Clinical Case: 68-Year-Old With Worsening Dyspnoea, Orthopnoea, and PND — Acute Decompensated Heart Failure for NEET PG

Clinical Case: 68-Year-Old With Worsening Dyspnoea, Orthopnoea, and PND — Acute Decompensated Heart Failure for NEET PG | NEETPGAI

Version 1.0 — Published August 2026

Quick Answer

Acute decompensated heart failure (ADHF) is one of the highest-yield medicine cases on NEET PG — the Nohria classification, IV loop diuretic dosing, ARNI-first GDMT, SGLT2i inclusion, and CRT-D criteria appear in nearly every paper. A 68-year-old with known dilated cardiomyopathy, worsening dyspnoea, orthopnoea, PND, +3 pedal oedema, JVP 12 cm, S3, crackles, BP 88/60, and rapid AF with LBBB needs the following 10-step workflow:

Classify the phenotype — Nohria Cold-Wet (hypoperfusion PLUS congestion — cardiogenic shock spectrum, highest mortality)
Work through FAILURE triggers — Forgot furosemide, AF-RVR, NSAID use, hyponatraemia, worsening renal function
Non-invasive ventilation — CPAP or BiPAP for hypoxia; sit up, oxygen to SpO2 over 92 percent
IV loop diuretic — furosemide 40-80 mg (or 2.5x home oral dose) bolus; add thiazide (metolazone, HCTZ) for diuretic resistance
Vasopressor and inotrope — norepinephrine to keep MAP over 65; dobutamine or milrinone for cold-wet with hypoperfusion; avoid dopamine first-line (DOPAMINE trial)
Rate control of AF-RVR — IV amiodarone loading, digoxin; AVOID verapamil/diltiazem in HFrEF; DC cardioversion if unstable; anticoagulate per CHA2DS2-VASc
GDMT 4 pillars — ARNI (sacubitril-valsartan) plus evidence-based beta-blocker plus MRA plus SGLT2i; initiate in parallel before discharge
Adjuncts — IV ferric carboxymaltose for iron deficiency (AFFIRM-AHF), vericiguat for worsening HF
CRT-D evaluation — LVEF at or below 35 percent plus LBBB plus QRS at or above 130 ms after 3 months of optimal GDMT
Discharge planning — 2 g Na and 1.5-2 L fluid restriction, daily weight (alert at 2 kg in 3 days), cardiac rehab, HF nurse follow-up, palliative-care discussion for advanced HF

The case

A 68-year-old retired bank manager is brought to the medicine emergency of a tertiary hospital in Bengaluru by his son with 3 days of progressively worsening breathlessness. He is a known patient with dilated cardiomyopathy diagnosed 3 years ago after an admission for pulmonary oedema; his last echocardiogram 4 months ago showed LVEF 28 percent, moderate mitral regurgitation, moderate tricuspid regurgitation, and a dilated left ventricle. He has been on guideline-directed medical therapy — enalapril 10 mg twice daily, carvedilol 12.5 mg twice daily, spironolactone 25 mg daily, furosemide 40 mg twice daily — and had been stable NYHA II with occasional NYHA III exacerbations.

Over the past 2 weeks he has had worsening knee pain from osteoarthritis and has been taking oral ibuprofen 400 mg three times daily on a neighbour's recommendation. Three days ago he missed his morning furosemide dose while travelling to a family wedding, then missed the next two doses because his medicine box was left at the wedding venue. The next day he noticed increasing breathlessness on climbing to the first floor; the following night he had to prop himself on 3 pillows to sleep; last night he woke up gasping around 3 a.m. — paroxysmal nocturnal dyspnoea — sat by the window for an hour to catch his breath.

He also noticed his legs and abdomen were swelling — his usual shoes no longer fit; his belt notch had moved out two holes over 5 days. Weight is up 4 kg in a week. Urine output has fallen. Appetite is poor; early satiety; two episodes of nausea today. No chest pain, no palpitations noticed by the patient (although his son felt an "irregular pulse" yesterday). No fever, no cough, no haemoptysis. Bowel habit normal.

Past medical history — dilated cardiomyopathy (3 years), hypertension (10 years), type 2 diabetes (12 years) on metformin and glimepiride, chronic kidney disease stage 3a (baseline creatinine 1.2), osteoarthritis of both knees, dyslipidaemia on atorvastatin, benign prostatic hyperplasia on tamsulosin. No prior myocardial infarction, no smoking history. Occasional social alcohol until 3 years ago; stopped after DCM diagnosis. Non-vegetarian diet with high sodium (typical South Indian filter coffee, pickle, fried snacks).

Family history — father died of heart failure at 72; mother alive with diabetes; no sudden cardiac deaths.

Medications on admission — enalapril 10 mg BD, carvedilol 12.5 mg BD, spironolactone 25 mg OD, furosemide 40 mg BD (last dose 3 days ago), atorvastatin 20 mg OD, metformin 500 mg BD, glimepiride 2 mg OD, tamsulosin 0.4 mg HS, ibuprofen 400 mg TDS (self-prescribed, 2 weeks).

On examination — sitting upright, distressed, unable to complete a full sentence without pause for breath. Temperature 37.0, pulse 118/min irregularly irregular, RR 28/min, BP 88/60, SpO2 87 percent on room air, capillary refill 4 seconds, extremities cool. Weight 78 kg (baseline 74 kg).

