Heart failure: systolic and diastolic dysfunction

Overview

Heart failure is a clinical syndrome in which a structural or functional heart problem prevents the heart from pumping enough blood for the body's needs, or allows it to do so only at raised filling pressures.

It is common in older people, is a leading cause of medical admission, and carries a poor outlook: about half of patients die within 5 years of diagnosis. Modern drugs and devices improve survival in the reduced-ejection-fraction type.

Classification

Other useful terms:

• Left-sided failure: pulmonary congestion (breathlessness, crackles).
• Right-sided failure: systemic congestion (raised JVP, oedema, liver enlargement, ascites). The commonest cause of right heart failure is left heart failure.
• Congestive cardiac failure: both sides failing.
• Acute vs chronic.
• High-output failure: normal heart overwhelmed by demand (anaemia, thyrotoxicosis, Paget disease, AV fistula, thiamine deficiency, pregnancy).

Causes

Common precipitants of decompensation

• Acute coronary syndrome or ischaemia.
• New AF or other arrhythmia.
• Infection (especially pneumonia).
• Stopping medicines or excess salt and fluid.
• Drugs: NSAIDs, steroids, verapamil/diltiazem, pioglitazone, some antiarrhythmics.
• Anaemia, thyroid disease, kidney failure, uncontrolled hypertension.

Pathophysiology (what explains the signs)

• A failing ventricle ejects less, so end-diastolic volume and pressure rise. By the Frank–Starling mechanism, stretch initially restores output, but the failing heart's curve is flattened.
• Low renal perfusion switches on the renin–angiotensin–aldosterone system: salt and water retention and vasoconstriction (raised preload and afterload).
• Sympathetic activation raises heart rate and contractility at first, but chronically damages myocytes.
• ANP (atria) and BNP (ventricles) are released in response to stretch; they promote salt loss and vasodilation and are useful blood tests.
• High ADH causes hyponatraemia, a poor prognostic sign.
• Remodelling: hypertrophy, myocyte loss and fibrosis change the shape of the ventricle.

Systolic dysfunction (HFrEF)

Symptoms

• Exertional breathlessness, orthopnoea (breathless lying flat; more pillows), paroxysmal nocturnal dyspnoea (wakes gasping).
• Fatigue, reduced exercise tolerance.
• Ankle swelling, abdominal swelling, weight gain.
• Nocturnal cough, wheeze ("cardiac asthma"), frothy pink sputum in pulmonary oedema.
• Late: anorexia, weight loss (cardiac cachexia), confusion.

Signs

• Tachycardia, small-volume pulse, pulsus alternans in severe failure.
• Raised JVP, positive hepatojugular reflux.
• Displaced apex beat (cardiomegaly).
• Third heart sound (S3) – gallop rhythm.
• Bibasal crackles, pleural effusions.
• Pitting oedema of ankles or sacrum, tender hepatomegaly, ascites.
• Cheyne–Stokes breathing in severe failure.

NYHA functional class

Diagnosis: laboratory and radiological findings

Diagnosis needs symptoms + signs + objective evidence of cardiac dysfunction, and the cause should always be sought.

Blood tests

• BNP or NT-proBNP: high in heart failure; a normal level makes heart failure unlikely (good rule-out test). In acute presentation, BNP above 100 pg/mL or NT-proBNP above 300 pg/mL suggests heart failure.
• FBC (anaemia), renal function and electrolytes (baseline before drugs; hyponatraemia), liver tests (congestion), thyroid function, glucose, lipids, troponin in acute cases.

Chest X-ray

Signs of left heart failure (remember ABCDE):

ECG

Rarely normal in HFrEF. May show previous MI (Q waves), ischaemia, LVH, LBBB, AF or other arrhythmia.

Echocardiography

The key test. It measures ejection fraction, chamber size, wall thickness, regional wall motion, valve disease and diastolic function, and often shows the cause.

Other tests

• Coronary angiography or CT coronary angiography (ischaemic cause).
• Cardiac MRI (cardiomyopathy, infiltration, viability).
• Stress echo or nuclear scan (hibernating myocardium that may recover after revascularisation).
• Holter monitoring (arrhythmia).

Acute management (acute pulmonary oedema)

The patient is breathless, sitting up, sweaty, with frothy sputum, crackles and low saturations.

1. Sit the patient upright.
2. Oxygen if hypoxic, aiming for saturations of about 95–98% (lower target if at risk of CO2 retention).
3. IV loop diuretic: furosemide (e.g. 40–80 mg IV, more if already taking it).
4. IV nitrate (GTN infusion) if systolic BP is above about 90 mmHg: reduces preload and pulmonary congestion.
5. CPAP / non-invasive ventilation if still hypoxic; intubation if exhausted.
6. IV opiate (small doses) only for distress; use cautiously.
7. Inotropes (dobutamine, milrinone, levosimendan) if hypotensive with poor perfusion; vasopressors (noradrenaline) in shock.
8. Treat the cause: ACS (PCI), fast AF (rate control or cardioversion), valve lesion, hypertension.
9. LMWH prophylaxis, fluid balance chart, daily weights, monitor urea, creatinine and potassium.

