Heat Exhaustion and Heatstroke

Heat exhaustion and heatstroke sit at opposite ends of a single continuum of heat-related illness, but the line between them is the single most important triage decision in this chapter: mental status. Heat exhaustion is a syndrome of significant fluid and electrolyte loss with an elevated core temperature — generally under 40°C, though some sources place the cutoff as high as 40.5°C — and, critically, an intact mental status.^[1][2] Heatstroke is the true emergency: a core temperature typically above 40°C together with altered mental status or other central nervous system dysfunction — confusion, delirium, ataxia, seizures, or coma.^[1][3] Any patient with heat exposure, an elevated temperature, and an altered mental status should be treated as heatstroke until proven otherwise; this single rule, more than any specific number on a thermometer, should drive the initial response (see Red Flags/Refer).

Heatstroke itself further divides into two genuinely different clinical pictures. Classic heat stroke typically affects older, sedentary, or chronically ill patients exposed passively to environmental heat — often with impaired thermoregulation, reduced ability to self-care, social isolation, and/or a contributing medication — and the skin is often hot and dry, since sweating has failed. Exertional heatstroke typically affects younger, physically active people (athletes, outdoor workers, military personnel) who generate heat faster than they can dissipate it during strenuous activity in a hot environment, and profuse sweating often persists even as core temperature climbs to dangerous levels — lack of sweating is therefore not a reliable way to rule out heatstroke.^[1][3] Reported mortality differs sharply between the two: roughly 10-65% for classic heat stroke versus roughly 3-5% for exertional heat stroke, reflecting both the underlying frailty of the classic-heatstroke population and how directly mortality tracks with delay to cooling.^[3]

This is also a chapter where pharmacotherapy plays a distinctly secondary role. The single most time-critical intervention in heatstroke is not a drug — it is rapid, active cooling, and mortality correlates directly with how long that cooling is delayed; reported short-term excess mortality during extreme heat events has ranged from about 4% to as much as 142% across studied events.^[1] What genuinely belongs to the pharmacist is upstream of the emergency: a long and often underappreciated list of common medications — anticholinergics, diuretics, beta-blockers, antipsychotics, stimulants — meaningfully raise heat-illness risk by interfering with sweating, volume status, or the cardiovascular compensation for heat stress, and a proactive medication review before and during a Canadian heat event is a genuinely concrete, pharmacist-actionable preventive intervention (see Risk Factors and Choose Initial Treatment).^[1][4] With Canadian extreme-heat events becoming more frequent, this is increasingly a home-grown clinical problem, not an imported one.^[5]

The heat-illness spectrum

Heat-related illness ranges from self-limited minor conditions through to heat exhaustion and, at the severe end, life-threatening heatstroke.^[1] Heat edema (transient peripheral swelling), miliaria rubra (a plugged-sweat-gland rash), heat cramps, and heat syncope are all generally benign and self-limited, but persistent or worsening symptoms despite rest and cooling should prompt reassessment for heat exhaustion or heatstroke rather than being assumed to simply need more time.^[1]

Heat exhaustion

Heat exhaustion is the most common heat-related illness and is not, by definition, associated with organ damage.^[1] It occurs when the cardiovascular system cannot simultaneously meet the combined demand of increased skin blood flow for cooling and blood flow to exercising muscle and vital organs — the resulting insufficient peripheral blood flow impairs thermoregulation.^[1] Two overlapping patterns are described: water-depletion heat exhaustion, from inadequate fluid intake during heat exposure, producing hypernatremia and small, concentrated urine; and sodium-depletion heat exhaustion, from replacing sweat losses with plain water while running an electrolyte deficit, with lower blood pressure and more prominent muscle weakness and fatigue.^[1] Symptoms are often vague — heavy sweating, fatigue, weakness, dizziness, headache, nausea, and sometimes vomiting — and patients frequently do not connect them to heat at all. Mental status is normal or, at most, mildly confused or agitated; any incoherence or loss of consciousness should be evaluated as possible heatstroke instead.^[1]

