Brugada And Cocaine_midwest Hospital Med Meeting

Brugada Electrocardiographic Pattern And Cardiovascular Complications Associated With Cocaine Toxicity M. 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 The Case

Cocaine induced dysrhythmias

Treatment of Cocaine Intoxication With Myocardial Complications

• 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.

• What is the diagnosis of this electrocardiogram (ECG)? 1. Acute ST-elevation myocardial infarction. 2. Bundle branch block (BBB) 3. Ventricular tachycardia 4. Accelerated AV junctional rhythm. 5. Brugada pattern.

• Which of the following agents considered first line for the management of cocaine induced myocardial injury? 1. Metoprolol 2. Lisinopril 3. Lorazepam 4. Phentolamine 5. Tissue plasminogen activator (t-PA)

• 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.

• 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.

• 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.

• Which of the following cardiac dysrhythmias and conductions disturbances reported with cocaine use? 1. Bundle-branch block 2. Accelerated idioventricular rhythm 3. Ventricular tachycardia 4. Torsade de pointes 5. Brugada pattern (right bundle-branch block with ST-segment elevation in leads V1, V2, and V3) 6. All of the above.

• 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

• 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)

Cocaine And Sodium Bicarbonate

• All of the choices in previous question are correct. But the precise arrhythmogenic potential of the drug is poorly defined. Suggested mechanisms: • As a sympathomimetic agent, it may increase ventricular irritability and lower the threshold for fibrillation. • Inhibits the generation and conduction of the action potential as a result of its sodium-channelblocking effects. • Increases the intracellular calcium concentration • 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. Quinidine 3. Procainamide 4. Disopyramide 5. 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.

Cocaine And Brugada syndrome

ECG 1 on arrival to ER

The 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.

Back To The Case

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

Cocaine-Induced Myocardial Infarction

ECG 2. six hours after arrival to ED

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.

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.

Conclusion 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 cocainerelated 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.