Heart Failure: When the Heart Cannot Pump Enough

Heart failure is a clinical syndrome in which the heart cannot fill or eject blood effectively without abnormal pressure. It can result from several heart diseases and may occur with reduced or preserved ejection fraction. Diagnosis requires clinical assessment, NT proBNP testing and cardiac imaging rather than symptoms alone.

What heart failure is Heart failure is a clinical syndrome rather than one single disease. It develops when an abnormality of heart structure or function prevents the circulation from meeting the body's needs normally. The heart may eject too little blood, fill under abnormally high pressure or have both problems. This can cause breathlessness, fatigue and fluid retention. Heart failure does not mean that the heart has stopped The term can sound as though the heart is no longer working. In reality, the heart continues beating but cannot support the circulation efficiently under ordinary conditions. Symptoms range from mild exertional limitation to life threatening pulmonary oedema or cardiogenic shock. Treatment can improve symptoms, reduce hospital admission and prolong life. Heart failure is not simply a weak pump Some people have weakened contraction and eject a reduced proportion of blood. Others eject a normal proportion but have a stiff ventricle that fills only under high pressure. Both patterns can cause congestion and impaired exercise capacity. Describing every case as a weak heart therefore creates an inaccurate mental model. The cardiac cycle During diastole, the heart muscle relaxes and the ventricles fill with blood. During systole, the ventricles contract and eject blood into the lungs and body. Efficient circulation requires adequate filling, coordinated contraction, functioning valves and a regular electrical rhythm. Disease affecting any of these components can contribute to heart failure. Cardiac output Cardiac output is the amount of blood pumped by a ventricle each minute. It depends on the amount ejected with each beat and the heart rate. A person can maintain cardiac output temporarily by increasing heart rate or retaining fluid. These compensations may later worsen congestion or increase the heart's workload. Congestion Congestion occurs when pressure builds behind a heart chamber and fluid moves into tissues. Raised pressure on the left side can contribute to fluid within the lungs. Raised pressure on the right side can contribute to leg swelling, liver congestion and abdominal fluid. Many people have involvement of both sides rather than a purely left sided or right sided problem. Ejection fraction Ejection fraction is the proportion of blood inside the left ventricle that is ejected during each contraction. It is usually estimated during an echocardiogram. Ejection fraction is not a percentage measure of the heart's total strength or overall health. A normal ejection fraction does not exclude heart failure. Heart failure with reduced ejection fraction Heart failure with reduced ejection fraction is usually shortened to HFrEF. Current NICE guidance defines it as symptomatic heart failure with a left ventricular ejection fraction of 40% or less. The ventricle has impaired systolic contraction and ejects a reduced proportion of its filled volume. HFrEF has several treatments that reduce hospital admission and premature death. Heart failure with preserved ejection fraction Heart failure with preserved ejection fraction is usually shortened to HFpEF. The left ventricular ejection fraction is 50% or more, but filling remains abnormal. The ventricle may be stiff, thickened or unable to relax efficiently. Pressure can rise within the heart and lungs despite the preserved percentage ejected. Diagnosis requires symptoms plus evidence of structural or functional cardiac abnormality. Heart failure with mildly reduced ejection fraction Heart failure with mildly reduced ejection fraction is usually shortened to HFmrEF. NICE defines this group as an ejection fraction between 41% and 49%. Its biology and treatment can overlap with both HFrEF and HFpEF. The three category model is more accurate than forcing every person into only reduced or preserved groups. Ejection fraction can change Heart function may improve after treatment of coronary disease, arrhythmia, inflammation or another reversible cause. A person previously diagnosed with HFrEF can later have an ejection fraction above 40%. This is sometimes described as heart failure with improved ejection fraction. Recovery does not automatically mean treatment should be stopped because deterioration can recur. Common causes Heart failure is the final clinical pathway of many cardiovascular diseases. Common causes include coronary heart disease, previous myocardial infarction and longstanding high blood pressure. Valve disease, cardiomyopathy and persistent arrhythmia are also important. Several causes can coexist in the same person. Coronary heart disease and myocardial infarction Coronary atherosclerosis can reduce blood supply to the myocardium. A heart attack can permanently damage part of the left ventricle. The remaining muscle must then work harder