AFib – Exam Prep, Short Answer, High Yield Questions

Atrial fibrillation (AF) is sustained by structural and electrical remodeling of the atria. Chronic atrial pressure overload, inflammation, and fibrosis lead to altered conduction properties and heterogeneous refractoriness, creating re-entry circuits. Calcium dysregulation and connexin remodeling contribute to ectopic activity and AF maintenance.

Class I indications include CHA₂DS₂-VASc score ≥2 in men or ≥3 in women. Direct oral anticoagulants (DOACs) are preferred over warfarin unless contraindicated. Anticoagulation is also indicated in patients with prior stroke, systemic embolism, or mechanical valves (warfarin required).

Large trials such as AFFIRM and RACE show that rhythm control offers no survival benefit over rate control in stable patients. However, rhythm control may improve symptoms and quality of life. Recent EAST-AFNET 4 trial suggests early rhythm control may reduce cardiovascular outcomes in select patients.

Beta-blockers are first-line for rate control due to their ability to suppress sympathetic tone, especially in hyperadrenergic states (e.g., post-op, sepsis). They provide superior AV nodal suppression. In heart failure with reduced EF, they are preferred over nondihydropyridine calcium channel blockers, which can worsen contractility.

TEE is used to exclude left atrial appendage thrombus prior to cardioversion in patients who are not anticoagulated for ≥3 weeks. If no thrombus is seen, early cardioversion can proceed with subsequent short-term anticoagulation. This reduces delay and hospital stay in acute settings.

AF is characterized by an irregularly irregular rhythm with no discernible P waves, replaced by fibrillatory waves. In contrast, atrial flutter shows sawtooth flutter waves, especially in leads II, III, and aVF, and may have regular or variable ventricular response depending on AV block.

The score assigns points for CHF, Hypertension, Age ≥75 (2 pts), Diabetes, Stroke/TIA (2 pts), Vascular disease, Age 65–74, and female sex. Limitations include overestimation of risk in older females and underperformance in younger populations. It does not account for dynamic risk changes over time.

SGLT2 inhibitors like dapagliflozin and empagliflozin reduce atrial pressure and fibrosis through natriuresis and anti-inflammatory effects. Post-hoc analyses suggest reduced new-onset AF in HF patients, though not a primary endpoint. Mechanistic trials are ongoing to confirm AF burden reduction.

The EAST-AFNET 4 trial demonstrated that early rhythm control (<1 year diagnosis) reduces cardiovascular events, including stroke and heart failure hospitalizations. Early intervention may prevent irreversible atrial remodeling and promote sinus rhythm maintenance long-term.

Paroxysmal AF terminates spontaneously within 7 days. Persistent AF lasts >7 days or requires pharmacological/electrical cardioversion. Long-standing persistent AF is continuous >12 months. These distinctions guide rhythm control strategies, particularly in procedural planning for ablation.

Catheter ablation is considered first-line in symptomatic paroxysmal AF when antiarrhythmic drugs are ineffective or poorly tolerated. It is increasingly considered early in younger patients, those with heart failure with reduced ejection fraction (HFrEF), and in those desiring rhythm control without medications.

Assess thromboembolic risk using CHA₂DS₂-VASc, and bleeding risk with HAS-BLED. Bridging is not needed for DOACs. Timing of last dose depends on renal function and procedural bleeding risk. Rate control must be optimized; consider withholding AV nodal blockers to prevent bradycardia under anesthesia.

Silent cerebral infarcts are MRI-detected ischemic lesions seen in up to 40% post-AF ablation. These are often subclinical but may impact cognitive function long-term. Risk factors include inadequate anticoagulation, prolonged procedural time, and use of non-irrigated catheters. Periprocedural anticoagulation is crucial.

Left atrial appendage occlusion (e.g., Watchman device) is an option for patients with contraindications to long-term anticoagulation. It reduces thromboembolic risk but is inferior to warfarin in early months post-implantation. Antithrombotic therapy is still required peri-procedurally.

Thyrotoxicosis increases β-adrenergic sensitivity and alters ion channel function, predisposing to AF. Acute management includes β-blockers (e.g., propranolol) for rate control and starting antithyroid therapy. Rhythm control is deferred until euthyroid state is achieved, as AF may spontaneously resolve.

Amiodarone is preferred in patients with structural heart disease, including ischemic or dilated cardiomyopathy. It is effective for both pharmacologic cardioversion and long-term rhythm maintenance, though limited by extracardiac toxicities (e.g., thyroid, pulmonary, hepatic) requiring monitoring.

Electrical or pharmacologic cardioversion transiently increases thromboembolic risk due to atrial stunning and pre-existing thrombi. Even short-duration AF (<48h) may harbor thrombus, particularly in elderly or high-risk patients. Guidelines recommend at least 4 weeks of anticoagulation post-cardioversion.

