Decompensated heart failure — structured viva

This scenario is fictional and invented for teaching; it does not describe a real person.

Stem

You are the admitting cardiologist. A 68-year-old man with known HFrEF presents with breathlessness that developed over a few hours: SpO₂ 86% on air, respiratory rate 30 breaths/min, BP 172/98 mmHg, crackles throughout both lungs, lactate 1.6 mmol/L. He takes furosemide 40 mg daily, ramipril and bisoprolol.^[1]

Branch A — Category and definition

Examiner: How would you classify this presentation under the 2026 ESC guideline? ^[1]

Strong answer: The 2026 guideline uses the term decompensated HF instead of acute HF. Its four clinical categories are decompensated left-sided HF, decompensated right-sided HF, acute pulmonary oedema and cardiogenic shock. This fits acute pulmonary oedema: respiratory distress with hypoxaemia and a respiratory rate above 25 breaths/min, from pulmonary congestion that developed over a short period. In APO the congestion is mainly from fluid redistribution, so such patients usually do not need high doses of diuretics but may need vasodilators.^[1]

Examiner (follow-up): What does the term "decompensated" add? ^[1]

Strong answer: DHF is acute or gradual onset of symptoms or signs severe enough to need urgent attention and new or intensified treatment. In pre-existing HF, worsening HF describes deterioration in symptoms or signs; DHF is specifically characterised by the need for treatment modification.^[1]

Branch B — The first hour

Examiner: Give me oxygen, ventilation and diuretic orders. ^{[1] [11]}

Strong answer: Oxygen, because SpO₂ is below 90% (Class I, Level C). NIPPV should be considered for respiratory distress and started as soon as possible (Class IIa, Level B2); Cochrane data show NPPV probably reduces intubation (RR 0.49).^{[1] [11]} If he has fluid overload, an i.v. loop diuretic is recommended (Class I, Level A); as he takes a loop diuretic, an i.v. dose of twice his usual oral dose (furosemide 80 mg i.v.) should be considered. APO with predominant fluid redistribution usually does not need high diuretic doses. With SBP above 110 mmHg, an i.v. vasodilator may be considered as initial therapy (Class IIb, Level C), with close blood-pressure monitoring. No routine opiates unless severe or intractable pain or anxiety (Class III, Level C).^[1]

Examiner (follow-up): What nitroglycerine regimen would you use? ^[1]

Strong answer: The ESC 2026 supplement gives a start of 10–20 μg/min, increased up to 200 μg/min, and lists tolerance with continuous use. Its text adds that nitroglycerine can be given as 1–2 mg boluses in severely hypertensive patients with acute pulmonary oedema.^[1]

Examiner (follow-up): Do vasodilators change outcome? ^[13]

Strong answer: ESC 2026 notes that no large-scale RCT has shown a clear benefit of vasodilatation on hard end points. A meta-analysis of 46 RCTs found no mortality reduction (RR 0.95) but less intubation (RR 0.54).^{[1] [13]} The AHA/ACC/HFSA guideline warns that nitroglycerin tachyphylaxis may develop within 24 hours.^[2]

Branch C — Diuretic response

Examiner: How do you know the diuretic is working, and what if it is not? ^{[1] [6]}

Strong answer: A satisfactory response can be defined as urinary sodium ≥70 mEq/L at 2 h or urine output ≥100 mL/h over the first 6 h. If not, the i.v. loop dose can be doubled and/or a non-loop diuretic added. If 24-hour diuresis is below 3 L and congestion persists, further escalation should be considered on day 2. The highest daily i.v. dose is generally considered to be furosemide 600 mg, although up to 1000 mg may be considered with severely impaired kidney function.^[1] If he has fluid overload despite previous loop diuretic treatment, adding short-term acetazolamide 500 mg i.v. once daily or oral hydrochlorothiazide dosed by eGFR should be considered (Class IIa, Level B1). ADVOR increased successful decongestion within 3 days (42.2% versus 30.5%) with no significant difference in death or HF rehospitalisation during 3 months of follow-up.^{[1] [6]}

Examiner (follow-up): Should urinary sodium guide therapy routinely? ^[8]

Strong answer: ESC 2026 says urinary sodium-guided therapy may be considered during the first days of treatment to improve natriuresis and diuresis (Class IIb, Level B1). PUSH-AHF increased 24-hour natriuresis, with no significant difference in death or HF rehospitalisation at 180 days (31% in both arms).^{[1] [8]}

Branch D — The shock pivot

Examiner: Overnight his BP falls to 80/55 mmHg, his peripheries are cold, he is confused and lactate is 4.8 mmol/L. What now? ^{[1] [15] [16]}

Strong answer: This is likely cardiogenic shock, critical end-organ hypoperfusion caused by primary cardiac dysfunction. Septic and hypovolaemic shock also cause hypotension with end-organ hypoperfusion, and mixed forms of shock often exist simultaneously. A lactate above 2 mmol/L (best measured arterially) meets the biochemical requirement for inadequate tissue perfusion. I consult the Shock Team because temporary MCS may be needed.^[1] A vasopressor, preferably norepinephrine, may be considered (Class IIb, Level C); in an RCT in patients with shock (De Backer 2010, dopamine versus norepinephrine as first-line vasopressor), arrhythmic events were more frequent with dopamine.^{[1] [16]} With SBP below 90 mmHg and hypoperfusion not responding to standard treatment, including fluid challenge, inotropes may be considered (Class IIb, Level C). Because he takes bisoprolol, levosimendan or a PDE-III inhibitor may be preferred over dobutamine. In cardiogenic shock, a milrinone-versus-dobutamine RCT (Mathew 2021) found no significant difference between milrinone and dobutamine in its primary composite outcome (49% versus 54%).^{[1] [15]}

Examiner (follow-up): Would you put in a balloon pump? ^[1]

Strong answer: IABP is not recommended in unselected cardiogenic shock (Class III, Level B1). Altshock-2 (routine early IABP in HF-related shock) stopped for futility. For HF-related haemodynamic instability, temporary MCS should be considered in selected patients as a bridge (Class IIa, Level C). A multidisciplinary Shock Team is recommended to guide the device modality and type (Class I, Level C).^{[1] [21]}

Branch E — Discharge

Examiner: He recovers. What must happen before and after discharge? ^{[1] [22]}

Strong answer: Start an SGLT2 inhibitor in hospital after stabilisation (Class I, Level B1). Before discharge, carefully evaluate for persistent congestion (Class I, Level C).^[1] Then rapidly start and up-titrate FMT before discharge and at frequent visits over the first 6 weeks (Class I, Level B2). STRONG-HF lowered 180-day HF readmission or death from 23.3% to 15.2%.^{[1] [22]} If he has iron deficiency, the pre-discharge phase may also be used to give iron, based on AFFIRM-AHF.^[1]