to maintain circulation. Progressive remodelling can enlarge the ventricle and reduce its pumping function. High blood pressure Longstanding hypertension forces the left ventricle to pump against increased resistance. The muscle can thicken in response. A thick ventricle may become stiff and fill poorly, contributing to HFpEF. Later, the muscle can dilate and contract less effectively. Good blood pressure treatment reduces the risk of developing heart failure. Heart valve disease Heart valves direct blood forwards through the chambers. A narrowed valve obstructs flow and increases pressure behind it. A leaking valve allows blood to move backwards and creates volume overload. Severe aortic stenosis and mitral regurgitation are important causes of heart failure. Valve treatment may improve heart failure when the valve abnormality is responsible. Cardiomyopathy Cardiomyopathy means disease of the heart muscle. Dilated cardiomyopathy causes enlarged chambers and impaired contraction. Hypertrophic cardiomyopathy causes abnormal thickening and can impair filling or blood flow. Restrictive cardiomyopathy makes the ventricles unusually stiff. Causes include inherited variants, inflammation, alcohol, toxins and some cancer treatments. Myocarditis Myocarditis is inflammation of the heart muscle. It can follow infection, immune disease or exposure to particular medicines. Some people recover completely, while others develop persistent ventricular dysfunction. Chest pain, arrhythmia and cardiogenic shock can accompany severe myocarditis. Arrhythmias Atrial fibrillation can reduce efficient ventricular filling and cause a persistently rapid heart rate. Longstanding rapid rhythms can weaken the heart muscle. Very slow rhythms can also reduce cardiac output. Heart failure can itself increase the likelihood of atrial and ventricular arrhythmias. The relationship can therefore operate in both directions. Other causes Congenital heart disease can eventually lead to heart failure. Pregnancy associated cardiomyopathy can develop towards the end of pregnancy or after birth. Thyroid disease, severe anaemia and iron overload can contribute. Alcohol, cocaine and some chemotherapy or targeted cancer medicines can damage heart muscle. Sleep apnoea, obesity, kidney disease and diabetes often increase risk or complicate management. Symptoms depend on pressure and output Congestion causes many fluid related symptoms. Reduced cardiac output and impaired muscle blood flow contribute to fatigue and exercise intolerance. Symptoms can fluctuate as fluid balance, rhythm and blood pressure change. No single symptom confirms heart failure. Exertional breathlessness Breathlessness during activity is a common presentation. Raised pressure within the lung circulation can make breathing harder during physical activity. Poor fitness, obesity, anaemia, lung disease and anxiety can cause similar symptoms. The pattern requires clinical assessment rather than diagnosis from breathlessness alone. Orthopnoea Orthopnoea means breathlessness that worsens when lying flat. Lying down moves fluid from the legs towards the chest and can increase pulmonary congestion. A person may need extra pillows or begin sleeping upright. Reflux, obesity and lung disease can also make lying flat uncomfortable. Paroxysmal nocturnal dyspnoea Paroxysmal nocturnal dyspnoea is sudden severe breathlessness that wakes someone from sleep. The person may need to sit or stand near an open window before symptoms settle. It usually develops after lying down for some time rather than immediately. This pattern raises concern for pulmonary congestion but is not unique to heart failure. Peripheral oedema Peripheral oedema is swelling caused by fluid within tissues. Heart failure swelling commonly affects both ankles and lower legs. It may leave an indentation after firm pressure, called pitting oedema. Venous disease, medicines, kidney disease and liver disease can produce similar swelling. One newly swollen painful leg raises a different concern, including deep vein thrombosis. Abdominal congestion Right sided congestion can enlarge the liver and cause upper abdominal discomfort. Fluid can collect within the abdomen, called ascites. Reduced appetite, nausea and early fullness can follow bowel or liver congestion. Rapid abdominal swelling requires assessment because liver and abdominal diseases have similar presentations. Fatigue and reduced exercise tolerance People may notice that ordinary activities take longer or require frequent rests. Reduced cardiac output, deconditioning, anaemia, iron deficiency and poor sleep can contribute. Fatigue is highly non specific and cannot establish heart failure alone. A change from the person's previous functional level is often more informative than the symptom word itself. Cough and wheeze Pulmonary congestion can cause a persistent cough or wheezing sound. Symptoms may worsen when lying down. Asthma, chronic obstructive pulmonary disease, infection and ACE inhibitor treatment are alternative causes. Pink frothy sputum with severe breathlessness can indicate acute pulmonary oedema. Palpitations and dizziness Palpitations may