Cocaine-associated chest pain: Difference between revisions

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*[[Benzos]] directed at symptom relief, not necessarily hypertension and tachycardia<ref name="McCord"></ref>
*[[Benzos]] directed at symptom relief, not necessarily hypertension and tachycardia<ref name="McCord"></ref>
*Consider [[Nitroglycerin]], [[Nitroprusside]], [[Phentolamine]] (1mg IV), or [[Calcium channel blockers|CCB]] (in benzodiazepine non-responders)  
*Consider [[Nitroglycerin]], [[Nitroprusside]], [[Phentolamine]] (1mg IV), or [[Calcium channel blockers|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<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 α activity. Labetolol although offering the theoretical advantage of blocking both α 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>
*Consider [[NaHOC3]] for Ventricular Arrythmias immediately following cocaine use  
*Consider [[NaHOC3]] for Ventricular Arrythmias immediately following cocaine use  

Revision as of 01:13, 24 July 2017

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

Emergent

Nonemergent

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 α activity. Labetolol although offering the theoretical advantage of blocking both α and beta receptors does not reverse coronary artery vasoconstriction[2][3]
    • Though not accepted in common practice, new evidence suggest no significant risk and a benefit to using beta blockade in these patients[4][5][6]
  • 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. ↑ 1.0 1.1 McCord J, et al. Management of cocaine-associated chest pain and myocardial Infarction. Circulation. 2008; 117:1897-1907.
  2. ↑ Boehrer JD. et al. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med. 1993; 94: 608– 610
  3. ↑ Lange RA. et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med. 1990; 112: 897–903
  4. ↑ Dattilo PB et al. β-blockers are associated with reduced risk of myocardial infarction after cocaine use. Ann Emerg Med. 2008; 51:117.
  5. ↑ Finkel JB and Marhefka GD. Rethinking cocaine-associated chest pain and acute coronary syndromes. Mayo Clin Proc. 2011; 86(12):1198-1207.
  6. ↑ Rangel C, et al. Marcus GM. Beta-blockers for chest pain associated with recent cocaine use. Arch Intern Med. 2010; 170(10):874-879.
  7. ↑ Kloner RA and Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003; 348:487-488.
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