18.4 — Heart Failure

The name is unfortunate. "Heart failure" sounds terminal, and patients hearing it frequently believe their heart is about to stop.

It means the heart cannot deliver enough output for the body's needs at normal filling pressures (Chapter 7.4) — a description of function, not of imminence.

And its treatment has improved more in the last decade than in the preceding three, to the point where the standard drug combination reduces mortality by around 60 to 70 percent compared with no treatment.

The two kinds

And the distinction determines the treatment entirely.

Reduced ejection fraction (HFrEF) — ejection fraction below 40 percent. The pumping is weak.

Causes: previous heart attack (much the commonest), dilated cardiomyopathy, long-standing hypertension, valve disease, alcohol, viral myocarditis, chemotherapy, and uncontrolled arrhythmia.

Preserved ejection fraction (HFpEF) — ejection fraction 50 percent or above. The ventricle is stiff and cannot fill properly, so the output is inadequate even though the percentage ejected is normal.

Associated with hypertension, age, obesity, diabetes and atrial fibrillation — and it accounts for around half of all heart failure.

HFpEF was for a long time the harder problem, because most heart failure drugs improve contraction and the defect here is relaxation. That changed with SGLT2 inhibitors, which are the first class to show clear benefit (Chapter 1.4).

Recognising it

The symptoms follow from where the blood backs up (Chapter 7.4).

Left-sided congestion — into the lungs:

Breathlessness on exertion, progressing to breathlessness at rest.

Orthopnoea — breathlessness lying flat, because fluid redistributes from the legs into the circulation. "How many pillows do you sleep on?" is a real clinical question, and an increase over months is significant.

Paroxysmal nocturnal dyspnoea — waking suddenly gasping, one to two hours after falling asleep, and having to sit up or go to a window. It is a strikingly specific symptom.

Cough, sometimes with frothy pink sputum.

Right-sided congestion — into the systemic veins:

Swollen ankles, worse by evening. Distended neck veins.Enlarged tender liver.Fluid in the abdomen.And in advanced disease, swelling over the sacrum in someone bedbound, because oedema follows gravity.

General: fatigue — frequently the dominant symptom and the least specific — reduced exercise tolerance, and weight gain from fluid.

**And daily weight is the most useful self-monitoring tool there is. A gain of 2 kg over 2 to 3 days is fluid, not fat, and it precedes symptoms — which is exactly why patients are taught to weigh themselves and act on it.

Diagnosis

BNP or NT-proBNP — released when the heart chambers are stretched (Chapter 12.7).

Its main value is as a rule-out test. A normal level in an untreated patient makes heart failure very unlikely, which spares a great many echocardiograms.

Echocardiography — the key test. Gives the ejection fraction, chamber sizes, valve function and wall motion.

ECG — rarely normal in heart failure, so a completely normal ECG argues against it.

Chest X-ray — cardiomegaly, pulmonary congestion, pleural effusions.

And investigating the cause matters — coronary disease, valve disease, arrhythmia, thyroid disease, alcohol, iron deficiency — because several are correctable.

Treatment of HFrEF

And this is genuinely one of the success stories of modern cardiology.

Four drug classes, now referred to as the four pillars, each reducing mortality independently:

1. ACE inhibitor or ARB — or, better, sacubitril/valsartan, which combines an ARB with a drug that blocks the breakdown of natriuretic peptides. It was superior to enalapril in a large trial and is now preferred in most patients.

2. Beta-blocker.

And this one is counter-intuitive. Beta-blockers reduce the force of contraction, which sounds like exactly the wrong thing in a weak heart.

They work because chronic sympathetic overactivity is itself damaging — driving remodelling, arrhythmia and progressive deterioration. Blocking it protects the heart over time.

They were contraindicated in heart failure until trials in the 1990s showed the opposite, and they are one of the clearest examples of physiological reasoning being overturned by evidence (Chapter 16.1).

They must be started at a very low dose and increased slowly, because the initial effect can transiently worsen symptoms.

3. Mineralocorticoid receptor antagonist — spironolactone or eplerenone.

4. SGLT2 inhibitor — dapagliflozin or empagliflozin.

And these were developed as diabetes drugs. Their benefit in heart failure — in people with and without diabetes — was an unexpected finding in cardiovascular safety trials, and it has changed practice completely (Chapter 1.4). The mechanism is still not fully explained.

Together, the four reduce mortality by around 60 to 70 percent relative to no treatment, and getting all four started and titrated is now the main quality measure in heart failure care.

Additionally:

Diuretics — for symptoms. They relieve congestion and do not improve survival, which is worth knowing: they make people feel better without changing the disease.

Iron infusion — iron deficiency is present in around half of heart failure patients, with or without anaemia, and correcting it intravenously improves symptoms and reduces admissions. It is under-tested for.

Devices:

Implantable defibrillator — for those at risk of sudden death (Chapter 7.3).

Cardiac resynchronisation therapy — pacing both ventricles in people whose conduction is delayed so the walls contract out of sequence. It genuinely improves both symptoms and survival in selected patients.

Advanced options — mechanical assist devices and transplantation.

Treatment of HFpEF

Historically limited, and it has improved.

SGLT2 inhibitors — the first class with clear benefit.

Diuretics for congestion.

Treating the associated conditions — hypertension, atrial fibrillation, obesity, sleep apnoea — which is where much of the benefit lies.

And weight loss in obesity-related HFpEF has produced substantial symptom improvement, including with GLP-1 drugs.

Living with it

Self-management, and the components are specific and effective:

Daily weights, with an action plan for a rise.

Fluid and salt awareness — and the evidence for strict fluid restriction is weaker than the traditional advice implied. Salt restriction is more clearly useful.

Taking the medication. And a specific point: NSAIDs cause fluid retention and worsen heart failure, and they are a common cause of decompensation bought over the counter.

Vaccination — influenza and pneumococcal, because respiratory infection is a leading trigger of admission.

Exercise. Supervised cardiac rehabilitation improves symptoms, quality of life and admission rates, and the old advice to rest was wrong.

Recognising deterioration: increasing breathlessness, more pillows, weight gain, increasing swelling.

The prognosis, honestly

And this deserves a direct paragraph, because it is frequently avoided.

Heart failure has historically carried a prognosis comparable to many cancers — around 50 percent five-year survival in older studies.

Modern treatment has improved that substantially, and the figures in the older literature substantially understate what is now achievable for a well-treated patient on all four drug classes.

The course is characteristically one of gradual decline punctuated by acute deteriorations, each of which is usually survivable and after which function is often slightly lower.

Which makes it well suited to advance care planning — discussing preferences while well, rather than during a crisis. And it is one of the conditions where palliative care alongside active treatment improves both symptoms and, in some studies, survival.

Deactivating an implantable defibrillator at the end of life is a specific and frequently overlooked conversation (Chapter 7.3).

Acute heart failure

The emergency version — acute pulmonary oedema.

Sudden severe breathlessness, unable to lie flat, distressed, sweating, with frothy sputum and crackles throughout the lungs.

Immediate management: sit the person upright with legs dependent — which reduces venous return — high-flow oxygen, intravenous diuretic, and nitrates if the blood pressure allows.

And non-invasive ventilation — CPAP — which reduces the need for intubation substantially by pushing fluid out of the alveoli and reducing the work of breathing.

Then look for the trigger: heart attack, arrhythmia, infection, missed medication, NSAIDs, excessive salt or fluid, anaemia, or thyroid disease.

What the next page fixes

Chapter 18.5 covers the electrical failures — the arrhythmias, from the harmless extra beat to the ones that stop the circulation.