This involves on-demand use of Class IC agents (e.g., flecainide, propafenone) for self-terminating AF episodes in highly symptomatic, infrequent paroxysmal AF. Contraindicated in structural heart disease or QT prolongation. Patients should first trial under monitoring to assess safety.

AF itself has a modest association with sudden death, but it's usually related to comorbidities such as LV dysfunction, CAD, or electrolyte disturbances. Antiarrhythmics (e.g., Class IC, sotalol) can provoke proarrhythmia in susceptible patients, particularly those with underlying structural disease.

Hemodynamic instability is defined by hypotension, altered mental status, ischemic chest pain, or signs of shock due to rapid ventricular response in AF. These patients require immediate synchronized DC cardioversion, regardless of anticoagulation status.

Common precipitants include sepsis, acute coronary syndrome, pulmonary embolism, thyrotoxicosis, alcohol binge ('holiday heart'), and post-operative states, especially cardiac or thoracic surgery.

Immediate synchronized cardioversion is indicated in patients with AF and hemodynamic instability, including hypotension, angina, pulmonary edema, or syncope. Delay for anticoagulation is not required in unstable patients.

IV magnesium may help control rate, particularly when associated with hypomagnesemia or in digoxin-toxic patients. It also stabilizes atrial myocytes and may assist rate control synergistically with AV nodal blockers.

The HAS-BLED score assesses bleeding risk using: Hypertension, Abnormal renal/liver function, Stroke, Bleeding history, Labile INRs, Elderly (>65), Drugs/alcohol. A score ≥3 indicates high bleeding risk, warranting caution and closer monitoring.

In patients with mechanical heart valves or moderate-to-severe mitral stenosis, DOACs are contraindicated; warfarin is the anticoagulant of choice. Non-valvular AF can be managed with DOACs if renal function permits.

Absolute contraindications include active major bleeding, recent hemorrhagic stroke, severe thrombocytopenia, or high fall risk with recent trauma. Relative contraindications include poor adherence or uncontrolled hypertension.

Atrial stunning after cardioversion increases the risk of thromboembolism for several weeks, even if sinus rhythm is restored. Anticoagulation should continue for at least 4 weeks post-cardioversion, regardless of baseline rhythm duration.

Withholding anticoagulation may be justified in patients with active bleeding, recurrent falls with injuries, severe hepatic failure, or intracranial malignancy, but this must be individualized. Alternatives like LAA closure may be considered.

Despite fall risk, the absolute benefit in stroke prevention often outweighs the bleeding risk unless falls are frequent and severe. DOACs offer a safer profile than warfarin in elderly patients. Fall risk should be addressed concurrently.

Rate control and anticoagulation take priority. Triple therapy (anticoagulant + dual antiplatelet) increases bleeding risk; thus, dual therapy with a DOAC and clopidogrel is often preferred post-PCI, with aspirin used short-term only.

Dose adjustments of DOACs are necessary based on renal function. Apixaban may be favored in advanced CKD due to safety profile. Warfarin remains standard in end-stage renal disease (ESRD), though bleeding risk is higher.

Subclinical AF lasting >5–6 minutes may increase stroke risk. The ASSERT trial showed these episodes correlate with future clinical AF and stroke. Long episodes (>24h) may warrant anticoagulation, depending on CHA₂DS₂-VASc score.

Anticoagulation can be cautiously resumed 1–2 weeks after hemostasis in high thromboembolic risk patients. Early resumption reduces stroke without significantly increasing rebleeding if the bleeding source is addressed.

DOACs are non-inferior to warfarin for stroke prevention, with reduced intracranial hemorrhage risk. They have more predictable pharmacokinetics and fewer dietary interactions but are contraindicated in mechanical valves or mitral stenosis.

For AF <48h duration and low stroke risk (CHA₂DS₂-VASc 0–1), cardioversion may proceed without anticoagulation. Otherwise, periprocedural DOAC dosing is preferred. Post-cardioversion anticoagulation for 4 weeks is recommended.

Early recurrence occurs within 3 months post-ablation due to inflammation or incomplete lesion formation. It does not indicate ablation failure. Short-term antiarrhythmic therapy and rate control are used during the 'blanking period'.

Obesity increases AF recurrence post-cardioversion or ablation due to left atrial enlargement and fibrosis. Weight loss improves sinus rhythm maintenance and enhances procedural success, as shown in the LEGACY and ARREST-AF studies.

Based on stroke size: small strokes resume at day 3, moderate at day 6–7, large after day 12–14. Early anticoagulation may risk hemorrhagic conversion, so timing balances stroke recurrence and bleeding risk.

Continue anticoagulation in low-bleeding-risk procedures. For high-risk procedures, stop DOACs 24–72 hours prior based on renal function. Resume when bleeding risk subsides. Rate control with β-blockers is preferred intraoperatively.