Heart Failure Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Davies is a 68-year-old retired builder who presents with progressive exertional dyspnoea (NYHA III), orthopnoea, and bilateral ankle swelling over four months. [1]

His past history includes:

• Ischaemic heart disease — anterior STEMI 2018, primary PCI to LAD
• Type 2 diabetes — HbA1c 72 mmol/mol on metformin and gliclazide
• Hypertension — previously on perindopril and amlodipine
• Stage 3A CKD — baseline creatinine 130 (eGFR 52)
• Ex-smoker — 40 pack-years, ceased 2018
• Obstructive sleep apnoea on CPAP [1]

His echo shows LVEF 30% with global hypokinesia and mild functional MR. ECG shows sinus rhythm, HR 76, old anterior Q waves, QRS 110ms. [1]

His main problems are:

1. Heart failure with reduced ejection fraction (HFEF), NYHA III — likely ischaemic origin
2. Suboptimally managed diabetes (HbA1c 72)
3. CKD stage 3A — cardiorenal overlap
4. OSA on CPAP — a comorbidity that worsens HF
5. Not on any GDMT for heart failure — a critical gap" [1]

Examiner probing questions and model answers

Q1: "What is your first pharmacological priority?" [1]

"Initiating the four pillars of GDMT. He is on no HF therapy currently, which is the most urgent gap. I would start all four at low dose simultaneously: sacubitril/valsartan 24/26mg BID (he is not on an ACEi so no washout needed), bisoprolol 1.25mg OD, spironolactone 12.5mg OD, and dapagliflozin 10mg OD. I would stop amlodipine as it has no HF mortality benefit. I would continue frusemide for congestion. I would monitor blood pressure, renal function, and potassium at 1–2 weeks." [1]

Q2: "His creatinine rises to 160 (eGFR drops to 42) after starting ARNI. What do you do?" [1]

"A 23% creatinine rise is within the acceptable threshold of 30%. I would continue the ARNI at the current dose and recheck in one week. If the rise exceeds 30% or potassium exceeds 5.5, I would reduce the dose and investigate other contributing factors — volume depletion, NSAID use, or contrast exposure. I would not stop the ARNI for a modest rise — the mortality benefit outweighs the renal risk, and SGLT2i will provide long-term renoprotection." [1]

Q3: "Why dapagliflozin in a non-diabetic... I mean, in this diabetic patient?" [1]

"DAPA-HF demonstrated that dapagliflozin reduces the composite of worsening heart failure hospitalisation or cardiovascular death by 26% in HFrEF patients, regardless of diabetes status. For this patient, it provides dual benefit — HF improvement and glycaemic control. It is also renoprotective per the DAPA-CKD trial. I would continue it even if his diabetes improves on other therapy." [1]

Q4: "Would you refer him for an ICD?" [1]

"Not yet. ICD primary prevention requires LVEF ≤35% after at least 3 months of optimal GDMT. His LVEF may improve with therapy — cardiac reverse remodelling can occur within 3–6 months. I would reassess his echo at 3 months. If LVEF remains ≤35% on optimal GDMT, with NYHA II–III and expected survival >1 year, I would refer for ICD. His QRS is 110ms, so he does not meet CRT criteria." [1]

Q5: "He develops iron deficiency (ferritin 55, TSAT 12%). How does this affect his management?" [1]

"Iron deficiency is present in approximately 50% of heart failure patients and independently worsens symptoms, exercise capacity, and quality of life — even without anaemia. I would treat with IV ferric carboxymaltose, which the FAIR-HF and AFFIRM-AHF trials showed improves symptoms and functional capacity in HFrEF. Oral iron is poorly absorbed and ineffective in HF. I would give 1000mg IV ferric carboxymaltose and reassess ferritin and TSAT at 3 months." [1]

Q6: "What is his prognosis and how would you discuss it?" [1]

"On optimal GDMT, his 1-year mortality is approximately 7–10%, down from 20–30% in the pre-GDMT era. However, his HbA1c, CKD, and ischaemic origin of HF are adverse prognostic markers. I would use the Seattle Heart Failure Model to generate a personalised estimate. I would discuss prognosis honestly but constructively — emphasising that modern therapy has transformed outcomes, that adherence to all four pillars is critical, and that advance care planning is appropriate but not urgent." [1]

Short Case Discussion

Scenario: "Examine this patient's cardiovascular system"

Candidate presentation (model): [1]

"I examined Mr Jones's cardiovascular system. He is comfortable at rest at 45 degrees. There is no clubbing, pallor, or cyanosis. The pulse is regular at 88 beats per minute, normal volume and character. Blood pressure is 125/75. The JVP is elevated 5 cm above the sternal angle, with a prominent V wave visible. [1]

The apex beat is displaced to the 6th intercostal space, anterior axillary line, and is diffuse in character, suggesting left ventricular dilatation. There is a parasternal heave present. On auscultation, the first heart sound is soft. There is a third heart sound audible at the apex. There is a pansystolic murmur at the apex radiating to the axilla, louder on expiration, consistent with functional mitral regurgitation. There is a separate pansystolic murmur at the lower left sternal edge, louder on inspiration, consistent with functional tricuspid regurgitation. [1]

Examination of the lungs reveals bilateral basal fine inspiratory crackles to mid-zones. There is pitting oedema to the knee bilaterally. Abdominal examination reveals a pulsatile liver edge 3 cm below the costal margin. [1]

In summary, these findings are consistent with biventricular heart failure with reduced ejection fraction, complicated by functional mitral and tricuspid regurgitation." [1]

Examiner: "What is the significance of the pulsatile liver?" [1]

"A pulsatile liver indicates tricuspid regurgitation — the regurgitant systolic wave is transmitted through the hepatic veins to the liver. In the context of heart failure, this reflects right ventricular dilatation and tricuspid annular stretching. It is a marker of advanced biventricular failure and is associated with a worse prognosis." [1]

Examiner: "Explain the third heart sound." [1]

"The S3 is a low-frequency sound produced in early diastole by rapid ventricular filling into a stiff, non-compliant ventricle with elevated filling pressure. In HFrEF, the dilated ventricle receives a large volume of blood rapidly during the passive filling phase, creating vibrations audible as the S3 gallop. It is highly specific for elevated left ventricular end-diastolic pressure and indicates decompensated heart failure." [1]