Cardiovascular — JVP elevated to 12 cm at 45 degrees with prominent V waves. Apex beat is displaced to the 6th intercostal space in the anterior axillary line, diffuse, heaving. S3 gallop clearly audible at the apex. Pansystolic murmur grade 3/6 at the apex radiating to the axilla (functional MR). No pericardial rub. Peripheral pulses irregular, weak volume.

Respiratory — bibasilar fine end-inspiratory crackles up to mid-zones bilaterally, worse on the right. Dullness on percussion at both bases (bilateral pleural effusions). No wheeze.

Abdomen — soft, mild diffuse tenderness, tender hepatomegaly 4 cm below the costal margin (pulsatile), shifting dullness suggesting ascites, mildly distended.

Extremities — bilateral pitting pedal oedema +3 up to the knees, sacral oedema present, cool peripheries, no calf tenderness.

CNS — alert, oriented, no focal deficits, mildly slow in mentation compared with son's baseline description.

The medicine registrar recognises the pattern and initiates simultaneous oxygen, IV access, cardiac monitor, urgent labs, ECG, chest X-ray, and bedside echo, with a working diagnosis of Nohria Cold-Wet acute decompensated heart failure precipitated by non-adherence, NSAID use, and new atrial fibrillation with rapid ventricular response.

Initial assessment and the time-critical principles

Three principles govern the first hour.

Principle 1 — Fix hypoxia early with non-invasive ventilation. CPAP or BiPAP in cardiogenic pulmonary oedema reduces preload, reduces work of breathing, and cuts intubation rates by roughly 50 percent (3CPO trial). Do not wait for the ABG in a patient with obvious respiratory distress and SpO2 under 90 percent on room air.

Principle 2 — Do not overdose vasodilators in the hypotensive patient. IV nitroglycerin and IV nitroprusside are effective in warm-wet ADHF but can precipitate shock in cold-wet. Our patient is hypotensive (BP 88/60) — vasodilators are contraindicated at this stage; norepinephrine and inotropes come first.

Principle 3 — Correct precipitants alongside the diuretic. IV furosemide alone will not fix a patient whose AF is at 118 and whose NSAID is blunting the diuretic response. Rate control, NSAID discontinuation, and electrolyte correction happen in parallel with diuresis.

ABCDE

A — Airway: patent, speaking short sentences.
B — Breathing: RR 28, SpO2 87 percent room air, bibasilar crackles up to mid-zones, bilateral effusions. High-flow oxygen 15 L via non-rebreather; escalate to CPAP or BiPAP at 8 cm H2O PEEP within 15 minutes if hypoxia persists.
C — Circulation: BP 88/60 (hypotensive), pulse 118 irregular, cool peripheries, prolonged CRT. Two 18G IV lines. Arterial line for beat-to-beat BP. Consider central line if norepinephrine needed.
D — Disability: alert, mild mentation slowing (hypoperfusion).
E — Exposure: as above; weight 78 kg (baseline 74 — 4 kg gain).

Tier 1 investigations (bedside, within 30 min)

ECG — atrial fibrillation with ventricular rate 118, LBBB morphology, QRS 148 ms, no acute ischaemic ST changes, no Q waves, no dynamic changes.
Chest X-ray — cardiomegaly with cardiothoracic ratio 0.68, upper-lobe blood diversion, Kerley B lines, perihilar bat-wing pulmonary oedema, bilateral small-to-moderate pleural effusions (right greater than left).
Bedside echocardiogram — LVEF 22 percent (severely reduced from baseline 28 percent), globally dilated LV, moderate-to-severe mitral regurgitation (functional), moderate tricuspid regurgitation, dilated right ventricle with reduced function, elevated pulmonary artery systolic pressure 55 mmHg, small pericardial effusion, IVC dilated 2.3 cm with less than 50 percent collapse (elevated CVP).
Point-of-care lung ultrasound — B-lines in all lung fields (over 3 per field bilaterally) — confirms pulmonary oedema.
Bedside troponin (high-sensitivity) — 22 ng/L (mildly elevated, within reference for age — not acute MI pattern).

Tier 2 laboratory investigations

CBC — Hb 10.2 g/dL (mild normocytic anaemia — supports iron studies later), WBC 9,800/microL (normal), platelets 210,000/microL.
BNP 3200 pg/mL (markedly elevated; over 400 supports ADHF, over 900 in over-75 year olds; the higher the BNP the worse the prognosis).
NT-proBNP would be an alternative marker; both fit ADHF here.
Renal panel — creatinine 1.8 mg/dL (baseline 1.2 — worsening), urea 68 mg/dL, eGFR 38 mL/min/1.73m2, Na 129 mEq/L (hyponatraemia — poor prognostic marker in ADHF), K 3.4 mEq/L (hypokalaemia — diuretic and secondary hyperaldosteronism), Cl 92, HCO3 24.
Liver panel — AST 62, ALT 78, ALP 210, GGT 96, total bilirubin 1.6 — mild cardiogenic hepatitis (congestive hepatopathy).
INR 1.5 (mildly elevated — congestive hepatopathy).
TSH 2.1 mIU/L (normal — thyroid excluded as trigger).
HbA1c 7.4 percent (moderate control).
Iron studies — serum iron 42 mcg/dL, TSAT 15 percent, ferritin 62 ng/mL — meets ESC HF iron deficiency criteria (ferritin under 100 OR ferritin 100-299 with TSAT under 20 percent) — candidate for IV ferric carboxymaltose after acute stabilisation.
Lactate 3.2 mmol/L (elevated — hypoperfusion marker).
Blood gas (arterial) — pH 7.34, pCO2 32, pO2 58 (on room air), HCO3 22, base excess -3.2 — mixed picture with mild metabolic acidosis (lactic from hypoperfusion) and respiratory alkalosis attempt.
ABG on CPAP 40 percent FiO2 after 20 min — pH 7.38, pCO2 34, pO2 82 — improved.
D-dimer — 1.8 mcg/mL (elevated but often elevated in ADHF; PE excluded by CT if clinical suspicion high).
Blood cultures x 2 — sent (rule out sepsis contributing).
Urine routine — mild proteinuria, no active sediment.

