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Cocaine-associated chest pain
From WikEM
(Redirected from Cocaine Chest Pain)
Contents
Background
- Cocaine causes vasoconstriction, which can precipitate MI
- Cocaine metabolites can persist for up to 24hrs and cause delayed or recurrent coronary vasoconstriction[1]
- 6% incidence of AMI with cocaine chest pain
- Cocaine associated with 24x risk of true MI
Clinical Features
- Chest pain in the setting of cocaine or related stimulant use
Differential Diagnosis
Chest pain
Critical
- Acute Coronary Syndromes
- Aortic Dissection
- Cardiac Tamponade
- Pulmonary Embolism
- Tension Pneumothorax
- Boerhhaave's Syndrome
- Coronary Artery Dissection
Emergent
- Pericarditis
- Myocarditis
- Pneumothorax
- Mediastinitis
- Cholecystitis
- Pancreatitis
- Cocaine-associated chest pain
Nonemergent
- Stable angina
- Asthma exacerbation
- Valvular Heart Disease
- Aortic Stenosis
- Mitral valve prolapse
- Hypertrophic cardiomyopathy
- Pneumonia
- Pleuritis
- Tumor
- Pneumomediastinum
- Esophageal Spasm
- Gastroesophageal Reflux Disease (GERD)
- Peptic Ulcer Disease
- Biliary Colic
- Muscle sprain
- Rib Fracture
- Arthritis
- Chostochondirits
- Spinal Root Compression
- Thoracic outlet syndrome
- Herpes Zoster / Postherpetic Neuralgia
- Psychologic / Somatic Chest Pain
- Hyperventilation
- Panic attack
Sympathomimetics
Evaluation
- 1-3hrs onset from last use
- If >3 hrs = lower risk of AMI
- Most with characteristic pain
- Dyspnea, diaploresis, and nausea
- Most have normal vitals
- ECG
Management
- ASA
- Benzos directed at symptom relief, not necessarily hypertension and tachycardia[1]
- Consider Nitroglycerin, Nitroprusside, Phentolamine (1mg IV), or CCB (in benzodiazepine non-responders)
- Avoid beta-blockers due to the possibility of unopposed alpha activity. Labetolol although offering the theoretical advantage of blocking both alpha and beta receptors does not reverse coronary artery vasoconstriction[2][3]
- Consider NaHOC3 for Ventricular Arrythmias immediately following cocaine use
- Reverses cocaine induced QRS prolongation by Na channel blockade
Disposition
- Consider discharge after 9-12 hour observation if pain free, no EKG changes and negative serial troponin
- In NEJM study, 334 patients studied. If both EKG and troponins negative, no deaths from cardiovascular events at 30 days. 4 patients did have non-fatal MI's but were using cocaine at the time.[7]
- Otherwise admit
See Also
References
- ↑ 1.0 1.1 McCord J, et al. Management of cocaine-associated chest pain and myocardial Infarction. Circulation. 2008; 117:1897-1907.
- ↑ Boehrer JD. et al. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med. 1993; 94: 608– 610
- ↑ Lange RA. et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med. 1990; 112: 897–903
- ↑ Dattilo PB et al. β-blockers are associated with reduced risk of myocardial infarction after cocaine use. Ann Emerg Med. 2008; 51:117.
- ↑ Finkel JB and Marhefka GD. Rethinking cocaine-associated chest pain and acute coronary syndromes. Mayo Clin Proc. 2011; 86(12):1198-1207.
- ↑ Rangel C, et al. Marcus GM. Beta-blockers for chest pain associated with recent cocaine use. Arch Intern Med. 2010; 170(10):874-879.
- ↑ Kloner RA and Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003; 348:487-488.
