SA Nodal Firing Rate in Atrial Fibrillation
The SA node firing rate becomes clinically irrelevant during atrial fibrillation because the chaotic atrial electrical activity completely overrides normal sinus node function, and the ventricular rate is instead determined entirely by AV nodal conduction properties, not by SA nodal impulses. 1
Mechanism of SA Node Suppression in AF
During atrial fibrillation, the normal pacemaker function of the SA node is functionally suppressed by the overwhelming atrial electrical chaos. The key physiological changes include:
- Multiple competing atrial wave fronts (300-600 per minute) bombard the AV node continuously, completely drowning out any organized SA nodal impulses 1
- The ventricular rate during AF is determined by: (1) AV nodal conduction properties and refractory period, (2) the sequence and timing of atrial wave fronts entering the AV node, and (3) autonomic tone—not by SA nodal firing 1
- Concealed conduction into the AV node explains rate control: each atrial impulse that partially penetrates the AV node renders those cells temporarily refractory, blocking subsequent impulses from conducting through 1, 2
Clinical Implications for Rate Control
The irrelevance of SA nodal firing during AF fundamentally shapes treatment strategy:
- Rate control targets the AV node exclusively, using beta-blockers, calcium channel blockers, or digoxin to prolong AV nodal refractoriness and slow ventricular response 1
- Target ventricular rates are 60-80 bpm at rest and 90-115 bpm during moderate exercise, achieved through AV nodal modulation alone 1, 3
- L-type calcium channels in AV nodal cells are the primary target, with sympathetic stimulation enhancing and vagal tone impeding AV nodal conduction 1
SA Node Dysfunction Associated with AF
A critical caveat: While SA nodal firing doesn't control ventricular rate during AF, the SA node itself often becomes damaged by AF:
- Up to 20% of AF patients develop sinus node dysfunction due to AF-induced atrial remodeling, including atrial fibrosis, altered calcium channel metabolism, and transformed gene expression in the SA nodal region 4
- AF patients with symptomatic bradycardia show abnormal response of the superior SA node to sympathetic stimulation, with failure of the earliest activation site to shift upward during isoproterenol infusion (only 20% vs 100% in controls) 5
- This creates tachycardia-bradycardia syndrome, where patients alternate between rapid AF and profound sinus bradycardia when AF terminates 4
Management Pitfalls
Critical warning about rate-control medications: Drugs that effectively slow ventricular rate during AF (beta-blockers, calcium channel blockers, digoxin, amiodarone) can cause severe symptomatic bradycardia when AF terminates and sinus rhythm resumes, particularly in patients with underlying SA node dysfunction 1
- This is especially problematic in paroxysmal AF where patients cycle between AF and sinus rhythm 1
- Amiodarone impairs SA node function in one-third of AF patients and further reduces heart rate in those with AF-induced sinus node dysfunction 6
- Some patients require permanent pacemaker implantation due to medication-induced bradycardia 1
Post-Ablation Considerations
After AV nodal ablation for rate control:
- The atria continue to fibrillate with the same chaotic electrical activity, but complete AV dissociation occurs with ventricular pacing providing a regular rate 7
- Anticoagulation remains mandatory because atrial fibrillation persists despite complete heart block, maintaining thromboembolic risk 7
- The SA node continues its irrelevant firing pattern in the fibrillating atria, completely isolated from ventricular function 7