Cardiac AP (fast response fibers)

Phase 0 and Phase 1 

Cardiac muscle and His-Purkinje System

Phase 0: Na+ channels open (depolarization)

Class I antiarrhythmics slow or block this phase

Phase 1: Na+ channels are inactivated (in His-Pukinje cells can get outward K+ and overshoot)

Antiarrhythmic drugs have NO effects  

Cardiac AP (fast-response fibers)

Phase 2-4 

Phase 2: plateau phase in which there is a slow influx of Ca2+ balanced by late occuring K+ out flux

NO effects of antiarrhythmics

Phase 3: Repolarization, the K+ outflow rapidly increases as the Ca2+ current dies out 

Class III antiarrhythmic drugs slow repolarization

Phase 4: return of membrane to resting potential 

Cardiac AP (slow response fibers)

Phase 0, 3, 4 

Phase 0: depolarization by Ca2+ channels NOT Na+

Class IV antiarrhythmics (CCB & beta blockers)

Phase 3: repolarization where K+ currents overcome Ca2+ currents (these opposing currents determine the shape of the AP)

Can use K+ channel blockers here

Phase 4: spontaneous depolarization (pacemaker potential) 

Class II and IV antiarrhythmics can slow this phase 

Effective Refractory Period  

No stimulus of any magnitude can elicit a response

Lasts into late phase 3 of AP b/c Na+ channels are inactivated

K+ channel blockers prolong the ERP & the AP duration  

Relative Refractory Period 

ANS regulation of the heart (M2 & B1) 

Phase 4 slope is increased by an increase in cAMP resulting from B1 receptor activation and slowed by a decrease in cAMP resulting from M2 receptor activation

Increase in cAMP:

Increase upstroke velocity in pacemakers by Ca influx

Shorten AP duration by increase of K+

Increases HR by increase of Na+ influx

Decrease in cAMP: 

Does the opposite plus produces a K+ current which slows the rate of diastolic depolarization and decreases HR