Cocaine-associated chest pain: Difference between revisions

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== Background ==
==Background==
Cocaine is a catalyst for CAD &amp; 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.<ref>Kloner RA and Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003; 348:487-488.</ref>


Cocaine is a catalyst for CAD &amp; 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).
===Epidemiology ===
 
=== Epidemiology ===
*Causes vasculitis  
*Causes vasculitis  
*6% incidence of AMI w/ cocaine CP  
*6% incidence of AMI w/ cocaine CP  
*Cocaine assoc c 24x risk of MI
*Cocaine assoc c 24x risk of true MI


==Clinical Features==
==Clinical Features==
*[[Chest pain]] in the setting of cocaine or related stimulant use
*[[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<ref>McCord J, et al. Management of cocaine-associated chest pain and myocardial Infarction. Circulation. 2008; 117:1897-1907.</ref>


== DDx  ==
==Differential Diagnosis==
 
[[Chest Pain (DDx)]]  
[[Chest Pain (DDx)]]  


== Workup  ==
==Diagnosis ==
 
*1-3hrs onset from last use
nl CP w/o (see disposition)
**If &gt;3 hrs = lower risk of MI
 
*Most with characteristic pain
== Diagnosis  ==
*Dyspnea, diaploresis, and nausea
*Most have nl vitals


#1- 3hrs onset from last use
==Management==
##if &gt;3 hrs = lower risk of MI
*ASA, NTG, O2
#Most with characterislnic pain
*Benzos
#Dyspnea, diaploresis, and nausea
*Consider Phentolamine or CCB (in benzo non responders)
#Most have nl vitals
*Labetalol?
**Theoretical contra-indication B-blocker 2nd to unopposed alpha
*Consider NaHOC3 for Ventricular Arrythmias immediately following cocaine use
**Reverses cocaine induced QRS prolongation by Na channel blockade


== Treatment  ==
==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


#ASA, NTG, O2
===Risk Stratification===
#Benzos
*Lower:  
#Consider Phentolamine or CCB (in benzo non responders)
**Also low risk if ecg normal and without ischemic changes  
#Labetalol?
**Cocaine can however cause AMI, dilated cardiomyopathy, CHF
##Theoretical contra-indication B-blocker 2nd to unopposed alpha
#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.
##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  ==


==See Also==
*[[Cocaine]]
*[[Cocaine intoxication]]
*[[Cocaine Withdrawal]]  
*[[Cocaine Withdrawal]]  
*[[Acute Coronary Syndrome (Main)]]
*[[Acute Coronary Syndrome (Main)]]


== Source  ==
==References==
 
</references>
10/07 DONALDSON (adapted from Lampe, Mistry)
 
7/12 N Engl J Med. 1995 Nov 9;333(19):1267-72. (adapted from Colorado compendium)


[[Category:Cards]] [[Category:Tox]]
[[Category:Cards]] [[Category:Tox]]

Revision as of 11:40, 20 June 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 (DDx)

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
  • Consider Phentolamine or CCB (in benzo non responders)
  • Labetalol?
    • Theoretical contra-indication B-blocker 2nd to unopposed alpha
  • 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

</references>

  1. ↑ Kloner RA and Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003; 348:487-488.
  2. ↑ McCord J, et al. Management of cocaine-associated chest pain and myocardial Infarction. Circulation. 2008; 117:1897-1907.
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