Atrial Fibrillation — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mrs Margaret Davies, 78 years old. [1]

Presenting complaint: Three months of intermittent palpitations, progressive exertional dyspnoea (now breathless walking 100 metres on flat ground), and two episodes of pre-syncope. One episode of waking at night breathless. No chest pain. No witnessed seizure activity. [1]

Past history:

• Hypertension for 20 years
• Type 2 diabetes for 15 years (HbA1c 68 mmol/mol)
• Ischaemic heart disease — NSTEMI 6 years ago, DES to LAD
• Stage 3B CKD (eGFR 35, baseline creatinine 155)
• Permanent pacemaker for sinus node dysfunction (implanted 3 years ago)
• Osteoarthritis (knees)
• Former smoker (40 pack-years, ceased 10 years ago) [1]

Current medications:

• Metformin 500mg BD
• Insulin glargine 20 units nocte
• Perindopril 10mg daily
• Amlodipine 10mg daily
• Atorvastatin 40mg nocte
• Aspirin 100mg daily
• Frusemide 20mg daily
• Paracetamol 1g QID PRN for knee pain [1]

Examination findings (trainee elicits):

• Alert, oriented, comfortable at rest at 45 degrees
• Irregularly irregular radial pulse, rate 96, pulse deficit of 8
• Blood pressure 152/88
• JVP: elevated 4 cm, no prominent waves
• Apex beat: not displaced, 5th ICS MCL
• S1 variable intensity, no murmurs
• S3 gallop present at the apex
• Bibasal fine inspiratory crackles to lower third
• Mild pitting oedema to ankles bilaterally
• Pacemaker generator palpable in left infraclavicular fossa
• Thyroid not enlarged, no eye signs [1]

Investigations:

• ECG: atrial fibrillation, ventricular rate 104 (undersensing noted with pacemaker), HR varies with pacemaker capture, old anterior Q waves (V1–V2)
• Echo: LVEF 42%, mild-moderate LA dilatation (LAA velocity 0.3 m/s), no significant valvular disease, RVSP 38 mmHg, pacemaker lead in RV apex
• Bloods: Hb 112, eGFR 35, K+ 4.8, TSH 2.1 (normal), troponin 18 (chronically elevated), BNP 620
• INR 1.0 (not currently anticoagulated) [1]

Candidate's structured presentation (model)

Opening statement: [1]

"Mrs Davies is a 78-year-old woman who presents with a 3-month history of palpitations, exertional dyspnoea, and pre-syncope, with echocardiographic evidence of atrial fibrillation, moderately reduced LV systolic function, and elevated filling pressures. She has a complex cardiovascular background including ischaemic heart disease, diabetes, CKD, and a permanent pacemaker for sinus node dysfunction. [1]

Her main problems are:

1. Atrial fibrillation, persistent, symptomatic — newly diagnosed on this presentation
2. Heart failure with mildly reduced ejection fraction (LVEF 42%) — NYHA III, with evidence of decompensation (S3 gallop, elevated JVP, basal crackles)
3. High thromboembolic risk — CHA₂DS₂-VASc requires formal calculation
4. Tachy-brady syndrome — she has a pacemaker for sinus node dysfunction and now has AF; this suggests sick sinus syndrome with paroxysmal AF
5. Type 2 diabetes with suboptimal control (HbA1c 68)
6. CKD stage 3B (eGFR 35) — affects DOAC dosing and drug choices
7. Hypertension — BP 152/88 is above target
8. Pacemaker — check function and programming in the setting of new AF" [1]

Investigation summary: [1]

"Her echocardiogram confirms LVEF 42% (HFmrEF) with mild-moderate LA dilatation and a low LAA velocity of 0.3 m/s, indicating significant thromboembolic risk from stasis. The elevated BNP of 620 and S3 gallop support a diagnosis of heart failure. Her TSH is normal, excluding thyrotoxicosis as a cause. Her troponin of 18 is chronically elevated in keeping with her known ischaemic heart disease and HF — it is not diagnostic of acute coronary syndrome without a rising trend. Her ECG shows AF with possible pacemaker undersensing — I would request a pacemaker check." [1]

Management plan: [1]

