Elsevier

Cardiology Clinics

Volume 24, Issue 1, February 2006, Pages 103-114
Cardiology Clinics

Evaluation and Management of the Patient Who Has Cocaine-associated Chest Pain

https://doi.org/10.1016/j.ccl.2005.09.003Get rights and content

Section snippets

Pharmacology

Cocaine is absorbed through application to the mucosa, ingestion, inhalation, and direct intravenous injection. Effects from nasal insufflation begin rapidly with peak concentrations typically reached within 30 to 60 minutes. Intravenous and inhalational routes of cocaine use produce near-immediate distribution throughout the circulation. “Crack” is the direct precipitate of free-base cocaine that results from alkalinization of aqueous cocaine hydrochloride.

The relative contributions of cocaine

Pathophysiology

Cocaine has diverse actions in humans. It directly blocks fast sodium channels, stabilizing the axonal membrane, with a resultant local anesthetic effect. Blockade of myocardial fast sodium channels causes cocaine to have type I antidysrhythmic properties [13], [14]. Cocaine interferes with the uptake of neurotransmitters at the nerve terminal. Cocaine functions as a vasoconstrictive agent. These three properties account for most of the toxicity seen in the clinical setting.

The initial effect

Initial approach to the patient in the emergency department

Patients who have potential cocaine toxicity should receive a complete evaluation including a history of cocaine use, recognition of signs and symptoms consistent with sympathetic nervous system excess, and evaluation of organ-specific complaints. It is imperative to determine whether signs and symptoms are caused by cocaine itself, underlying unrelated structural abnormalities, or cocaine-induced structural abnormalities.

The differential diagnosis of cocaine-associated chest pain is similar to

Electrocardiography

Interpretation of the EKG in patients who have cocaine-associated chest pain can be difficult, because patients can have nondiagnostic EKGs in the setting of ischemia as well as abnormal EKGs in the absence of ischemia. MI occurs in patients who have normal or nonspecific EKGs [37], [48]. In one series, patients who had MI were as likely to present with normal or nonspecific EKGs as with ischemic EKGs, thereby, resulting in the emergency department release of 15% of patients who have MI [37].

Initial disposition decision

Patients who have acute STEMI should receive immediate reperfusion therapy. Direct percutaneous coronary intervention (PCI) is preferred in light of the frequently complex clinical presentation and risk of thrombolytics. Patients who have cocaine-associated MI who are likely to develop complications can be identified with a high degree of accuracy during the initial 12 hours of hospitalization [58]. Patients who have cocaine-associated chest pain and do not have infarction have an extremely low

Initial treatment considerations

The initial treatment should focus on airway, breathing, and circulation. Specific treatments are based on the specific sign, symptom, or organ system affected. Because of the direct relationship between the neuropsychiatric and other systemic complications, management of neuropsychiatric manifestations affects the systemic manifestations of cocaine toxicity.

Patients who have suspected cocaine-induced ischemia or MI should be treated similarly to those with traditional acute coronary syndromes,

In-hospital management

There is limited specific information available regarding the in-hospital management of patients who have cocaine-related cardiovascular disease. Therefore, as a general rule, treatment guidelines follow those recommended for patients who have acute coronary syndromes not associated with cocaine Table 1 [105], [106].

ST-elevation myocardial infarction

The diagnosis of STEMI can be more challenging in patients who have acute cocaine toxicity because of the atypical presentation and challenges with interpretation of the EKG, including left ventricular hypertrophy and early repolarization. Patients who have acute cocaine toxicity frequently are younger than expected and are hypertensive, and aortic dissection must be considered in the differential diagnosis. Therefore cardiac catheterization with direct PCI is the preferred method of

High-risk unstable angina/non–ST-segment elevation myocardial infarction

Patients who have elevated cardiac enzymes or abnormal EKGs are at higher risk for subsequent events and benefit from an early invasive approach with cardiac catheterization and revascularization [107]. Although no specific data exist for cocaine-related unstable angina/non-STEMI, it is reasonable to believe these patients would benefit from a similar approach. It is important to use drug rehabilitation as well as aggressive risk factor modification in these patients, because there is a high

Low-risk unstable angina

Most patients who have cocaine-related chest pain have low-risk unstable angina and can be treated satisfactorily with a 12-hour observation protocol [59].

Patients who have cocaine-associated chest pain have a 1-year survival rate of 98% and an incidence of late MI of only 1% [49]. Most deaths occur because of concurrent medical problems (such as HIV disease). Because patients who have cocaine-associated chest pain are not at high risk for MI or death during the ensuing year, urgent cardiac

Secondary prevention

Cessation of cocaine use is the hallmark of secondary prevention. Recurrent chest pain is less common and MI and death are rare in patients who discontinue cocaine use [49]. Aggressive risk factor modification is indicated in patients who have MI or evidence of premature atherosclerosis, coronary artery aneurysm, or ectasia. This risk factor modification includes smoking cessation, hypertension control, diabetes control, and aggressive lipid-lowering therapy with a target low-density

Summary

Patients who have chest pain following the use of cocaine have become more common in emergency departments throughout the United States, with approximately 6% of these patients sustaining an acute MI. The authors have described the rationale for recommending aspirin, benzodiazepines, and nitroglycerin as first-line treatments and calcium-channel blockade or phentolamine as possible second-line therapies and have summarized the controversies surrounding the use of fibrinolytic agents. Admission

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