Mechanism of Arrhythmia Flashcards
What are the clinical consequences of arrhythmia?
inadequate pump function, leading to low cardiac output and symptoms
Describe the APs generated by SA and AV nodes
slow potential, mediated by Ca ions
Describe the APs generated by atria, ventricles, and His-Purkinje system
fast potential, mediated by Na ions
Describe the manifestations of K channel blockade in the heart
- increase in AP duration, increase in QT interval
What are the two general mechanisms of arrhythmia?
- disturbance of impulse formation (initiated somewhere besides the SA node)
- disturbance of impulse conduction (too slow, too fast, or blocked)
What are some conditions that can cause a brady arrhythmia? What about a tachyarrhythmia?
Brady bunch: sinus bradycardia, SA exit block, sick sinus syndrome, sinus arrest, type I, II, or III degree heart block
Tricky tachy: supraventricular tachycardia or ventricular tachycardia
How does each type of heart block appear on EKG?
1st degree: increased P-R interval
2nd degree, type I (Wenckebach): gradual increase in P-R interval until a beat is skipped
2nd degree, type II: constant P-R interval with intermittent skipped beats
3rd degree: no conduction present from atria to ventricles, no relationship between P wave and R-S waves… why can’t we all just get along?
What are the three specific potential mechanisms of tachyarrhythmia?
- increased automaticity (impulse from somewhere besides SA node - atrial, junctional, ventricular)
- triggered automaticity (impulse starts too early)
- reentry (impulse through different tissues)
What is the most common mechanism of ventricular arrhythmia?
- reentry: 3 or more consecutive beats at the rate of 100+ bpm, wide but regular QRS
What are two examples of triggered automaticity?
- Early Afterdepolarization: interrupts phase 3
- Delayed Afterdepolarization: interrupts phase 4
A new patient comes in that has been on digoxin for the past few years. What type of arrhythmia are they most at risk for?
- delayed afterdepolarization
In about 10% of the population, there are two pathways that lead into the AV node. What does this put them at risk for?
- reentry
- there is a fast and slow conduction pathway
- requires a unidirectional block
- there must be a final common destination of the two paths
- usually this is harmless, but a premature beat can disrupt the homeostasis
You’re looking at an EKG and you see delta waves. What could this indicate?
- Wolff Parkinson White Syndrome
- cells with conduction properties are abherrently around mital and tricuspid annulus to create an accessory pathway for conduction
- conduction down this tissue is faster than AV node conduction
- can also cause reentry
- in the context of A fib, this can really mess a person up and progress to v fib
You look at an EKG and see no organized atrial activities! What is going on?!
- atrial fibrillation
- QRS is irregularly irregular
- thankfully, there is a safety mechanism in the AV node to peak at 200 bpm
I say saw tooth, you say…
- atrial flutter
- rate can be 240-340 bpm
- QRS is regular