Epidemiology: 2nd most common narrow-complex tachycardia in the ED (1st: sinus tachy)

Pathophysiology:
Multiple, small areas of atrial myocardium continuously discharging and contracting → no
uniform atrial depolarization and contraction (only a quivering of the atrial chamber walls) →
ineffective ventricular filling and diminished cardiac output.

ECG Features:
● Absence of discernible P waves with flat or chaotic isoelectric baseline, most
prominent in V1
● QRS complexes narrow unless preexisting bundle branch block or preexcitation
syndrome
● Irregularly irregular ventricular rhythm

Atrial rate > 600 beats/min

Ventricular rate 120-170 beats/min (ventricular rate is slower due to the refractory period of
the AV node)
Illnesses or medications may reduce AV node conduction and markedly slow ventricular
response.
A very rapid ventricular response (>200 beats/min) may be seen in patients with accessory
or bypass tracts.

Clinical Significance:
AF is usually associated with ischemic and valvular heart diseases. Less common causes
include congestive cardiomyopathy, myocarditis, alcohol binge (“holiday heart”),
thyrotoxicosis, and blunt chest trauma.

Left atrial enlargement is a common feature of patients with chronic AF.

AF classification according to duration/episode persistence:

● Paroxysmal: AF lasting < 7 days terminating spontaneously or with treatment
● Persistent: AF lasting > 7 days OR requiring treatment to terminate
● Long-standing persistent: AF lasting continuously > 1 year
● Permanent: decision was made not to cardiovert to SR
● New-onset: symptomatic patient without prior history of AF

AF classification according to underlying pathophysiology:

The likelihood of developing AF varies across physiological and pathological states. Within
this context AF may be considered as:
● Primary: If AF has an established pathophysiologic process.
● Secondary: If AF is caused by a self-limited or acutely reversible (or at least partially
reversible) precipitant.
○ Common causes of secondary AF are:
The clinical consequences of atrial fibrillation include:
● Loss of atrial contraction: in patients with compromised cardiac function, left atrial
contraction contributes significantly to left ventricular filling, so the loss of effective
atrial contractions may produce heart failure in these patients
● Potential for rapid ventricular rates: a rapid ventricular rate can impact ventricular
filling as well as coronary and systemic perfusion
● Risk of venous and arterial thromboembolism

Risk of conversion-induced thromboembolic events according to duration:

● NOAF < 12 hours → 0.3%
● NOAF 12-48 hours → 1% (9.8% in HF and DM)
● NOAF > 48 hours → increased risk across all patient groups, anticoagulation for 3-4
weeks prior to cardioversion is recommended

Treatment:
ED treatment of AF involves 3 issues:
1. Ventricular rate control
2. Rhythm conversion
3. Anticoagulation

Ventricular Rate Control Approach

● Initiating medications that block the AV node to control the ventricular response,
initiating oral anticoagulants to prevent thromboembolism (if appropriate), and
reevaluation after 3 to 4 weeks for elective cardioversion.
● Using:
○ Calcium-channel blockers (diltiazem)
○ Beta-blockers (metoprolol, esmolol)
○ IV procainamide
○ IV amiodarone
● The goal for rate control is a ventricular rate of <100 beats/min at rest.

Rhythm Conversion Approach

● Using electrical (150-200 J) or pharmacologic methods to convert the patient back
into SR while in the ED.
● The antiarrhythmics procainamide, ibutilide, flecainide, propafenone, and vernakalant
can chemically convert atrial fibrillation to SR
○ Ibutilide has the highest consistent success rate for conversion.
○ Ibutilide should not be given in the presence of hypokalemia, prolonged QT
interval, or history of HF, as torsades de pointes may be initiated (risk persists
for 4 to 6 hours after the ibutilide is given)

Anticoagulation
● Calculate CHA2DS2-VASc score to risk-stratify the potential for future arterial
embolic complications.
 ● For unstable patients requiring cardioversion who are at increased risk for embolic
complications, administer an initial dose of a DOAC for nonvalvular AF or LMWH for
patient with mechanical prosthetic valve, rheumatic mitral stenosis, or serious renal
impairment before or immediately after electrical cardioversion.
● For patients treated with heparin, transition to warfarin is begun on discharge with
continued heparin treatment until the INR is in the therapeutic range.

