Cardiovascular signatures
Acute effects (0–3 h)
Heart rate
- Cocaine alone: +11 ± 2 bpm (controlled study, Circulation AHA 1999)
- Cocaine + ethanol: +20–40 bpm (synergistic, not additive)
- Task performance + cocaine/ethanol: up to +40 bpm
- Dose-dependent tachycardia; route matters (IV/smoked > intranasal > oral)
Blood pressure
- Hypertension via ↑ myocardial oxygen demand exceeding supply → ischemia/infarction risk
- BP biphasic: early sympathetic rise, possible orthostatic drop later
HRV
- ↓ during acute intoxication (sympathetic predominance from catecholamine surge)
- No published wearable HRV data — all autonomic data from lab settings
- HRV during intoxication is not a reliable recovery metric
Temperature
- Hyperthermia risk, especially with physical activity
Arrhythmia: 4 mechanisms {#arrhythmia}
- Sodium channel blockade — reduces rapid depolarisation (phase 0); follows use-dependent kinetics → higher HR (from catecholamine surge) exacerbates Na⁺ blockade → pro-arrhythmic positive feedback loop
- Potassium channel blockade — prolongs repolarisation
- Catecholamine excess — further ↑ HR and myocardial O₂ demand
- MI/myocarditis — ischaemic or inflammatory myocardial damage
Positive feedback loop: Cocaine → catecholamine surge → ↑ HR → worsens use-dependent Na⁺ blockade → worsens arrhythmia risk → more catecholamine release.
Cocaethylene amplification
See Cocaethylene — half-life 2–3× longer than cocaine, synergistic cardiotoxicity. Most users (~92%) co-use alcohol, making this the majority risk profile, not the exception.
Cardiovascular recovery
- Next-day HR/HRV: likely suppressed but exact timeline not well characterised
- Sustained cocaine use → risk of cardiomyopathy (direct myocardial toxicity + microvascular spasm, distinct from ischaemic MI)
- Cocaine crash associated with possible hypotension/bradycardia rebound after acute tachycardia
Related
Cocaine, Cocaine crash, DAT blockade, Cocaethylene, Cocaine risk profile, Cocaine sleep architecture