GENERAL MECHANISMS OF ARRHYTHMIAS

I. Normal cardiac conduction:

  1. Sinus node==>Atrium==>AV node (delay)==>His bundle==>RBB(RV) and LBB
  2. LBB splits into L. anterior fascicle (ant LV) and L. posterior fascicle (septum and post-lat LV)

II. Mechanisms of arrhythmias:

  1. Passive
  1. Results from depressed automaticity or conductivity of structures responsible for rhythm, so usually cause bradyarrhythmias
  2. Examples include AV block, IVCD
  1. Automatic/ectopic
  1. Due to increased automaticity of a structure, so it udergoes spontaneous depolarization during diastole, therefore acting as a pacemaker
  2. Examples include PVCs and tachyarrhythmias, e.g. VT
  1. Reentrant
  1. The reentrant circuit involves an impulse going antegrade down one arm, exciting myocardium, and continuing retrograde up the other arm to start the cycle again
  2. Requires the following:
  1. 2 pathways over which impulse is conducted, usually close together
  2. Different conduction properties across the 2 pathways: the retrograde arm of circuit has delayed or blocked antegrade conduction but intact retrograde conduction
  1. Most premature beats and tachyarrhythmias are produced this way
  2. Results from various causes, including anatomical dual pathyways (e.g. WPW), myocardial injury
  3. If circuit is in the junction or the ventricles, can cause retrograde atrial activation and thus p waves on EKG!
  1. "Triggered activity"
  1. Repetitive electrical activity due to delayed afterdepolarization
  2. Clinical significance not yet established

III. Approach to diagnosis:

  1. EKG
  1. Cherchez la "p"-II, III, F, and V1 are best to see it
  2. Other atrial activity-flutter/fib waves
  3. AV dissociation?
  4. QRS width
  5. Regular or irregular ventricular rhythm
  6. Any early beats or pauses?
  1. Px
  1. Signs of AV dissociation: cannon jugular venous waves; fluctuating systolic BP, fluctuating heart sounds, intermittent S3 and S4