Article by Dr. Thomas Burnell and Dr. Bethany Turner
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Core
Heart failure is the inability of the heart to meet the body’s demands. It is a clinical syndrome (a recognised pattern of symptoms and signs) caused by a structural or functional abnormality of the heart. This leads to raised pressures inside the heart and/or inadequate cardiac output (CO), at rest or during exercise. The result can be tissue hypoperfusion (too little blood flow to the tissues) and tissue congestion (fluid backing up in the tissues).
There are many causes of heart failure, including:
- Ischaemic heart disease - this causes myocardial damage which causes myocardial dysfunction, reducing the cardiac output.
- Hypertension - increases the afterload (the pressure the ventricle has to pump against). This causes the ventricles to undergo hypertrophy in order to generate more force to pump blood out against the higher pressure.
- The thickened myocardium results in the heart being less efficient at pumping blood, as there is reduced space in the ventricle, reducing the amount of filling.
- Aortic stenosis (narrowing of the aortic valve) - increases the afterload on the ventricle.
- Other valvular (heart valve) and myocardial (heart muscle) structural diseases
- Cardiomyopathies (diseases of the heart muscle) - e.g. dilatation (stretching and enlargement of the chambers) or hypertrophy.
- Arrhythmias (abnormal heart rhythms)
- Pericardial disease
- Cor pulmonale - right ventricular heart failure secondary to chronic lung disease, e.g. chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, bronchiectasis (permanent widening of the airways).
- If the body’s demands become excessive, requiring a grossly elevated cardiac output e.g. sepsis, severe anaemia, thyrotoxicosis (too much thyroid hormone).
A main cause of heart failure is a reduction in stroke volume (SV). The causes of this can be split into three categories:
- Reduced pre-load - less filling of the ventricles (pre-load is the stretch on the ventricle as it fills), so less blood is pumped out. Once heart failure is established, fluid retention raises pre-load instead (see Pathophysiology).
- Reduced myocardial activity - heart muscle can no longer produce the same force of contraction for a given volume so less blood is pumped out.
- Increased after-load - the heart is pumping against a higher pressure leading to hypertrophy.
Heart failure has two main classifications based on the equation:
Ejection fraction = (Stroke Volume) / (End Diastolic Volume). Ejection fraction is therefore the proportion of the blood in the ventricle at the end of filling that is pumped out with each beat. NICE defines heart failure with reduced ejection fraction as an ejection fraction of 40% or less, mildly reduced as 41% to 49%, and preserved as 50% or more (plus structural changes in the heart).
The classifications are:
- Heart failure with reduced ejection fraction, HFrEF - where there is systolic dysfunction.
- In HFrEF, there is a problem with heart contraction and therefore the heart cannot pump with enough force, so there is systolic dysfunction.
- Causes include: thin/fibrosed walls, enlarged chambers, abnormal/uncoordinated contraction.
- It is also known as systolic heart failure.
- Heart failure with preserved ejection fraction, HFpEF - where there is diastolic dysfunction.
- In HFpEF, there is a problem with the heart where it does not fill properly, so there is diastolic dysfunction.
- One cause of diastolic dysfunction is hypertrophy (thickening of the heart muscle). Hypertrophy makes the chambers stiff, so they cannot relax enough to allow adequate filling of the ventricles.
Diagram - The classification of heart failure
SimpleMed original by Dr. Bethany Turner
Heart failure can also be classified based on the symptoms that patients experience, using the New York Heart Association (NYHA) classification. The classes are:
- Class I - no symptomatic limitation of physical activity.
- Class II - slight limitation of physical activity. No symptoms at rest.
- Class III - marked limitation of physical activity. No symptoms at rest.
- Class IV - inability to carry out any physical activity without symptoms. Symptoms are present at rest.
Heart failure on one side of the heart can lead to heart failure on the other side of the heart. When there is both left and right sided heart failure, this is called biventricular heart failure. NICE CKS notes that the older terms "congestive heart failure" (heart failure with sodium and water retention), "left heart failure" and "right heart failure" are potentially misleading and no longer routinely used. This article still uses left and right sided heart failure to describe patterns of symptoms and signs.
