Cocaine-associated chest pain: Difference between revisions
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*ASA, NTG, O2  
*ASA, NTG, O2  
*Benzos directed at symptom relief, not necessarily HTN and tachycardia<ref name="McCord"></ref>
*Benzos directed at symptom relief, not necessarily HTN and tachycardia<ref name="McCord"></ref>
*Consider NTG, Nitroprusside, Phentolamine, or CCB (in benzo non responders)  
*Consider NTG, Nitroprusside, Phentolamine (1mg IV), 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>
*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>
**Though not accepted in common practice, new evidence suggest no significant risk and a benefit to using beta blockade in these patients<ref>Dattilo PB et al. β-blockers are associated with reduced risk of myocardial infarction after cocaine use. Ann Emerg Med. 2008; 51:117.</ref><ref>Finkel JB and Marhefka GD. Rethinking cocaine-associated chest pain and acute coronary syndromes. Mayo Clin Proc. 2011; 86(12):1198-1207. </ref><ref> Rangel C, et al. Marcus GM. Beta-blockers for chest pain associated with recent cocaine use. Arch Intern Med. 2010; 170(10):874-879.</ref>
**Though not accepted in common practice, new evidence suggest no significant risk and a benefit to using beta blockade in these patients<ref>Dattilo PB et al. β-blockers are associated with reduced risk of myocardial infarction after cocaine use. Ann Emerg Med. 2008; 51:117.</ref><ref>Finkel JB and Marhefka GD. Rethinking cocaine-associated chest pain and acute coronary syndromes. Mayo Clin Proc. 2011; 86(12):1198-1207. </ref><ref> Rangel C, et al. Marcus GM. Beta-blockers for chest pain associated with recent cocaine use. Arch Intern Med. 2010; 170(10):874-879.</ref>

Revision as of 22:43, 14 September 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

Chest pain

Critical

Emergent

Nonemergent

Sympathomimetics

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[2]
  • Consider NTG, Nitroprusside, Phentolamine (1mg IV), 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[3][4]
    • Though not accepted in common practice, new evidence suggest no significant risk and a benefit to using beta blockade in these patients[5][6][7]
  • 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

  1. ↑ Kloner RA and Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003; 348:487-488.
  2. ↑ 2.0 2.1 McCord J, et al. Management of cocaine-associated chest pain and myocardial Infarction. Circulation. 2008; 117:1897-1907.
  3. ↑ Boehrer JD. et al. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med. 1993; 94: 608– 610
  4. ↑ Lange RA. et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med. 1990; 112: 897–903
  5. ↑ Dattilo PB et al. β-blockers are associated with reduced risk of myocardial infarction after cocaine use. Ann Emerg Med. 2008; 51:117.
  6. ↑ Finkel JB and Marhefka GD. Rethinking cocaine-associated chest pain and acute coronary syndromes. Mayo Clin Proc. 2011; 86(12):1198-1207.
  7. ↑ Rangel C, et al. Marcus GM. Beta-blockers for chest pain associated with recent cocaine use. Arch Intern Med. 2010; 170(10):874-879.
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