Atrial Fibrillation

Atrial fibrillation occurs when the atria fibrillate and send rapid impulses to the atrioventricular node. The atrioventricular node serves as the “gatekeeper,” deciding which signals get through to the infranodal conduction system. It causes an irregularly irregular rhythm, the differential of which includes includes atrial fibrillation, multifocal atrial tachycardia, and atrial flutter with variable conduction. Causes include any disturbance of atrial architecture (e.g., inflammation, fibrosis, hypertrophy) increases susceptibility. These changes occur most commonly in the setting of heart disease associated with hypertension, coronary artery disease, valvular heart disease, cardiomyopathies, and heart failure (which tend to increase left atrial pressure and alter wall stress). Extracardiac factors that promote atrial fibrillation include sleep apnea, obesity, alcohol/drugs, and hyperthyroidism.

“Lone AF” is a historical descriptor that has been variably applied to younger persons without clinical or echocardiographic evidence of cardiopulmonary disease, hypertension, or diabetes mellitus. If the duration of onset is reliably less than 48 hours, it is reasonable to offer the patient a rhythm control strategy – either pharmacologic with amiodarone, dofetilide, flecainide, ibutilide, propafenone, or procainamide, or electrical cardioversion. If the onset is longer than 48 hours, pursue a rate control strategy with either beta blockers or non-dihydropyridine calcium channel blockers as first line agents with a heart rate goal of < 110 bpm.

Also, consider anticoagulation after risk stratification with the CHADSVASC score for stroke prevention. Always consider secondary causes of atrial fibrillation (i.e., sepsis, pulmonary embolism, etc.) prior to pursuing a rate control strategy as the heart rate could be compensatory.

Examples

Atrial Fibrillation

Atrial fibrillation with rapid ventricular response.

Atrial Fibrillation

Atrial fibrillation with rapid ventricular response. The apparent atrial activity in V1, at first glance, appears to represent flutter waves, but flutter waves are very regular in appearance and cause ventricular activation (R-R intervals) at intervals that at multiples of atrial activation (P-P interval) - not the case here. Therefore, the apparent atrial activity in V1 is just baseline artifact and this is atrial fibrillation

Atrial Fibrillation

Slow atrial fibrillation due to digoxin toxicity. Digoxin slows conduction through the atrioventricular node and increases automaticity. Slow atrial fibrillation is a common rhythm with digoxin toxicity. Also note the "scooped" ST-segments typical of the digoxin-effect.

Atrial Fibrillation with WPW

The QRS morphologies are inconsistent owing to the variable transmission of signals from the atria to the ventricles.

Atrial Fibrillation with WPW

Atrial fibrillation with Wolf-Parkinson-White. The QRS morphology is inconsistent owing to the variable transmission of signals from the atria to the ventricles. Normally, the atrioventricular node serves as the “gatekeeper” for signals arising from the atria – it has a refractory period that does not allow ventricular rates much faster than about 190. Accessory pathways have short refractory periods; therefore, signals can be transmitted at much faster rates with R-R intervals as low as 200 ms (i.e., 300 bpm)

Atrial Fibrillation with WPW

Notice the more-rapid-than-usual rate for atrial fibrillation and changing QRS morphologies consistent with pre-excitation (i.e., Wolf-Parkinson-White). This patient was electrically cardioverted and admitted for a successful accessory pathway ablation.

Right Bundle Branch Block & Left Posterior Fascicular Block

The rhythm is irregularly irregular as a result of atrial fibrillation. There is a right bundle branch block and a left posterior fascicular block.

Third Degree Atrioventricular Block

This patient had known atrial fibrillation yet has a regular rhythm (aside from the final premature complex). Atrial fibrillation with complete heart block will characteristically have a fibrillatory baseline but with a regular escape rhythm.

Bifascicular Block

Right bundle branch block and left anterior fascicular block with atrial fibrillation. This patient ultimately progressed to complete heart block.

Right Bundle Branch Block

Rate-dependent right bundle branch block. At higher rates, disease fascicles can fail.

Sinus Node Dysfunction

Atrial fibrillation alternated with sinus arrest and junctional escape in this patient with sick sinus syndrome.

Right Bundle Branch Block

In addition to the right bundle branch block, the left anterior fascicular block, and atrial fibrillation, the patient was also hyperkalemic.

Left Bundle Branch Block

Atrial fibrillation with rapid ventricular response and a left bundle branch block. The left bundle branch block resolved after rate control. In most cases, rate-related bundle branch blocks occur due to a prolonged refractory period of a diseased bundle. When a critical heart rate is exceeded, the diseased bundle fails. Rate-related bundle branch blocks can be especially challenging to diagnose when the rate is regular and fast (e.g., supraventricular tachycardia), creating a regular, wide complex tachycardia that appears like ventricular tachycardia.

Ashman Phenomenon

There are two aberrantly conducted beats with wide QRS complexes and unifocal morphology. In both instances, a prolonged R-R interval is followed by a relatively short R-R interval, which is then terminated by an aberrant beat, consistent with Ashman phenomenon.

Hypothermia

Osborn waves can mimic ST-segment elevation as was the case with this post-arrest ECG. Slow atrial fibrillation is another hallmark of hypothermia. The core temperature was 76 deg F (24.4 deg C).

Digoxin Effect

There is atrial fibrillation with baseline artifact, and a sagging or scooped ST segment best seen in the lateral precordial leads. These findings are expected of someone who takes digoxin, which this patient did.

References

January CT, Wann LS, Alpert JS, et al. AHA / ACC / HRS Practice Guideline 2014 AHA / ACC / HRS Guideline for the Management of Patients With Atrial Fibrillation A Report of the American College of Cardiology / American Heart Association Task Force on Practice Guidelines and the Heart Rhythm So. Circulation. 2014;130(23):199-267.
Van Gelder IC, Groenveld H, Crijns H, et al. Lenient versus Strict Rate Control in Patients with Atrial Fibrillation. New England Journal of Medicine. 2010;362(15):1363-1373.
Stiell IG, Clement CM, Perry JJ, et al. EM Advances Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter. 2010;12(3):181-191.
January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: A report of the American College of cardiology/American heart association task force on practice guidelines and the heart rhythm society. Circulation. 2014;130(23):e199-e267.
Bosch NA, Cimini J, Walkey AJ. Atrial Fibrillation in the ICU. Chest. 2018;154(6):1424-1434.