Heatstroke

Heatstroke reflects failure of the thermoregulatory system itself: once cooling mechanisms are overwhelmed, core temperature rises in an uncontrolled way that will not reverse spontaneously without external cooling, even in patients who retain some ability to sweat.^[1][3] The physiological injury is direct as well as functional — high core temperature denatures intracellular proteins and disrupts cell membranes, triggers a large heat-shock-protein response, and drives cellular apoptosis, with the brain particularly vulnerable.^[1][6] This is why heatstroke, unlike heat exhaustion, carries a genuine risk of permanent organ damage and death, and why the duration of hyperthermia — not simply its peak — is the dominant driver of outcome.^[1]

^[1]

Differential diagnosis

Several other causes of hyperthermia and/or altered mental status deserve explicit consideration, especially given how many of the same medications discussed in Risk Factors can themselves cause a hyperthermic syndrome independent of ambient heat:^[1]

• Neuroleptic malignant syndrome — antipsychotic-associated; generally rigidity, hyperthermia, autonomic instability, and altered mental status, independent of environmental heat exposure, though heat exposure can precipitate or worsen it in a patient already taking an antipsychotic.
• Serotonin syndrome — serotonergic drug exposure (SSRIs and combinations); hyperreflexia, clonus, agitation.
• Sepsis or a central nervous system infection (meningitis, encephalitis) — fever with altered mental status but typically without a specific heat-exposure history.
• Thyroid storm — hyperthermia, tachycardia, and altered mental status in a patient with underlying or undiagnosed hyperthyroidism.
• Malignant hyperthermia — a specific anesthesia-triggered hypermetabolic emergency, not heat-exposure-related.
• Sympathomimetic or anticholinergic toxidrome — stimulant or anticholinergic overdose can independently produce hyperthermia and altered mental status; in a patient with a genuine heat-exposure history who is also on one of these drug classes, the two may be difficult to fully separate, and both should be treated as present.

Complications of heatstroke

Severe heatstroke can progress to multi-organ dysfunction syndrome, including rhabdomyolysis (more common in exertional heatstroke) with a real risk of acute kidney injury, disseminated intravascular coagulation, hepatocellular injury or failure, pulmonary edema and acute respiratory distress syndrome, cardiac arrhythmias, and seizures.^[1][3] Even reversible complications can take a genuinely long time to resolve — published recovery courses longer than 7 weeks are described — so "the patient cooled down and looks better" is not the same as "fully recovered," and follow-up should reflect that (see Monitoring/Follow-up).^[3]

Heat-illness risk is rarely due to a single factor — it is the interaction of physiological vulnerability, environmental exposure, and, very often, medication effects, and patients frequently have more than one of these at once.^[1]

Medications that increase heat-illness risk — genuinely high-yield pharmacist content

This is one of the most concretely pharmacist-actionable parts of this chapter. A wide range of common medications interfere with thermoregulation through distinct mechanisms, and Health Canada's own technical guide for health care workers — co-authored with the Institut national de santé publique du Québec — was written specifically because health care workers, including pharmacists, are "often uninformed about the potential risks associated with the use of certain drugs in extreme heat."^[1]

Two points matter as much as the list itself. First, the relationship between any single drug and heat illness is genuinely difficult to quantify — heatstroke can occur in patients on no medications at all, and case reports of heat-related death very often involve more than one of these drug classes at once, making it difficult to attribute risk to one agent specifically.^[1] Second, and just as important: the correct response to identifying one of these medications on a patient's list is very rarely simply "stop it." Abruptly discontinuing a diuretic, antipsychotic, or antidepressant carries its own real risk of destabilizing the condition it is treating — minimizing heat exposure, reinforcing hydration, and involving the prescriber in any dose change is generally the safer course of action (see Choose Initial Treatment).^[1]

