Why Heat Stroke Causes Low BP (Hypotension) and High Heart Rate (Tachycardia)

1. Massive Peripheral (Cutaneous) Vasodilation

"The hyperthermia is accompanied by marked generalized vasodilation, with peripheral pooling of blood and a decreased effective circulating blood volume."

• Robbins, Cotran & Kumar Pathologic Basis of Disease

BP = Cardiac Output × SVR

"Excessive cutaneous vasodilation can lead to a fall in arterial pressure and therefore to a decrease in brain perfusion."

2. Dehydration and Volume Depletion

• Loss of intravascular fluid volume
• Reduced venous return to the heart (preload falls)
• Less blood available to fill the ventricles, so stroke volume drops
• Blood pressure falls further

"The hypotension that is initially common among patients with heat-stroke results from both dehydration and high-output cardiac failure caused by peripheral vasodilation."

3. Tachycardia - the Compensatory Response

Cardiac Output = Heart Rate × Stroke Volume

• Tachycardia shortens diastolic filling time, limiting stroke volume further
• High temperatures directly impair myocardial contractility
• Right-sided heart failure can develop due to the volume overload from peripheral pooling

4. Direct Myocardial Damage (Late Stage)

"ECG abnormalities are common in heat stroke; pulmonary edema and transient right and/or left ventricular dysfunction may occur, along with hypotension and circulatory collapse. Sinus tachycardia is invariably present."

Summary Diagram of the Mechanism

High ambient temperature
        ↓
Hypothalamus triggers thermoregulation
        ↓
Massive cutaneous vasodilation + profuse sweating
        ↓                            ↓
Low SVR                         Volume depletion (dehydration)
        ↓                            ↓
        └─────────→ ↓ Venous return (preload) ←─────┘
                            ↓
                     ↓ Stroke Volume
                            ↓
               Baroreceptor reflex activated
                            ↓
              ↑ Heart Rate (tachycardia)  ← sympathetic drive
                            ↓
          Still → ↓ Blood Pressure (hypotension)
          (because SVR collapse dominates)
                            ↓
               High-output cardiac failure

Clinical Note

• Harrison's Principles of Internal Medicine, 22e, p. 3819
• Robbins, Cotran & Kumar - Pathologic Basis of Disease
• Braunwald's Heart Disease, p. 272
• Medical Physiology (Boron & Boulpaep)
• Tintinalli's Emergency Medicine, A Comprehensive Study
• Miller's Anesthesia, 10e

Exertional Heat Stroke (EHS)

Definition

• Core body temperature >40°C (>104°F)
• Profound central nervous system (CNS) dysfunction (confusion, ataxia, coma, seizures)
• Occurring during or immediately after vigorous physical exertion

Who Gets It?

Pathophysiology

Step 1 - Heat Stress Inputs

• Physical exercise generates massive metabolic heat
• High ambient temperature and humidity prevent dissipation
• Heavy clothing, equipment, lack of air movement compound the load

Step 2 - Physiological Strain

• Cardiovascular system is challenged: blood must simultaneously supply working muscles AND perfuse the skin for cooling
• Blood pressure regulation fails as peripheral vasodilation overwhelms cardiac reserve
• Tissue hyperthermia, ischemia, and oxidative/nitrosative stress develop

Step 3 - Pathophysiology (the gut-endotoxemia axis)

• Gut permeability increases - splanchnic blood flow is diverted to working muscle and skin, making the gut ischemic
• Intestinal barrier breaks down → endotoxemia (bacterial LPS enters blood)
• This triggers an exaggerated acute-phase response
• Leads to Systemic Inflammatory Response Syndrome (SIRS)
• SIRS drives coagulopathy → DIC
• Then necrosis/apoptosis of cells across multiple organs

