Clinical Differentiation of Cocaine vs Alcohol Intoxication Based on Objective Findings

Cardiovascular Manifestations

Cocaine induces tachycardia and hypertension by inhibiting catecholamine re‑uptake at postsynaptic α‑ and β‑adrenergic receptors (American Heart Association) 1.
Cocaine causes wide‑complex tachycardia and QRS prolongation through sodium‑channel blockade (American Heart Association) [1][2].
Cocaine leads to QT‑interval prolongation via potassium‑channel blockade (American Heart Association) 3.
Cocaine carries a risk of coronary vasospasm and myocardial infarction (American Heart Association) 4.

Cocaine intoxication is characterized by increased psychomotor activity, agitation, and aggressiveness (American Heart Association) 1.
Cocaine can precipitate seizures owing to central nervous system stimulation (American Heart Association) [1][3].
Diaphoresis (excessive sweating) is a common autonomic sign of cocaine toxicity (American Heart Association) [1][4].

Cocaine intoxication may produce hyperthermia that can become rapidly life‑threatening (American Heart Association) [1][2].

The presence of hypertension + tachycardia + hyperthermia strongly suggests cocaine intoxication (American Heart Association) [2][1].
Agitation, hyperactivity, and diaphoresis on mental‑status exam point toward cocaine rather than alcohol (American Heart Association) [2][1].
QRS widening or wide‑complex tachycardia on ECG is indicative of cocaine‑related sodium‑channel blockade (American Heart Association) [2][1].
Blood alcohol concentration (BAC) measurement and urine drug screen should be obtained to definitively identify the ingested substance(s) (American Heart Association) 2.

Cocaine induces both hypertension (e.g., systolic ≈ 160 mm Hg) and tachycardia (≈ 125 bpm) by inhibiting catecholamine reuptake at postsynaptic α‑ and β‑adrenergic receptors, producing peripheral α‑adrenergic vasoconstriction and β‑adrenergic cardiac stimulation【5】.
Sympathetic stimulation from cocaine causes mydriasis (dilated pupils) in affected individuals【5】.
Central nervous system activation due to blockade of norepinephrine, epinephrine, dopamine, and serotonin reuptake leads to agitation and heightened psychomotor activity【5】.
Hyperthermia (e.g., ≥ 104 °F) is a life‑threatening complication of cocaine intoxication that necessitates rapid external cooling measures【5】.

The simultaneous presence of hypertension, tachycardia, hyperthermia, mydriasis, diaphoresis, and agitation is virtually pathognomonic for cocaine intoxication and should trigger immediate recognition of a sympathomimetic toxidrome【5】.

Benzodiazepines are recommended as first‑line therapy to control agitation, hypertension, and psychomotor symptoms in patients with cocaine intoxication【5】.
Rapid external cooling should be instituted promptly for patients with life‑threatening hyperthermia secondary to cocaine use【5】.

Pure β‑blockers (e.g., propranolol) should be avoided because they may precipitate paradoxical severe hypertension via unopposed α‑adrenergic vasoconstriction【5】.
If β‑blockade is clinically required, combined α/β‑blockers such as labetalol or carvedilol are preferred to mitigate the risk of unopposed α‑stimulation【5】.