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  Cocaine has sympathomimetic effetc due to blockade of presynaptic norepinephrine and dopamine reuptake.
  Cocaine has local anesthetic effect due to sodium channel blockade, similar to Class 1 antiarrhythmic agents. Inhibition of this channel slows impulse conduction
(in a manner similar to class I antiarrhythmics), thereby prolonging the QRS and HV intervals.
  Cocaine can block IKr channels (rapid delayed rectifier potassium currents) resulting in QT interval prolongation.
  Cocaine use has acute, chronic and withdrawal effects.
  Cardiovascular effects of Cocaine are dose-dependent, which may account for much of the conflicting data to date.
  Concurrent drug use with Cocaine (alcohol, marijuana, methadone, etc.) may be present.
  Any type of atrioventricular (AV) block.
  ST segment elevation: More frequent than ST depression. May be asymptomatic.
  ST segment depression.
  Negative T waves (most common), flattened T waves, prominent T waves (least common)
  J waves.
  U waves.
  Widened QRS (rare).
  Prolonged QT interval
  Right bundle branch block (more common) or left bundle branch block.
  Brugada pattern (commonly associated with acidosis).
  Sinus tachycardia
  Sinus bradycardia
  Sinus arrest
  Ectopic atrial rhythm
  Accelerated junctional rhythm
  Atrial fibrillation
  Supraventricular tachycardia
  Wide QRS tachycardia
  Torsades de Pointes
  Asystole
  Ventricular fibrillation
  Frequent episodes of ST segment elevation by ambulatory ECG (rhythm Holter) monitoring was observed during the first 2 weeks of Cocaine withdrawal.
Most of these episodes were silent.
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