Phys Vivas · cardiovascular
Heart Failure — Viva Defence
Structured DCE viva for heart failure: long-case defence and short-case discussion covering GDMT reasoning, device therapy, cardiorenal syndrome, and examination findings.
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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:
- Heart failure with reduced ejection fraction (HFrEF), NYHA III — likely ischaemic origin
- Suboptimally managed diabetes (HbA1c 72)
- CKD stage 3A — cardiorenal overlap
- OSA on CPAP — a comorbidity that worsens HF
- 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 10–15%, 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]
References2ShowHide
- [1]McMurray JJV, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure N Engl J Med, 2014.PMID 25176015
- [2]McMurray JJV, et al. Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction N Engl J Med, 2019.PMID 31535829