Other risk factors

• Age extremes — infants and young children (higher body-surface-area-to-mass ratio, dependence on a caregiver to recognize and respond to heat exposure) and older adults, especially those over 75 (impaired thermoregulation, higher prevalence of chronic illness and polypharmacy).^[1]
• Chronic illness — cardiovascular disease, respiratory disease, renal disease, neurological disease (including Parkinson's disease), diabetes, and obesity all independently reduce heat tolerance.^[1]
• Lack of heat acclimatization — sudden exertion or exposure without a gradual build-up meaningfully increases risk, particularly for exertional heat illness.^[1]
• Psychiatric illness, particularly when combined with social isolation or living alone — patients with a psychiatric illness who are also taking an antipsychotic and living alone are at meaningfully greater risk than those with only one of these three factors.^[1]
• Poor access to cooling — air conditioning is highly protective when available and a real, independent risk factor when it is not; this is a genuine social-determinants issue, not simply a comfort issue.^[1]
• Homelessness and low income — people who are homeless carry a disproportionate share of the risk factors above (higher prevalence of poorly controlled chronic disease, mental illness, and substance use) plus direct environmental exposure, limited transportation to cooling services, limited hydration access, and a higher probability of social isolation.^[1]
• Physical or social isolation more broadly — confinement to bed, reduced independence, and infrequent contact with others all delay recognition and help-seeking.^[1]

History

Characterize the exposure (ambient temperature and humidity, duration, exertional versus passive), ask specifically about fluid and electrolyte intake, and take a focused medication and substance history targeting every drug class in Risk Factors plus alcohol. Ask about prior heat-illness episodes — recurrence on an unchanged medication regimen is itself a signal that a medication review is overdue.^[7]

Examination — mental status is the central finding

Assess mental status explicitly, not only as a general impression. Simple orientation questions (name, date, location) and, where relevant, questions about a recent past event can help characterize whether a patient was confused during the acute illness even after partly recovering by the time of assessment; standard tools such as the Glasgow Coma Scale or the AVPU scale (Alert, Voice, Pain, Unresponsive) are reasonable depending on the setting.^[1]

Measure core temperature with a rectal thermometer wherever possible — oral, tympanic, and aural-canal measurements correlate poorly with true core temperature in heat-injured patients and can meaningfully underestimate it (oral temperature can read roughly 3°C lower, and aural-canal measurement up to roughly 5°C lower, than rectal temperature in collapsed patients).^[1] Because cooling often begins as soon as heat injury is suspected — appropriately, since delay is the dominant driver of poor outcomes — the first recorded temperature may already be below the true peak; interpret a lower-than-expected temperature in a patient who looks unwell with appropriate caution rather than reassurance.^[1]

Investigations

For heat exhaustion without red flags, investigations are often unnecessary beyond basic clinical assessment. For suspected heatstroke, or heat exhaustion with moderate-to-severe symptoms or in an older patient, obtain:^[1][3]

• Electrolytes and renal function — sodium in particular, given the risk of both hypernatremia (water-depletion heat exhaustion) and hyponatremia (diuretic/SSRI effect, or sodium-depletion heat exhaustion).
• Creatine kinase (CK) and urine myoglobin — to assess for rhabdomyolysis, more common in exertional heatstroke.
• Liver enzymes (AST/ALT) — hepatocellular injury is a recognized heatstroke complication.
• Coagulation studies (PT/INR, aPTT) — to assess for disseminated intravascular coagulation.
• Complete blood count and blood gas as clinically indicated.

Differential diagnosis

See Recognize the Condition for neuroleptic malignant syndrome, serotonin syndrome, sepsis/central nervous system infection, thyroid storm, malignant hyperthermia, and sympathomimetic/anticholinergic toxidrome as the principal alternatives — or genuine co-existing diagnoses — to actively consider.

