Basic Cardiac Electrical Activity

5 Phases of Cardiac AP

Rapid depolarization

Early partial repolarization

Plateau phase

Repolarization

Resting Membrane potential

Phase 0: Rapid Polarization

Rapid depolarization (upstroke) driven by fast Na+ influx (iNa) in fast response cells

Phase 1: Early Partial Repolarization

driven by outward K+ current (ito)

Phase 2: Plateau Phase

Maintained by inward L-type Ca2+ current (iCa-c) balancing outward K+ currents

Phase 3: Repolarization

Driven by outward K+ currents (iki)

Phase 4: Resting Membrane Potential

or diastolic depolarization in pacemaker cells

Pharmacological effects:

Blocking Ca2+ channels (e.g with Diltiazem) depresses the plataeu phase

Fast Response Cells (Atrial and Ventricular Myocytes, Purkinje Fibers)

Feature a steep Phase 0 upstroke (dv/dt) dependent on fast Na+ channels, a higher amplitude, and a highly negative resting potential (-90 mV)

Slow Response (SA node and AV node)

Phase 0 upstroke is slow and mediated by Ca2+ channels (iCa-c), with a less negative resting potential (-60 mV) and smaller amplitude

Prevention of Tetanization

The long Effective (Absolute) Refractory Period (ERP) prevents tetanic contractions and guards against premature re-excitation during a single beat

AV Node Frequency

In slow response cells, the Relative Refractory Period (RRP) extends well into Phase 4 beyond the action potential duration, allowing the AV node to act as a frequency filter during rapid atrial arrhythmias (e.g atrial fibrilation)

Heart Rate Dependence

Higher heart rates shorten ADP and refractory periods, preserving diastolic filling time at fast rates

Phase 4 Diastolic Depolarization

Spontaneous depolarization in pacemaker cells reaches threshold via the funny current (If, net Na+ influx) and inward Ca2+ currents

Pacemaker Hierarchy and Overdrive Suppression

The Sa node has the fastest intrinsic firing rate and suppresses secondary/latent pacemakers (AV node, Purkinge fibers) via overdrive suppression

Autonomic Control

Firing rate is altered by changing Phase 4 slope, maximum diastolic potential, or threshold potential

Sympathetic (Norepinephrine)

Increases Phase 4 Slope—>Increases HR

Parasympathetic (ACh)

Conduction is lowest in the AV Node (creating a necessary delay for ventricular filling) and fastest in the Purkinje system and ventricular myocardium

Conduction Pathway

SA node—>Atrial Myocardium—>AV node—>Bundle of His—>Bundle branches—>Purkinje fibers—>Ventricular myocardium

Conduction Velocity Variations

Conduction is slowest in the AV node (creating a necessary delay for ventricular filliing) and fastest in the Purkinje system and ventricular myocardium

PR interval

Represents SA to His bundle conduction line (AV node delay)

QRS Complex

Represents ventricular depolarization

QT Interval

Corresponds to ventricular action potential duration (APD)

Ischemia and Hyperlikemia

Local elevated extracellular K partially depolarizes the membrane, inactivating fast Na+ channels, converting fast APs to slow APs and markedly slowing conduction

Re entry and AV Blocks

Unidirectional conduction block paired with slow conduction can trigger reentry loops. AV conduction blocks present in 1st, 2nd or 3rd degrees

Long QT Syndrome and Early Afterdepolarizations

Prolonged ADP or dispersion of repolarization across the wall can trigger EADs, predisposing to Ventricular Tachycardia (Torsades de Pointes)