Interpretation: advanced ADHF with cardiogenic shock spectrum (BP 88/60, lactate 3.2, worsening renal function), atrial fibrillation with rapid ventricular response and LBBB, functional MR, dilated poorly contracting LV, hyponatraemia, hypokalaemia, mild anaemia with iron deficiency, congestive hepatopathy. Three FAILURE triggers stacked — Forgot furosemide, Arrhythmia (AF-RVR), and NSAID (ibuprofen).

Nohria phenotyping and the Forrester counterpart

NEET PG tests both classifications.

Nohria-Stevenson bedside 2 x 2

Perfusion \ Congestion	DRY (no congestion)	WET (congestion)
WARM (well-perfused)	Warm-Dry (compensated)	Warm-Wet (commonest ADHF)
COLD (hypoperfused)	Cold-Dry (low output)	Cold-Wet (cardiogenic shock spectrum)

Congestion signs (Wet): orthopnoea, elevated JVP, S3 gallop, rales, hepatomegaly, ascites, pedal oedema, rising weight
Hypoperfusion signs (Cold): narrow pulse pressure (under 25 percent of systolic), cool extremities, altered mentation, hyponatraemia, worsening renal function, hypotension, elevated lactate
Warm-Wet — the commonest phenotype (roughly 65-70 percent of ADHF); IV diuretic plus vasodilator (nitroglycerin or nitroprusside) plus GDMT continuation
Cold-Wet — highest in-hospital mortality (over 20 percent); IV diuretic plus inotrope (dobutamine, milrinone) plus vasopressor (norepinephrine) to maintain MAP; consider mechanical circulatory support
Cold-Dry — inotrope plus cautious volume; often chronic advanced HF; usually not our acute admission

Forrester classification (invasive haemodynamics)

Uses cardiac index (CI) and pulmonary capillary wedge pressure (PCWP) from a Swan-Ganz catheter. Rarely used routinely now.

Subset	CI (L/min/m2)	PCWP (mmHg)	Clinical
I	over 2.2	at or below 18	Normal
II	over 2.2	over 18	Pulmonary congestion — Warm-Wet
III	at or below 2.2	at or below 18	Peripheral hypoperfusion — Cold-Dry
IV	at or below 2.2	over 18	Cardiogenic shock — Cold-Wet

Our patient sits in Nohria Cold-Wet / Forrester IV — the highest-risk phenotype.

The FAILURE mnemonic — precipitants of decompensation

Letter	Trigger	Notes
F	Forgot medications	Non-adherence is the commonest precipitant
A	Arrhythmia	AF-RVR, VT/VF, high-grade AV block, loss of AV synchrony
I	Ischaemia and Infarction	Exclude ACS with troponin, ECG, imaging
L	Lifestyle	Dietary sodium, fluid excess, alcohol binge
U	Upregulation	Thyroid, pregnancy, fever, anaemia, high-output states
R	Renal failure	Worsening GFR reduces diuretic response
E	Embolism	PE precipitates right-sided decompensation
R (also)	Medications	NSAIDs, glitazones, verapamil/diltiazem in HFrEF, steroids

Our patient has three triggers stacked — Forgot furosemide, AF-RVR, NSAID (ibuprofen).

Diagnosis

Acute decompensated heart failure — Nohria Cold-Wet / Forrester IV — in a 68-year-old man with pre-existing dilated cardiomyopathy (LVEF 22 percent), precipitated by (1) 3 missed furosemide doses, (2) new atrial fibrillation with rapid ventricular response and LBBB, and (3) 2 weeks of NSAID (ibuprofen) use; complicated by hypotension (BP 88/60), worsening renal function (creatinine 1.8, baseline 1.2), hyponatraemia (Na 129), hypokalaemia (K 3.4), congestive hepatopathy, and iron deficiency — for CPAP, IV loop diuretic, norepinephrine plus dobutamine, IV amiodarone for AF rate/rhythm, NSAID discontinuation, and staged initiation of 4-pillar GDMT with CRT-D evaluation after 3 months of optimal therapy.

