Cardiac Arrythmia

mechanisms and definitions note: Arrythmias with "Variable" rhythm characteristics were not added

Arrythmia

* Any SIGNIFICANT deviation from normal cardiac rhythm
* If left untreated: impair of cardiac pumping ability, cardiac failure, CVA.

Cardiac Electrophysiology Phase 0

Rapid depolarization; rapid influx of Na.

Cardiac Electrophysiology Phase 1

Brief period of repolarization; efflux (exit) of K.

Cardiac Electrophysiology Phase 2

plateau; opening of Ca channels; diastole.

Cardiac Electrophysiology Phase 3

end of plataeu; repolarization complete; close of Ca channels.

Cardiac Electrophysiology Phase 4

SLOW AF spontaneous depolarization

Pacemaker Cells

Cell found in the SA and AV node that has the ability to depolarize spontaneously because of a rising phase 4

Components of the heart that allow depolarization

* SA node
* Atria
* AV node
* Bundle of His
* Purkinje fibers

Factor that affect the development of Arrythmia

* Metabolic and electrolyte imbalance
* Abnormal autonomic influence on the heart
* Digitalis toxicity
* Myocardial ischemia and Myocardial infarction
* Abnormal impulse generation
* Abnormal impulse conduction
* Simultaneous abnormalities of impulse generation and conduction

Sinus Tachycardia

Sinus Arrythmia

>100 bpm

Sinus Bradycardia

Sinus Arrythmia

Sick Sinus Syndrome

Sinus Arrythmia

Junctional Rhythm

Atrioventricular Junctional Arrhythmias

40-55 bpm

Junctional Tachycardia

Atrioventricular Junctional Arrhythmias

100-200 bpm

Atrial fibrillation and flutter

Supraventricular Arrhythmias

Atrial rate > 300 bpm

Atrial tachycardia

Supraventricular Arrhythmias

Atrial rate > 140-200 bpm

Ventricular tachycardia

Ventricular Arrhythmia

140-200 bpm

Ventricular Fibrillation

Ventricular Arrhythmia

Irregular, totally uncoordinated rhythm

Sodium Channel Blockers

* Class 1
* Will go for **sodium channels** in nerve and muscles.
* Directly bind to channel or effect on cell membrane.
* Inhibit channel opening = **decrease membrane excitability**
* May affect myocardial excitation and conductance.

Sodium Channel Blockers: Subclass 1A

* **Moderate** slowing of phase 0 depolarization: Moderate slowing of action potential propagation
* Prolonged repolarization of cardiac cell = increase in effective refractory period

Sodium Channel Blockers: Subclass 1B

* **Minimal** ABILITY TO SLOW phase 0 depolarization: Minimal slowing of cardiac conduction.
* Shorten cardiac repolarization of cardiac cell = decrease in effective refractory period
* used to treat ventricular arrhythmia.

Sodium Channel Blockers: Subclass 1C

* Marked decrease in rate of phase 0 depolarization: Marked slowing of conduction
* Little effect on repolarization
* Best for ventricular arrhythmia

Adverse Effects of Sodium Channel Blockers

* Aggravation of cardiac rhythm disturbances
* Dizziness, visual disturbances, and GIT problems (nausea, vomitting, diarrhea)

Beta Blockers

* Class 2
* **Mainstay** in the treatment of arrhythmias
* **Blocks Beta 1 receptors**
* Decrease cardiac automaticity prolong effective refractory period = decrease in HR
* Slow down conduction through myocardium
* Most effective in treating HR problems that originated in the Atria especially AV node.

Adverse Effects of Beta Blockers

* Heart failure
* Excessive slowing of cardiac conduction: increase in arrhythmias.

Drugs that Prolong Repolarization

* Class 3
* Delays repolarization: prolonging effective refractory period
* MOA:

> -Inhibits sympathetic adrenergic discharge
>
> \-Decreasing myocardial excitability
>
> \-Slowing down cardiac conduction
* Used to treat ventricular arrhythmias.

Adverse Effects of Drugs that Prolong Repolarization

* Amiodarone - can cause pulmonary toxicity (interstitial pneumonitis, pulmonary fibrosis, liver damage)
* Bretylium - orthostatic hypotension

Calcium Channel Blockers

* Class 4
* Selective ability to **block calcium entry** into myocardial and vascular smooth muscle after excitability and conduction of cardiac tissues: Decrease rate of discharge of SA node.
* Inhibit conduction velocity through the AV node
* Most successful in treating arrhythmias caused by atrial dysfunction: SVT and Af

Adverse Effects of Calcium Channel Blockers

* Excessive bradycardia (low HR)
* Peripheral vasodilation (dizziness and headaches)

Digitalis Glycosides

Can also be used to prevent or treat certain arrhythmias, including severe atrial fibrillation and paroxysmal AV nodal reentrant tachycardia

Large doses of Magnesium (1-2 gm)

Can be infused intravenously to treat severe ventricular arrhythmias such as torsades de pointes (tachycardia that starts at the lower chambers).

This is thought to control these arrhythmias by normalizing cardiac ion channel function, but the exact mechanism of its effects is not fully understood.

Adenosine

A substance found naturally in the body, can also be administered intravenously to terminate severe arrhythmias such as reentrant supraventricular tachycardia.

Binds to specific adenosine receptors on the heart, and it affect HR by decreasing calcium entry into myocardial tissues.

Ranolazine (Ranexa)

Has complex effects on sodium and calcium movement across myocardial cell membrane – may help control atrial and ventricular arrhythmias with minimal proarrhythmic effects.

Non-Pharmacological Tx for Arrhythmia

* Implantable Devices
* Pacemakers
* Cardioverter Defribillator
* Surgical Intervention (Electrode Catheter Ablation)