Cocaine is a powerful sympathomimetic and ⇑O2 demand:
- Blocking re-uptake of norepinephrine and dopamine at the pre-synaptic adrenergic terminals
- Cocaine causes ↑HR and ↑BP in a dose-dependent fashion.
The chronotropic effects of cocaine are intensified in the setting of alcohol use.
Cocaine ↓left ventricular function and increase end-systolic wall stress.
By ↑ HR, BP, and contractility, cocaine leads to ↑ myocardial demand.
Cocaine is a potent coronary vasoconstrictor:
- Vasoconstriction worse with pre-existing CAD - particularly smokers.
- Direct coronary art wall myocyte adrenergic stimulation.
- Cocaine ↑ levels of endothelin-1 (a powerful vasoconstrictor) and ↓ nitric oxide (vasodilator).
Cocaine is pro-thrombotic:
- It increases platelet count, activation and platelet hyper-aggregability.
- Aspirin & nitrates are strongly recommended
- β-blockers are contraindicated
- Theoretically, β-blockade might induce or worsen hypertension and vaso-spasm.
- Benzodiazepines are recommended as the primary treatment for anxiety, tachycardia, and hypertension.
- Calcium channel blockers are not recommended.
- Early percutaneous coronary intervention is particularly preferred over fibrinolysis in patients with cocaine-associated MI
- Increased risk for intracranial haemorrhage after fibrinolytic agents in cocaine users.
- Chest pain (often "cardiac sounding") is the commonest (56%) presenting complaint amongst cocaine users.
- Dyspnoea and shortness of breath are commonly associated.
- Beware - up to half of cocaine associated AMIs do NOT report chest pain (palpitations or SOB etc).
- Cocaine associated chest pain may be due to aortic dissection, pneumothorax or pneumomediastinum.
- General features of cocaine intoxication
Investigations / Management
- An abnormal ECG has been reported in 56% to 84% of patients with cocaine-associated chest pain.
- ECG sensitivity in revealing ischaemia or MI to predict a true MI is only 36%.
- Specificity, positive predictive value, and negative predictive value of the ECG are 89.9%, 17.9%, and 95.8%, respectively.
- Cocaine may cause rhabdomyolysis (raised myoglobin and total CK in up to 75% of patients).
- Cardiac troponins are the most sensitive and specific markers.
- As only 0.7% to 6% of patients with cocaine-associated chest pain progress to an AMI, risk stratification of these patients in the CDU may be appropriate.
- High risk patients or those with positive ECG / markers should be admitted to CCU.
- Low risk patients with normal initial investigations should be transferred to the CDU.
- Exercise Stress Testing is optional (decision by emergency medicine consultant) for patients with cocaine-associated chest pain who have had an uneventful 9 to 12 hours of observation. (Ref)