Management — first hour, first 24 hours, first week, discharge, and long-term

First hour — stabilisation

Non-invasive ventilation — start CPAP at 8 cm H2O PEEP (or BiPAP 12/6) with FiO2 40-60 percent. Continue for 2-6 hours until oxygenation improves and work of breathing settles. Intubate if failing (rising CO2, deteriorating mentation, exhaustion).
Position — sit upright, legs dependent (reduces venous return).
IV access — two 18G peripheral lines; consider arterial line and central line if norepinephrine required.
Loop diuretic — IV furosemide 80 mg bolus (double the missed home dose OR 2.5x the total daily oral dose per DOSE trial). Reassess urine output over 2 hours; if under 100 mL/hr, repeat bolus with double dose (160 mg) or start continuous infusion 5-10 mg/hr. Target 3-5 L negative in first 24 hours.
Vasopressor — norepinephrine 0.05-0.5 mcg/kg/min titrated to MAP over 65 mmHg. Do NOT start dopamine first-line (DOPAMINE trial showed more arrhythmia and higher mortality vs norepinephrine).
Inotrope — dobutamine 2.5-10 mcg/kg/min OR milrinone 0.125-0.75 mcg/kg/min for cold-wet with persistent hypoperfusion after norepinephrine and diuresis. Milrinone is preferred if there is right ventricular failure or pulmonary hypertension (pulmonary vasodilator).
Rate control of AF — IV amiodarone 150 mg bolus over 10 min, then 1 mg/min for 6 hours then 0.5 mg/min (rate and rhythm control with minimal negative inotropy). OR IV digoxin 0.25-0.5 mg loading then repeat 0.25 mg every 6-8 hours to total 0.75-1.5 mg (slows AV node without lowering BP). AVOID verapamil, diltiazem, and non-selective beta-blocker acutely in HFrEF.
DC cardioversion — if the AF is haemodynamically decompensating despite the above (worsening BP, worsening pulmonary oedema), synchronised DC cardioversion at 200 J biphasic.
Anticoagulation — start therapeutic-dose LMWH (enoxaparin 1 mg/kg SC BD or 1.5 mg/kg OD, adjusted for renal function). Plan DOAC (apixaban 5 mg BD adjusted for age/weight/creatinine, or rivaroxaban 20 mg OD) — CHA2DS2-VASc will be at least 3 in this patient (age 65-74 = 1, CHF = 1, HTN = 1, DM = 1 — score 4).
Withhold NSAIDs, hold ACEi (enalapril) temporarily given hypotension and worsening renal function (do not restart until BP and creatinine stabilise; will convert to ARNI at discharge), hold spironolactone temporarily (K 3.4 first, then reassess); continue carvedilol at half-dose if tolerated (do not fully withdraw beta-blocker unless symptomatic bradycardia, high-grade AV block, or cardiogenic shock refractory to inotropes).
Correct electrolytes — IV KCl 40 mEq slow infusion (for K 3.4); IV MgSO4 2 g (co-supplement to help K retention and rate control).
Foley catheter — to accurately measure urine output.

First 24 hours — active decongestion

Target 3-5 L net negative fluid balance in the first 24 hours in cold-wet ADHF, then 1-2 L/day until euvolemic
Continuous furosemide infusion if intermittent boluses fail to produce over 100 mL/hr urine output
Diuretic resistance strategies (if urine output remains under 100 mL/hr despite escalating IV furosemide):
- Add thiazide-type diuretic — oral metolazone 5-10 mg once daily OR IV chlorothiazide 500 mg OR oral HCTZ 25-50 mg (sequential nephron blockade); most powerful adjunct
- Add acetazolamide 500 mg IV daily — ADVOR trial showed 4-day acetazolamide plus IV loop diuretic increased decongestion vs loop alone
- Add empagliflozin 10 mg — EMPULSE trial showed benefit initiating SGLT2i in-hospital
- Consider hypertonic saline plus high-dose furosemide (Paterna protocol) in refractory diuretic resistance
- Ultrafiltration — for true diuretic-refractory volume overload with worsening renal function
Wean vasopressor and inotrope as MAP recovers and lactate falls
Reassess NIV every 2-4 hours; wean off oxygen when SpO2 above 92 percent on room air
Serial K, Mg, creatinine every 6-12 hours during aggressive diuresis
Daily weight (target 0.5-1 kg loss per day)
Serial NT-proBNP or BNP (falling trend is reassuring)

First week — GDMT initiation and up-titration

Once euvolemic and haemodynamically stable (BP above 100/60, off vasopressor and inotrope for at least 24 hours, creatinine stable within 30 percent of baseline), start the 4 pillars in parallel at low doses.

Pillar	Drug	Starting dose	Target dose
1. ARNI (RAAS)	Sacubitril-valsartan	24/26 mg BD (if hypotension or elderly) or 49/51 mg BD	97/103 mg BD
2. Beta-blocker	Bisoprolol or carvedilol or metoprolol succinate	Bisoprolol 1.25 mg OD, carvedilol 3.125 mg BD, metoprolol 12.5-25 mg OD	Bisoprolol 10 mg, carvedilol 25 mg BD, metoprolol 200 mg OD
3. MRA	Spironolactone or eplerenone	Spironolactone 12.5-25 mg OD, eplerenone 25 mg OD	50 mg OD
4. SGLT2i	Dapagliflozin or empagliflozin	10 mg OD (no titration)	10 mg OD

Sacubitril-valsartan — hold ACEi (enalapril) for at least 36 hours before starting ARNI to avoid additive angio-oedema risk. Start at the lower dose in the elderly, hypotensive, or renal impairment. Monitor BP, K, creatinine at 1-2 weeks.
Beta-blocker — do NOT initiate during acute decompensation. Once euvolemic and stable, start LOW and titrate every 2 weeks. If patient was on beta-blocker at admission, continue at half-dose unless bradycardia, high-grade block, or refractory shock.
MRA — start when K under 5.0 AND eGFR above 30. Monitor K weekly for first month.
SGLT2i — no titration needed. Benefit is independent of diabetes. Watch for genitourinary infections, euglycaemic DKA (rare), volume depletion.

