Current Heart Failure Reports

, Volume 11, Issue 2, pp 139–145

Cardiovascular Responses to Heat Stress in Chronic Heart Failure


  • Jian Cui
    • Penn State Hershey Heart and Vascular Institute, H047, Milton S. Hershey Medical CenterPennsylvania State University College of Medicine
    • Penn State Hershey Heart and Vascular Institute, H047, Milton S. Hershey Medical CenterPennsylvania State University College of Medicine
Pathophysiology: Neuroendocrine, Vascular, and Metabolic Factors (SD Katz, Section Editor)

DOI: 10.1007/s11897-014-0191-y

Cite this article as:
Cui, J. & Sinoway, L.I. Curr Heart Fail Rep (2014) 11: 139. doi:10.1007/s11897-014-0191-y


Clinical reports have suggested that patients with heart diseases may be particularly vulnerable to heat injury. This review examines the effects of heat stress on cardiovascular and autonomic functions in patients with chronic heart failure (CHF). Laboratory investigations have shown that cutaneous vasodilator responses to heating are impaired in patients, whereas activation of skin sympathetic nerve activation is not attenuated in CHF as compared to controls. Attenuated cutaneous vasodilation may increase the risk of a heat related illness when CHF subjects are exposed to hyperthermic conditions.


Heart failureAutonomic controlThermoregulationSkin blood flowSkin sympathetic nerve activityCutaneous vasodilationHeat stress


Healthy individuals have a great capacity to withstand exposure to a hot environment and are able to survive increases in internal temperature of up to ~3 °C. However, many clinical reports demonstrate that thermal tolerance to heat stress is impaired in patients with cardiovascular diseases. In particular, cardiovascular conditions associated with ventricular dysfunction and chronic heart failure (CHF) are predisposed to heat intolerance. Elevations in skin blood flow (SkBF) and sweating are the primary heat exchange mechanisms in humans that protect against heat-related injury. These heat-dissipating responses are accompanied by critical cardiovascular adjustments, which are under autonomic control. If these adjustments are ineffectual, then thermal regulation can be compromised during exercise and/or exposure to elevated environmental temperatures. Thus, the severely impaired cardiovascular and autonomic function in CHF could contribute to heat intolerance. On the other hand, heat exposure, as a stimulus to the cardiovascular system, has been suggested as a therapeutic intervention in patients with cardiovascular diseases including CHF. The objective of this article is to present findings pertaining to cardiovascular and autonomic responses associated with passive heat stress in CHF.

Patients with Cardiovascular Diseases in Heat Waves or Summer

Heat waves defined as a period of abnormally and uncomfortably hot and (usually) humid weather are associated with death and injury especially in those with prior medical conditions such as heart failure or hypertension [1, 2]. A classic example of the increased risk of heat stress was the 1995 Chicago heat wave in which 700 “excess” deaths were reported. Of the deaths investigated, 39 % had a prior “heart condition” [1]. The 2003 heat wave in Europe caused many thousands of “excess” deaths [35]. The 2006 heat wave in California also caused a large number of deaths and heat injuries [6]. Of note, the excess mortality associated with a heat wave increases with age [4].

In contrast to the effects of an acute period of extreme heat, the epidemiological evidence regarding seasonal effects of temperature is controversial. Some reports show that the adverse cardiac events occur at a higher frequency during summer months than spring and autumn [79]. In contrast, other reports suggest a lower hospitalization rate and a lower prevalence of mortality for CHF patients in summer than in winter [10, 11•]. In general, blood pressure tends to be lower in the summer than in the winter and/or the spring, and this effect is most prominent in the elderly [12, 13]. We speculate these seemingly contradictory observations are due to a variety of different factors (e.g., the level and length of the heat exposure), which must be viewed with each other. Therefore, well-controlled and monitored laboratory investigations into passive heat stress have greatly added to our understanding of heat-induced illness and deaths in patient populations.

Typically, laboratory investigators have utilized a variety of methods to evoke passive heat stress. Specific approaches may employ climatic chambers; total body or limb water immersion; or using water-perfused suits, in which hot water is perfused through a tube-lined suit worn by human volunteers. In all cases, an elevation in skin temperature is the primary stimulus by which internal temperature is raised.