• Cool the patient as rapidly as safely possible — the single most time-critical intervention in heatstroke, since mortality correlates directly with time-to-cooling and the total duration of hyperthermia.^[1]
• Correctly and rapidly distinguish heat exhaustion (mental status intact) from heatstroke (altered mental status) at first contact, since this single distinction determines urgency and disposition.^[1]
• Restore intravascular volume and correct electrolyte derangements without causing iatrogenic harm — cerebral edema from overly rapid sodium correction, or pulmonary edema from overzealous fluid administration.^[1]
• Identify and manage heatstroke complications early: rhabdomyolysis, acute kidney injury, disseminated intravascular coagulation, hepatic injury, and multi-organ dysfunction.^[1][3]
• Recognize and, where appropriate and safe, address modifiable medication risk factors (anticholinergics, diuretics, beta-blockers, antipsychotics, stimulants) — a genuinely pharmacist-actionable preventive intervention, balanced against the real risk of destabilizing the underlying condition being treated.^[1]
• Prevent recurrence through patient and caregiver education, especially for patients with a prior heat-illness episode or ongoing high-risk medication therapy.^[7]

Heat exhaustion — supportive care, rapid improvement expected

Reduce the cardiovascular workload with rest and gentle cooling (cool environment, cold compresses, fanning; active cooling matters most when core temperature is between roughly 38.5°C and 40°C), and correct fluid/electrolyte depletion with oral rehydration — an oral electrolyte solution or water, as directed by the prescriber or clinical context — reserving IV normal saline for nausea/vomiting or evidence of significant tissue hypoperfusion.^[1] Patients with heat exhaustion retain the ability to cool spontaneously once removed from heat, and should improve meaningfully with rest, cooling, and rehydration; anyone who does not improve, or who worsens, needs re-evaluation for heatstroke rather than simply more time.^[1] Where water-depletion heat exhaustion has produced significant hypernatremia, correct it slowly (a commonly cited rate is approximately 2 mEq/L per hour) — rapid correction risks iatrogenic cerebral edema.^[1] Older adults and patients with moderate-to-severe symptoms should generally be considered for a more complete workup and possible admission rather than routine outpatient management.^[1]

Heatstroke — cool first, ask questions later

The primary and most time-critical goal is rapid reduction of core temperature; published target cooling rates vary somewhat by source and method (Health Canada's technical guide cites a general target of roughly 0.15-0.30°C per minute; StatPearls specifies approximately 0.13°C per minute for ice-water immersion and approximately 0.05°C per minute for evaporative cooling) — the exact number matters less than the underlying principle that cooling should start immediately and continue by the fastest available method.^[1][6] For exertional heatstroke specifically, cooling to under 39°C within 30 minutes of collapse has been associated with 100% survival in published series — a striking illustration of just how much time-to-cooling matters.^[8]

Choosing a cooling method

Preferred, exertional heatstroke cold- or ice-water immersion is the fastest and most effective method and is described by the Wilderness Medical Society as the "gold standard" for rapid temperature reduction; submerge the torso — and as much of the body as feasible — in cold water (roughly 2-4°C), keeping the core submerged, with continuous monitoring of vital signs and core temperature.^[1][8][6] Classic heatstroke, or where immersion is not feasible or tolerated evaporative cooling — wetting the skin (ideally with warm-to-tepid water, to avoid triggering vasoconstriction) combined with vigorous fanning to promote evaporation — is a reasonable and better-tolerated alternative, particularly in frail older patients where immersion can be logistically difficult and where cooling is generally undertaken more gradually to avoid destabilizing existing chronic conditions; ice packs to the groin, axillae, and neck are a reasonable adjunct or field alternative when neither immersion nor a full evaporative setup is available.^[1][6] Whichever method is used, monitor core temperature continuously (rectal, checked at least every 15 minutes) and stop active cooling once the patient reaches approximately 38-39°C to avoid overshooting into iatrogenic hypothermia.^[1][6]

Suppressing shivering during active cooling

Shivering generates heat and can directly work against the cooling effort. A benzodiazepine (see Pharmacologic Treatment Options) is a reasonable adjunct specifically to control shivering and agitation during active cooling, rather than routine first-line pharmacotherapy for heatstroke itself.^[6][3]

