Congestive cardiac failure — aetiology, clinical features, evaluation and management; drug categories, indications and side effects; approach to refractory heart failure

Heart failure (HF) is a clinical syndrome of symptoms and signs caused by a structural or functional cardiac abnormality resulting in reduced cardiac output or raised filling pressures.

Prevalence rises with age — HF is present in 13–14% of people over 80. Lifetime risk at age 40 is about 21% for men and 20% for women. Two-year and five-year mortality are approximately 60% and 75%, comparable to many common cancers.

Indian and developing-country context: ischaemic aetiology is proportionally less common; rheumatic heart disease, hypertension, idiopathic dilated cardiomyopathy and cor pulmonale contribute more. Patients present younger and at a more advanced stage.

Commonest causes in the elderly: ischaemic heart disease and hypertension — together they account for more than 75% of overt heart failure in older patients.

Others: valvular disease (calcific aortic stenosis, mitral annular calcification), atrial fibrillation, cardiomyopathies (including cardiac amyloidosis), thyroid disease, anaemia, chronic kidney disease, alcohol, chemotherapy (anthracyclines, trastuzumab) and cor pulmonale.

Ageing changes that predispose: myocardial fibrosis and collagen deposition, reduced beta-adrenergic responsiveness, impaired ventricular relaxation, reduced maximum heart rate, and increased afterload from arterial stiffening.

Typical: exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, ankle oedema, raised JVP, third heart sound, basal crackles, hepatomegaly, pleural effusion, ascites.

Atypical presentations in old age (high-yield): confusion or delirium, falls, anorexia and weight loss, nocturia, functional decline, unexplained fatigue. Pathy's notes that one-third of older patients with HF do not display the classical signs.

Individual symptoms and signs have low sensitivity; it is the constellation that supports the diagnosis. Essentials warns that HF is over-diagnosed in older adults — pedal oedema alone is not sufficient, as venous stasis mimics it.

Step 1 — clinical probability: symptoms, signs, prior cardiac history, abnormal ECG. A completely normal ECG makes HF very unlikely.

Step 2 — natriuretic peptides. ESC thresholds for further investigation: BNP >35 pg/mL or NT-proBNP >125 pg/mL in the non-acute setting. Normal levels virtually exclude HF; raised levels also carry prognostic weight. Equally predictive in HFrEF and HFpEF.

Step 3 — echocardiography to define ejection fraction, chamber size, wall thickness, valve disease and diastolic function. NICE: echocardiography first in those with previous MI; natriuretic peptide first in those without.

Supportive tests: chest X-ray (excludes COPD, fibrosis, malignancy), full blood count, renal function and electrolytes, thyroid function, glucose/HbA1c, iron studies, liver function, urinalysis.

Patient and carer education, daily weight monitoring, salt and fluid moderation, alcohol and smoking cessation, treatment of anaemia and iron deficiency, immunisation (influenza and pneumococcal), supervised cardiac rehabilitation and exercise training, adherence support, and multidisciplinary HF nurse follow-up. Pathy's stresses these are "often overlooked". Drug Categories — Indications and Side Effects (HFrEF) Class Indication / evidence Key adverse effects in the elderly ACE inhibitors All HFrEF irrespective of NYHA Hypotension, hyperkalaemia, rising creatinine, cough, angioedema. (enalapril, ramipril) class; cornerstone since Contraindicated in bilateral renal artery stenosis. CONSENSUS. Low doses still give benefit. ARBs (candesartan, ACE-inhibitor intolerance (cough). Hyperkalaemia, hypotension. Never combine with ACE inhibitor. valsartan) Beta blockers Symptomatic HFrEF NYHA I–IV Fatigue, bradycardia, worsening exercise tolerance, bronchospasm in (carvedilol, bisoprolol, added to ACE inhibitor; benefit severe COPD. Start low, go slow. nebivolol, metoprolol MR) shown up to age 80 (SENIORS used nebivolol in the elderly). MRAs (spironolactone, Persisting symptoms despite ACE Hyperkalaemia, renal impairment, gynaecomastia (spironolactone). Monitor eplerenone) inhibitor + beta blocker. K⁺ and creatinine. Loop diuretics Congestion and fluid overload — Dehydration, hypokalaemia, hyponatraemia, gout, ototoxicity, incontinence, (furosemide, torsemide) symptomatic benefit, no mortality falls. benefit. Digoxin Persisting symptoms, especially Nausea, anorexia, heart block, arrhythmia, confusion. Toxicity increased by with AF. In over-70s use 0.125 renal impairment and hypokalaemia. mg/day, target level 0.5–0.9 ng/mL. Ivabradine NYHA II–III, sinus rhythm, heart Headache, dizziness, phosphenes (visual brightness), bradyarrhythmia. rate >70/min despite optimal therapy (SHIFT). ARNI NYHA II–III already on optimal Hypotension, hyperkalaemia, angioedema. 36-hour washout required (sacubitril/valsartan) therapy (PARADIGM-HF; 20% after the last ACE inhibitor dose. reduction in CV death/HF admission). Hydralazine + nitrate ACE inhibitor/ARB intolerance; Headache, tachycardia, lupus-like syndrome. African-ancestry patients.

Cardiac resynchronisation therapy (CRT) for HFrEF with ventricular conduction delay; ICD for selected patients with reduced ejection fraction and reasonable life expectancy; consider left ventricular assist devices and transplantation only in highly selected younger-biological-age patients.

Pathy's Table 34.8 summarises the historically negative HFpEF trials: CHARM-Preserved, I-PRESERVE, PEP-CHF, SENIORS, DIG-ancillary, TOPCAT and PARAGON-HF — none reduced mortality; several reduced hospitalisations. Management therefore centred on diuretics plus treatment of hypertension, ischaemia, AF and diabetes.

Confirm it is truly refractory: check adherence, excess salt/fluid intake, and drugs that worsen HF (NSAIDs, glitazones, non-dihydropyridine calcium channel blockers, some antiarrhythmics).

Search for a reversible precipitant: uncontrolled AF or other arrhythmia, silent ischaemia, anaemia, iron deficiency, infection, thyroid dysfunction, renal failure, uncontrolled hypertension, severe valve disease, pulmonary embolism, cardiac amyloidosis.

Escalate therapy: optimise/uptitrate disease-modifying drugs; combine loop diuretic with a thiazide for sequential nephron blockade; switch oral to intravenous furosemide (infusion) for gut oedema; consider ultrafiltration; consider CRT; consider inotropes for short-term bridging only.

Palliative approach: as the disease reaches the terminal stage, prioritise symptom relief and quality of life — withdraw unnecessary drugs and blood tests, treat breathlessness and anxiety with judicious opioids and benzodiazepines, provide multidisciplinary emotional support, and consider home- or institution-based hospice care.