Cocaine-associated chest pain: Difference between revisions
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*Benzos directed at symptom relief, not necessarily HTN and tachycardia<ref>McCord J, et al. Management of Cocaine-associated chest pain and myocardial infarction. Circulation. 2008; 117:1897-1907.</ref> | *Benzos directed at symptom relief, not necessarily HTN and tachycardia<ref>McCord J, et al. Management of Cocaine-associated chest pain and myocardial infarction. Circulation. 2008; 117:1897-1907.</ref> | ||
*Consider NTG, Nitroprusside, Phentolamine, or CCB (in benzo non responders) | *Consider NTG, Nitroprusside, Phentolamine, or CCB (in benzo 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<ref>Boehrer JD. et al. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med. 1993; 94: 608– 610</ref><ref> Lange RA. et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med. 1990; 112: 897–903</ref> | ||
*Consider NaHOC3 for Ventricular Arrythmias immediately following cocaine use | *Consider NaHOC3 for Ventricular Arrythmias immediately following cocaine use | ||
**Reverses cocaine induced QRS prolongation by Na channel blockade | **Reverses cocaine induced QRS prolongation by Na channel blockade | ||
Revision as of 02:37, 16 July 2015
Background
Cocaine is a catalyst for CAD & up to 6% of cocaine related CP develop an MI, however, a 9-12 hour period of ECG's and serial troponins can be safe. Of the 334 pts studied, if both were negative, no deaths from CV events occurred at 30 days. 4 pts did have non-fatal MI's but were using coc at the time.[1]
Epidemiology
- Causes vasculitis
- 6% incidence of AMI w/ cocaine CP
- Cocaine assoc c 24x risk of true MI
Clinical Features
- Chest pain in the setting of cocaine or related stimulant use
- Cocaine metabolites can persist for up to 24hrs and cause delayed or recurrent coronary vasoconstriction[2]
Differential Diagnosis
Diagnosis
- 1-3hrs onset from last use
- If >3 hrs = lower risk of MI
- Most with characteristic pain
- Dyspnea, diaploresis, and nausea
- Most have nl vitals
Management
- ASA, NTG, O2
- Benzos directed at symptom relief, not necessarily HTN and tachycardia[3]
- Consider NTG, Nitroprusside, Phentolamine, or CCB (in benzo 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[4][5]
- Consider NaHOC3 for Ventricular Arrythmias immediately following cocaine use
- Reverses cocaine induced QRS prolongation by Na channel blockade
Disposition
- May discharge after: 9-12 hour period of ECG's and serial troponins, if both are negative
- In NEJM 2/03; n=334; outcome of zero events at 30dys if no more cocaine
Risk Stratification
- Lower:
- Also low risk if ecg normal and without ischemic changes
- Cocaine can however cause AMI, dilated cardiomyopathy, CHF
See Also
References
- ↑ Kloner RA and Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003; 348:487-488.
- ↑ McCord J, et al. Management of cocaine-associated chest pain and myocardial Infarction. Circulation. 2008; 117:1897-1907.
- ↑ 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