Cocaine and ECG

What it looks like on ECG

The most common finding is sinus tachycardia, reflecting the sympathomimetic effect of cocaine (blockade of catecholamine reuptake). In some patients experiencing chest pain, ST-T changes are recorded: ST depression or elevation, a flattened or biphasic T wave. These changes are variable and can be either nonspecific or correspond to a specific coronary territory — the absence of typical territoriality does not rule out ACS and does not allow the finding to be dismissed as benign.

The QT/QTc interval may be prolonged, especially in overdose, electrolyte disturbances, and in combination with other QT-prolonging substances; the mechanism involves potassium channel blockade alongside other toxic effects on repolarization. This is not a universal ECG sign of cocaine intoxication — the degree of prolongation varies significantly and depends on the dose and concomitant factors, rather than solely on the direct action of cocaine. At high doses and pronounced sodium channel blockade, QRS complex widening may occur, which clinically and electrographically resembles poisoning with tricyclic antidepressants or other sodium channel blockers — up to the appearance of a tall R wave in aVR. QRS is measured as the maximum duration across all 12 leads, rather than specifically in one or two; ≥120 ms is the generally accepted threshold for a wide QRS. The threshold of ≥100 ms as an alarm sign of toxic sodium channel blockade is taken mainly from tricyclic antidepressant data and has not been separately validated for cocaine — such widening on its own does not prove cocaine intoxication and is evaluated together with the clinical picture.

Some patients develop true ST-segment elevation consistent with STEMI: it can be the result of coronary vasospasm (cocaine-induced vasospasm, including in intact arteries) or thrombosis against the background of atherosclerosis and increased platelet aggregation. The leads with ST elevation correspond to the affected wall by standard localization: anterior — V3–V4, inferior — II, III, aVF, lateral — I, aVL, V5–V6.

Mechanism

Cocaine blocks the reuptake of norepinephrine, dopamine, and serotonin in the synaptic cleft, enhancing sympathetic stimulation of the heart and vessels — hence tachycardia and arterial hypertension. At the same time, cocaine has a membrane-stabilizing action similar to local anesthetics: it blocks fast sodium channels of cardiomyocytes, slowing depolarization and widening the QRS. The effect on potassium channels and other toxic effects on repolarization can prolong QT, but this effect is inconstant and depends on the dose, electrolyte background, and concurrent medications — describing cocaine simply as an agent with class III antiarrhythmic-like action is inaccurate. At the coronary vessel level, cocaine causes marked vasospasm via alpha-adrenergic stimulation and promotes thrombosis through platelet activation and endothelial injury — the combination of these effects produces the clinical picture of ACS even in young people without advanced atherosclerosis.

Causes

• Acute cocaine intoxication (inhalation, crack smoking, intravenous administration)
• Chronic cocaine use as a factor contributing to the earlier development of coronary atherosclerosis (along with vasospasm, increased myocardial oxygen demand, thrombosis, and dissection as independent mechanisms of ACS)
• Concomitant use of cocaine with alcohol (formation of cocaethylene, which enhances cardiotoxicity)
• Overdose against the background of underlying coronary artery disease

Differential diagnosis

• True STEMI unrelated to cocaine — age and the absence of traditional risk factors do not reliably differentiate cocaine-associated ACS from conventional ACS; a positive toxicological screen confirms use but does not prove a causal relationship, while coronary angiography establishes anatomy and the presence of occlusion, but not whether the spasm was triggered by cocaine
• Tricyclic antidepressant poisoning — the ECG pattern of similar sodium channel blockade (QRS widening, tall R in aVR) by itself does not reliably differentiate the two conditions; differentiation is based primarily on history, physical examination, and the clinical toxicrome, while toxicological screens have auxiliary value — they may fail to detect the substance, yield cross-reactivity, and do not establish what specifically caused the current toxicity, especially in poly-substance use. In the presence of widened QRS and signs of sodium channel blockade, emergency treatment is initiated based on clinical indications regardless of the screening result
• Early repolarization syndrome — diffuse concavo-ascendent ST elevation in a young person without pain, most commonly with sinus rhythm and may increase with bradycardia; with pain, ECG dynamics, or troponin elevation, ischemia cannot be ruled out solely by ST shape, and the standard ACS algorithm is required
• Myocarditis — diffuse ST-T changes without a clear coronary territory, but without a history of stimulant use

Clinical significance and management

ECG findings during cocaine intoxication require interpretation in the clinical context: chest pain in a young patient with tachycardia and ST-T changes is always considered a possible ACS until proven otherwise. Cocaine-associated ACS is managed like conventional ACS: serial ECGs and high-sensitivity troponin, echocardiography as indicated, and an immediate reperfusion strategy in the presence of persistent ST elevation or suspected occlusion. A history of recent use helps identify a potential trigger but does not rule out conventional coronary occlusion and is no reason to delay standard ACS management.

When coronary vasospasm is suspected, in addition to standard ACS therapy, benzodiazepines are used as indicated to control agitation, tachycardia, and arterial hypertension, nitrates for ischemia or hypertension, and calcium channel blockers. Beta-blockers are not routinely administered during acute cocaine intoxication until acute sympathomimetic toxicity is resolved due to the risk of exacerbating uncompensated alpha-adrenergic vasoconstriction; after stabilization and in the absence of signs of acute intoxication, the decision is individualized.

In clinically significant QRS widening due to toxic sodium channel blockade, sodium bicarbonate administration according to the toxicological protocol is considered, assessing the risk in combination with hypotension, seizures, arrhythmias, and altered mental status, rather than based solely on QRS duration. When torsades de pointes develops, intravenous magnesium, correction of hypokalemia and hypomagnesemia, discontinuation of other QT-prolonging drugs, and immediate defibrillation for hemodynamic instability are indicated.

Common interpretation errors

• Attributing ST-elevation or ST-T changes solely to a "cocaine effect" without ruling out true occlusion — coronary angiography is required if STEMI is persistently suspected
• Failing to obtain a history of psychoactive substance use in a young patient presenting with chest pain and an atypical ECG pattern
• Relying on toxicological screening as the decisive criterion for differential diagnosis instead of the clinical toxidrome and medical history
• Prescribing a beta-blocker routinely without addressing signs of acute sympathomimetic toxicity
• Limiting management to rhythm monitoring in the presence of significant QT prolongation or QRS widening without considering specific therapy (magnesium for torsades, sodium bicarbonate for sodium blockade)

Frequently asked questions

Related terms

More in "Pharmacology and Toxicology"

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Sources

• Goldberger's Clinical Electrocardiography, current edition
• Surawicz, Knilans — Chou's Electrocardiography in Clinical Practice
• ESC Guidelines for the management of acute coronary syndromes, 2023

Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.