Episode 210: Heat Stroke Basics Written by Jacob Dunn, MS4, American University of the Caribbean. Edits and comments by Hector Arreaza, MD.
Episode 210: Heat Stroke Basics
Written by Jacob Dunn, MS4, American University of the Caribbean. Edits and comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
Definition:
Heat stroke represents the most severe form of heat-related illness, characterized by a core body temperature exceeding 40°C (104°F) accompanied by central nervous system (CNS) dysfunction.
Arreaza: Key element is the body temperature and altered mental status.
Jacob: This life-threatening condition arises from the body's failure to dissipate heat effectively, often in the context of excessive environmental heat load or strenuous physical activity.
Arreaza: You mentioned, it is a spectrum. What is the difference between heat exhaustion and heat stroke?
Jacob: Unlike milder heat illnesses such as heat exhaustion, heat stroke involves multisystem organ dysfunction driven by direct thermal injury, systemic inflammation, and cytokine release. You can think of it as the body's thermostat breaking under extreme stress — leading to rapid, cascading failures if not addressed immediately.
Arreaza: Tell us what you found out about the pathophysiology of heat stroke?
Jacob: Pathophysiology:
Under normal conditions, the body keeps its core temperature tightly controlled through sweating, vasodilation of skin blood vessels, and behavioral responses like seeking shade or drinking water. But in extreme heat or prolonged exertion, those mechanisms get overwhelmed.
Once core temperature rises above about 40°C (104°F), the hypothalamus—the brain’s thermostat—can’t keep up. The body shifts from controlled thermoregulation to uncontrolled, passive heating. Heat stroke isn’t just someone getting too hot—it’s a full-blown failure of the body’s heat-regulating system.
Arreaza: So, it’s interesting. the cell functions get affected at this point, several dangerous processes start happening at the same time.
Jacob: Yes:
Arreaza: Yikes. Cytokines play a big role in the pathophysiology of heat stroke too.
Jacob:
Arreaza: What other systems are affected?
Arreaza: And one of the key features is neurologic dysfunction.
Jacob:
Arreaza: Cell injury, inflammation, coagulopathy, circulatory collapse and neurologic dysfunction.
Jacob: Ultimately, heat stroke is a multisystem catastrophic event—a combination of thermal injury, inflammatory storm, coagulopathy, and circulatory collapse. Without rapid cooling and aggressive supportive care, these processes spiral into irreversible organ failure.
Background and Types:
Arreaza: Heat stroke is part of a spectrum of heat-related disorders—it is a true medical emergency. Mortality rate reaches 30%, even with optimal treatment. This mortality correlates directly with the duration of core hyperthermia. I’m reminded of the first time I heard about heat stroke in a baby who was left inside a car in the summer 2005.
Jacob: There are two primary types:
-nonexertional (classic) heat stroke, which develops insidiously over days and predominantly affects vulnerable populations like children, the elderly, and those with chronic illnesses during heat waves;
-exertional heat stroke, which strikes rapidly in young, otherwise healthy individuals, often during intense exercise in hot, humid conditions.
Arreaza: In our community, farm workers are especially at risk of heat stroke, but any person living in the Central Valley is basically at risk.
Jacob: Risk factors amplify vulnerability across both types, including dehydration, cardiovascular disease, medications that impair sweating (e.g., anticholinergics), and acclimatization deficits. Notably, anhidrosis (lack of sweating) is common but not required for diagnosis. Hot, dry skin can signal the shift from heat exhaustion to stroke.
Arreaza: What other conditions look like heat stroke?
Differential Diagnosis:
Jacob: Presenting with altered mental status and hyperthermia, heat stroke demands a broad differential to avoid missing mimics.
-Environmental: heat exhaustion, syncope, or cramps.
-Infectious etiologies like sepsis or meningitis must be ruled out.
-Endocrine emergencies such as thyroid storm, pheochromocytoma, or diabetic ketoacidosis (DKA) can overlap.
-Neurologic insults include cerebrovascular accident (CVA), hypothalamic lesions (bleeding or infarct), or status epilepticus.
-Toxicologic culprits are plentiful—sympathomimetic or anticholinergic toxidromes, salicylate poisoning, serotonin syndrome, malignant hyperthermia, neuroleptic malignant syndrome (NMS), or even alcohol/benzodiazepine withdrawal.
When it comes to differentials, it is always best to cast a wide net and think about what we could be missing if this is not heat stroke.
Arreaza: Let’s say we have a patient with hyperthermia and we have to assess him in the ER. What should we do to diagnose it?