Cardiovascular and Autonomic Responses to Passive Heating in Healthy Individuals

When individuals are exposed to a hot environment, core temperature rises and heat must be transferred to the environment. This necessitates a marked increase in SkBF. Specifically SkBF is estimated to increase from 300 mL/min in thermo-neutral conditions to upwards of 7,500 mL/min [14, 15] or from 5-10 to 50-70 % of total cardiac output [16]. In order to maintain arterial blood pressure in the presence of such an impressive cutaneous vasodilation, cardiac output must increase (e.g., up to 13 L/min in healthy individuals [14, 15]) and flow to noncutaneous beds must decrease. The increase in cardiac output is due mainly to an increase in heart rate as stroke volume remains constant or rises by roughly 10 % or less in young healthy heat-stressed subjects [1719]. The redistribution of blood flow to the skin is accomplished in part by reduction in splanchnic and renal blood flow [15, 20, 21]. Passive whole body heating has been reported to have little effect on muscle blood flow [2225]. This occurs in the face of significant elevations in muscle sympathetic nerve activity (MSNA) [2630]. Thus, the individual is functioning in what has been termed a “hyperadrenergic state” [18, 31]. Considering that local (limb) heating increases muscle blood flow [22] (i.e., the direct effect of heating), and alpha-adrenergic vasoconstrictor responsiveness is preserved [32], MSNA activation evoked by whole body heating is a crucial determinant of flow distribution seen with heat stress. In young healthy individuals, the increases in SkBF, cardiac output and the reduction in splanchnic flow results in either no change, or only minimal reductions in arterial blood pressure [27, 29, 3337].

Autonomic control of SkBF occurs via skin sympathetic nerve activity (SSNA), which includes vasoconstrictor, vasodilator and sudomotor activities. Sympathetic vasoconstrictor nerve activity leads to the release of norepinephrine and subsequent cutaneous vasoconstriction [16, 38, 39]. This vasoconstrictor component is engaged in response to cold and thermal neutral conditions [40]. The second system is a non-adrenergic sympathetically mediated vasodilator system that is engaged in warm environments [14, 16, 41, 42]. Classic studies [41, 43] demonstrate that human skin is innervated by sympathetic vasodilator nerves, since nerve blockade prevents large increases in SkBF seen with core hyperthermia in the absence of nerve blockade. However, it has never been possible to definitively confirm the specific pathways and processes involved in the skin sympathetic dilator response seen in human subjects [44]. It has been hypothesized that cholinergic sudomotor nerve activity [45] or a co-transmitter system [44, 46] are involved in the cutaneous active vasodilation, although the precise systems involved in this process remain unknown. Upon exposure to a warm/hot environment and/or exercise, the initial increase in SkBF occurs via withdrawal of the cutaneous vasoconstrictor activity [35, 47]. As internal temperature continues to increase, an active cutaneous vasodilator system is engaged [16], and accounts for 85–95 % of the rise in SkBF in hairy skin during whole-body heating [16]. Thus, a functioning cutaneous sympathetic active vasodilator system is vital for appropriate thermoregulatory responses seen during heat exposure. Moreover, a functioning sudomotor (i.e., sweating) system is absolutely necessary in order for human subjects to effectively respond to heat exposure. Under hyperthermic conditions, sudomotor/vasodilator activity is the predominant component in SSNA discharge [38, 40], and less cutaneous vasoconstrictor activity is detected in healthy individuals [38].

