IM1.1-27 | Heart Failure — Graded Quiz

Correct. In acute decompensated HFrEF with haemodynamic compromise (low BP), rising creatinine, and signs of low cardiac output, the immediate priority is haemodynamic stabilisation. ACE inhibitors and aldosterone antagonists should be held (both lower blood pressure further and the ACE inhibitor contributes to renal impairment in low-flow states). The beta-blocker should be reduced in dose rather than abruptly stopped — abrupt discontinuation risks rebound adrenergic activation and arrhythmia. Increasing diuresis in the setting of low blood pressure and rising creatinine worsens cardio-renal syndrome.

ADHF management hierarchy: stabilise haemodynamics first. In low-output states: hold ACE inhibitor/ARB and aldosterone antagonist; halve (not stop) beta-blocker; optimise diuresis without pushing into cardio-renal syndrome. Abrupt beta-blocker withdrawal in HF causes rebound tachycardia and arrhythmia.

In ADHF with hypotension (BP 90/60) and rising creatinine, increasing diuresis further worsens cardio-renal syndrome. ACE inhibitors and aldosterone antagonists should be held — both reduce BP further and the ACE inhibitor contributes to pre-renal impairment in low-output states. Beta-blockers should be reduced rather than stopped abruptly to avoid rebound adrenergic activation. Stabilisation of haemodynamics takes priority over maximising neurohormonal blockade.

Correct. CRT-D is indicated when LVEF is 35% or less, QRS is 130 ms or more (especially with left bundle branch block morphology, where benefit is greatest), and the patient remains symptomatic (NYHA Class II-IV) despite optimal medical therapy. This patient has LVEF 25%, QRS 170 ms with LBBB, and persistent symptoms — all three criteria are met. CRT-D provides both biventricular pacing (resynchronisation) and defibrillation for prevention of sudden cardiac death, and has demonstrated reductions in mortality and hospitalisation.

CRT-D indications: LVEF 35% or less + QRS 130 ms or more (especially LBBB) + NYHA Class II-IV despite optimal therapy. CRT corrects interventricular dyssynchrony; the widened QRS (especially LBBB) identifies mechanical dyssynchrony that responds to biventricular pacing.

CRT indication: LVEF 35% or less + QRS 130 ms or more (greatest benefit with LBBB morphology) + symptomatic on optimal medical therapy. ICD alone addresses sudden cardiac death but does not treat dyssynchrony. Permanent pacemaker provides only rate control. CRT-D is superior to ICD alone in patients who also meet CRT criteria.

Correct. PBMV is generally the preferred intervention for severe mitral stenosis (MVA below 1.5 cm2) with favourable valve morphology (pliable, non-calcified, without significant MR or LA thrombus). However, the presence of moderate mitral regurgitation is a contraindication to PBMV — PBMV can worsen MR by tearing the valve leaflets during balloon inflation. In this patient with moderate MR, MVA 0.9 cm2, and recurrent decompensations, surgical mitral valve replacement is the definitive intervention.

PBMV indications: severe MS (MVA below 1.5 cm2) + favourable valve morphology + no significant MR + no LA thrombus. Contraindications to PBMV include significant MR, LA thrombus, heavily calcified valve. Surgical MVR is indicated when PBMV criteria are not met or PBMV is contraindicated.

PBMV is contraindicated when there is significant mitral regurgitation (PBMV risks worsening MR by traumatising leaflets). With MVA 0.9 cm2 (severe stenosis), moderate MR, and recurrent hospitalisation, surgical mitral valve replacement is indicated. Medical therapy alone does not address the structural obstruction and cannot prevent further decompensations.

Correct. Transesophageal echocardiogram (TOE) has significantly higher sensitivity for vegetations (approximately 96%) compared to transthoracic echocardiography (TTE, approximately 60-70%), particularly for small vegetations (<5 mm), prosthetic valve IE, and posterior structures. In a patient with suspected staphylococcal endocarditis and a new murmur, early TOE is required to identify vegetations, assess valve destruction, and detect perivalvular complications (abscess, fistula) that change management and predict the need for urgent surgery.