reflect atrial fibrillation, ectopic beats or another rhythm disturbance. Low blood pressure or poor cardiac output can cause dizziness or fainting. Medicines can also reduce blood pressure or heart rate. Syncope in someone with known heart disease requires prompt assessment because a dangerous arrhythmia is possible. Older adults may present subtly Older adults do not always report clear breathlessness or ankle swelling. Presentation can include reduced mobility, falls, confusion, poor appetite or loss of independence. A person may simply stop completing activities they previously managed. Frailty, kidney disease, lung disease and medicine effects can obscure the pattern. A sudden functional decline should not be attributed automatically to ageing. Heart failure can be chronic or acute Chronic heart failure develops or persists over time. Symptoms may remain stable for months with appropriate treatment. Acute heart failure means new or rapidly worsening symptoms requiring urgent hospital assessment. Acute decompensated heart failure describes deterioration in someone with established disease. Triggers for acute decompensation A chest infection or another systemic infection can increase cardiac workload. A heart attack, uncontrolled blood pressure or a new arrhythmia can trigger deterioration. Kidney injury, anaemia and thyroid disease are additional possibilities. Missed medicines, excess fluid or very high salt intake may contribute, but deterioration should not be blamed on behaviour without assessment. Acute pulmonary oedema Acute pulmonary oedema occurs when fluid rapidly enters the lung tissue and air spaces. The person can become severely breathless, distressed and unable to lie flat. Breathing may sound wet or wheezy, and pink frothy sputum can appear. This is a medical emergency requiring a 999 call. Cardiogenic shock Cardiogenic shock develops when the heart cannot maintain blood flow to vital organs. Possible features include very low blood pressure, confusion, cold clammy skin and reduced urine output. It can follow a large myocardial infarction, severe myocarditis, valve failure or advanced cardiomyopathy. Emergency critical care and cardiology treatment are required. Clinical assessment The clinician asks about breathlessness, sleeping position, swelling, weight change and exercise tolerance. They review coronary disease, hypertension, valve disease, rhythm problems and previous cardiac treatment. Examination assesses pulse, blood pressure, oxygen level, fluid status, heart sounds and lung sounds. These findings guide probability but cannot confirm the syndrome alone. NT proBNP N terminal pro B type natriuretic peptide is usually shortened to NT proBNP. The heart releases natriuretic peptides when its walls experience increased stretch or pressure. NICE recommends measuring NT proBNP in adults with suspected chronic heart failure. The test helps decide how quickly specialist assessment and echocardiography are needed. It does not identify the underlying cause or heart failure subtype. NICE referral thresholds An untreated person with NT proBNP above 2,000 nanograms per litre needs urgent specialist assessment and echocardiography within two weeks. A result from 400 to 2,000 nanograms per litre leads to assessment and echocardiography within six weeks. A result below 400 nanograms per litre makes chronic heart failure less likely in an untreated person. Persistent clinical concern still requires discussion with a heart failure specialist. Limits of NT proBNP A raised NT proBNP does not prove heart failure. Age, atrial fibrillation, kidney disease, pulmonary disease, sepsis and liver disease can increase the level. Obesity and African or African Caribbean ethnicity can be associated with lower concentrations. Diuretics and several heart failure medicines can also lower the result. NT proBNP cannot distinguish HFrEF from HFpEF. NT proBNP in acute heart failure Hospitals use a different rule out threshold for new suspected acute heart failure. An NT proBNP below 300 nanograms per litre makes new acute heart failure less likely within the NICE pathway. An elevated result supports urgent echocardiography but remains non specific. Acute treatment is guided by the full clinical picture and must not wait for one laboratory result when the person is critically unwell. Echocardiography Transthoracic echocardiography uses ultrasound to examine heart structure and function. It measures ejection fraction and assesses ventricular size, wall thickness and movement. It evaluates valve disease, filling patterns, pulmonary pressures and some congenital abnormalities. Echocardiography helps confirm cardiac dysfunction and classify the heart failure pattern. Diagnosing HFpEF requires more than a normal ejection fraction A person does not have HFpEF merely because breathlessness accompanies an ejection fraction above 50%. Evidence of abnormal filling pressure or structural heart disease is also needed. Examples include left atrial enlargement, ventricular thickening or abnormal Doppler measurements. Alternative causes of breathlessness must be considered. The ECG A 12 lead electrocardiogram