncope, very little reductions in cutaneous vascular conductance occurred. *Significantly different from normothermia. ¥Significantly different from heat stress just prior to LBNP/upright tilt. Data adapted, with permission, from Crandall et al. (36).


Figure 17. Cerebral blood velocity from the middle cerebral artery (MCAvmean) and calculated cerebrovascular conductance (CBVC) during heat stress and lower‐body negative pressure (LBNP) where subjects inhaled either a hypercapnic gas mixture (solid squares) or room air (open circles—Sham). Notice that at tolerance, both MCAvmean and CBVC were significantly elevated with during the hypercapnic trial relative to the Sham trial. ‡Significantly different from Sham trial; 1Significantly different from 0 mmHg LBNP; 2Significantly different from 20 mmHg LBNP. Figure adapted, with permission, from Lucas et al. (142).
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Article Title: Human Cardiovascular Responses to Passive Heat Stress
 

How to Cite

Craig G. Crandall, Thad E. Wilson. Human Cardiovascular Responses to Passive Heat Stress. Compr Physiol 2014, 5: 17-43. doi: 10.1002/cphy.c140015