Modified Duke criteria for IE: major criteria include positive blood culture (specific organisms or persistent bacteraemia) and evidence of endocardial involvement on echocardiography (vegetation, abscess, new regurgitation). TOE is preferred when TTE is negative or inconclusive in high clinical suspicion, or for all prosthetic valve suspected IE. Blood cultures must be drawn BEFORE antibiotics.

TOE is superior to TTE for detecting vegetations (sensitivity 96% vs 60-70%), particularly for small vegetations, posterior structures, and prosthetic valves. In suspected IE with Gram-positive cocci in clusters (consistent with Staphylococcus aureus), TOE is the investigation of choice because it more reliably detects vegetations and perivalvular complications (abscess — indicated by PR prolongation on ECG) that may require urgent surgery.

Correct. Fixed, irreversible pulmonary hypertension (pulmonary vascular resistance above 5-6 Wood units unresponsive to vasodilators) is an absolute contraindication to orthotopic heart transplantation. The transplanted right ventricle, which is adapted to normal pulmonary pressures, cannot overcome severely elevated pulmonary vascular resistance and will acutely fail (right ventricular failure immediately post-transplant). This is the principal cardiopulmonary contraindication to transplant.

Cardiac transplantation: indication = end-stage HF (NYHA III-IV, LVEF below 25%) refractory to optimal therapy. Key absolute contraindication = irreversible pulmonary hypertension (PVR >5-6 Wood units). This must be tested with vasodilator (nitroprusside, inhaled nitric oxide) to confirm irreversibility before listing.

Irreversible pulmonary hypertension (PVR >5-6 Wood units, unresponsive to vasodilators) is the key absolute contraindication to cardiac transplantation. The donor right ventricle, conditioned to normal pulmonary pressures, fails acutely against a high-resistance pulmonary bed. Mild-to-moderate renal impairment and prior cardiac surgery are relative rather than absolute contraindications.

Correct. This is a classic presentation of digoxin toxicity: xanthopsia (yellow-green visual disturbance), nausea, and bradyarrhythmia. Hypokalaemia (potassium 2.9 mmol/L) potentiates digoxin toxicity by increasing myocardial sensitivity to the drug — both digoxin and hypokalaemia compete for the same binding site on the Na+/K+ ATPase. The concurrent aldosterone antagonist might be expected to raise potassium, but this patient has hypokalaemia — likely from inadequately replaced potassium with the loop diuretic.

Digoxin toxicity triggers: hypokalaemia (most important), hypomagnesaemia, renal impairment (digoxin is renally cleared), hypothyroidism, age. Classic symptoms: anorexia, nausea, xanthopsia (yellow-green vision), bradyarrhythmia. Therapeutic window: 0.5-0.9 ng/mL (lower target reduces toxicity). Antidote: Digifab (digoxin-specific Fab fragments).

Digoxin toxicity: nausea, vomiting, xanthopsia (yellow-green vision), arrhythmia (bradycardia, heart block, ventricular arrhythmias). Hypokalaemia potentiates digoxin toxicity by increasing Na+/K+ ATPase inhibition. Serum digoxin level, ECG (bradycardia, regularisation of AF, SVT with heart block), and potassium correction are immediate priorities. Digoxin-specific antibody fragments (Digifab) are the antidote for severe toxicity.

Correct. The immediate management of acute pulmonary oedema follows LMNOP: Lasix (furosemide IV), Morphine (judiciously — reduces preload and anxiety but can cause hypotension and respiratory depression, now used selectively), Nitrates (GTN IV or sublingual — potent venodilators that reduce preload and, at higher doses, afterload; particularly beneficial when BP is elevated as in this patient), Oxygen (non-invasive ventilation preferred over intubation as first-line), Position (sit upright). Oxygen is the immediate first step to correct life-threatening hypoxia. IV furosemide and GTN simultaneously reduce preload and afterload.