records the heart's electrical activity. It can identify atrial fibrillation, previous infarction, ventricular hypertrophy and conduction delay. It helps assess whether beta blockers or devices may be appropriate. The ECG does not directly measure ejection fraction, filling pressure or cardiac output. Additional investigations A chest X ray can show heart enlargement, pulmonary congestion or another lung diagnosis. Blood tests assess kidney function, electrolytes, thyroid function, liver function, glucose and blood count. Iron studies are important because iron deficiency can worsen symptoms, particularly in HFrEF. Urinalysis and lung function testing may identify alternative or contributing conditions. Coronary imaging or cardiac MRI is selected when the underlying cause remains uncertain. Finding the cause matters Heart failure is not a complete diagnosis until its likely cause has been assessed. Coronary disease may need anti ischaemic or revascularisation decisions. Severe valve disease can require repair or replacement. An arrhythmia may need rate control, rhythm treatment or ablation. Inherited cardiomyopathy can have implications for relatives. Treatment has several goals Treatment aims to relieve congestion and improve daily function. It also aims to prevent hospital admission, slow disease progression and prolong life. The treatment combination depends on ejection fraction, cause, kidney function, blood pressure and rhythm. Medicines are introduced and increased according to tolerance rather than through one rigid order for everyone. The four core HFrEF medicine classes Current NICE guidance offers four core medicine classes for HFrEF. These are an ACE inhibitor, an evidence based beta blocker, a mineralocorticoid receptor antagonist and an SGLT2 inhibitor. The four classes act through different biological pathways. Using them together provides greater protection than relying on one medicine alone. The renin angiotensin pathway medicine An ACE inhibitor reduces harmful hormonal signalling, blood vessel resistance and cardiac remodelling. Examples include ramipril, lisinopril and enalapril. An ARNI combines an angiotensin receptor blocker with neprilysin inhibition. Current NICE guidance considers switching from the ACE inhibitor to an ARNI when symptoms continue despite maximum tolerated doses of the four core medicines. An ARNI may also replace an ACE inhibitor when ACE inhibitor intolerance makes this appropriate. ACE inhibitors and ARNIs are not taken together Combining an ACE inhibitor with an ARNI increases the risk of serious angioedema. A planned washout period is required when switching from an ACE inhibitor to an ARNI. Blood pressure, kidney function and potassium require monitoring. These changes should occur through the prescribing team rather than by independent medicine substitution. Beta blockers Evidence based beta blockers protect the heart from excessive sympathetic stimulation. They slow the heart rate, reduce arrhythmia risk and support ventricular recovery. Treatment begins at a low dose and increases after clinical review. Beta blockers are started or increased cautiously when the person is stable rather than severely congested or in shock. Mineralocorticoid receptor antagonists Mineralocorticoid receptor antagonists are usually shortened to MRAs. Spironolactone and eplerenone block harmful effects of aldosterone. They reduce sodium retention, fibrosis, hospital admission and mortality in appropriate HFrEF. Potassium and kidney function must be monitored because hyperkalaemia and kidney deterioration can occur. SGLT2 inhibitors SGLT2 inhibitors were first developed as glucose lowering medicines. Dapagliflozin and empagliflozin also improve heart failure outcomes in people with or without diabetes. They reduce hospital admission and cardiovascular risk across several ejection fraction groups. Possible adverse effects include genital infection, dehydration and rare ketoacidosis. The prescriber reviews kidney function, illness management advice and diabetes treatment. Four pillars does not mean four tablets for everyone immediately The four classes are core HFrEF treatment, but introduction must be individualised. Low blood pressure, kidney disease, potassium changes, frailty and rhythm problems affect sequencing and dose. Some people cannot tolerate every medicine at a full trial dose. The aim is to establish the most complete tolerated combination without creating avoidable harm. Monitoring medicines Kidney function and electrolytes are measured before starting ACE inhibitors, ARNIs, ARBs or MRAs. They are checked again one to two weeks after starting and after dose increases. Blood pressure, heart rate and symptoms are reviewed throughout optimisation. Stable people still need regular monitoring because health and kidney function can change. Diuretics Diuretics help the kidneys remove sodium and water. Loop diuretics such as furosemide reduce ankle swelling, breathlessness and other congestive symptoms. They are titrated to the lowest dose that maintains a stable fluid state. Diuretics relieve congestion but are not one of the four disease modifying HFrEF