Prevalence trend of atrial fibrillation
Prevalence directly related to age (older = more)
What determines the APD in fast channel tisue?
Na+ channel recovery
What determines the APD in slow channel tissue?
Ca++ channel recovery
Atrial fibrillation exhibits mostly what kidn of reentry?
Irregularly irregular reentry
Describe the rate of firing in atrial fibrillation
Rapid and irregular firings at 400 - 600 bpm
Maximum beat rate that the AV node can conduct. What effect does this have on atrial fibrillation?
AV node filtering since the 400 - 600 bpm firing in the atria cannot pass into the ventricles
Typical untreated ventricular response to atrial fibrillation
130 - 150 bpm
Ventrical response to atrial fibrillation involving a fast channel tissue bypass
Firing > 150 bpm = increased response
3 potential negative consequences of atrial fibrillation
Impaired cardiac performance
Symptoms (palpitations, chest discomfort, dyspnea)
Potential consequence of maintaining beat rate over 100 bpm due to atrial fib
Congestive heart failure
Potential concentration of maintaining beat rate over 120 bpm due to atrial fib
Cause of stroke due to atrial fibrillation
Stasis of blood in left atrial appendage leads to clot formation. Dislodgment of thrombus --> brain = stroke
NOTE: single most important cause of stroke in elderly
What is the method to predict stroke risk for atrial fib patients?
Note that age 65 may also be a good cutoff
If CHADS = 1 or higher, what kind of treatment is recommended?
Classic proposed mechanism for atrial fib
Multiple simultaneous functional reentrant circuits
2 mechanisms proposed for atrial fib apart from the classic mechanism
Rapidly firing single ectopic focus, driving atria so fast that different regions respond at different rates according to max frequency they can support, producing fibrillatory response
Single very rapid local reentry circuit, producing fib response as in 1
2 treatment approaches for atrial fibrillation
How to control rate in atrial fib
Leave patient in AF, but control ventricular response (i.e. slow conduction in AV node, for example)
How to control rhythm in atrial fib
Stop AF if needed (usually by electrical cardioversion)
If needed to prevent recurrence (often is), give antiarrhythmetic drugs, or if they fail, perform atrial tissue ablation targeted to arrhythmogenic regions
3 types of drugs for rhythm control (i.e. in atrial fib)
Class I (propafenone, flecainide)
Class II/ beta-blocker (sotalol)
3 types of drugs frp rate control (i.e. in atrial fib)
Calcium channel blockers (diltiazem, verapamil)
Purpose of electrica cardioversion
Synchronise cardiac electrical activity and "resetting it" = effective for terminating >99% of sustained tachyarrythmias, including atrial fib
How to deliver electrical cardioversion for supraventricular arrhythmias (such as atrial fib)
Shock should be synchronized with the QRS to avoid delivery during T wave (when some ventricular muscle is repolarized and some not)
Potential consequence of delivering electrical cardioversoin during T wave
Can induce chaotic ventricular reentry and ventricular fibrillation
How to prevent recurrance of atrial fibrillation
Increase refractory period
Describe the firing in atrial flutter
A single atrial macroreentrant circuit in atrium (most commonly right), typically at 250 - 300 bpm
Atrial flutter exhibits mostly what kind of reentry and why?
Rate is slower than in atrial fib, so atria cn respond 1:1 (rapid and regular)
Atrial fibrillation ECG
Atrial flutter ecg
Which type of control approach is more used in treating atrial flutter?
Rate control is harder for AFL, so rhythm control more commonly used (best response to class I and class III antiarrhythmics)
Most successful and curative method for atrial flutter
Why is ablation most often the first choice for prevention of recurrance over antiarrhythmic drugs for atrial flutter?
Single circuit usually allows critical anatomical component to be identified so easy to ablate
Stroke risk for atrial flutter
Comparable to atrial fib (same principles apply, i.e. CHAS2 > 1 = anticoagulants)
Define ventricular tachycardia
Rapid rhythm arising from a region in the ventricles, most typically 150 - 180 bpm
Causes of ventricular tachycardia
VT due to enhanced automaticity is seen most likely in what condition?
What does VT due to enhanced automaticity repond well to?
Class I antiarrhythmetics (i.e. intravenous lidocaine)
VT due to DADs is most likely seen in which conditions?
Conditions of cardiac hypertrophy and failure (i.e. hypertrophic cardiomypathies, CHF), which cause abnormal Ca++ handling
Give an example of a specific genetic context in which DAD-induced VT is seen
Ryanodine receptor mutation in catecholaminergic polymorphic VT (CPVT)
DAD-induced VT responds to what kind of antiarrhythmic drug?
Class I effect (i.e. relevant to DAD-induced VT)
Prevents DAD from reaching threshold and may also prevent abnormal RyR2 Ca++ release
Conditions associated with EAD-induced VT
Conditions that prolong APD/QT interval (i.e. Long QT Syndrome); can be congenital or acquired
Example of acquired EAD-VT
Drugs that prolong APD, especially class III drugs
Examples of congenital EAD-VT
Genetic conditions that enhance plateau Na+ current (LQT3) or reduce phase 3 K+ current (LQT1, LQT2)
What exacerbates the risk of EAD-induced VT?
Concomitant factors tending to prolong QT (slow heart rate, hypokalemia, hypomagnesemia)
How to treat EAD-induced VT
Focus on underlying conditions:
- Beta-blockers useful in LQT1 and 2
- Increasing HR rate induces QT and may help (i.e. temp. pacemaker in emergency situation)
When does reetrant VT tend to occur?
In presence of reentry substrate like a myocardial scar, most commonly post-MI
Drugs that reetrant VT is most likely to respond to
Drugs that reetrant VT is unlikely to respond to
When can direct-current cardioversion be used for VT?
Terminate VT when severe hemodynamic compromise is life-threatening
Define ventricular fibrillation
Chatoci ventricular rhythm with no effective cardiac pumping
Lethality of ventricular fibrillation
Lethal within minutes in the absence of cardiac massage/ CPR (requires emergency cardioversion)
How does ventricular fibrillation occur?
De novo as a result of a predisposing condition (acute MI, congenital ion-channel mutation)
A result of degeneration of VT
How to prevent recurrence of ventricular fibrillation
Resuscitated individuals from VF generally require implantation of a defibrillator (drug therapy not reliable enough)