What does NOT work — a genuine and important myth to correct

Antipyretics (e.g., acetaminophen) have no meaningful role in heatstroke and should not be given expecting them to lower temperature. This is a genuinely important counseling point because it runs against intuition: fever is a regulated, hypothalamic-set-point-driven response, and antipyretics work by resetting that set point — but heatstroke is not a fever, it is a failure of the thermoregulatory system itself, so there is no elevated set point for an antipyretic to act on. Antipyretics add risk without benefit here, including a possible contribution to coagulopathy and organ dysfunction in a patient who may already have organ involvement.^[1][2][6] Dantrolene is also not recommended — it has not been shown to improve heatstroke outcomes and is not an effective substitute for direct external cooling; reserve it for its actual indication, malignant hyperthermia, which is a distinct diagnosis (see Recognize the Condition).^[1][2]

Fluid and electrolyte management

Give IV crystalloid (0.9% sodium chloride, or lactated Ringer's) for significant volume depletion, but avoid overzealous administration — heatstroke patients may be less dehydrated than they appear, and brisk fluid administration can precipitate pulmonary edema or congestive heart failure, particularly in older adults; a commonly cited approach is roughly 0.5-2.5 L of crystalloid titrated to clinical response rather than a fixed large-volume protocol.^[1] Monitor serum sodium and renal function closely, and correct any significant sodium abnormality slowly to avoid cerebral edema, exactly as in heat exhaustion.^[1]

The pharmacist's preventive action: medication review before and during a heat event

Before and during a heat alert proactively review the medication list of any patient with one or more risk factors above for the drug classes in Risk Factors, and involve the prescriber in any change — Ontario's provincial heat-alert guidance explicitly directs patients to "ask your doctor or pharmacist if it increases your health risk in the heat," and this is exactly the conversation a community pharmacist is positioned to start.^[4] As above, the goal is very rarely outright discontinuation; reinforcing hydration, heat-avoidance behaviour, and closer monitoring is often the safer course, with dose adjustment reserved for genuine, prescriber-directed clinical judgment.^[1]

• Move to the coolest available environment — air-conditioned space where possible; even a few hours a day in air conditioning is meaningfully protective during a heat event.^[1]
• Remove excess or constrictive clothing to promote heat loss.
• For heat exhaustion, oral rehydration with water or an electrolyte-containing drink is generally as effective as IV rehydration in a patient who can tolerate oral intake.^[1]
• For heatstroke, active cooling is the central, highest-yield intervention in this entire chapter — more so than any medication (see Choose Initial Treatment for method selection).
• Encourage pre-emptive hydration before thirst develops — by the time thirst is perceived, meaningful dehydration (roughly 2% body water loss) has typically already occurred; water is appropriate for most people, and sports drinks offer little additional benefit for typical heat-event hydration.^[1]
• Loose-fitting, light-coloured, breathable clothing supports evaporative cooling and dry heat exchange.^[1]
• Encourage gradual heat acclimatization (roughly 5-10 days of progressively increasing heat/activity exposure) rather than sudden strenuous activity in the heat, particularly for outdoor workers and athletes.^[1]
• Reschedule strenuous outdoor activity away from peak-heat hours where possible.
• Encourage awareness of, and response to, official heat warnings — in Canada these are issued by Environment and Climate Change Canada, typically 18-24 hours in advance, using temperature and/or humidex thresholds that vary by region, and provincial systems such as Ontario's Harmonized Heat Warning and Information System layer additional local response triggers on top.^[5][4]
• Connect patients who are homeless, low-income, or otherwise without reliable access to cooling with community cooling centres and other local heat-response resources — this is a genuine, actionable social-determinants intervention, not a side issue (see Special Populations).^[1][4]
• Encourage regular check-ins on older, chronically ill, or socially isolated neighbours, friends, and patients during a heat event — physical and social isolation is an independent, well-documented risk factor for fatal heat illness.^[1]

Older adults

The predominant classic-heatstroke population — impaired thermoregulation, a higher prevalence of the chronic illnesses and polypharmacy discussed in Risk Factors, and a real risk of pre-existing cardiovascular or renal disease being destabilized by aggressive fluid administration. Cool more gradually than in exertional heatstroke, where full immersion may be poorly tolerated, and apply a lower threshold for admission and workup.^[1]

Infants and young children

Children have a higher body-surface-area-to-mass ratio, absorb heat more readily under hot conditions, and are entirely dependent on a caregiver to notice environmental risk and respond — increasing fluids, adjusting clothing, moving to a cooler space; repeat education for caregivers, since a single conversation is often not enough.^[1] Never leave a child unattended in a parked vehicle, even briefly — vehicle interior temperatures can rise to dangerous levels within minutes.