pillars. Excessive dosing can cause dehydration, low blood pressure, electrolyte disturbance and kidney injury. Treatment of HFmrEF Current NICE guidance advises considering an ACE inhibitor, beta blocker, MRA and SGLT2 inhibitor for HFmrEF. An ARB can replace the ACE inhibitor when intolerance makes this appropriate. Treatment remains individualised according to the cause, symptoms and comorbidities. Treatment of HFpEF HFpEF treatment includes relieving congestion and managing the conditions driving high filling pressure. Current NICE guidance advises considering an MRA and an SGLT2 inhibitor. Diuretics treat fluid retention. Blood pressure control, atrial fibrillation management, coronary care, weight management and treatment of sleep apnoea can be important. HFpEF should not be treated as though a preserved ejection fraction means no treatment is available. Treating the underlying cause Coronary heart disease requires cardiovascular prevention and selected revascularisation decisions. Valve disease may require intervention when severe and responsible for symptoms. Atrial fibrillation requires assessment of rate, rhythm and stroke prevention. Thyroid disease, anaemia and infection need specific treatment. Alcohol or cardiotoxic medicines may need reduction, withdrawal or specialist review. Atrial fibrillation and anticoagulation Atrial fibrillation commonly coexists with heart failure. Anticoagulation is used when stroke risk assessment indicates benefit. Heart failure alone in sinus rhythm does not automatically require an anticoagulant. Kidney and liver function influence anticoagulant choice and dose. Intravenous iron Iron deficiency can worsen exercise tolerance even when severe anaemia is absent. Current NICE guidance recommends checking haemoglobin, ferritin and transferrin saturation in HFrEF. Intravenous iron is considered for selected people meeting defined deficiency criteria. Iron deficiency still requires assessment for causes such as gastrointestinal blood loss. Implantable cardioverter defibrillators An implantable cardioverter defibrillator is usually shortened to ICD. It monitors the heart rhythm continuously. The device can deliver pacing or a shock when it detects a life threatening ventricular rhythm. It is considered for selected people with persistent reduced ejection fraction and sufficient risk of sudden cardiac death. An ICD does not improve the heart's pumping strength or prevent every cause of death. Cardiac resynchronisation therapy Cardiac resynchronisation therapy is usually shortened to CRT. It uses pacing leads to coordinate contraction of the right and left ventricles. It is considered when reduced ejection fraction accompanies a prolonged electrical conduction pattern, particularly a broad QRS complex. CRT can improve symptoms, ventricular function and survival in appropriately selected people. Some devices combine CRT with an ICD. Devices require careful selection Device eligibility depends on ejection fraction, ECG findings, symptoms and expected benefit. Treatment is assessed after appropriate medicine optimisation when possible. Implantation has risks including infection, bleeding and lead complications. The decision includes future review and discussion of possible ICD deactivation when care goals change. Advanced heart failure treatment A minority of people remain severely symptomatic despite optimised medicines and devices. Specialist centres may assess mechanical circulatory support or heart transplantation. Eligibility depends on reversibility, organ function, frailty and likely benefit. Palliative care support can occur alongside advanced treatment assessment. Acute decompensated heart failure is an emergency Severe or rapidly worsening heart failure requires hospital assessment. The team identifies the precipitating cause and evaluates oxygenation, blood pressure, rhythm and organ function. Intravenous loop diuretics are the main initial treatment for acute congestion. Weight, urine output, kidney function and electrolytes are monitored closely. Respiratory support in acute heart failure Oxygen is used when oxygen levels are below the appropriate target or respiratory failure is present. Non invasive ventilation is considered for cardiogenic pulmonary oedema with severe breathlessness and acidaemia. Invasive ventilation may be required when respiratory failure, exhaustion or reduced consciousness develops. Vasoactive medicines Inotropes increase the force of cardiac contraction, while vasopressors support blood pressure. They are not routine treatments for ordinary congestive deterioration. NICE reserves them for selected potentially reversible cardiogenic shock within monitored critical care settings. These medicines can provoke arrhythmia and increase myocardial oxygen demand. Treatment after stabilisation Long term HFrEF treatment is started, restarted or optimised after the acute condition becomes stable. A beta blocker is not usually increased while someone remains in shock or requires intravenous diuresis for severe congestion. Discharge requires a management plan, medicine monitoring and access to the specialist heart failure