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“There are hills, rounded, blunt, burned, squeezed up out of chaos, chrome and vermilion painted, aspiring to the snow-line.”
With very basic introductions to heat transfer, the cardiovascular response to heat stress and the distinction between heat exhaustion and heatstroke, this final section addresses fundamental aspects of treating heat-related illness. These musings are certainly not authoritative and the reader is referred to these, excellent primary resources to imbibe, metabolize and produce his or her own neuronal heat.
Returning to the heat transfer equation, the ultimate goal when treating heat-related illness is to dissipate stored heat within the body – in other words, the clinician wants to point the value of S [i.e., stored heat] downwards. This is, very simply, achieved by reducing metabolic heat gain and increasing dry, evaporative and respiratory heat transfer. The urgency and vigour with which the clinician facilitates the aforementioned is dictated by the severity of the clinical presentation.
In the setting of heat exhaustion, relatively rapid therapy is essential to prevent progression to heatstroke. The patient should be rested to remove metabolic heat energy. Mechanisms to augment dry heat transfer from the patient include: loosening or removing insulating clothing or equipment, placing the patient upon a cool surface [i.e., conductive transfer], in a cool ambient temperature with ventilation [i.e., convective transfer] out of the sun [i.e., radiant transfer]. Misting the patient will help evaporative heat transfer and oral or intravenous hydration itself cools the patient, preserves blood flow to the skin and maintains sweating mechanisms. Additionally, some recommend laying the patient supine with legs raised to augment venous return and cardiac output but care should be taken if the patient is at risk for aspiration.
In conjunction with the basic principles of heat mitigation above, at risk organ systems such as the central nervous system and kidneys should be monitored. Electrolytes, and especially sodium, should be measured so as not to miss severe hyponatremia as a cause of central nervous dysfunction. Symptoms of heat exhaustion typically resolve relatively quickly.
When heatstroke is the diagnosis, rapid cooling should be instituted immediately, even in the prehospital setting; that is, ‘cool and run’ or ‘cool first, transport second’ rather than ‘scoop and run’ is endorsed. Rapid cooling is critical considering that mortality from classic or passive heatstroke in the elderly is greater than 50%, an order of magnitude greater than that of exertional heatstroke.
The aforementioned cooling mechanisms described for heat exhaustion may be employed for heatstroke though more aggressive external, conductive, immersion measures including cooling blankets, ice packs, or iced-water bath should be attempted. Notably, there are limitations to ice bath immersion including shivering and peripheral vasoconstriction when the skin temperature falls below 30 degrees C as well as bradycardia from the diving reflex and limited patient access especially in the setting of cardiac arrest. Nevertheless, in young, healthy patients suffering from acute, exertional heatstroke, cold water immersion is safe, effective and recommended with the goal of reducing core temperature by 0.20 to 0.35 degrees Celsius per minute. If ice is unavailable, large amounts of plain water poured over the body with fanning can reduce core body temperature by 0.1 degree Celsius per minute.
While iced-water bath immersion has been employed successfully in exertional heatstroke [e.g., young, healthy patients], it is poorly tolerated in classic heat stroke as it induces agitation and combativeness. Thus, experts in the field suggest other external conduction, convection and evaporation techniques in classic heatstroke such as ice packs, or coating the body in gauze wetted to room temperature with fanning. Internal, conductive cooling mechanisms such as infusions of chilled [i.e., 4 degrees Celsius] crystalloid, cooling catheters and even cooled extracorporeal circulation have been reported. There is no definitive core temperature target, though 38-to-40 degrees Celsius is often used as a guidepost for peeling back active cooling measures.
Notably, while the paragraph above considers external and internal mechanisms of heat energy dissipation – primarily via conduction, convection and evaporation – the heat transfer equation also predicts that diminishing metabolic heat pushes heat storage downwards. Nevertheless, there is no supportive data for pharmacological cooling in heat exhaustion or heatstroke. For example, dantrolene has been proposed, but found to be ineffective. Further, given that fever raises core temperature via a separate physiological pathway, acetaminophen is unhelpful and may aggravate hepatic toxicity. Similarly, there is no role for non-steroidal anti-inflammatories.
While often a lever out-of-reach of the intensivist, prevention of heat-related illness is almost certainly the best mechanism to reduce its burden. This will be at the forefront of human health in the coming years and decades. While there will undoubtedly be technological advancements to help predict the onset of heat-related illness [e.g., smart thermostats, smartphone technology, artificial intelligence and the like] these are all symptom abatement rather than disease eradication. Until atmospheric carbon dioxide retention becomes a human priority, cooling centres and increased social interaction with elderly members of the community will be required during heat waves to reduce the burden of heat-related illness in emergency departments and intensive care units. For sporadic, exertional heatstroke, preventive measures such as avoiding work during the warmest times of the day, eliminating insulating clothing and equipment, proper hydration and close attention to early signs of heat-related illness are effective courses.