Adjuncts:

IV ferric carboxymaltose — for iron deficiency (ferritin under 100 OR ferritin 100-299 with TSAT under 20 percent) even if Hb is normal. AFFIRM-AHF and IRONMAN trials show fewer HF hospitalisations. Dose 500-1000 mg IV single infusion; repeat at 6 weeks and every 6-12 months as needed.
Vericiguat 2.5 mg OD titrated to 10 mg OD — soluble guanylate cyclase stimulator; VICTORIA trial in worsening HF (recent hospitalisation or IV diuretic) despite optimal GDMT showed 10 percent RRR in CV death or HF hospitalisation.
Ivabradine 5 mg BD — if sinus rhythm with resting HR at or above 70 despite maximally tolerated beta-blocker; not indicated in our patient (AF).
Digoxin — reduces hospitalisation but not mortality; consider for persistent symptoms despite optimal GDMT or for rate control in AF (target level 0.5-0.9 ng/mL).

Discharge planning (typically days 5-10)

Salt and fluid restriction — 2 g Na (5 g salt) per day; 1.5-2 L fluid per day
Daily weight monitoring — alert card: gain of 2 kg in 3 days = call clinic / take extra diuretic
Medication reconciliation — confirm 4-pillar GDMT started, appropriate doses, no re-introduction of NSAIDs; hand over a printed medication list
Patient and family education — recognise early warning signs (worsening dyspnoea, orthopnoea, PND, weight gain, ankle swelling)
Cardiac rehabilitation — 8-12 week supervised programme (limited availability in India — refer to metros; home-based programme if not available)
HF nurse follow-up — call at 48-72 hours post-discharge; clinic follow-up at 1-2 weeks then 4 weeks then 3 months
Vaccinations — influenza (annual), pneumococcal (PCV13 then PPSV23), COVID-19 booster, RSV (over 60)
Advanced HF and palliative care discussion — for NYHA IIIb-IV patients; discuss goals of care, LVAD, transplant, ICD/CRT-D deactivation at end-of-life

Long-term — CRT-D, LVAD, transplant

CRT-D indications (after 3 months of optimal GDMT):
- LVEF at or below 35 percent PLUS sinus rhythm PLUS LBBB PLUS QRS at or above 150 ms — class I
- LVEF at or below 35 percent PLUS sinus rhythm PLUS LBBB PLUS QRS 130-149 ms — class IIa
- LVEF at or below 35 percent PLUS non-LBBB PLUS QRS at or above 150 ms — class IIa (weaker signal)
- Our patient has LBBB and QRS 148 ms — meets class IIa if in sinus rhythm and NYHA II-IV after optimisation; may need AF rhythm control or ablation first because CRT benefits are diluted in poorly rate-controlled AF
ICD alone (for primary prevention of SCD) — LVEF at or below 35 percent plus NYHA II-III despite optimal GDMT for 3 months, expected survival over 1 year
LVAD — bridge to transplant OR destination therapy in NYHA IV refractory HF; limited availability in India (AIIMS, CMC Vellore, Fortis Escorts, Narayana, Kokilaben) and prohibitive cost (Rs 60-100 lakh)
Orthotopic heart transplant — end-stage HF (NYHA IV, LVEF under 20 percent, refractory to all therapies); India has ROTTO/SOTTO organ-sharing network with programmes at AIIMS, CMC Vellore, Fortis, MMHRC, Global; long waiting lists
Advanced HF palliative care — NYHA IV with recurrent hospitalisations; symptom control, opioids for dyspnoea, dobutamine at home in some centres, comprehensive advance care planning

HFpEF differences

Heart failure with preserved ejection fraction (HFpEF, LVEF at or above 50 percent) and mid-range EF (HFmrEF, 41-49 percent) share many features with HFrEF but differ in evidence base.

Diuretics — symptomatic only; loop diuretics for congestion; goal euvolaemia
SGLT2i (dapagliflozin, empagliflozin) — now proven in HFpEF (EMPEROR-Preserved, DELIVER); reduces HF hospitalisation
MRA (spironolactone) — TOPCAT trial showed regional heterogeneity (positive in North America, negative in Russia/Georgia); AHA guidelines give a class IIb recommendation for spironolactone in HFpEF
ARNI (sacubitril-valsartan) — PARAGON-HF just missed the primary endpoint but signal in LVEF 45-57 percent subgroup and in women; class IIb consideration in HFmrEF and HFpEF at the lower end of the EF range
Beta-blockers, ACE inhibitors, ARBs — no robust mortality benefit in pure HFpEF; used for co-morbid indications (hypertension, coronary disease, arrhythmia)
Treat co-morbidities aggressively — hypertension (target BP under 130/80), atrial fibrillation, obesity, sleep apnoea, coronary disease, iron deficiency

Right heart failure

Causes — left HF (commonest), pulmonary hypertension (WHO group 1-5), pulmonary embolism, RV infarction, tricuspid valve disease, arrhythmogenic RV cardiomyopathy
Presentation — raised JVP, hepatomegaly, ascites, pedal oedema, but relatively preserved lung fields
Treatment — treat the underlying cause; diuretics for congestion; AVOID over-diuresis in RV-dependent physiology (drops preload and cardiac output); PDE5 inhibitors (sildenafil, tadalafil) or endothelin receptor antagonists (bosentan, ambrisentan) or prostacyclin analogues (epoprostenol, iloprost, treprostinil) for PAH-related RV failure

