- Clinical science
Atrial fibrillation (Afib) is a commonly seen type of supraventricular tachyarrhythmia that is characterized by uncoordinated atrial activation resulting in an irregular ventricular response. While the exact mechanisms are still poorly understood, associations with a number of cardiac (e.g., valvular heart disease, coronary artery disease) and noncardiac (e.g., hyperthyroidism, electrolyte imbalances) risk factors have been established. Individuals with Afib are typically asymptomatic. However, when symptoms do occur, these usually include palpitations, lightheadedness, and shortness of breath. Physical examination typically reveals an irregularly irregular pulse. Ineffective atrial emptying as a result of Afib can lead to stagnation of blood and clot formation in the atria, which in turn increases the risk of stroke and other thromboembolic complications. The diagnosis is confirmed by an ECG showing indiscernible P waves and a narrow QRS complex with irregular QRS intervals. Echocardiography is used in patients with Afib to rule out structural heart disease and detect the presence of atrial thrombi. Immediate synchronized cardioversion is required in hemodynamically unstable patients. In stable patients, treatment involves the correction of modifiable risk factors, rate or rhythm control strategies, and anticoagulation. Rate control therapy typically involves the use of beta-blockers or nondihydropyridine calcium channel blockers. Rhythm control strategies involve elective synchronized cardioversion and/or the use of antiarrhythmics (e.g., flecainide, propafenone, or amiodarone). The need for anticoagulation therapy is determined based on the CHA2DS2-VASc score. Catheter-directed or surgical ablation of the arrhythmogenic tissue is used in refractory or severe Afib.
Atrial flutter is another type of commonly seen supraventricular tachyarrhythmia that is usually caused by a single macroreentrant rhythm within the atria. The risk factors for atrial flutter are similar to those of Afib. In atrial flutter, the atrial rate is slower than in Afib and the ventricular rhythm is usually regular. Treatment is similar to that of Afib, consisting of anticoagulation and strategies to control heart rate and rhythm. Atrial flutter frequently degenerates into atrial fibrillation.
The exact causes of atrial fibrillation are unknown, but several risk factors have been identified (see table below).
|Risk factors for atrial fibrillation|
|Cardiovascular risk factors|
|Intrinsic cardiac disorders|
|Noncardiac disorders|| |
Approx. 15% of individuals who develop Afib have none of the above mentioned risk factors (idiopathic/lone Afib).
Remember PARASITE to memorize the major risk factors for acute Afib: P – Pulmonary disease; A – Anemia; R – Rheumatic heart disease; A – Atrial myxoma; S – Sepsis; I – Ischemia; T – Thyroid disease; E – Ethanol.
|Hemodynamic stability||Unstable Afib||Afib presenting with signs of hemodynamic instability (e.g., chest pain, altered mental status, acute pulmonary edema, hypotension, or cardiogenic shock)|
|Stable Afib||Afib without signs of hemodynamic instability|
|Heart rate||Afib with rapid ventricular response||Afib with a ventricular rate > 100 bpm (tachycardic Afib)|
|Slow Afib||Afib with a ventricular rate < 60 bpm (bradycardic Afib)|
|Onset and duration of Afib||New-onset Afib||Afib less than 48 hours in duration|
|Paroxysmal Afib||Afib that resolves within 7 days of onset either following treatment or spontaneously|
|Persistent Afib||Continuous Afib for > 7 days|
|Long-standing persistent Afib||Continuous Afib for > 1 year|
|Permanent Afib||Long-standing persistent Afib that is not treated unless the patient and the treating physician agree to do so|
|Mitral valve involvement||Valvular Afib||Afib in patients with mitral valve stenosis, artificial heart valves, and/or repaired mitral valves|
|Nonvalvular Afib||Afib in patients without mitral valve involvement|
Patients with Afib should always be evaluated for mitral valve involvement!
- Atrial fibrillation is a .
- The exact mechanisms of Afib are not well understood. Suggested mechanisms include:
The new onset of Afib triggers a vicious circle that can ultimately lead to long-standing Afib with atrial remodeling:
- Afib is triggered by one or both of the following
- Afib is sustained by re-entry rhythms and/or rapid focal ectopic firing
- Electrophysiological changes in the atria occur within a few hours of Afib onset (electrical modeling).
- If Afib persists, atrial fibrosis and dilatation (structural remodeling) occur within a few months.
- Electrical and structural remodeling increase susceptibility to Afib, resulting in a vicious circle.
- Effects of Afib
- Most affected individuals are asymptomatic.
- Less commonly, affected individuals develop symptoms of such as palpitations, dizziness, syncope, fatigue, and or dyspnea.
- Signs of underlying disease (e.g., murmurs of mitral stenosis)
- Tachycardia with an irregularly irregular pulse
- Apex-pulse deficit: difference between the rate of apex heart beat and that of the peripheral pulse
- Complications of long-standing Afib
Individuals with Afib may be asymptomatic for a long time before diagnosis is made.
