Arrhythmias (B 2: W 1) Flashcards
What is the definition of an arrhytmia?
Arrhythmias are any disorder of rate, rhythm, origin, or conduction of impulses within the heart
What are some of the consequences of arrhythmias?
- Compromised mechanical performance - tachycardias, extrasystoles, bradycardias, AV block, fibrillation
- Triggers for more serious arrhythmias
- Formation of thrombi
What precipitating factors can contribute to arrhythmias?
- Ischemia with pH and electrolyte abnormalities
- Excessive myocardial fiber stretch
- Excessive discharge or sensitivity to autonomic neurotransmitters
- Exposure to foreign chemicals (e.g. digitalis)
What are the two major mechanisms involved in generating arrhythmias?
- Abnormal impulse formation
- Reentrant excitation
What are the sub-categories of abnormal impulse formation (automaticity)?
- No change in pacemaker site: sinus bradycardia and sinus tachycardia
- Changes in pacemaker site: ectopic pacemakers
- Emergence of latent pacemakers - AV node, Purkinje fibers
- Automaticity resulting from “injury current”
- Oscillatory after-depolarizations
What is an example of slowed conduction without reentry?
AV block
No reentry
What are the requirements for reentry in disorders of impulse conduction?
- Unidirectional block
- Conduction time around alternative pathways must exceed the effective refractory period of the tissue
What factors favor the development of reentry in cardiac arrhythmias?
- Long reentrant pathway
- Slow conduction
- Short effective refractory period
What are the two kinds of abnormal triggered activity in ventricular cells?
- Delayed-Afterdepolarizations (DADs)
- Early-Afterdepolarizations (EADs)
What causes a DAD?
Elicited by abnormal Calcium release event which induces a transient membrane depolarization
Activates Na-Ca exchanger (3:1): one positive charge moving in –> delayed afterdepolarization (arises from the resting potential)
Often seen in conditions favoring intracellular Ca overload
What causes EADs?
Delayed repolarization favoring reopening of Calcium channels
During plateau of action potential
How does digitalis lead to arrhythmias?
**Causes increase in calcium **
Delayed-Afterdepolarization
Also strengthens force in heart beat
What factors promote DADs?
- Cardiac glycosides (digitalis) in Purkinje fibers: agents used as posiive inotropic agents in heart failure
- Catecholamines in atrial and ventricular tissues
- Elevated heart rate - Ca cannot return to resting level
- Low K or high Ca - narrow window
- Caffeine - opens Ca release channels
- Hypoxia - elevates intracellular Ca
- Cardiac hypertrophy and failure - cells are compromised so have depressed Ca regulation
What conditions favor the development of EADs?
- Hypoxia - stimulation of Ca ion channels
- Acidosis - prolonged action potential, K channels sensitive to low pH
- Catecholamines - phosphorylate Ca channels by ß adrenergic stimulation
- Current injections
- Pharmacological agents:
- Antiarrhytmic agents
- Cardiac hypertrophy and failure
Why do antiarrhythmic agents produce arrhythmia?
They block repolarizing K channels, which can lead to ventricular arrhythmias
Creates longer repolarization
Which ions have an impact on EADs and how so?
Potassium and Sodium
Block in potassium channel means the ventricular cell can’t repolarize
Increase in sodium channels - They are normally closed, but fail to inactivate - Na channels open throughout action potential, leads to a prolonged action potential
What can trigger torsades de pointes?
- Increase in sodium channels - prolonged AP
- QT dispersion as a result of longer QT interval - prolonged AP
What is long QT syndrome (LQT)?
- 12 types
- Inherited or congenital (rare): genetic mutations affecting the expression and/or function of voltage-gated ion channels determining the cardiac action potential
- Aquired (more common: drug-induced, but could involve a genetic predisposition
- Triggers EADs –> arrhythmias
- Prolonged action potential due to increase in Ca, increase in Na, or decrease in K