Jacob: Workup:
Diagnosis is primarily clinical, hinging on documented hyperthermia (>40°C) plus CNS changes (e.g., confusion, delirium, seizures, coma) in a hot environment.
Arreaza: No single lab confirms it, but targeted testing allows us to detect complications and rule out alternative diagnosis.
Jacob:
-Start with ECG to assess for dysrhythmias or ischemic changes (sinus tachycardia is classic; ST depressions or T-wave inversions may hint at myocardial strain).
-Labs include complete blood count (CBC), comprehensive metabolic panel (electrolytes, renal function, liver enzymes), glucose, arterial blood gas, lactate (elevated in shock), coagulation studies (for disseminated intravascular coagulation, or DIC), creatine kinase (CK) and myoglobin (for rhabdomyolysis), and urinalysis. Toxicology screen if history suggests.
Arreaza: I can imagine doing all this while trying to cool down the patient. What about imaging?
-Imaging: chest X-ray for pulmonary issues, non-contrast head CT if neurologic concerns suggest edema or bleed (consider lumbar puncture if infection suspected).
It is important to note that continuous core temperature monitoring—via rectal, esophageal, or bladder probe—is essential, not just peripheral skin checks.
Arreaza: Treatment
Management:
Time is tissue here—initiate cooling en route, if possible, as delays skyrocket morbidity. ABCs first: secure airway (intubate if needed, favoring rocuronium over succinylcholine to avoid hyperkalemia risk), support breathing, and stabilize circulation.
-Remove the patient from the heat source, strip clothing, and launch aggressive cooling to target 38-39°C (102-102°F) before halting to prevent rebound hypothermia.
-For exertional cases, ice-water immersion reigns supreme—it's the fastest method, with immersion in cold water resulting in near-100% survival if started within 30 minutes.
-Nonexertional benefits from evaporative cooling: mist with tepid water (15-25°C) plus fans for convective airflow.
-Adjuncts include ice packs to neck, axillae, and groin;
-room-temperature IV fluids (avoid cold initially to prevent shivering);
-refractory cases, invasive options like peritoneal lavage, endovascular cooling catheters, or even ECMO.
-Fluid resuscitation with lactated Ringer's or normal saline (250-500 mL boluses) protects kidneys and counters rhabdomyolysis—aim for urine output of 2-3 mL/kg/hour.
Arreaza: What about medications?
Jacob: Benzodiazepines (e.g., lorazepam) control agitation, seizures, or shivering; propofol or fentanyl if intubated. Avoid antipyretics like acetaminophen. For intubation, etomidate or ketamine as induction agents. Hypotension often resolves with cooling and fluids; if not, use dopamine or dobutamine over norepinephrine to avoid vasoconstriction.
Jacob: What IV fluid is recommended/best for patients with heat stroke?
Both lactated Ringer’s solution and normal saline are recommended as initial IV fluids for rehydration, but balanced crystalloids such as LR are increasingly favored due to their lower risk of hyperchloremic metabolic acidosis and AKI. However, direct evidence comparing the two specifically in the setting of heat stroke is limited.
Arreaza: Are cold IV fluids better/preferred over room temperature fluids?
Cold IV fluids are recommended as an adjunctive therapy to help lower core temperature in heat stroke, but they should not delay or replace primary cooling methods such as cold-water immersion. Cold IV fluids can decrease core temperature more rapidly than room temperature fluids. For example, 30mL/kg bolus of chilled isotonic fluids at 4 degrees Celsius over 30 minutes can decrease core temperature by about 1 degree Celsius, compared to 0.5 degree Celsius with room temperature fluids.
Arreaza: Getting cold IV sounds uncomfortable but necessary for those patients. Our favorite topic.
Screening and Prevention:
-Heat stroke prevention focuses on public health and individual awareness rather than routine testing.
-High-risk groups—elderly, children, athletes, laborers, or those on impairing meds—should acclimatize gradually (7-14 days), hydrate preemptively (electrolyte solutions over plain water), and monitor temperature in exertional settings.
-Communities during heat waves need cooling centers and alerts.
-For clinicians, educate patients with CVD or obesity about early signs like dizziness or nausea.
-No formal "screening" exists, but vigilance in EDs during summer surges saves lives.
-Arreaza: I think awareness is a key element in prevention, so education of the public through traditional media like TV, and even social media can contribute to the prevention of this catastrophic condition.
Jacob: Ya so heat stroke is something that should be on every physician’s radar in the central valley especially in the summer time given the hot temperatures. Rapid recognition is key.
Arreaza: Thanks, Jacob for this topic, and until next time, this is Dr. Arreaza, signing off.
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