Three Clinical Phases of Severe EHS

1. Hyperthermic-neurologic acute phase: Elevated tissue temperature → GI dysfunction + CNS dysfunction (confusion, ataxia, seizure, coma)
2. Hematologic-enzymatic phase: Mild-to-severe DIC + elevated CK and aminotransferases (liver/muscle damage)
3. Late renal-hepatic phase: Diffuse end-organ failure (AKI, hepatic failure, ARDS)

Clinical Features

Vital Signs

• Core temperature >40°C (must be measured rectally - oral/axillary/tympanic are unreliable in EHS)
• Tachycardia, widened pulse pressure, arrhythmia
• Hypotension
• Tachypnea

CNS (most important diagnostic feature)

• Inability to continue exercise, disorientation, emotional lability
• Ataxia, altered gait (cerebellar sensitivity to heat)
• Confusion, delirium, behavioral changes, aggression
• Seizures (common, especially during cooling)
• Coma

Skin

• Profuse sweating (unlike classic HS where skin is dry) - absence of sweating is NOT required
• Pallor

GI

• Nausea, vomiting, diarrhea

Musculoskeletal

• Muscle flaccidity, cramps
• Rhabdomyolysis (muscle breakdown)

Urine

• Oliguria; dark/brown urine (myoglobinuria from rhabdomyolysis)

Fig: EHS causes multiorgan failure - coma, arrhythmia/sudden death, liver failure, kidney failure from rhabdomyolysis (Miller's Review of Orthopaedics)

Laboratory Findings

Treatment

Golden Rule: Cool First, Transport Second

1. Immediate Cooling (highest priority)

• Cooling rate of ≥0.155°C/min is the target
• Stop cooling at 39°C to avoid overcooling/hypothermia
• Cooling causes peripheral vasoconstriction, which helps redirect blood to the heart - a beneficial side effect

2. Airway

• Endotracheal intubation if unconscious or altered airway reflexes
• Avoid depolarizing agents (succinylcholine) - risk of hyperkalemia from rhabdomyolysis

3. IV Fluid Resuscitation

• EHS patients require far more aggressive isotonic crystalloid (normal saline) than classic HS
• Monitor urine output closely
• If rhabdomyolysis + myoglobinuria: maintain urine flow to protect kidneys

4. Seizure Management

• Lorazepam 1-2 mg IV (safe - low hepatotoxicity)
• Avoid: chlorpromazine (lowers seizure threshold, anticholinergic, worsens hypotension)

5. Cardiovascular Support

• Dopamine or dobutamine if cardiac output remains depressed despite adequate CVP
• Avoid norepinephrine - alpha-adrenergic vasoconstriction impedes skin cooling
• Cardiac arrhythmias during hyperthermia usually resolve spontaneously with cooling; antiarrhythmics rarely needed

6. Monitoring for Complications

• ECG monitoring for arrhythmia
• Watch for hyperkalemia (from rhabdomyolysis)
• DIC monitoring: PT/PTT, fibrinogen, platelets, d-dimer
• Liver and renal function
• Glucose (hypoglycemia common)

What NOT to Use

• Antipyretics (NSAIDs, aspirin, acetaminophen) - completely ineffective; aspirin worsens coagulopathy; acetaminophen is hepatotoxic in this setting
• Dantrolene - effective in malignant hyperthermia but not heat stroke
• Anticholinergic drugs (including atropine) - inhibit sweating

Complications

Prognosis

• EHS mortality: 3-5% (much better than classic HS, because patients are young and healthy with rapid recognition)
• Classic HS: up to 60% die before reaching hospital; ICU mortality 10-65%
• 10-28% mortality at 1-2 years post-treatment
• Persistent neurologic deficits (ataxia, cerebellar signs) in a significant proportion

• Goldman-Cecil Medicine, International Edition - Chapter 95
• Miller's Anesthesia, 10e
• Miller's Review of Orthopaedics, 9th Ed
• Harrison's Principles of Internal Medicine, 22e
• Tintinalli's Emergency Medicine