In heart failure the decreased CO causes a decreased BP (BP = CO x TPR, where TPR is total peripheral resistance, the resistance to blood flow in the blood vessels). Reduced BP causes:
- Baroreceptors (pressure sensors in the artery walls) to detect the low BP and stimulate an increased sympathetic drive that leads to:
- Increased heart rate
- Increased peripheral resistance
- Activation of the Renin-Angiotensin-Aldosterone System (RAAS, a hormone system that raises blood pressure) that causes:
- Increased sodium retention leading to increased water retention (water follows sodium) and this increases the circulating volume
- Anti-Diuretic Hormone (ADH) release, which makes the kidneys keep water
- Vasoconstriction
- Enhanced sympathetic activity
This is all an attempt to increase BP, but in reality it culminates in increased after-load and pre-load, placing even more strain on the failing heart.
Signs and Symptoms of Heart Failure
The signs and symptoms of heart failure depend on the side of the heart affected. This determines whether the pulmonary or systemic circulation is predominantly affected.
Right sided heart failure signs and symptoms:
- Fatigue/lethargy
- Breathlessness
- Peripheral pitting oedema (swelling that leaves a dent when pressed)
- Raised jugular venous pressure (the pressure in the neck veins is higher than normal)
- Tender, smooth and enlarged liver (hepatomegaly)
Left sided heart failure signs and symptoms:
- Fatigue/lethargy
- Breathlessness
- Pulmonary oedema which can manifest as:
- Orthopnoea (breathlessness on lying flat)
- Paroxysmal nocturnal dyspnoea - attacks of breathlessness at night that wake the patient from sleep
- Basal pulmonary crackles (crackling sounds heard with a stethoscope at the lung bases)
- Cardiomegaly (enlarged left ventricle leads to a displaced apex beat (the lowest and outermost point where the heartbeat can be felt) on examination)
Investigations for Heart Failure
Full Blood Count - check for anaemia as the symptoms of anaemia are similar to heart failure. Anaemia can worsen heart failure as it puts further strain on the heart to meet the body's demands.
Electrolytes and renal function - advanced chronic kidney disease can cause fluid overload because the kidneys do not remove enough fluid from the body. Fluid overload can cause the symptoms of heart failure. NICE also advises measuring renal function and electrolyte levels before starting, and regularly while taking, heart failure medicines that can affect them (see Management).
B-type (brain) Natriuretic Peptide (BNP) - BNP is produced by the stretching of ventricles. It is produced to try and reduce BP by increasing sodium loss and therefore increasing water loss. In the UK, NICE advises measuring N-terminal pro-B-type natriuretic peptide (NT-proBNP, a related peptide also released when the ventricles are stretched) in people with suspected heart failure.
- A raised level suggests heart failure. In suspected chronic heart failure, an NT-proBNP of less than 400 nanogram/litre in an untreated person makes the diagnosis less likely. In new suspected acute heart failure, NICE uses a BNP of less than 100 nanogram/litre or an NT-proBNP of less than 300 nanogram/litre to rule out the diagnosis. Obesity, African or African-Caribbean ethnic background and some heart failure medicines can lower the level. Other conditions, for example kidney disease or chronic obstructive pulmonary disease, can raise it.
- The NT-proBNP level helps to decide how soon a person needs specialist assessment and echocardiography (an ultrasound scan of the heart). This is within 2 weeks for an NT-proBNP above 2,000 nanogram/litre, and within 6 weeks for 400 to 2,000 nanogram/litre. Very high levels carry a poor prognosis.
ECG - an abnormal ECG with a raised BNP provides evidence for heart failure.
Chest X-Ray - pulmonary oedema can be classically seen on a chest X-ray as batwing shadowing (white shadowing that spreads out from the centre of both lungs, like the wings of a bat). An enlarged heart can also be seen as an increased cardiothoracic ratio. This is the maximal horizontal diameter of the heart divided by the maximal horizontal diameter of the thorax (chest) on the X-ray.
Echocardiogram - can be used to measure the ejection fraction to help determine the type of heart failure. It can also assess the valve and ventricular function to help determine the causative factor.