team. Specialist follow up should occur promptly after an acute admission. Cardiac rehabilitation NICE recommends personalised exercise based cardiac rehabilitation for people with heart failure. Assessment occurs before exercise begins to ensure that the programme is suitable. Rehabilitation includes education and psychological support as well as physical activity. It can be delivered at home, in the community, in hospital or through accessible digital services. Exercise and activity Regular activity can improve exercise capacity, confidence and quality of life. The programme should start at a level appropriate for the person's symptoms and stability. Severe breathlessness, chest pain, dizziness or sustained palpitations during exercise require review. Heart failure should not automatically lead to permanent inactivity. Monitoring symptoms at home A care plan should explain which changes need routine, urgent or emergency contact. Useful observations include breathlessness, sleeping position, ankle swelling and ability to complete usual activities. A noticeable deterioration from the person's stable pattern is more important than one isolated symptom. People should know how to contact the heart failure nurse or another responsible service. Weight monitoring Some people are advised to record weight regularly using the same scales and similar conditions. A rapid upward trend can reflect fluid retention before swelling becomes obvious. Weight can also change because of appetite, muscle loss, clothing or measurement variation. The individual care plan should define the change that requires contact. Diuretic doses should not be altered independently unless a clinician has provided an agreed flexible plan. Fluid intake NICE does not recommend routine fluid restriction for everyone with heart failure. Restriction may be appropriate for dilutional hyponatraemia or unusually high fluid intake. Too little fluid can contribute to dehydration, low blood pressure and kidney injury. Individual advice becomes particularly important during hot weather, vomiting, diarrhoea or acute illness. Salt and sodium NICE does not recommend a strict routine sodium restriction for every person with heart failure. Very high salt intake can increase thirst and promote fluid retention. A balanced diet avoiding excessive added salt and heavily salted foods is usually appropriate. Advice should be individualised rather than imposing an extreme low sodium diet. Potassium containing salt substitutes can be dangerous with ACE inhibitors, ARNIs, ARBs or MRAs. Medicines that can worsen heart failure Non steroidal anti inflammatory medicines can cause sodium retention and kidney injury. Some calcium channel blockers, antiarrhythmics and diabetes medicines are unsuitable in particular heart failure patterns. Over the counter and herbal products can interact with prescribed treatment. A pharmacist or clinician should review new medicines rather than the person stopping essential therapy independently. Vaccination and infection prevention Influenza and pneumococcal vaccination reduce the risk of infections that can destabilise heart failure. Prompt assessment is important when infection causes worsening breathlessness, fever or confusion. Emotional health Heart failure can cause anxiety, low mood and fear of exertion or breathlessness. Symptoms can restrict employment, relationships and social participation. Rehabilitation and specialist nursing should address psychological and practical needs. Depression and anxiety deserve active treatment rather than being accepted as inevitable. Prognosis varies The course depends on cause, ejection fraction, kidney function, rhythm, frailty and treatment response. Some people remain stable for many years. Others experience repeated admissions or progressive symptoms. Modern multidrug and device treatment has improved outcomes substantially. Prognostic estimates remain uncertain for an individual person. Palliative and supportive care Palliative care focuses on symptoms, quality of life and the person's priorities. It can be provided alongside active heart failure medicines and device treatment. Referral is based on need rather than one predicted survival score. Breathlessness, pain, anxiety and advance care planning can all be addressed. What this lesson should not be used for This lesson cannot diagnose heart failure from breathlessness, ankle swelling or weight change. NT proBNP identifies probability and urgency but does not confirm the subtype or cause. A preserved ejection fraction does not exclude heart failure, and a reduced ejection fraction does not explain every symptom. Do not start, stop or adjust diuretics or heart failure medicines without an agreed clinical plan. Call 999 for severe breathlessness, pulmonary oedema, collapse or signs of cardiogenic shock.

Heart failure is a syndrome caused by impaired cardiac filling, ejection or both. HFrEF has reduced contraction, while HFpEF causes raised filling pressure despite a preserved ejection fraction. Diagnosis combines NT proBNP, ECG and echocardiography, while treatment matches the subtype, cause, congestion and individual tolerance.