ADHF management: sit upright + oxygen (target SpO2 94-98%) + IV furosemide + nitrates (if BP adequate). Non-invasive ventilation (CPAP/BiPAP) reduces intubation rates. IV morphine: selective use only (respiratory depression risk). Dobutamine reserved for cardiogenic shock with low cardiac output. NEVER use beta-blockers, CCBs, or NSAIDs in acute decompensation.

Acute pulmonary oedema immediate priorities: (1) oxygen — correct hypoxia immediately; (2) IV furosemide — reduce venous congestion; (3) IV GTN/nitrates — particularly beneficial when BP is elevated (as here) to reduce afterload and preload. Morphine is no longer first-line (can suppress respiratory drive and cause hypotension). Dobutamine is used only in low-output/cardiogenic shock, not in hypertensive pulmonary oedema.

Correct. Streptococcus bovis (now renamed S. gallolyticus) bacteraemia has a strong and well-established association with colorectal neoplasm — polyps and carcinoma. This association is explained by mucosal disruption of the colonic epithelium by a neoplasm allowing translocation of S. bovis into the bloodstream. In all patients with S. bovis endocarditis or bacteraemia, colonoscopy should be performed urgently to exclude an underlying colorectal cancer.

S. bovis (S. gallolyticus) endocarditis = mandate colonoscopy to exclude colorectal neoplasm. Organisms with specific associations: HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella) = subacute, slow-growing, blood culture-negative; S. aureus = acute, prosthetic valves, IVDU; S. viridans = dental procedures, rheumatic valves; Enterococcus = GI/GU procedures; Candida = immunosuppressed/IVDU.

S. bovis (S. gallolyticus) bacteraemia has a well-established association with underlying colorectal neoplasm. Any patient with S. bovis endocarditis must have colonoscopy to exclude colorectal cancer — a principle tested in clinical examinations and essential for preventing a missed malignancy diagnosis. The murmur is consistent with aortic regurgitation (early diastolic, right sternal edge), which is a complication of aortic valve endocarditis.

Correct. In chronic severe mitral regurgitation, the LVEF is misleadingly elevated because part of the stroke volume is ejected backwards into the low-pressure left atrium. An LVEF of 48% in severe MR represents significant underlying LV dysfunction. The threshold for intervention in severe MR includes: LVEF 60% or less (some guidelines: below 60%), or LVESD above 40-45 mm. Once LVEF falls below 30-35% in MR, post-operative LV function often does not recover — intervening before this threshold prevents irreversible dysfunction.

Severe MR surgical thresholds: LVEF below 60% (note: in MR, LVEF appears higher than true function) OR LVESD above 40 mm, even if asymptomatic. Severe AS: intervention when symptomatic or LVEF below 50% even if asymptomatic. Severe MS: MVA below 1.5 cm2 with symptoms, or below 1.0 cm2 even without symptoms.

In severe MR, the LV ejects into the low-pressure LA — LVEF is falsely elevated relative to true forward output. An LVEF of 48% in severe MR (guideline threshold: LVEF below 60% or LVESD above 40 mm) indicates impending irreversible LV dysfunction. Surgery should be performed before LVEF falls further — late surgery (when LVEF is below 30-35%) risks permanent LV dysfunction. ACE inhibitors do not halt structural progression of primary (organic) MR.

Correct. The clinical triad of a dynamic LVOTO murmur (increases with Valsalva — which reduces preload and worsens obstruction; decreases with squatting — which increases preload), jerky carotid pulse, and family history of sudden cardiac death in young relatives is characteristic of hypertrophic obstructive cardiomyopathy (HOCM). The dynamic nature of the murmur distinguishes it from fixed aortic stenosis (which does not change with position). ICD implantation is the intervention with the strongest evidence for reducing sudden cardiac death in HOCM with high-risk features, including family history of SCD in first-degree relatives.

