Arrhythmia Flashcards
1
Q
Normal Conduction
A
- Normally begins at SA-node in right atria
- SA node depolarizes atrial muscles
- AV-node between atria and ventricles is activated and (after a delay) initiates the conduction impulse through ventricles
- Purkinje fibers carry signal through septum to the apex and the rest of the ventricular mass
2
Q
PR Interval
A
- 100-200 ms normally
- Long: heart block (drugs, electrolytes)
- Represents AV-node conduction
- Drugs and disease states may increase time interval/conduction that may cause blockage of impulse
- Monitor PR with certain drugs
3
Q
QRS Interval
A
- 80-120 ms normally
- Long: conduction abnormalities (bundle branch block)
4
Q
QT Interval
A
- Normal range varies with HR
- > 450 ms leads to ventricular tachycardia
- Long: repolarization abnormalities, ion channelopathies (long QT syndrome)
- Represents time for ventricular polar/repolarization
- Rate dependent on HR (QT/ sqrt(R-R))
- *NEED TO MONITOR FOR DRUGS THAT PROLONG QT INTERVAL**
5
Q
Phase 0
A
- Na+ Dependent: Atrium, ventricles
- Ca++ Dependent: SA and AV node
6
Q
Impulse Generation “Leak”
A
- During Phase 4, gradual slope in potentials leads to activation of voltage-gated Na channels (THRESHOLD POTENTIAL and Phase 0!!!)
- Electrical energy and start of one heartbeat
- Altering characteristics of this slope or sensitivities of channels can alter cardiac pacing
7
Q
Phase 4 Slope
A
- Increasing => increases automaticity (HR)
- Sympathetic activity increases slope
- Cholinergic activity decreases slope/HR
- Some antiarrhythmics change slope and HR
8
Q
Impulse Generation
A
- SA node: 60-100 beats/min (most leaky ion channels thus is primary pacemaker)
- AV node: 30-50 beats/min
- Ventricles: <30 beats/min
9
Q
Tachycardias
A
- Sinus tachycardia (SA)
- Atrial tachycardia
- Atrial fibrillation/flutter (fib: HR = 500, flutter: HR = 350)
- AV-nodal re-entry tachycardia (HR = 150-250)
- Wolff-Parkinson White Syndrome (WPW: HR = 150-250)
- Ventricular tachycardia
- Ventricular fibrillation (fib: HR = 500, flutter: HR = 350)
10
Q
Bradycardia
A
-Sinus bradycardia (SA)
-AV node block (1st, 2nd, or 3rd degree)
-Asystole
(Mild-Mod: HR = 40, Severe: HR = 20)
11
Q
Etiology Classifications
A
Metabolic Abnormalities
- Ectopic conduction (early after depolarization)
- Ischemic tissue
- Genetic abnormalities (QT-prolongation)
- Electrolyte abnormalities
- Drug Toxicity
Structural Abnormalities
- Scarring/fibrotic area of no conduction
- Hypertrophy and cardiomyopathy
- Accessory pathways/block/congenital malformations
12
Q
Mechanisms of Arrhythmia Formation
A
Disorder of Impulse Generation
- Abnormal automaticity
- Triggered activity, early or delayed after depolarizations (EAD or DAD)
Abnormal Impulse Conduction
- Block
- Reentry
13
Q
EAD vs DAD
A
- EAD: altered opening of Ca++ or Na+ channels, also K+ channels
- DAD: elevated systolic [Ca++]
14
Q
Heart Blocks
A
- Area of tissue that does not conduct electrical impulse (action potential)
- Most important areas: SA node, AV node, or His-purkinje system (bundle brunch)
- 3rd degree: atria and ventricles are depolarizing independently, no association between the two
15
Q
Reentry Abnormality
A
- Unidirectional block caused by myocardial injury or a prolonged refractory period resulting in abnormal conduction pathway
- Reentry is most common cause of arrhythmias, and it can occur at any level of conduction system
- Impulses travel in retrograde direction and cause extra or irregular heart beats
- AV-nodal reentry arrhythmia is common, premature beat can set it up (node has embedded slow and fast pathways)
- Terminate by increase refractoriness (two-way block) or slow conduction (abnormal impulse hit refractory tissue out of damaged area)
