• The event: A previously healthy 27-year-old man ingested the content of a bag of cocaine as an impulsive gesture to avoid police detection. One hour later, he developed psychomotor agitation and generalized seizures. Within seconds, patient found pulseless and the electrocardiogram (ECG) monitoring showed ventricular asystole. CPR started and ventilation with supplemental oxygen by endotracheal (ET) intubation two ampules of Epinephrine and two ampules of Sodium Bicarbonate delivered by EMS immediately restored spontaneous heart beats.

• Vitals signs: Temperature of 39oC peripheral pulse of 70 bmp, blood pressure 90/70mm Hg, respiratory rate 32, SpO2 98% with full ventilator support (FiO2 100%), and Glasgow Coma scale of 5/15.

• Physical exam: Pupils were fixed, dilated and non-reactive to light bilaterally. The fundoscopic exam showed arterial narrowing. His skin was warm and flushed and his oral mucosa was dry with no signs of tongue laceration. Bilateral crackles more on the right than the left side heard on chest examination. Heart exam was significant for regular rate and rhythm with frequent escaped beats. The abdominal exam was negative.

• Initial work-up: Severe anion-gap metabolic acidosis with elevated lactic acid, creatinine kinase and myocardial Troponin I.

• Electrocardiogram: serial ECG’s done and shown below (ECG 1 and ECG 2)

• What is the diagnosis of this electrocardiogram (ECG)?1. Acute ST-elevation myocardial infarction.2. Bundle branch block (BBB)3. Ventricular tachycardia4. Accelerated AV junctional rhythm. 5. Brugada pattern.

• The electrocardiograms are showing accelerated idioventricular rhythm at 66 beats/min, QRS (0.44 sec), QTc (0.533 sec) with right bundle branch block (RBBB) and left anterior hemiblock (LAHB) configuration, and rSR' pattern with coved ST-segment elevation in V1 and more clearly in V2 mimicking Brugada pattern. However, underlying ischemia/infraction can’t be ruled out.

• Which of the following cardiac dysrhythmias and conductions disturbances reported with cocaine use? 1. Bundle-branch block2. Accelerated idioventricular rhythm3. Ventricular tachycardia4. Torsade de pointes5. Brugada pattern (right bundle-branch block with ST-segment elevation in leads V1, V2, and V3)6. All of the above.

• All of the choices in previous question are correct. But the precise arrhythmogenic potential of the drug is

poorly defined. Suggested mechanisms:1. As a sympathomimetic agent, it may increase ventricular irritability and lower the threshold for

fibrillation.2. Inhibits the generation and conduction of the action potential as a result of its sodium-channel-

blocking effects.3. Increases the intracellular calcium concentration4. It reduces vagal activity, which potentiates cocaine’s sympathomimetic effects.

• Which one of the following antiarrhythmics safe in patients with cocaine induced ventricular tachycardia or fibrillation?1. Lidocaine 2. Quinidine3. Procainamide4. Disopyramide5. Non of the above

• Lidocaine has been used safely in patients with cocaine induced ventricular tachycardia or fibrillation. Class IA antiarrhythmic drugs, such as quinidine, procainamide, and disopyramide, should be avoided, since they may exacerbate prolongation of the QRS and QT intervals and slow the metabolism of cocaine and its metabolites.

Brugada Electrocardiographic Pattern And Cardiovascular Complications Associated With Cocaine ToxicityBrugada Electrocardiographic Pattern And Cardiovascular Complications Associated With Cocaine ToxicityM. Chadi Alraies M.D., Abdul Hamid Alraiyes M.D., Samer Alhindi M.D., Richard Christie M.D.

Internal Medicine Residency Program, Department of Internal Medicine Case Western Reserve University - St. Vincent Charity Hospital – Cleveland, Ohio

• Which of the following agents considered first line for the management of cocaine induced myocardial injury?1. Metoprolol2. Lisinopril3. Lorazepam4. Phentolamine5. Tissue plasminogen activator (t-PA)

• Cocaine has no known antidote. Lorazepam supportive care and benzodiazepines such as lorazepam is the cornerstone of therapy. Furthermore, benzodiazepines considered first line treatment of cocaine related myocardial injury. Review the following table for the agents recommended by AHA for treatment.

The CaseThe Case

ECG 1 on arrival to ER

ECG 2. six hours after arrival to ED

Cocaine induced dysrhythmias Cocaine induced dysrhythmias

From: N Eng J Med, Lange RA, cardiovascular Complications of Cocaine. Vol. 345 No. 5

Cocaine-Induced Myocardial InfarctionCocaine-Induced Myocardial Infarction

Three suggested mechanisms:1. An increased myocardial oxygen demand in the face of a limited or fixed supply.2. Marked vasoconstriction of the coronary arteries.3. Enhanced platelet aggregation and thrombus formation.

Treatment of Cocaine Intoxication With Myocardial ComplicationsTreatment of Cocaine Intoxication With Myocardial Complications

Cocaine And Brugada syndromeCocaine And Brugada syndromeThe syndrome is characterized by (ECG) pattern of right bundle branch block (RBBB) with coved or occasionally saddleback ST-segment elevation in leads V1 through V3, the absence of demonstrable structural heart disease, and a propensity for ventricular tachycardia, ventricular fibrillation, and sudden cardiac death.

The arrhythmogenic potential of cocaine is extremely complex and poorly understood. Theses characteristic ECG changes occasionally are transient and may be exposed by sodium channel blocker, such as cocaine, or procainamide in patients with “latent” Brugada syndrome.

There is considerable debate in the literature whether an incidental finding of the Brugada pattern on the ECG of asymptomatic individuals with no family history of sudden death warrants an electrophysiologic evaluation.

• Several reports have described the treatment of cocaine-induced wide-complex tachycardia including Brugada pattern, associated with drugs having sodium channel blocking action, such as cocaine with the administration of sodium bicarbonate

Cocaine And Sodium BicarbonateCocaine And Sodium Bicarbonate

Cocaine can unmask latent Brugada syndrome in patient with the susceptible gene. Cocaine associated seizures and severe metabolic acidosis is multifactorial. Electrocardiogram has a low sensitivity in detecting cocaine-related myocardial ischemia and infarction. Sodium bicarbonate has more than one indication in the management of cocaine toxicity, reversal of the metabolic acidosis, treatment of rhabdomyolysis, and reversal of the sodium channel blocking property of cocaine on myocardium.

Conclusion Conclusion

Back To The Case Back To The Case

The patient was treated with IV fluids boluses and continuous infusion, sodium bicarbonate and lorazepam (1 mg/h) drips. All this led to hemodynamic stabilization and almost normalization of serum bicarbonate and PH levels. Subsequently, repeated ECG showed normal sinus rhythm. Cardiac catheterization showed normal coronary arteries with normal LV EF of 60%. Patient discharged back to the jail and to follow up with electrophysiology clinic.