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What are arrhythmias due to enhanced automaticity?

- Pacemaker hierarchy: SA fires at more rapid rate than atrial, AV, or purkinje fibers 

- Latent pacemakers prone to acceleration in response to beta stimulation, hypokalemia, fiber stretch, hypoxemia, acidosis, and injury 

- Enhanced automaticity results in premature/rapid firing of cells, resulting in: 

1. Sinus tachycardia (SA node) 

2. Atrial premature beats (APB; atrial conducting fibers) 

3. Ventricular premature beat (VPB; purkinje fibers) 


68-y/o AA M with shortness of breath and leg swelling. Prominent third heart sound and bilateral rales to mid lung fields, both signs of CHF. Pulse is rapid and regular at 100 bpm. ECG shows sinus tachy. 

What is the mechanism of the arrhythmia, and what would you use to treat it?

- Enhanced automaticity (INC SYM activity) 

- Focus on CHF tx, and reduce BB if on one 

- Don't give BB for decompensated CHF, or Verapamil for CHF 


Class III anti-arrhythmics

- Suppress ectopic pacemakers and interrupt reentry by blocking K+ channels 

- Phase 2, 3 repolarization delayed, extending APD and ERP, making it harder for ectopic pacemakers to fire and for reentry to be sustained 

1. ERP (in phase 3) is the time during AP when cell won't respond to a new stimulus -> by prolonging ERP in slow-conducting limb or reentrant circuit, reentry is interrupted 

- As a result of delayed repolarization, QT interval can be prolonged -> INC risk of EAD and torsade 


What is re-entry? What conditions are required for it to occur?

- Occurs when an impulse repetitively activates the same area of the heart 

- Conditions required

1. Anatomic or physiological obstacle (circuit) 

2. Unidirectional block 

3. Conduction time must exceed effective refractory period in the "slow" circuit

- Typically initiated by a premature impulse (automaticity) -> circulating impulse gives off daughter impulses, resulting in rapid activation of the ventricle (or atrium) 


Procainamide (Class IA)

- Action: suppresses ectopic pacemaker activity in partially depolarized cells, reduces conduction velocity (prolongs QRS), prolongs APD (class III)

- Use: acute control of atrial, ventricular arrhythmias; little effect on normal SA, AV node 

1. Short-term tx, i.e., post-op atrial fibrillation 

- Side effects: drug-induced lupus (rash, arthralgia, pleural effusions, etc.), torsades (limit long-term use)

Metabolism/prep: hepatic acetylation (50% of ppl slow acetylators -> INC likelihood of lupus), renal excretion; IV ONLY 


Lidocaine (Class IB)

Action: binds open/inactivated Na+ channels with rapid on/off kinetics (

Use: acute tx of vtach (NOT atrial arrhythmias)

Side effects: CNS, agitation, confusion, seizures (usually missed in CCU)

Metabolism/prep: only effective IV; elim via hepatic biotransformation



- Endogenous nucleoside in all cells in the body

- Used to terminate acute PSVT by blocking AV node

- Rapid admin via IV -> T(1/2) of 10 seconds 

- Chest tightness, transient asystole (

- Can be diagnostic for PSVT: if reverts, confirms dx; if not, allows dx of other cause, i.e., atrial flutter