1. Anticoagulation (urgent priority):

   • CHA₂DS₂-VASc: age 75+ (2), hypertension (1), diabetes (1), vascular disease/prior MI (1), heart failure (1), female sex (1) = 7. Anticoagulation is strongly indicated.
   • HAS-BLED: uncontrolled hypertension (1), abnormal renal function (1), age over 65 (1), concomitant aspirin (1) = approximately 4. High bleeding risk — correct modifiable factors.
   • Start apixaban 2.5mg BID — she meets two dose-reduction criteria: age 78 is approaching 80 but not quite; however creatinine 155 is over 133 micromol/L (one criterion). At 78 and with creatinine 155, she meets only one formal criterion, so standard dose 5mg BID may be appropriate — but given her frailty, CKD, and bleeding risk, many clinicians would use 2.5mg BID conservatively. I would discuss with cardiology.
   • Stop aspirin — she is over 12 months post-stent and the bleeding risk of combining aspirin with a DOAC is significant. [1]

2. Rate and rhythm strategy:

   • She is symptomatic with LVEF 42% and a pacemaker for sinus node dysfunction. Her pacemaker means bradycardia is covered, allowing aggressive rate control without risk of symptomatic bradycardia.
   • Rate control: increase beta-blockade. She is not currently on a beta-blocker — add bisoprolol 1.25mg OD (cautious given LVEF 42% and borderline BP, but bisoprolol is evidence-based for HFmrEF). Continue frusemide for congestion; may need to uptitrate.
   • Rhythm consideration: given her symptoms, recently diagnosed AF, HFmrEF, and pacemaker backup, she is a candidate for rhythm control per EAST-AFNET 4 (PMID 32865375). Amiodarone is the safe antiarrhythmic choice given her ischaemic heart disease and reduced EF. If she fails pharmacological rhythm control, catheter ablation is supported by CABANA HF data. However, her multiple comorbidities and age make a shared decision essential.
   • Consider cardioversion after 3 weeks of therapeutic anticoagulation or TOE-guided approach — but given her pacemaker for sinus node dysfunction, she may have poor sinus node function and may not maintain sinus rhythm well. [1]

3. Heart failure management:

   • LVEF 42% (HFmrEF): initiate/up-titrate GDMT. Add bisoprolol (beta-blocker), ensure she is on ACEi (already on perindopril — uptitrate), add SGLT2 inhibitor (empagliflozin 10mg — safe at eGFR 35, dual benefit for HF and diabetes), consider spironolactone.
   • Increase frusemide for current congestion.
   • Stop amlodipine — no HF mortality benefit and adds to polypharmacy. [1]

4. Pacemaker review:

   • Check pacemaker function — the ECG suggests possible undersensing. May need reprogramming to optimise AF detection and rate response. [1]

5. Comorbidity optimisation:

   • Diabetes: add SGLT2 inhibitor, optimise insulin regimen.
   • Hypertension: uptitrate perindopril, add thiazide-like if needed (cautious with CKD).
   • Check sleep study for OSA. [1]

Examiner discussion questions

Q: "Why does she have a pacemaker, and how does that affect your AF management?" [1]

"She has a permanent pacemaker for sinus node dysfunction — likely sick sinus syndrome, where the sinus node fails to generate adequate impulses. Sick sinus syndrome is commonly associated with AF — the 'tachy-brady syndrome' — where periods of sinus bradycardia or sinus pauses alternate with paroxysmal AF. The pacemaker prevents symptomatic bradycardia and sinus pauses. [1]

This actually facilitates my AF management: because the pacemaker protects against bradycardia, I can use higher doses of rate-control agents (beta-blockers, digoxin) without fear of symptomatic pauses. It also means cardioversion is less likely to result in symptomatic post-shock bradycardia, as the pacemaker will provide backup pacing." [1]

Q: "You mentioned her LVEF is 42%. What does HFmrEF mean for your drug choices?" [1]

"HFmrEF — heart failure with mildly reduced ejection fraction (LVEF 41–49%) — is an intermediate phenotype. The evidence base is less robust than for HFrEF, but the 2021 ESC and 2022 ACC/AHA guidelines recommend SGLT2 inhibitors for HFmrEF based on extrapolation from DELIVER and EMPEROR-Preserved data. Beta-blockers, ACEi/ARNI, and MRAs are recommended with lower evidence levels. SGLT2 inhibitors are particularly attractive here because of her diabetes. I would start all four pillars cautiously and monitor her renal function and blood pressure." [1]

