Atrial Fibrillation in PACES: Signs, Causes and the Viva

How it presents in PACES

Atrial fibrillation rarely arrives as a standalone "spot diagnosis" — it is usually the finding you make while examining a cardiovascular patient for something else. In the cardiology station it commonly sits behind a murmur (mitral disease is the classic pairing), a prosthetic click, or heart failure. In consultation and communication scenarios it appears as palpitations, a new irregular pulse, or a counselling problem about anticoagulation.

The examiner is testing two things: can you recognise the rhythm at the bedside, and can you then reason about its cause and consequences? The rhythm itself is easy marks if you slow down and feel it properly. The higher marks come from the story you build around it — the scar, the goitre, the malar flush, the hemiparesis — and from a crisp management framework when you are asked to discuss.

Signs to look for

Feel the pulse deliberately for at least fifteen seconds before you commit. The discriminating findings are:

• A pulse that is irregularly irregular in both rate and volume — this is the bedside hallmark. Beats vary in both timing and strength.
• An apical–radial pulse deficit — the apical rate exceeds the radial rate because short-filling beats fail to transmit to the wrist. Count by auscultating the apex, not the radial.
• A variable-intensity first heart sound, reflecting variable diastolic filling, and loss of the JVP 'a' wave.
• Ventricular rate: describe it as controlled (resting rate under about 90) or uncontrolled (over 90) — a phrase examiners like to hear.
• Clues to the cause on inspection: goitre, exophthalmos or tremor (thyrotoxicosis); malar flush with a tapping apex and mid-diastolic murmur (mitral stenosis); a metallic prosthetic click or valvotomy/thoracotomy scar; a hemiparesis from previous embolic stroke; and signs of heart failure.
• Beware: controlled AF can feel deceptively regular at first pass. Concentrate on beat-to-beat variation before you call it sinus rhythm.

Confirming the diagnosis and differential

The 12-lead ECG settles it: absolutely irregular RR intervals, absent distinct P waves, and a fibrillatory baseline (atrial rate 300–600/min) with an irregular ventricular response. If you are describing an ECG in the viva, lead with irregularity and the absent P waves.

The main mimics of an irregular pulse are frequent ventricular ectopics (exercise abolishes ectopics but worsens AF), atrial flutter with variable AV block (a more regular, sawtooth pattern), and multifocal atrial rhythm — the ECG distinguishes all of these. For paroxysmal palpitations, keep a wider net: paroxysmal AF, atrial flutter, a regular re-entrant SVT (look for a WPW delta wave), and ventricular arrhythmia as the can't-miss diagnosis, especially with syncope or structural heart disease.

A crucial teaching point: a normal resting ECG never excludes paroxysmal AF. If the history fits, the key investigation is ambulatory monitoring — a Holter escalating to a patch, event recorder or implantable loop recorder for elusive symptoms.

The viva: what examiners ask

Structure your answer around four parallel jobs: document the rhythm, treat reversible drivers, prevent stroke, and control rate or rhythm for symptoms.

• Causes (a sieve they love): ischaemic heart disease, hypertension, mitral valve disease, heart failure and cardiomyopathy, thyrotoxicosis (the classic reversible driver — always send a TFT), sepsis or pneumonia, PE, alcohol ("holiday heart"), electrolyte disturbance, OSA, obesity and diabetes. "Lone AF" means no identifiable cause or structural disease.
• Classification: first-diagnosed; paroxysmal (self-terminating, usually within 48 hours); persistent (over 7 days); long-standing persistent (over a year); and permanent.
• Investigations: 12-lead ECG, ambulatory monitoring for paroxysmal disease, bloods (TFT, FBC, U&E with K and Mg, glucose, renal and liver function for anticoagulant dosing), and an echocardiogram to assess LV function, LA size and — critically — valve disease.
• Stroke prevention is the answer that changes prognosis. Score with CHA2DS2-VASc and anticoagulate at ≥2 in men / ≥3 in women. A DOAC is first-line for non-valvular AF; warfarin is reserved for moderate–severe mitral stenosis or a mechanical valve ("valvular AF"), targeting INR 2.0–3.0. Antiplatelets are not stroke prevention in AF.
• Rate control (first-line for most): a beta-blocker or rate-limiting calcium-channel blocker, adding digoxin if sedentary or in heart failure. Rhythm control for younger, symptomatic patients: flecainide only if there is no structural or ischaemic disease, otherwise amiodarone or sotalol, with catheter ablation / pulmonary-vein isolation for drug-refractory paroxysmal AF.
• Complications: cardioembolic stroke, worsening heart failure, and a tachycardia-mediated cardiomyopathy if the rate runs uncontrolled.

Common pitfalls and how to score

The commonest error is under-treating "only paroxysmal" AF. Anticoagulation is decided by CHA2DS2-VASc, not by AF burden — paroxysmal AF carries the same stroke risk as persistent or permanent AF, and atrial flutter is anticoagulated identically. Say this explicitly and you separate yourself from weaker candidates.

Know that HAS-BLED identifies and corrects modifiable bleeding risk — it does not veto anticoagulation. In pre-excited AF (WPW), avoid all AV-node blockers (adenosine, digoxin, verapamil, diltiazem, beta-blockers), which can precipitate VF; use flecainide or DC cardioversion. And remember cardioversion timing: if AF has lasted over 48 hours or the duration is unknown, anticoagulate for at least three weeks first or exclude left atrial appendage thrombus with a TOE, then continue anticoagulation for at least four weeks afterwards because of atrial stunning.

Finally, do not miss the reversible endocrine driver. New-onset AF mandates a TFT, and in a thyrotoxic patient you treat the thyroid, rate-control cautiously, anticoagulate, and defer cardioversion until euthyroid.