SkBF Response to Heat Stress in CHF

To examine the thermoregulatory responses to whole body heat stress in patients with CHF, Cui et al. [48] assessed cutaneous vasodilation in 13 patients with stable class II–III CHF and in 13 matched healthy subjects during passive whole-body heating with a water-perfused suit. Forearm SkBF was measured from an area not covered by the tube-lined suit with laser-Doppler probes. The SkBF was also measured via venous occlusion plethysmography. Previous studies suggested that the increase in forearm blood flow during passive heat stress is predominately due to increases in SkBF [2325]. Whole body heating induced a similar increase in skin (~4 °C) and internal temperature (~0.85 °C) in the two groups. Of note, the heat induced elevation in forearm SkBF and cutaneous vascular conductance (CVC) was much less in the CHF subjects than in the control subjects. In fact, the increase in CVC was less than half as great in CHF as in the control subjects. Additionally, the slope of the relationship between the elevations in forearm CVC and the elevation in internal temperature was reduced in patients with CHF relative to control subjects. The maximal cutaneous vasodilator capacity to direct local heating in patients with CHF was also significantly lower than that in control subjects. However, the impaired cutaneous vasodilator response to whole body heat stress was not due to a vasodilatory ceiling effect. These results suggest that patients with CHF exhibit an attenuated cutaneous dilator response to heat stress; this is a result that is consistent with observations of Green and colleagues [49]. We posit that the attenuated cutaneous vasodilation occurs as part of an integrated response designed to prevent a reduction in blood pressure in patients with CHF who have limited cardiac output reserve. We further suggest that the tendency to protect blood pressure makes CHF patients particularly sensitive to heat injury.

SSNA Response to Heat Stress in CHF

It is well known that autonomic control is impaired in CHF patients [50] yet resting SSNA is similar [5153] in CHF and control subjects. To examine if the neural control of the cutaneous circulation in heat stress is altered in CHF, Cui and colleagues assessed SSNA during passive whole body heating in nine patients with stable class II-III CHF and in matched healthy subjects. Whole body heating induced similar increases in skin (~4 °C) and internal (~0.6 °C) temperature in the two groups. Consistent with previous observations [48, 49], the elevation in forearm CVC in patients with CHF was significantly lower than that in healthy control subjects. However, whole body heat stress evoked similar SSNA activation in CHF patients and the control subjects (Fig. 1). Thus, SSNA activation during a modest whole body heat stress is not attenuated in CHF.
Fig. 1

Mean skin sympathetic nerve activity (SSNA), cutaneous vascular conductance (CVC), and sweat rate (SR) responses to whole body heating. During the initial period of heating, mean skin temperature (Tsk) increased, but the internal temperature (Tcore) did not rise. In the later period of whole-body heating, Tsk was clamped at ~38 °C, whereas the Tcore increased. Mean body temperature (Tbody) was calculated as follows: 0.9*Tcore + 0.1*Tsk. CHF indicates chronic heart failure (From Cui J, et al., “Chronic Heart Failure Does Not Attenuate the Total Activity of Sympathetic Outflow to Skin During Whole-Body Heating,” Circ Heart Fail., 2013;6: 271–278, with permission from the American Heart Association)

We are surprised by these results since skin dilation is neurally mediated [16]. We suspect these results suggest that no-SSNA components of the dilatory response are abnormal. For example, whether CHF was due to a difference in sweating capacity in CHF and controls, we compared CVC at the same sweat rates in the two groups and found that, for a given sweat rate, CVC was much lower in CHF than in controls. These data support the concept that for a given level cholinergic nerve activity [45], cutaneous vasodilator responses are attenuated in CHF. Studies are necessary to further identify the determinants of the impaired dilatory response in CHF [38].

Roles of Endothelial Dysfunction of CHF in Heat Stress

Endothelium-dependent vasodilation plays a key role in vasodilatory response, while it is known that CHF induces endothelial dysfunction. The maximal peripheral vasodilator responses to forearm ischemia (the reactive hyperemia response) are known to be impaired in CHF [54, 55]. Structural changes in the cutaneous vasculature are seen in CHF [56]. CHF impairs endothelium-dependent vasodilation of the peripheral circulation [5759] including skin [60] and nitric oxide production, and reduces the vascular responsiveness to nitric oxide [57, 61, 62]. The local heating induced cutaneous vasodilation was attenuated in patients with CHF [48], while sustained local heating causes cutaneous vasodilation via nitric oxide dependent mechanisms [63, 64]. Green and colleagues have shown a significant nitric oxide contribution to heat-induced skin vasodilation in control subjects, but not in CHF patients [49]. Studies have shown that ~30 % of the elevation in CVC during indirect whole-body heating is mediated by nitric oxide-dependent mechanisms [65, 66]. Thus, the impaired SkBF response to whole body heating observed in CHF patients may be in part explained by impaired nitric oxide function [58, 67].