Q: "What if she had presented with a stroke instead of palpitations?" [1]

"If she presented with an ischaemic stroke and AF was diagnosed during the workup, the timing of anticoagulation would be critical. The 1-3-6-12 day rule applies: TIA (1 day), small infarct (3 days), moderate infarct (6 days), large infarct (12–14 days). The delay balances thromboembolic protection against haemorrhagic transformation of the infarct. AF is the most common cause of cardioembolic stroke, and AF-related strokes are larger, more disabling, and more likely to haemorrhically transform. Early detection of AF post-stroke (using prolonged cardiac monitoring or implantable loop recorders) is important because silent paroxysmal AF is found in 10–30% of cryptogenic stroke patients." [1]

DCE Short Case — Cardiovascular Examination (Irregular Pulse)

Instruction

"Examine this patient's cardiovascular system. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates

• Irregularly irregular pulse — the cardinal finding
• Pulse deficit — apical rate exceeds radial rate
• Variable first heart sound intensity — reflecting varying diastolic filling time
• Absent "a" waves in JVP — no organised atrial contraction
• Possible murmur of underlying valvular disease (mitral stenosis, mitral regurgitation)
• Signs of heart failure if present (elevated JVP, S3, basal crackles, oedema)
• Signs of thyroid disease if AF is thyrotoxic in origin (tremor, thyroid bruit, eye signs) [1]

Examination routine (step by step)

1. General inspection: comfortable at rest? Breathless? Cyanosed? Thyroid status?
2. Hands: radial pulse — rate, rhythm, character. State immediately: "The pulse is irregularly irregular." Check for thyroid signs (fine tremor, thyroid acropachy, palmar erythema).
3. Blood pressure: note the variability. Systolic BP varies with beat-to-beat stroke volume.
4. Neck: JVP — look for absent "a" waves. Thyroid — palpate for goitre, listen for bruit.
5. Face: conjunctival pallor (anaemia), facial plethora. Eyes — exophthalmos, lid lag (thyroid).
6. Precordordium:
   • Inspect for scars (pacemaker, thoracotomy), apex impulse.
   • Palpate apex beat — position and character. Palpate for parasternal heave (RV overload, pulmonary hypertension, tricuspid disease).
   • Auscultate: note variable S1. Listen carefully for murmurs — mitral stenosis (loud S1, opening snap, diastolic rumble), mitral regurgitation (pansystolic at apex to axilla). Listen for S3 (heart failure).
7. Back: basal crackles (heart failure).
8. Abdomen: hepatomegaly, ascites (right heart failure), pulsatile liver (tricuspid regurgitation).
9. Legs: peripheral oedema, peripheral pulses (check all four). [1]

Presentation template

"I examined this patient's cardiovascular system. The key finding is an irregularly irregular radial pulse with a pulse deficit of approximately 8 beats. The blood pressure is [X]. The JVP shows absent 'a' waves. The first heart sound varies in intensity. [Describe any murmurs or additional findings.] These findings are consistent with atrial fibrillation. I would now investigate for the underlying cause and assess for complications, including an ECG to confirm the rhythm, an echocardiogram to assess for structural heart disease, and thyroid function testing." [1]

Discussion questions

Q: "What is your differential for an irregularly irregular pulse?" [1]

"Atrial fibrillation is the most common cause. Other causes include: atrial flutter with variable AV block, multifocal atrial tachycardia (common in COPD — multiple different P wave morphologies), and frequent atrial or ventricular ectopics (usually a regularly irregular pattern with normal underlying sinus rhythm interrupted by premature beats). The ECG distinguishes these: AF has absent P waves and a chaotic baseline; flutter has sawtooth waves; MAT has multiple P wave morphologies; ectopics show premature QRS complexes with compensatory pauses." [1]

Q: "How would you confirm the diagnosis?" [1]

"A 12-lead ECG is the definitive diagnostic test. The diagnostic features are: absent P waves, atrial fibrillatory waves at 350–600 per minute (fine or coarse baseline undulations), irregularly irregular R-R intervals, and usually narrow QRS (unless aberrancy, pre-excitation, or bundle branch block). For paroxysmal AF not captured on the 12-lead, I would use ambulatory monitoring — a 24–48 hour Holter for frequent episodes, or an event recorder or implantable loop recorder for infrequent episodes." [1]