Treatment varies according to:

● Patient stability
● Duration of symptoms
● Chronicity of atrial fibrillation (paroxysmal, persistent, or permanent)
● Whether there’s an underlying medical condition or not (For NOAF, check thyroid
function)

In complex AF (AF + RVR with significant underlying acute medical issues, e.g.: sepsis,
severe hypovolemia, PE, alcohol withdrawal, etc), management priority is focused on
treating the underlying medical issue while not employing standard rate and rhythm control
therapies in the early stages of care. Because, it is significantly more difficult to achieve rate
or rhythm control in complex AF and such attempts are associated with an increased
incidence of adverse events.

Recent-onset AF + RVR in unstable patients, treat with urgent electrical cardioversion.

Long-standing AF + RVR in unstable patients, electrical cardioversion is not likely to

succeed, and instead, initiate hemodynamic resuscitation and ventricular rate control
treatment.

For stable low-risk patients NOAF, either rate-control or rhythm-conversion strategies are
appropriate. But no proven benefit for conversion of all NOAF patients to SR while in the ED,
because: rate of spontaneous conversion is high (70% within 48-72%) and AF trials
demonstrating that rate control is similar to rhythm control in terms of several key endpoints.
So, stable NOAF → rate control alone, either as an inpatient or outpatient depending on
overall clinical condition

Paroxysmal AF → a period of observation and treatment in the ED is appropriate as the AF

may spontaneously convert. Ventricular rate control may help control symptoms until
conversion.

Recurrent paroxysmal AF → pill in a pocket approach: oral medications (usually flecainide

or propafenone) taken at the onset of the dysrhythmia
Exclude SA or AV node dysfunction, conduction disturbance (bundle branch block, Brugada
syndrome), and structural heart disease before starting this approach.

Successful cardioversion to SR is more likely in:

● AF of short duration (<48 hours) and atria are not dilated
● No rate control or medical rhythm conversion attempts were made prior
Atrial Flutter:
● Atrial flutter is a form of supraventricular tachycardia caused by a re-entry circuit
within the right atrium.
● Atrial flutter most often is a regular rhythm. Rarely, it can be irregular due to variable
AV nodal block.
● P waves are present and of a single morphology, typically a downward deflection,
called flutter waves resembling a saw blade with a “sawtooth” pattern, best seen in
the inferior leads, upright flutter waves are present in V1.
● Most commonly, the atrial rate is regular, classically around 300 beats/min, +/- 50
beats/min
● The ventricular rhythm is frequently regular and is a function of the AV block.
○ AV ratios of 2:1 are common and produce a ventricular rate around 150
beats/min
 ○ 3:1 AV ratio will result in a ventricular rate of 100 beats/min.
○ Although the degree of AV conduction is often fixed, it may also be variable
and create an irregular ventricular response.
● Managed the same way as AF: either rhythm conversion or ventricular rate control
with β-blockers or calcium channel blockers.
● Very responsive to electrical cardioversion; as little as 25 to 50 J is often effective.
● Atrial flutter patients tend to better tolerate the dysrhythmia hemodynamically than
patients with AF, which results from the organized atrial contraction seen with atrial
flutter, as opposed to the lack of organized atrial contraction with AF.
● Despite organized atrial activity, there is a risk of arterial embolism with atrial flutter,
and corresponding recommendations for anticoagulation are based on the same
criteria used for AF.

https://recapem.com/atrial-fibrillation-in-critically-ill-patients-innocent-bystander-or-criminal/
https://emcrit.org/squirt/af/