Arrhythmias: Classification, Mechanisms, & Treatment Approach

Front 1

Outline the most common types of arrhythmias and, for each, describe a possible mechanism and the strategies for acute and chronic treatment.

Back 1

Atrial Fibrillation: Functional re-entry (multiple foci in atria); acute: control ventricular rate by reducing AV conduction (beta blockers and verapamil, a Ca2+ channel blocker) / maintain sinus rate with DC conversion or pharmacologic cardioversion; chronic: control ventricular rate by reducing AV conduction/maintain sinus rhythm with K+ or Na+ channel block/ablation of triggers int he left atrium, near the pulmonary veins

Atrial Flutter: stable anatomic re-entrant circuit; acute: control ventricular rate by reducing AV conduction/restore sinus rate with DC conversion; chronic: same as Afib + ablation (80% success rate)/if pharacologic approach is needed, same as atrial fibrillation

AV nodal re-entry (PVST: Paroxysmal Supraventricular Tachycardia): Re-entrant circuit within or near the AV node; acute: control ventricular rate by reducing AV conduction/restore sinus rate with adenosine or DC; chronic: suppress PAC or PVC triggers with beta blockers or other anti arrhythmic drugs/ablation of the accessory or slow pathway in the AV node.

Ventricular tachycardia in patients without structural heart disease: increased SANS activity, resulting n calcium overload, afterdepolarizations and triggered automaticity; acute: restore sinus rhythm with defibrillation/reduce Ca-induced triggers with verapamil or beta blockers

Ventricular tachycardia in patients with a history of MI: reentry near the rim of the healed MI; acute: Restore sinus rhythm with defibrillation or with K+ and/or Na+ channel block; chronic: ICD, beta blocker, K+ channel block

Ventricular fibrillation: functional reentry; acute: restore sinus rhythm with defibrillation or K+ and/or Na+ channel block; chronic: ICD, beta blocker, K+ channel block

Torsades de pointes: prolonged AP, resulting in afterdepolarizations and triggered automaticity; acute: restore sinus rhythm with defribillation, pacing, magnesium correction of electrolyte abnormalities; chronic: beta blockade, pacing, ICD if underlying irreversible cause

Front 2

Briefly describe the association between abnormalities of impulse formation and arrhythmias, and between abnormalities of conduction and arrhythmias

Back 2

Abnormalities of impulse formation (aka automaticity)

1) Reduced Automaticity: failure or inhibition of impulse formation
- sinus bradycardia caused by inhibited impulse formation in SA node

2) Enhanced Automaticity: Cells have an increased tendency to undergo an AP
- AV node cells can pace the heart under pathologic conditions (beta-adrenergic stimulation, hypokalemia, mechanical stretch)
- myocardial atrium or ventricle cells can acquire pacemaker abilities (usually due to depolarization as a result of ischemia)

3) Triggered Automaticity: when a normal cardiac AP is interrupted or imediately followed by an early depolarization event, which, if of sufficient strength may propagate into a sustained arrythmia
-EAD (Early afterdepolarization): triggered when AP is prolonged during repolarization phase, shows up as a prolonged QT interval. These can lead to torsade de pointes, a dangerous form of ventricular tachycardia with polymorphic waves caused by a "twisting" reentry current (Long QT Syndrome is a term fro the clinical syndrome associated with a genetic condition that interferes with K+ channels or activates Na+ channels resulting in prolonged QT interval due to inhibited repolarization after an AP
- DAD (delayed afterdepolarization): triggered from the resting potential, think "calcium burp" caused by excessive intracellular Ca, often underlies arrhythmias caused by ischemia, heart failure, excess catecholamines, and digitalis OD

Hint 2

Abnormalities of conduction:

Conduction blocks (1st, 2nd type 1, 2nd type 2, 3rd degree): AV node abnormalities can block the AV node to varying degrees (slowed conduction all the way to total block), leading to the conduction block arrythmias listed in parentheses

Reentry pathways
-anatomically determined accessory pathways (congenital WPW syndrome or acquired permanent changes in conducting properties of a certain area of the heart, leading to self-sustaining conduction loops
- Functionally determined accessory pathways (no distinct, anatomically defined pathway, instead distressed myocardial tissue (ie ischemia) see example of unidirectional block)

Front 3

Explain why the presence of an abnormal electrical connection between the ventricles and atria seen in Wolff-Parkinson-White syndrome predisposes to a reentry arrhythmia

Back 3

Example of reentrant pathway due to an anatomically-determined accessory pathway. In WPW syndrome, fast conduction fibers are present in teh fibrous skeleton that normally electrically divides atria from ventricles, a congenital condition. A premature atrial impulse has a high chance of inciting a sustained reentry circuit, because the premature beat will depolarize the atria up to the accessory pathway and be blocked by the ventricles which are still refractory from the previous beat. Meanwhile, the premature impulse is delayed normally by the AV node, propogates through the ventricles which have now recovered, and loops through the accessory pathway to the atrium, which has now repolarized due to the abnormal AV conduction delay.