Complications

Acute (hospitalisation)

Cardiogenic shock (10-15 percent of ADHF admissions)
Acute kidney injury (cardiorenal syndrome — commonest in-hospital complication)
Arrhythmias — new AF, VT, VF
Electrolyte disturbances — hypokalaemia, hyponatraemia, hypomagnesaemia
Nosocomial infection — pneumonia, urinary tract infection, catheter-related
VTE / pulmonary embolism (immobility, congestion)
Diuretic-induced hyperuricaemia and gout flare

Subacute (weeks-months)

Recurrent hospitalisation (30-day readmission rate 20-25 percent — major quality metric)
Progressive renal dysfunction
Persistent congestion

Long-term

Progressive LV dilation and worsening EF
Sudden cardiac death (10-15 percent per year in HFrEF NYHA III-IV without ICD)
End-stage HF requiring LVAD or transplant
Cardiac cachexia (poor prognosis marker)

India-specific considerations

Rising HF hospitalisation burden — the Trivandrum Heart Failure Registry and CSI-HFR data show HF admissions doubling over the last decade with in-hospital mortality of 8-10 percent, driven by delayed presentation, under-diagnosis, under-prescribed GDMT, and cost-driven non-adherence
GDMT under-prescription — Indian registries show only 25-40 percent of eligible HFrEF patients are on ARNI, 60-70 percent on beta-blocker, 40-50 percent on MRA, 20-30 percent on SGLT2i; systematic in-hospital initiation is the largest lever
Cost and access — sacubitril-valsartan (Vymada) at Rs 60-80 per tablet, dapagliflozin (Forxiga) at Rs 40-50 per tablet, empagliflozin (Jardiance) at Rs 30-40 per tablet; PMJAY (Ayushman Bharat) and state schemes (Chief Minister's Comprehensive Health Insurance in Tamil Nadu, MJPJAY in Maharashtra) cover HF admission but out-of-pocket outpatient medication cost is a major barrier
Rheumatic heart disease — remains a common cause of HF in India; mitral stenosis and mixed mitral disease need separate management (rate control, anticoagulation, valve intervention) — GDMT does not apply to valvular HF
Peripartum cardiomyopathy — a specific cause of ADHF in postpartum women; bromocriptine is a proposed adjunct in some series; anticoagulation for LV thrombus (higher risk than DCM); LVEF may recover
Chagas disease is absent in India but arsenic-related cardiomyopathy is reported in some regions (West Bengal); rheumatic and ischaemic aetiologies dominate
Cardiac rehabilitation — limited availability outside metros; home-based programmes and mobile-app-supported rehab are gaining traction
LVAD and transplant — programmes at AIIMS, CMC Vellore, Fortis Escorts, Narayana, Kokilaben; extremely limited numbers relative to need; cost approaches Rs 60-100 lakh for LVAD; transplant less costly but organ availability is the bottleneck
Palliative care — under-developed in India; advance care planning conversations for NYHA IV HF are rare; hospices with cardiology-informed care are few

How NEET PG tests acute decompensated heart failure

Nine recurring patterns.

Pattern 1 — The Nohria phenotyping question: Vignette gives BP 88/60, cool extremities, JVP raised, S3, crackles; asks the classification. Cold-Wet. Highest mortality phenotype.

Pattern 2 — The FAILURE trigger question: Vignette describes a HF patient decompensating after a wedding season (dietary salt) OR after starting NSAIDs OR after new-onset AF OR after skipping medications; asks the trigger. Trace through the mnemonic and pick.

Pattern 3 — The IV loop diuretic dose question: Best initial IV furosemide dose in ADHF on 40 mg BD oral? 2.5 times total daily oral dose per DOSE trial — so around 80-160 mg IV bolus. Continuous infusion if inadequate.

Pattern 4 — The 4-pillar GDMT question: What is the correct 4-pillar therapy for HFrEF (LVEF at or below 40 percent)? ARNI (or ACEi/ARB), beta-blocker (bisoprolol, carvedilol, metoprolol succinate), MRA (spironolactone, eplerenone), SGLT2i (dapagliflozin, empagliflozin). Parallel initiation, not sequential.

Pattern 5 — The ARNI switch question: Patient on enalapril 10 mg BD switching to sacubitril-valsartan — what is the required washout? At least 36 hours (to avoid additive angio-oedema).

Pattern 6 — The rate control in AF-RVR plus HFrEF question: Which nodal blocker to AVOID? Verapamil and diltiazem (negative inotropy). Preferred agents — amiodarone, digoxin, cautious beta-blocker after euvolaemia.

Pattern 7 — The CRT-D question: LVEF 30 percent, LBBB, QRS 155 ms, NYHA III despite 3 months optimal GDMT — next step? CRT-D (biventricular pacing plus ICD) — meets class I indication.

Pattern 8 — The SGLT2i indication question: Does dapagliflozin help HFpEF? Yes — EMPEROR-Preserved and DELIVER trials; class I recommendation for HFpEF and HFmrEF now.

Pattern 9 — The BNP interpretation question: BNP 3200 in a 68-year-old with dyspnoea — likely diagnosis? Acute decompensated HF (BNP over 400 supports; over 900 in over-75). Rule out obesity (falsely low), atrial fibrillation (falsely high), renal impairment (falsely high).