Pregnancy

Maternal hyperthermia, particularly during the first several months of pregnancy, has been associated with fetal effects including neural tube and other congenital malformations; treat any significant heat exposure or confirmed hyperthermia in a pregnant patient as warranting prompt clinical assessment rather than reassurance.^[1] Women generally have efficient heat-dissipation mechanisms during moderate heat stress, but this should not be taken as reassurance in a patient with frank heat exhaustion or heatstroke symptoms.^[1]

Psychiatric illness and antipsychotic therapy

This population carries genuinely compounded risk: the antipsychotic (or other psychotropic) medication itself impairs thermoregulation (see Risk Factors), the underlying illness can reduce self-care and heat-avoidance behaviour, and social isolation or living alone independently adds further risk — patients with all three factors together are at substantially higher risk than those with only one.^[1] A published case report describes a patient on combination antipsychotic therapy hospitalized twice in a single summer — once for heatstroke, once for heat exhaustion — a genuine illustration of how a heat-risk medication regimen left unaddressed can produce recurrent, preventable illness.^[7] Consider neuroleptic malignant syndrome in the differential for any such patient (see Recognize the Condition), and involve the prescriber in a proactive medication review before and during heat events rather than only after a first episode.

Homelessness, low income, and inadequate cooling access

This is not a peripheral demographic note — people who are homeless carry a disproportionate share of nearly every risk factor in this chapter at once (poorly controlled chronic disease, mental illness and substance use, direct and prolonged environmental exposure, limited transportation to cooling resources, limited hydration access, and a high likelihood of social isolation).^[1] Build any discharge or follow-up plan around where the patient will actually be able to access cooling, not around an assumption of stable housing with air conditioning, and connect proactively with community cooling centres and local heat-response services during a heat alert.^[1][4]

Outdoor workers and athletes (exertional heat illness)

Encourage gradual acclimatization (roughly 5-10 days), scheduled rest and hydration breaks, and awareness that heavy protective equipment or uniforms add meaningful thermal insulation. Onset can be rapid, but can also build over a second or third consecutive day of heat exposure, particularly when overnight cooling — including the sleeping environment — is inadequate to allow full recovery between exposures.^[1] For this population, cold-water immersion is generally well tolerated and should be used preferentially when heatstroke occurs.^[8][6]

Renal and hepatic impairment

Monitor renal function closely in any heatstroke patient given the rhabdomyolysis/acute-kidney-injury risk described in Recognize the Condition, and avoid dantrolene given its hepatotoxicity potential and lack of demonstrated benefit (see Choose Initial Treatment). Adjust benzodiazepine dosing cautiously in hepatic impairment given reduced clearance.

During active cooling for heatstroke, monitor core (rectal) temperature at least every 15 minutes to confirm the cooling rate and avoid overshooting into iatrogenic hypothermia — stop active cooling at approximately 38-39°C.^[1][6] Monitor urine output (a commonly cited target is roughly 50-100 mL/hour) as a marker of adequate renal perfusion, and trend renal function, CK, liver enzymes, and coagulation studies over the following days in any patient who had a significant heatstroke episode, since complications such as acute kidney injury and DIC can evolve over that window rather than being apparent immediately.^[1]

• Reassess heat-exhaustion patients within a defined, short interval — improvement should be evident with rest, cooling, and rehydration; a patient who is not improving needs re-evaluation for heatstroke, not simply more time.^[1]
• Set expectations honestly for heatstroke recovery — even reversible complications can take longer than 7 weeks to fully resolve, and "the fever broke" is not the same as "fully recovered."^[3]
• Before the patient returns to strenuous activity or heat exposure, confirm medical clearance — a repeat episode significantly raises future risk and should specifically prompt the medication review described in Choose Initial Treatment if it has not already happened.^[7]
• At every follow-up during heat-alert season, ask specifically about access to cooling, hydration, and whether the risk-factor medication list has actually been reviewed since the last heat event — not only whether it was recommended.