Sweating Response in CHF

Whole body heating induces significant sweating responses in CHF patients [48], while the sweat rate toward the end of the moderate whole body heating in CHF patients was marginally lower (~20 %) than the control subjects [48, 68•]. It should be noted that in CHF patients both SSNA and sweat rate increased during the initial period of whole body heating (e.g., internal temperature increase ~0.2–0.3 °C), while neither increased in healthy controls during this period [68•]. These data support the clinical observation of excessive sweating in CHF patients when they perform simple activities of daily living. Prior clinical reports have suggested that an increased sweating rate may be an important symptom in CHF [69]. Sweat function in CHF patients is an area that should be further examined and understood.

Possible Roles of Pharmacologic Therapy on the Impaired Responses to Heat Stress

Of note, all patients in the studies described above [48, 49, 68•] were receiving a variety of vasoactive medications. Specifically, most patients were receiving beta-blockers as per clinical guidelines. Beta-blockers have been shown to attenuate the cutaneous vasodilator response seen with exercise. Thus, it is possible that the impaired cutaneous dilation seen in CHF with heat stress could have been due to beta-blockers. However, we noted impaired cutaneous dilation in CHF patients not on beta-blockers [48]. It is also possible that beta-blockers might alter the subject sweat rates [70]. However, studies performed in healthy subjects do not paint a consistent picture of the effects of blocking a sweat rate. [7072].

Whatever the mechanism, it is important to understand that CHF patients are at a higher risk for heat stress related injury due to altered cutaneous vasodilation responses.

Cardiac Function During Heat Stress in CHF, and Possible “Thermal Therapy”

During heat stress, cardiac output must rise so that cutaneous beds remain perfused [15, 16]. This increase in cardiac output is associated with increased ejection fraction and tissue Doppler determinants of systolic function [73, 74], presumably these findings are due to a direct inotropic effect of heat stress [15, 16]. Heat stress also decreases ventricular filling pressures [18, 19, 75, 76] and central blood volume [73]. Of note, heat stress does not appear to alter diastolic function [74].

We pose the question of whether cutaneous vasodilation evoked by heat exposure may decrease afterload, and in turn improve vasodilatory response to stress. In CHF, reductions in cardiac output lead to an increase in vascular resistance, which over time may adversely affect the ability of the peripheral vascular to dilate in response to heat and exercise stress. We raise the possibility that warm temperatures may beneficially affect peripheral resistance and cardiac output in CHF subjects. We further wonder whether these beneficial effects of temperate warmth are responsible for lower death rates during summer months [10, 11•]. Others have previously suggested that thermal therapy (e.g., warm water baths, sauna or dry sauna, etc.) can be considered in CHF subjects [77•, 7883]. Some have suggested that this approach increases cardiac output [81] and ejection fraction [77•], improves left ventricular function [77•, 83], improves endothelial function [79, 80, 84, 85], and improves the quality of life in CHF [78]. This type of beneficial modest thermal intervention has been termed “hormesis” [86, 87]. We believe controlled physiologic studies are needed to better understand heat therapy in CHF.

Conclusions and Future Directions

In conclusion, cutaneous vasodilator and sweating responses to heat stress are impaired in patients with CHF. Interestingly, modest whole body heat stress does not evoke an attenuated SSNA response in CHF patients. Attenuated cutaneous vasodilation may represent an intrinsic vascular abnormality. Whatever the cause, it is clear that heat waves increase the risk of cardiac illness. Against this background, it is also important to note that modest heat exposure might be beneficial in patients with cardiac disease. Heat therapy will need to be understood and tested in subjects with CHF.

Compliance with Ethics Guidelines

Conflict of Interest

Jian Cui and Lawrence I. Sinoway declare that they have no conflict of interest.

Human and Animal Rights and Informed Consent

This article does not contain any new studies with human or animal subjects performed by any of the authors.

Copyright information

© Springer Science+Business Media New York 2014