Cocaine-associated chest pain: Difference between revisions
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==Background== | ==Background== | ||
Cocaine | *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 | *6% incidence of AMI with cocaine chest pain | ||
*Cocaine associated with 24x risk of true MI | *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== | ==Clinical Features== | ||
*[[Chest pain]] in the setting of cocaine or related stimulant use | *[[Chest pain]] in the setting of cocaine or related stimulant use | ||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
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*[[ASA]] | *[[ASA]] | ||
*[[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 [[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 | *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 | ||
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==Disposition== | ==Disposition== | ||
* | *Consider discharge after 9-12 hour observation if pain free, no EKG changes and negative serial troponin | ||
**In NEJM | **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== | ==See Also== | ||
*[[Cocaine]] | *[[Cocaine]] | ||
*[[Cocaine toxicity]] | *[[Cocaine toxicity]] | ||
*[[Cocaine | *[[Cocaine withdrawal]] | ||
*[[Acute Coronary Syndrome (Main)]] | *[[Acute Coronary Syndrome (Main)]] | ||
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<references/> | <references/> | ||
[[Category:Cardiology]] [[Category:Toxicology]] | [[Category:Cardiology]] | ||
[[Category:Toxicology]] | |||
Latest revision as of 16:13, 26 March 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
- Acute coronary syndromes (ACS)
- Aortic dissection
- Cardiac tamponade
- Coronary artery dissection
- Esophageal perforation (Boerhhaave's syndrome)
- Pulmonary embolism
- Tension pneumothorax
Emergent
- Cholecystitis
- Cocaine-associated chest pain
- Mediastinitis
- Myocardial rupture
- Myocarditis
- Pancreatitis
- Pericarditis
- Pneumothorax
Nonemergent
- Aortic stenosis
- Arthritis
- Asthma exacerbation
- Biliary colic
- Costochondritis
- Esophageal spasm
- Gastroesophageal reflux disease
- Herpes zoster / Postherpetic Neuralgia
- Hypertrophic cardiomyopathy
- Hyperventilation
- Mitral valve prolapse
- Panic attack
- Peptic ulcer disease
- Pleuritis
- Pneumomediastinum
- Pneumonia
- Rib fracture
- Stable angina
- Thoracic outlet syndrome
- Valvular heart disease
- Muscle sprain
- Psychologic / Somatic Chest Pain
- Spinal Root Compression
- Tumor
Sympathomimetics
- Cocaine
- Amphetamines
- Synthetic cathinones (khat)
- Ketamine
- Ecstasy (MDMA)
- Synthetic cannabinoids
- Bath salts
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]
- 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
- ↑ 1.0 1.1 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
- ↑ Dattilo PB et al. β-blockers are associated with reduced risk of myocardial infarction after cocaine use. Ann Emerg Med. 2008; 51:117.
- ↑ Finkel JB and Marhefka GD. Rethinking cocaine-associated chest pain and acute coronary syndromes. Mayo Clin Proc. 2011; 86(12):1198-1207.
- ↑ Rangel C, et al. Marcus GM. Beta-blockers for chest pain associated with recent cocaine use. Arch Intern Med. 2010; 170(10):874-879.
- ↑ Kloner RA and Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003; 348:487-488.