High-yield one-liners:

ADHF Cold-Wet has the highest in-hospital mortality (over 20 percent)
IV furosemide 2.5x oral home dose per DOSE trial; continuous infusion for resistance
NIV (CPAP/BiPAP) cuts intubation rates by 50 percent in cardiogenic pulmonary oedema (3CPO trial)
Norepinephrine first-line vasopressor in cardiogenic shock (DOPAMINE trial)
Dobutamine or milrinone for cold-wet with hypoperfusion after norepinephrine
ARNI (sacubitril-valsartan) is now first-line RAAS blockade for HFrEF, replacing ACEi/ARB
36-hour washout when switching from ACEi to ARNI
SGLT2i benefit is independent of diabetes and now proven in HFpEF (EMPEROR-Preserved)
IV ferric carboxymaltose for iron deficiency reduces HF hospitalisation (AFFIRM-AHF)
Vericiguat for worsening HF despite optimal GDMT (VICTORIA)
Ivabradine only for sinus rhythm with HR at or above 70 despite max beta-blocker
CRT-D — LVEF at or below 35 percent plus LBBB plus QRS at or above 130 ms after 3 months of optimal GDMT
AVOID verapamil/diltiazem in HFrEF (negative inotropy)
AVOID NSAIDs, glitazones in HF
Daily weight — 2 kg gain in 3 days = warning sign
30-day readmission rate 20-25 percent is a key quality metric

Frequently Asked Questions

What is the Nohria-Stevenson bedside classification of acute decompensated heart failure and why is it useful?

The Nohria-Stevenson classification is a bedside 2-by-2 grid used to phenotype a patient with acute decompensated heart failure (ADHF) at the point of contact, without waiting for echocardiogram or invasive haemodynamics. Two clinical axes are assessed. Congestion (Wet vs Dry) is judged by orthopnoea, elevated JVP, S3 gallop, rales, hepatomegaly, ascites, pedal oedema, and rising weight. Perfusion (Warm vs Cold) is judged by narrow pulse pressure (under 25 percent of systolic), cool extremities, altered mentation, hyponatraemia, worsening renal function, and hypotension. The four profiles are Warm-Dry (compensated, no acute intervention), Warm-Wet (congested but perfusing — most ADHF; treat with IV diuretics and vasodilators), Cold-Dry (hypoperfused but not congested — treat with inotropes carefully, cautious fluids), and Cold-Wet (congested AND hypoperfused, cardiogenic shock spectrum — inotropes plus diuretics plus vasopressors as needed). Cold-Wet carries the highest in-hospital mortality (over 20 percent). The parallel Forrester classification uses invasive haemodynamics — cardiac index and pulmonary capillary wedge pressure — but Nohria is bedside-first and is what NEET PG tests. Our 68-year-old with hypotension (BP 88/60), hypoperfusion signs, and clear congestion (elevated JVP, S3, crackles, ascites, +3 oedema) is Cold-Wet.

What is the FAILURE mnemonic for triggers of acute decompensated heart failure and how does it change management?

The FAILURE mnemonic identifies precipitants of decompensation in a patient with previously compensated chronic heart failure and it should be worked through in every admission. F is for Forgot medications — non-adherence to diuretics, ARNI/ACE/ARB, beta-blocker, or MRA is the single most common precipitant. A is for Arrhythmia — new atrial fibrillation with rapid ventricular response is classic; also ventricular arrhythmias, high-degree AV block, or loss of AV synchrony after a paced-rhythm change. I is for Ischaemia and Infarction — acute coronary syndrome must be excluded with troponin, ECG, and often coronary imaging in first presentations. L is for Lifestyle — dietary sodium load (festival meals, restaurant sodium), fluid excess, alcohol binge. U is for Upregulation — thyroid dysfunction, pregnancy, fever, anaemia, high-output states (severe iron deficiency, arteriovenous fistula). R is for Renal failure — worsening GFR reduces diuretic response, drives fluid retention, and demands dose adjustment. E is for Embolism — pulmonary embolism can precipitate right-sided decompensation and is often missed. Also often added is a second R for medications like NSAIDs, glitazones, negative-inotropic verapamil/diltiazem in reduced-EF disease, and steroids. Identifying the trigger changes management — rate control for AF, revascularisation for ACS, iron for iron deficiency, thyroid treatment for thyrotoxicosis. Our vignette patient has three FAILURE triggers stacked — Forgot furosemide (3 missed doses), Arrhythmia (rapid AF), and NSAID use (renal salt-water retention plus reduced diuretic response). Correcting all three is as important as the diuretic itself.

What is the current 4-pillar GDMT for HFrEF and what is the recommended sequence of initiation?