ECG (initial investigation)
- Irregularly irregular RR intervals
- P-waves are indiscernible
- Narrow QRS complex (< 0.12 seconds)
- Transthoracic echocardiogram (TTE)
Transesophageal echocardiogram (TEE)
- Indicated in patients who meet all of the following criteria:
- Visualizes the atria and the left atrial appendage (hotspots for thrombogenesis) to identify thrombi before attempting cardioversion
- Further assesses heart function and rules out underlying structural disease
- TSH, fT4: to screen for hyperthyroidism
- Serum electrolytes (Na+, K+, Mg2+, and Ca2+): to identify electrolyte imbalances
- Troponin levels: to rule out myocardial infarction
- D-dimer levels: if risk factors (e.g., DVT) or clinical features of pulmonary embolism are present
- Brain-natriuretic peptide (BNP): to rule out heart failure
- CBC: to identify anemia, infection
- BUN, serum creatinine: to identify chronic kidney disease
- Ethanol levels, digoxin levels, and/or urine toxicology (e.g., cocaine, amphetamines)
The general principles of treating atrial fibrillation include:
- Correcting reversible causes and/or treatable conditions (e.g., hyperthyroidism, electrolyte imbalances)
- Controlling heart rate and/or rhythm
- Providing anticoagulation
Controlling heart rate and/or rhythm
- Unstable AF: emergent
- Stable AF: rate control or rhythm control strategies to control AF and prevent long-term recurrence (see table below)
|Treatment strategy||Rate control||Rhythm control|
|Goal and rationale|| || |
|Indications|| || |
|Contraindications|| || |
|Therapeutic measures||1st line|
|2nd line (ablative procedures)|| |
Patients with unstable AF should be treated with immediate cardioversion!
Prerequisites for cardioversion of AF
New onset AF (< 48 hours) in patients with:
- Low thromboembolic risk (see cardioversion below) → consider anticoagulation directly before or after
- High thromboembolic risk → start anticoagulation immediately before or after cardioversion
- Anticoagulation options: IV heparin or LMWH, direct thrombin inhibitors (e.g., dabigatran), or factor Xa inhibitors (e.g., rivaroxaban, apixaban)
AF ≥ 48 hours or of unknown duration in patients with:
Unstable AF (require urgent cardioversion): IV heparin or LMWH immediately before cardioversion followed by warfarin for up to 4 weeks after cardioversion
- TEE to rule out atrial thrombi recommended if anticoagulation has not been administered at least 3 week prior to cardioversion
- Stable AF (do not require urgent cardioversion): warfarin with bridging therapy for 3 weeks before and up to 4 weeks after cardioversion
- Unstable AF (require urgent cardioversion): IV heparin or LMWH immediately before cardioversion followed by warfarin for up to 4 weeks after cardioversion
Anticoagulation therapy should be considered in all patients who are about to undergo cardioversion.
|CHA2DS2-VASc score||Indications for long-term anticoagulation|
|C||CHF or left-sided heart failure||1|| |
|A2||Age ≥ 75||2|
|S2||Stroke or TIA or thromboembolism||2|
|V||Vascular disease (prior MI, peripheral artery disease, or aortic plaque)||1|
|Sc||Sex category (female sex)||1|
|CHA2DS2-VASc scores of 1, 2, 3, 5, and ≥6 carry an annual stroke risk of approx. 1%, 2%, 3%, 7%, and >9% respectively.|
Long term anticoagulation for patients with AF in order to prevent thromboembolic complications is indicated if the patient has an underlying valvular disease and/or a CHA2DS2-VASc score ≥ 2
The risk of bleeding due to anticoagulation should always be taken into consideration when initiating anticoagulation therapy
- Atrial flutter is a that is usually caused by a single macroreentrant rhythm within the atria.
- Incidence: 88 per 100,000 person-years (increases with age)
- Sex: ♂ > ♀ (5:2)
- Etiology: similar to atrial fibrillation (see “Etiology” above)
- Type I (common; ; typical or isthmus-dependent flutter): caused by a counterclockwise (more common) or clockwise (less common) macroreentrant activation of cardiac muscle fibers in the right atrium that travels along the tricuspid annulus and passes through the cavotricuspid isthmus
- Type II (rare, atypical atrial flutter): various reentrant rhythms that do not involve the cardio-tricuspid isthmus, are not well defined, and/or occur in the left atrium
- Clinical features
Diagnostics: similar to atrial fibrillation; see “Diagnostics” above
- Sawtooth appearance of P waves: identical flutter waves (F waves) that occur in sequence at a rate of ∼ 300 bpm
- Regular, narrow QRS complexes
- The rhythm may be:
- Treatment: similar to atrial fibrillation (see “Therapy” below)
- Frequently degenerates into atrial fibrillation (see “Clinical features” above)
- 1:1 conduction leading to life-threatening ventricular tachycardia
- Immediate synchronized cardioversion (see DC cardioversion)
- Urgent cardiology consultation
- ICU/CCU transfer
- Identify and treat the underlying cause.
- Continuous cardiac telemetry.
- Consider indications for nonemergency cardioversion (e.g., first episode).
- Establish rate control.
- Consider rhythm control.
- ICU/CCU consultation and transfer in refractory rapid ventricular rate
- Identify and treat the underlying cause.
- TTE to evaluate for valvular/structural heart disease
- Assess the risk of stroke and consider indications for anticoagulation.
- Patients with nonvalvular Afib: Assess stroke risk with the CHA2DS2-VASc score and weigh risks of bleeding with the HAS-BLED score.
- Patients with a mechanical heart valve: Start warfarin.
- Patients undergoing nonemergency cardioversion 
- New-onset Afib (< 48 hours): Start anticoagulation before cardioversion.
- Afib > 48 hours or duration unknown
- At least 4 weeks of oral anticoagulation and then cardioversion
- TEE to look for thrombi if cardioversion is required earlier