Coronary angiography - this technique (an X-ray scan of the coronary arteries after injecting contrast dye) allows for imaging of the coronary arteries and can be used to determine if they are blocked by an atherosclerotic plaque (a fatty deposit in the artery wall). If there is a blockage of a coronary artery, the oxygen delivery to the myocardium is reduced, putting strain on the heart. Blockage can lead to ischaemia and acute coronary syndromes (sudden reduced blood flow to the heart muscle, such as a heart attack).
Management of heart failure depends on whether it is acute or chronic.
Acute heart failure is managed in hospital in the following way:
- Give oxygen if the patient is hypoxaemic (has a low blood oxygen level).
- Give an IV loop-diuretic, Furosemide. This causes diuresis (water loss) to reduce the volume of fluid in the circulation. This will reduce preload and can improve cardiac output.
- Giving a diuretic also helps to reduce oedema.
- Consider heparin only if there is another indication, such as atrial fibrillation, venous thromboembolism, or acute coronary syndrome.
- Ventilator support is not used routinely. Consider non-invasive ventilation (breathing support through a mask, such as CPAP, which gives continuous positive airway pressure) without delay if there is pulmonary oedema with severe breathlessness and acidaemia (too much acid in the blood). Consider invasive ventilation (a breathing tube) if respiratory failure, reduced consciousness or exhaustion develops.
- IV nitrates (drugs that widen blood vessels) are not offered routinely. They are used in specific circumstances, such as myocardial ischaemia, severe hypertension, or regurgitant (leaking) aortic or mitral valve disease.
Chronic heart failure is managed by:
- Treating the underlying cause and, where needed, surgery or devices:
- E.g. surgery to repair or replace a damaged heart valve.
- A pacemaker or an implantable cardioverter defibrillator (ICD, a device that shocks the heart out of a dangerous rhythm) can control the heart rate or fix an irregular heartbeat. Cardiac resynchronisation therapy (CRT, a pacemaker that helps the ventricles contract together) is another device option. NICE recommends ICDs and CRT as options for heart failure with reduced ejection fraction.
- In severe heart failure, a left ventricular assist device (a mechanical pump that helps the heart pump blood) or a heart transplant may be offered.
- Non-pharmacological management:
- NICE advises offering a personalised, exercise-based cardiac rehabilitation programme, which also includes psychological and educational support.
- NICE advises not to restrict salt or fluid routinely. Ask about intake and reduce it if it is high. Restrict fluid for dilutional hyponatraemia (a low blood sodium level caused by too much water). Avoid salt substitutes that contain potassium.
- Cut down on alcohol and stop smoking. NICE advises offering an annual influenza vaccination and a once-only pneumococcal vaccination.
- Pharmacological therapy (drug treatment) - this relieves symptoms and, for several of the drugs below, reduces hospital admissions and deaths.
- For heart failure with reduced ejection fraction, NICE advises offering four medicines together: an ACE (angiotensin-converting enzyme) inhibitor, a β-blocker, a mineralocorticoid receptor antagonist (MRA, such as spironolactone, which blocks the action of aldosterone) and an SGLT2 inhibitor (a sodium-glucose cotransporter-2 inhibitor, which makes the kidneys pass more glucose into the urine).
- If an ACE inhibitor is not tolerated (other than because of angioedema, swelling of the face, lips or throat), an angiotensin receptor-neprilysin inhibitor (ARNI, for example sacubitril with valsartan) is offered instead. An angiotensin II receptor blocker (ARB) can be considered after angioedema with an ACE inhibitor, or if an ARNI is not tolerated. If symptoms continue on the maximum tolerated doses, NICE suggests considering a switch from the ACE inhibitor to an ARNI.
- For mildly reduced ejection fraction, NICE advises considering the same four medicines. For preserved ejection fraction, it advises considering an MRA and an SGLT2 inhibitor.
- Diuretics relieve congestive symptoms and fluid retention.
- The aims of pharmacological therapy are to relieve symptoms, reduce admissions to hospital and improve survival. Several of these drugs act on the hormonal and sympathetic responses described in Pathophysiology. For example, MRAs block the action of aldosterone.
Edited by: Dr. Ben Appleby
Reviewed by: Dr. Marcus Judge
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