Guideline-Directed Medical Therapy (GDMT) for heart failure with reduced ejection fraction (HFrEF, LVEF at or below 40 percent) is now built on four foundational pillars, each of which independently reduces cardiovascular death and heart-failure hospitalisation. Pillar 1 is renin-angiotensin system inhibition — sacubitril-valsartan (an angiotensin receptor-neprilysin inhibitor, ARNI) is now first-line, replacing ACE inhibitor (enalapril, ramipril) or ARB (losartan, valsartan) based on PARADIGM-HF; hold ACEi 36 hours before switching to ARNI to avoid angio-oedema. Pillar 2 is beta-blocker — evidence-based agents only (bisoprolol, carvedilol, or metoprolol succinate); start LOW when the patient is euvolemic and titrate every 2 weeks; do NOT abruptly withhold beta-blocker in acute decompensation unless there is symptomatic bradycardia, high-degree AV block, or cardiogenic shock. Pillar 3 is mineralocorticoid receptor antagonist — spironolactone or eplerenone; monitor potassium and creatinine; contraindicated if K over 5.0 or eGFR under 30. Pillar 4 is SGLT2 inhibitor — dapagliflozin or empagliflozin; benefit is independent of diabetes status; also reduces HF hospitalisation in HFpEF (EMPEROR-Preserved, DELIVER). The traditional slow-sequencing approach (ACEi first over months, then beta-blocker, then MRA) has been abandoned. The current strategy is parallel simultaneous initiation at low doses within days-to-weeks of admission, before discharge whenever safe, then rapid up-titration to target or maximally tolerated doses over 2-4 weeks. Adjuncts include IV iron (ferric carboxymaltose for iron deficiency regardless of anaemia — AFFIRM-AHF, IRONMAN), vericiguat for worsening HF despite optimal GDMT (VICTORIA), and ivabradine for sinus rhythm with heart rate at or above 70 despite maximally tolerated beta-blocker. NEET PG tests all four pillars, the parallel-initiation shift, and the ARNI-over-ACEi upgrade.

How is atrial fibrillation with rapid ventricular response managed in acute decompensated heart failure?

Atrial fibrillation with rapid ventricular response (AF-RVR) in acute decompensated heart failure requires a management approach that differs from AF-RVR in a haemodynamically stable outpatient. Step 1 is haemodynamic assessment — hypotension, chest pain, altered mentation, or acute pulmonary oedema not responding to initial therapy defines unstable AF and mandates urgent synchronised DC cardioversion (200 J biphasic, escalate as needed). Step 2 in a stable patient with reduced EF and acute HF is rate control WITHOUT negative-inotropic nodal blockade — verapamil and diltiazem are relatively contraindicated in HFrEF because they worsen cardiac output. First-line choices are intravenous amiodarone (150 mg IV bolus over 10 min, then 1 mg/min infusion for 6 hours then 0.5 mg/min) which acts as rate AND rhythm control with minimal negative inotropy, or intravenous digoxin (0.25-0.5 mg IV then repeat 0.25 mg every 6-8 hours to a total loading dose of 0.75-1.5 mg) which slows the AV node without lowering blood pressure. Beta-blockers can be used cautiously once euvolemic and haemodynamically stable. Step 3 is stroke prevention — CHA2DS2-VASc score guides anticoagulation; in a 68-year-old man with CHF (1) plus hypertension (if present) plus age 65-74 (1) the score is already 2 or more and warrants a DOAC (apixaban, rivaroxaban, dabigatran, edoxaban) unless contraindicated (mechanical valve, moderate-severe mitral stenosis, severe renal impairment for some agents). Step 4 is trigger correction — treat the precipitant (electrolyte disturbance, thyroid dysfunction, ischaemia). Step 5 is longer-term rhythm strategy — rate vs rhythm control in HFrEF has shifted toward early rhythm control (EAST-AFNET 4) and catheter ablation (CASTLE-AF showed mortality benefit in HFrEF plus AF). NEET PG tests the avoidance of verapamil/diltiazem in HFrEF, the amiodarone/digoxin choice, the CHA2DS2-VASc cut-off, and the CASTLE-AF ablation signal.

What are the indications for cardiac resynchronization therapy (CRT) and ICD in chronic heart failure?

Cardiac resynchronization therapy (CRT) and implantable cardioverter-defibrillator (ICD) are electrical device therapies that reduce mortality and hospitalisation in selected HFrEF patients. ICD indications for PRIMARY prevention of sudden cardiac death in HFrEF are LVEF at or below 35 percent despite at least 3 months of optimal GDMT plus NYHA II-III symptoms plus expected survival over 1 year with good functional status; some guidelines add LVEF at or below 30 percent for NYHA I ischaemic cardiomyopathy. SECONDARY prevention is indicated after a sustained VT/VF arrest not due to reversible cause. CRT (biventricular pacing) indications are LVEF at or below 35 percent plus sinus rhythm plus LEFT BUNDLE BRANCH BLOCK (LBBB) morphology plus QRS at or above 150 ms (class I) or 130-149 ms (class IIa) plus NYHA II-IV symptoms despite optimal GDMT for at least 3 months. LBBB morphology is the strongest predictor of CRT response; non-LBBB (RBBB, IVCD) has a weaker signal and typically needs longer QRS (at or above 150 ms) for benefit. Most patients meeting CRT criteria also meet ICD criteria, so a CRT-D (defibrillator plus resynchronization) is the usual device. Our vignette patient has LBBB and rapid AF at 118; he needs LVEF reassessment after acute optimisation, rate control (target under 100), 3 months of optimal GDMT (ARNI, beta-blocker, MRA, SGLT2i), and only THEN a CRT-D evaluation — never during acute decompensation and never before optimising GDMT. NEET PG tests the LVEF 35 percent cut-off, the LBBB requirement, the 130-150 ms QRS bands, and the 3-month optimal-GDMT waiting period.

This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.

Written by: NEETPGAI Editorial Team Reviewed by: Pending SME Review Last reviewed: August 2026