Chronic heart failure is essentially the chronic version of acute heart failure. It is caused by either impaired left ventricular contraction (“systolic heart failure”) or left ventricular relaxation (“diastolic heart failure”). This impaired left ventricular function results in a chronic back-pressure of blood trying to flow into and through the left side of the heart.
There are some key features that patients with chronic heart failure present with:
- Breathlessness worsened by exertion
- Cough. They may produce frothy white/pink sputum.
- Orthopnoea (the sensation of shortness of breathing when lying flat, relieves by sitting or standing). Ask them how many pillows they use at night.
- Paroxysmal Nocturnal Dyspnoea (see below)
- Peripheral oedema (swollen ankles)
Paroxysmal Nocturnal Dyspnoea (PND)
Paroxysmal nocturnal dyspnoea is a term used to describe the experience that patients have of suddenly waking at night with a severe attack of shortness of breath and cough.
Patients will describe waking up and feeling acutely short of breath, with a cough and wheeze. They have to sit on the side of the bed or walk around the room and gasp for breath. They feel like they are suffocating and may want to open a window in an attempt to get air. Symptoms improve over several minutes.
PND is caused by a few proposed mechanisms:
Firstly, fluid settling across a large surface area of their lungs as they sleep lying flat. As they stand up the fluid sinks to the lung bases and their upper lungs clear and can be used more effectively.
Secondly, during sleep the respiratory centre in the brain becomes less responsive so their respiratory rate and effort does not increase in response to reduced oxygen saturation like it normally would when awake. This allows the person to develop more significant pulmonary congestion and hypoxia before waking up and feeling very unwell.
Thirdly, there is less adrenalin circulating during sleep. Less adrenalin means the myocardium is more relaxed and this worsens reduces the cardiac output.
- Clinical presentation
- BNP blood test (specifically “N-terminal pro-B-type natriuretic peptide” – NT‑proBNP)
- Ischaemic Heart Disease
- Valvular Heart Disease (commonly aortic stenosis)
- Arrhythmias (commonly atrial fibrillation)
This is based on NICE guidelines 2018. See the full guidelines before implementing treatment.
- Refer to specialist (NT-proBNP > 2,000 ng/litre warrants urgent referral)
- Careful discussion and explanation of the condition
- Medical management (see below)
- Surgical treatment in severe aortic stenosis or mitral regurgitation
- Heart failure specialist nurse input for advice and support
- Yearly flu and pneumococcal vaccine
- Stop smoking
- Optimise treatment of co-morbidities
- Exercise at tolerated
First Line Medical Treatment (ABAL)
- ACE inhibitor (e.g. ramipril titrated as tolerated up to 10mg once daily)
- Beta Blocker (e.g. bisoprolol titrated as tolerated up to 10mg once daily)
- Aldosterone antagonist when symptoms not controlled with A and B (spironolactone or eplerenone)
- Loop diuretics improves symptoms (e.g. furosemide 40mg once daily)
Extra details on medical treatment:
An Angiotensin Receptor Blocker (ARB) can be used instead of an ACE inhibitor if ACE inhibitors are not tolerated (for example candesartan titrated up to 32mg once daily).
Avoid ACE inhibitors in patients with valvular heart disease until indicated by a specialist.
Aldosterone antagonists are used when there is a reduced ejection fraction and symptoms are not controlled with an ACEi and beta blocker.
Patients should have their U&Es monitored closely whilst on diuretics, ACE inhibitors and aldosterone antagonists as all three medications can cause electrolyte disturbances.
Last updated October 2018