2 - Cardiac Electrophysiology and Autonomic Pharmacology Review

What does the myocardium muscle tissue do?

Performs the major work of the heart → contraction to pump blood

Atrial and ventricular muscle makes up most of it

What are the specialized tissues of the heart?

SA node, AV node, His-Purkinje system, and accessory pathways

They conduct electrical impulses / action potentials through the heart

What do myocytes do in the heart?

Conduct electrical impulses and help the heart contract

SA node starts it → myocytes conduct it → heart contracts

What happens during Phase 0?

Na⁺ enters the cell → rapid depolarization

Cardiac muscle cell is activated and begins to contract

What happens during Phase 1?

K⁺ briefly leaves the cell → repolarization begins → but the heart muscle is still contracted

What happens during Phase 2?

Ca²⁺ enters while K⁺ leaves → creates the plateau and maintains the heart muscle's contraction

What happens during Phase 3?

K⁺ continues to leave and Ca²⁺ is removed from the cell → repolarization finishes → contraction ends and the muscle relaxes

What happens during Phase 4?

Na⁺/K⁺ ATPase moves Na⁺ out and K⁺ in → restores the resting state → cell is ready for the next heartbeat

What determines conduction velocity in the SA and AV nodes?

Ca²⁺ channel current → determines how fast the electrical impulse conducts through the SA and AV nodes

What determines conduction velocity everywhere else in the heart, NOT the SA and AV nodes?

Na⁺ channel current → determines how quickly the electrical impulse spreads / conducts

Which cardiac cells have fast potentials, and why are they “fast”?

They act fast because rapid Na⁺ influx during Phase 0 causes rapid depolarization and fast electrical conduction

Ex → Atrial and ventricular myocytes, Bundle of His, and Purkinje fibers

Which cardiac cells have slow potentials, and what makes them “slow”?

Their electrical activity spreads more slowly → important for controlling the heart’s rhythm and slowing conduction through the AV node

Ex → SA and AV nodes

How are the fast action potential and Phases 0–4 connected?

The fast action potential is the electrical activity in atrial/ventricular myocytes, Bundle of His, and Purkinje fibers

The Phases 0–4 describe what happens during that fast action potential

What causes the small deflection between Phase 1 and Phase 2?

The voltage-gated Na⁺ channels close/inactivate after Phase 0 → causing a brief drop in membrane voltage before the Phase 2 plateau → when Ca²⁺ enters the cell.

How can genetic variations affect cardiac electrophysiology?

Genetic variations in genes that control cardiac ion channels or electrical signaling can change how the heart’s electrical impulses work

Creating a predisposition to different arrhythmias

What is arrhythmogenesis?

The process by which abnormal electrical activity develops in the heart and causes arrhythmias

What are the 2 major mechanisms of arrhythmogenesis?

Impulse generation → Early/late afterdepolarizations

Impulse conduction → Reentry

What are issues with impulse generation mostly caused by?

Sympathetic/parasympathetic disturbances → can influence impulse generation → increased automaticity and/or afterdepolarizations → arrhythmia

How can disturbances in sympathetic/parasympathetic activity be mitigated?

Vagal maneuvers → techniques that increase vagus nerve activity → slowing HR / AV conduction

β-blockers

What are early afterdepolarizations (EADs)?

Occur during Phases 2–3

Intensify at slow heart rates

Can contribute to long QT-related arrhythmias

What are late/delayed afterdepolarizations (DADs)?

Occur after phase 3

Caused by → increased intracellular Ca²⁺ and intensify at fast heart rates

Can occur with digitalis toxicity, catecholamines, or myocardial ischemia.

What is automaticity and afterdepolarizations?

Automaticity → ability of a cardiac cell to spontaneously generate an impulse.

Afterdepolarization → abnormal depolarization during or after an action potential that can trigger an extra impulse

Can mess with impulse generation → causing arrhythmias

What is a unidirectional block?

An electrical impulse is blocked in one direction but can still travel in another direction.

How can reentry cause an arrythmia?

A unidirectional block forces the impulse to travel in the opposite direction → the impulse eventually loops back and reactivates tissue out of synch → reentry → arrhythmia

Examples of cardiac arrhythmias?

Supraventricular Tachycardia

Atrial Flutter

Atrial Fibrillation

Ventricular Tachycardia

Ventricular Tachycardia and Torsades de Points → monomorphic v polymorphic

What is supraventricular tachycardia (SVT)?

A rapid heart rhythm that starts in the atria or other areas above the ventricles

What happens during atrial flutter?

Rapid, regular atrial electrical activity causes the atria to beat very quickly

The AV node acts as a gatekeeper → limiting how many impulses reach the ventricles, so the ventricles are not the source of the problem

What happens during atrial fibrillation (AFib)?

he atria have rapid, irregular electrical activity → causing no effective atrial beating

Fatal!

What are ventricular tachycardia (VT) and torsades de pointes?

VT → rapid rhythm originating in the ventricles.

Torsades de pointes → a type of polymorphic VT → VT can be monomorphic or polymorphic

What can cause Long QT syndrome?

Genetic mutations

Certain medications → antibiotics and antidepressants

Electrolyte imbalances

What is Long QT syndrome?

A condition where the QT interval is prolonged

So the ventricular electrical activity takes longer than normal to recover → increased risk of ventricular arrhythmias

What is Torsades de Pointes?

A ventricular arrhythmia associated with prolonged QT

It is a polymorphic VT → very fast ventricular rhythm with (poly) changing QRS shapes

What is commotio cordis?

Polymorphic VT caused by a sudden impact to the chest during the T-wave upstroke → when the heart is electrically vulnerable

How do the sympathetic and parasympathetic nervous systems compare?

Sympathetic → speed up → increases heart rate, contractility, and AV conduction.

Parasympathetic → slow down → decreases heart rate and AV conduction.

What are the main parasympathetic ANS receptors?

Nicotinic and Muscarinic

What are the main sympathetic ANS receptors?

Adrenergic receptors → α1, α2, β1, β2, β3

How does the parasympathetic nervous system affect the heart?

Cholinergic

Acts on the SA node, atrial wall, AV node, and ventricular conducting system → mainly affects heart rate and conduction

How does the sympathetic nervous system affect the heart?

Noradrenergic

Acts on the SA node, atrial wall, AV node, ventricular conducting system, and ventricular wall → affects heart rate, conduction, and force of contraction