Cardiogenic shock (systolic BP below 90 mmHg with poor perfusion) is covered in its own chapter.

Chronic management of HFrEF

General measures

• Explain the condition; daily weights (sudden gain = fluid).
• Salt restriction; fluid restriction in severe failure.
• Stop smoking; limit alcohol (negative inotrope).
• Regular gentle exercise and cardiac rehabilitation.
• Influenza and pneumococcal vaccines.
• Review drugs that worsen failure (NSAIDs, verapamil, diltiazem, pioglitazone).
• Multidisciplinary heart failure team; palliative care in advanced disease.

Drugs

Devices and surgery

• Cardiac resynchronisation therapy (CRT): biventricular pacing for HFrEF with a wide QRS (LBBB) despite drugs; improves symptoms and survival.
• Implantable cardioverter-defibrillator (ICD): prevents sudden arrhythmic death in selected patients with low EF or previous VT/VF; often combined with CRT (CRT-D).
• Revascularisation if there is hibernating myocardium.
• Valve surgery for a correctable valve lesion.
• Left ventricular assist device and heart transplantation for selected young patients with end-stage disease.

Diastolic dysfunction (HFpEF)

Who gets it

• Elderly, often women, with hypertension and LVH.
• Diabetes, obesity, AF, chronic kidney disease.
• Hypertrophic, restrictive and infiltrative cardiomyopathy (amyloid); constrictive pericarditis is an important mimic.

Pathophysiology

The ventricle is stiff and thick: it contracts well but relaxes and fills poorly. Filling pressures rise, so lungs congest even though the EF is normal. Atrial contraction contributes more to filling, so loss of atrial kick in AF causes sudden deterioration, and tachycardia (shorter diastole) is poorly tolerated.

Signs and symptoms

• Same symptoms as systolic failure: exertional breathlessness, orthopnoea, PND, oedema, fatigue.
• Often hypertensive, sometimes with episodes of "flash" pulmonary oedema.
• Fourth heart sound (S4) from atrial contraction into a stiff ventricle; apex not displaced but may be heaving.

Diagnosis

Four conditions:

1. Symptoms of heart failure.
2. Signs of heart failure.
3. Normal or near-normal EF with a non-dilated left ventricle.
4. Evidence of structural heart disease (LVH, left atrial enlargement) and/or diastolic dysfunction on echo.

Raised BNP supports it. Echo shows thick LV walls, big left atrium, abnormal relaxation (Doppler) and normal EF. ECG often shows LVH or AF.

Management

• Control blood pressure (ACE inhibitors or ARBs are commonly used, especially with LVH).
• Diuretics for congestion, used carefully: these patients depend on filling pressure and become hypotensive if over-dried.
• Rate control and anticoagulation for AF; restore sinus rhythm where possible.
• Treat ischaemia, diabetes, obesity and sleep apnoea.
• SGLT2 inhibitors now have a place in current guidelines for HFpEF.
• Unlike HFrEF, older drugs (ACE inhibitors, beta-blockers) have no proven survival benefit in HFpEF.

Complications and prognosis

• Sudden death from ventricular arrhythmias.
• AF, thromboembolism (stroke; anticoagulate in AF or LV thrombus).
• Renal impairment (cardiorenal syndrome), hyponatraemia, hypokalaemia from diuretics.
• Cachexia, depression.
• Poor outlook signs: NYHA IV, low EF, hyponatraemia, high BNP, renal failure, repeated admissions.

Quick revision

• HFrEF EF <40%; HFmrEF 40–49%; HFpEF ≥50%.
• Commonest cause: ischaemic heart disease; commonest cause of right failure: left failure.
• Symptoms: breathlessness, orthopnoea, PND, oedema, fatigue. Signs: raised JVP, S3, crackles, oedema.
• Normal BNP/NT-proBNP rules heart failure out; echo confirms and finds the cause.
• CXR: alveolar oedema, Kerley B lines, cardiomegaly, upper lobe diversion, effusions.
• Acute: sit up, oxygen, IV furosemide, GTN if BP ok, CPAP; inotropes if hypotensive.
• Chronic HFrEF: ACE-I/ARNI + beta-blocker + aldosterone antagonist + SGLT2i; diuretics for symptoms.
• HFpEF: elderly hypertensive, LVH, S4; control BP, diuretics with care, rate-control AF.

Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).

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