HOCM murmur manoeuvres: increases with Valsalva, standing, tachycardia (all reduce preload or ventricular volume); decreases with squatting, lying down, beta-blockers (all increase preload or volume). HOCM SCD risk factors: prior cardiac arrest, family history SCD, extreme LVH (>30 mm), unexplained syncope, NSVT. ICD is the most effective SCD prevention.

HOCM: dynamic murmur at left sternal edge that increases with Valsalva (reduced preload worsens obstruction) and decreases with squatting (increased preload reduces obstruction). Fixed AS murmur does not show this dynamic variation. Family history of SCD in two first-degree relatives is a high-risk feature for HOCM — ICD implantation reduces SCD risk. Myomectomy reduces obstruction but does not prevent SCD.

Correct. Peripartum cardiomyopathy (PPCM) is defined as new-onset heart failure in the last month of pregnancy or within 5 months of delivery, without a pre-existing cardiac condition or identifiable cause. LVEF is typically below 45%. ACE inhibitors and ARBs are absolutely contraindicated in pregnancy due to severe foetotoxicity — they cause oligohydramnios, renal agenesis, skull ossification defects, and foetal death. Beta-blockers (metoprolol is preferred) and hydralazine plus nitrates are used as alternatives to ACE inhibitors during pregnancy in PPCM.

PPCM: defined as new-onset HF (LVEF below 45%) in the last month of pregnancy or within 5 months postpartum, no prior cardiac disease. ACE inhibitors/ARBs = absolutely contraindicated in pregnancy (Pregnancy Category X for foetal renal/ossification toxicity). Safe alternatives during pregnancy: hydralazine + isosorbide dinitrate (instead of ACE inhibitor); beta-1 selective blockers (metoprolol). Bromocriptine: emerging therapy for PPCM (suppresses prolactin, which is implicated in PPCM pathogenesis).

Peripartum cardiomyopathy: new HF (LVEF below 45%) in the last month of pregnancy or within 5 months postpartum, no prior cardiac disease. ACE inhibitors and ARBs are absolutely contraindicated in pregnancy (foetotoxicity: oligohydramnios, renal malformation, skull defects). Alternatives in pregnancy: hydralazine + nitrates (instead of ACE inhibitor) + metoprolol. Post-delivery: standard HFrEF therapy including ACE inhibitor can be initiated.

Correct. Cardio-renal syndrome Type 1 describes acute kidney injury occurring as a consequence of acute cardiac decompensation. The mechanisms include reduced renal perfusion pressure (low cardiac output), venous congestion transmitted to the renal vasculature (elevated JVP reduces renal perfusion), and neurohormonal activation (RAAS, vasopressin, sympathetic) that causes renal vasoconstriction. The persistent JVP elevation despite diuretic therapy indicates inadequate decongestion — in this context, renal worsening is primarily driven by renal venous hypertension and low forward flow, not direct furosemide toxicity.

Cardio-renal syndrome (CRS): Type 1 = acute cardiac decompensation causing AKI; Type 2 = chronic HF causing CKD; Type 3 = AKI causing acute cardiac dysfunction; Type 4 = CKD causing chronic cardiac dysfunction; Type 5 = systemic disease causing both. Elevated JVP (renal venous congestion) is a key mechanism of AKI in ADHF — not just low output. Treatment: optimise cardiac output + careful diuresis + consider vasodilators.

Cardio-renal syndrome Type 1: acute worsening of cardiac function causes AKI. Mechanisms: reduced cardiac output (reduced renal perfusion), elevated central venous pressure transmitted to renal veins (venous congestion reduces net filtration pressure), and neurohormonal activation. Persistent JVP elevation indicates ongoing venous congestion as the dominant mechanism. Furosemide ototoxicity is rare at standard doses and causes hearing loss, not AKI.