Diferencia entre revisiones de «Cocaine-associated chest pain»

(Created page with "==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...")
 
 
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==Background==
==Background==
*Cocaine causes vasoconstriction, which can precipitate MI
**Cocaine metabolites can persist for up to 24hrs and cause delayed or recurrent coronary vasoconstriction<ref name="McCord">McCord J, et al. Management of cocaine-associated chest pain and myocardial Infarction. Circulation. 2008; 117:1897-1907.</ref>
*6% incidence of AMI with cocaine chest pain
*Cocaine associated with 24x risk of true MI
*Be aware of cocaethylene metabolites in the setting of EtOH use, will produce longer symptoms and potentially be more directly cardiotoxic


==Clinical Features==
*[[Chest pain]] in the setting of cocaine or related stimulant use


*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 (NEJM 2/03).
==Differential Diagnosis==
{{Chest Pain DDX}}


{{Sympathomimetic types}}


===Epidemiology===
==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==
1) causes vasculitis
*[[ASA]]
 
*[[Benzos]] directed at symptom relief, not necessarily hypertension and tachycardia<ref name="McCord"></ref>
2) 6% incidence of AMI w/ cocaine CP
*Consider [[Nitroglycerin]], [[Nitroprusside]], [[Phentolamine]] (1mg IV), or [[Calcium channel blockers|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<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>
3) Cocaine assoc c 24x risk of MI
**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
**Reverses cocaine induced QRS prolongation by Na channel blockade
 
==Diagnosis==
 
 
1) 1- 3hrs onset from last use
 
-if >3 hrs = lower risk of MI
 
2) Most with characterislnic pain
 
3) Dyspnea, diaploresis, and nausea
 
4) Most have nl vitals
 
 
==Workup==
 
 
= nl CP w/o (see disposition)
 
 
==Treatment==
 
 
1) Benzos
 
2) Labetalol?
 
*Theoretical contra-indication B-blocker 2nd to unopposed alpha
 


==Disposition==
==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.<ref>Kloner RA and Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003; 348:487-488.</ref>
*Otherwise admit


==See Also==
*[[Cocaine]]
*[[Cocaine toxicity]]
*[[Cocaine withdrawal]]
*[[Acute Coronary Syndrome (Main)]]


May discharge after: 9-12 hour period of ECG's and serial troponins.
==References==
 
<references/>
If both are negative.
 
(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
 
 
==Source ==
 
 
10/07 DONALDSON (adapted from Lampe, Mistry)
 
 
 


[[Category:Cards]]
[[Category:Cardiology]]
[[Category:Toxicology]]

Revisión actual - 16:13 26 mar 2018

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
  • Be aware of cocaethylene metabolites in the setting of EtOH use, will produce longer symptoms and potentially be more directly cardiotoxic

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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