1. Heat exhaustion not improving within a reasonable period of rest, cooling, and oral rehydration: re-evaluate for heatstroke and escalate rather than continuing the same management and waiting longer.
2. Heatstroke with persistent altered mental status despite reaching target core temperature (approximately 38-39°C): consider that active cooling alone has not addressed the whole picture — reassess for a complication (cerebral edema, ongoing organ dysfunction) or an alternative/co-existing diagnosis such as neuroleptic malignant syndrome, serotonin syndrome, or a central nervous system infection (see Recognize the Condition).
3. Core temperature not falling despite active cooling: confirm the cooling method is actually being applied correctly (adequate body-surface contact with cold water, genuine core submersion, fanning actually promoting evaporation) before assuming the method itself has failed.
4. Rising creatinine, climbing creatine kinase, or falling urine output: escalate for aggressive fluid/electrolyte management and nephrology involvement rather than assuming this will resolve with cooling alone.
5. New bleeding, bruising, or coagulation abnormalities: evaluate for disseminated intravascular coagulation and escalate to critical care.
6. A second heat-illness episode in the same season on an unchanged medication regimen: this is a clear signal, not a coincidence — trigger a formal, prescriber-involved medication review rather than repeating the same counseling.

• Giving acetaminophen, or another antipyretic, expecting it to lower temperature in heatstroke — it has no meaningful role, since heatstroke is thermoregulatory failure, not a hypothalamic-set-point fever.
• Reaching for dantrolene as if it were an effective heatstroke treatment — it has not been shown to improve outcomes and is not a substitute for active cooling.
• Assuming a sweating patient cannot have heatstroke — profuse sweating is common in exertional heatstroke and does not rule it out.
• Delaying active cooling to complete a full diagnostic workup or wait for transport — cooling should begin immediately and continue during transport, not after it.
• Using an oral, tympanic, or aural-canal temperature to make or exclude a heatstroke diagnosis — these correlate poorly with true core temperature; use a rectal thermometer.
• Continuing active cooling past the point of overshoot, or not monitoring temperature frequently enough during cooling, risking iatrogenic hypothermia.
• Giving large-volume IV fluids by default in heatstroke without titrating to clinical response, particularly in older adults — this can precipitate pulmonary edema rather than help.
• Correcting hypernatremia or hyponatremia too quickly, risking cerebral edema.
• Reflexively telling a patient to simply stop a heat-risk medication (a diuretic, antipsychotic, or antidepressant) without prescriber involvement — abrupt discontinuation carries its own real risk.
• Overlooking the medication list entirely during a heat-alert consultation — this is one of the most concretely preventable pieces of this entire chapter, and it is easy to skip when the visit is focused on an unrelated concern.
• Missing neuroleptic malignant syndrome or serotonin syndrome as an alternative or co-existing diagnosis in a patient on antipsychotic or serotonergic therapy who presents with hyperthermia.
• Treating a homeless or socially isolated patient's heat-illness episode purely as a medical event without addressing the underlying access-to-cooling problem that will otherwise cause it to recur.

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

IV Fluid and Electrolyte Repletion

Titrate to clinical response rather than a fixed large-volume protocol — heatstroke patients may be less dehydrated than they appear, and brisk administration can precipitate pulmonary edema, especially in older adults.

Benzodiazepines — Adjunct for Shivering/Agitation During Active Cooling

Shivering generates heat and can directly work against active cooling. Use as an adjunct to cooling, not as routine first-line pharmacotherapy for heatstroke itself.

Agents With No Meaningful Role in Heatstroke — Do Not Use for This Purpose

Heatstroke is thermoregulatory failure, not a hypothalamic-set-point fever — antipyretics have no elevated set point to act on, and dantrolene is not an effective substitute for active external cooling.

Supportive Care

For accompanying symptoms rather than the underlying thermoregulatory problem itself.