What are the cardiovascular complications and treatment options for a patient with cocaine toxicity, considering their potential underlying medical history of substance abuse or mental health issues?

Cardiovascular Complications of Cocaine Toxicity

Major Cardiovascular Complications

Cocaine causes life-threatening cardiovascular complications through multiple mechanisms including coronary vasospasm, accelerated atherosclerosis, thrombosis, arrhythmias, and direct myocardial toxicity. 1, 2

Acute Coronary Syndromes

• Myocardial infarction is the most common cardiovascular manifestation, occurring through coronary artery vasoconstriction, in situ thrombosis formation, and platelet aggregation 1, 3, 2
• Cocaine-induced coronary vasospasm can cause severe, reversible arterial spasm leading to ST-elevation MI and life-threatening ventricular arrhythmias 4
• Chronic cocaine use accelerates atherosclerosis through endothelial dysfunction, with significant coronary disease common even in young users 2

Arrhythmias and Sudden Death

• Cocaine blocks potassium channels, increases L-type calcium channel current, and inhibits sodium influx during depolarization, all contributing to arrhythmogenesis 1
• Ventricular arrhythmias can be recurrent and severe, sometimes requiring cardioverter-defibrillator implantation 4
• Sudden cardiac death is a frequent outcome, making cocaine intoxication the most common cause of drug-related death reported by medical examiners 1

Structural Heart Disease

• Left ventricular hypertrophy, myocarditis, and dilated cardiomyopathy develop with continued use and lead to heart failure 1, 5
• Irreversible structural damage to the heart occurs with chronic exposure 1

Vascular Complications

• Aortic dissection can occur due to severe hypertension and generalized vasoconstriction 6, 5
• Coronary artery dissection is a life-threatening complication requiring screening 6

Treatment Algorithm

Immediate Stabilization

Benzodiazepines (lorazepam or diazepam) are first-line treatment for cocaine-induced hypertension, tachycardia, chest pain, and agitation by reducing sympathetic outflow and treating underlying agitation. 7, 6

• Diazepam specifically demonstrated improved autonomic findings and resolution of chest pain in cocaine-associated presentations 8, 7
• Benzodiazepines effectively control blood pressure, heart rate, and reduce coronary vasospasm through anxiolysis and sedation 7

Management of Persistent Hypertension and Coronary Vasospasm

If hypertension or vasospasm persists after benzodiazepines, use phentolamine as the preferred second-line agent because it directly reverses cocaine-induced coronary artery vasospasm without risk of unopposed alpha-stimulation. 8, 7, 6

• Verapamil effectively resolves cocaine-induced coronary vasospasm and may be used as an alternative when alpha-blockers are unavailable 8, 7
• Nitroglycerin reverses cocaine-induced coronary vasospasm (45% of patients reported chest pain reduction), but use with caution due to risk of severe hypotension and reflex tachycardia 8, 7
• Morphine partially reverses cocaine-induced coronary artery vasospasm and can be used for chest pain 8

Critical Contraindications

Pure beta-blockers are absolutely contraindicated in acute cocaine intoxication because they cause unopposed alpha-adrenergic stimulation leading to paradoxical hypertension and severe coronary vasospasm. 7, 6

• Propranolol worsened cocaine-induced coronary artery vasoconstriction in clinical trials 8, 7
• Esmolol showed no consistent improvement and caused adverse effects including hypertension, hypotension, and CNS depression 8, 7
• Avoid beta-blockers within 72 hours of cocaine use due to risk of potentiating coronary vasospasm 6, 9

Cardiac Arrest Management

Apply standard BLS and ACLS algorithms without modification for cocaine-induced cardiac arrest, as there is insufficient evidence to suggest changes to resuscitation protocols. 8, 6

• Standard therapy achieved 55% overall and neurologically intact survival in cocaine-associated cardiac arrest 8

Wide-Complex Tachycardia and Arrhythmias

For wide-complex tachycardia or cardiac arrest with suspected sodium channel blockade, administer sodium bicarbonate (1-2 mEq/kg IV bolus) to reverse QRS prolongation. 6

• Lidocaine is reasonable for wide-complex tachycardia as it competitively binds cocaine at sodium channels; 29 patients treated with lidocaine (including 8 with wide-complex tachycardia) had no complications and all survived 8, 6

Acute Coronary Syndrome Protocol

Obtain immediate 12-lead ECG to identify ST-segment elevation. 6

High-risk features requiring monitored admission include:

• ST-elevation or depression ≥1 mm
• Elevated cardiac markers
• Recurrent chest pain
• Hemodynamic instability 6

Use troponin I and T as preferred biomarkers over CK-MB, since CK can be falsely elevated from skeletal muscle activity and rhabdomyolysis. 6

ST-Elevation MI Management

Proceed immediately to PCI rather than fibrinolytic therapy, as cocaine users frequently have contraindications to thrombolytics. 6

• Use bare-metal stents rather than drug-eluting stents due to shorter required duration of dual antiplatelet therapy and poor medication adherence in this population 6
• Antiplatelet therapy and vasodilators (nitrates, nifedipine) are appropriate treatment strategies 3

Life-Threatening Complications Requiring Screening

Screen for complications beyond MI: aortic dissection, coronary artery dissection, myocarditis, and cardiomyopathy. 6

For life-threatening hyperthermia, rapidly cool patients using evaporative or immersive cooling modalities, as hyperthermia results from cocaine-induced hypermetabolism and significantly increases toxicity and mortality. 6

Critical Pitfalls to Avoid

• Carefully dose medications to avoid hypotension after cocaine metabolism, as cocaine's effects are transient (minutes to hours) but treatment effects persist 6
• ECG and serial cardiac markers are less accurate in identifying MI in cocaine users experiencing chest pain; maintain high clinical suspicion especially in younger males 1
• The combination of cocaine with alcohol or cigarettes intensifies cardiovascular effects 6
• Class Ia and III antiarrhythmics are strongly discouraged if the patient is likely to continue cocaine use due to documented adverse effects 1

Monitoring and Follow-Up

• Serial vital sign assessment is crucial in patients with cardiovascular complications 6
• Patients who develop myocardial injury have increased risk of cardiac and all-cause mortality lasting at least 7 years; cardiology follow-up is recommended 8
• Evaluate and treat coexisting psychiatric disorders (depression, anxiety, bipolar disorder) that are common in cocaine users 6