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Effect of temperature and stress on heart

Heat and cold stress have direct impact on many of the fundamental control mechanisms of stroke volume such as preload, afterload, diastolic function or compliance, and systolic function or inotropy. 


Cardiac output increases during whole-body heating but does not significantly change during whole-body cooling. In contrast, stroke volume is maintained or slightly increased by both thermal stressors.


Whole-body heating decreases right-sided preload (right atrial pressure and central venous pressure, as well as left-sided preload (left-ventricular end diastolic volume and pulmonary capillary wedge pressure. In healthy animals exposed to heat stress, right- and left-sided preload decrease by a similar magnitude. This indicates that central venous pressure can be used to predict changes in left-ventricular filling pressure during thermal stress

The reason for this decrease in preload during heat stress is likely multifactoral being related to blood volume distribution, cardiac output/venous return, and systemic vascular conductance. Heat stress increases cutaneous vascular volume and translocates blood volume out of the splanchnic, renal, and central reservoirs.

Cold stress marginally increases both right (central venous pressure; and left (pulmonary capillary wedge pressure; sided preload. In healthy humans, right- and left-sided preload increase by a similar magnitude and thus indicates that central venous pressure can be used to predict changes in left-ventricular filling pressure during cold stress.


Heat stress does not change or slightly decreases mean arterial pressure despite large increases in cardiac output, while systemic vascular conductance increases substantially due primarily to large increases in cutaneous vascular conductance.

Cold stress increases mean arterial pressure and decreases systemic vascular conductance. This increase in mean arterial pressure is related to decreases in vascular conductance in both glabrous and non-glabrous cutaneous vasculature, and in the brachial, renal, celiac, and superior mesenteric arteries.

Compliance and Diastolic Function

No significant alteration in left-ventricular compliance is observed during acute thermal perturbations, as represented when we express pulmonary capillary wedge pressure to left-ventricular end-diastolic volume


Heat stress decreases preload, yet stroke volume is maintained or slightly increased. Radionucleotide multi-gated acquisition and echocardiography data indicate increases in ejection fraction and isovolumic acceleration of the septal and lateral mitral annulus with the imposition of a heat stress


Cardiac output increases to values often well above 10 L•min?1 during whole-body heating. Because stroke volume is maintained or only slightly increased during heat stress, the increase in heart rate is the primary driving force behind these increases in cardiac output. The control and regulation of heart rate during heat stress may be related to:

1) direct effects of temperature on the sinoatrial node, and

2) sympathetic and parasympathetic effects on the heart due to either the baroreflexes or a global hyperadrenergic state. During cold stress heart rate does not significantly change.


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