- Failure of the heart to maintain adequate cardiac output to meet the body's demands. It's a clinical syndrome rather than a specific diagnosis.
- Causes are multiple and it's important to determine the exact aetiology as this will guide treatment. The 2 main categories are valvular diseases and impairment of ventricular function (e.g. coronary artery disease, MI). Prognosis is poor and 50% of patients will die within 2 years.
- Cardiac output is a function of preload and afterload.
- Preload: Volume and pressure of blood in the heart at the end of diastole.
- Afterload: Volume and pressure of blood in the heart at the beginning of systole.
- Starling’s Law: Under normal circumstances, the more the myocardium stretches (for instance from increasing blood volume or pressure), the harder it contracts hence maintaining cardiac output. However there is a limit to how much the myocardium will comply with this rule i.e. overstretching the heart will cause it to lose the ability to pump harder and therefore fail.
Once the heart fails, the body will try and increase the afterload and preload through counter-regulatory neurohormonal mechanisms (renin-angiotensin-aldosterone system mainly) which under normal circumstances will support cardiac function by maintaining cardiac output. It does this in 3 ways:
- Retain sodium and water to increase intravascular volume and preload
- Vasoconstriction of arteries to increase blood pressure and afterload
- Increased sympathetic activation leading to increased cardiac contractility
But in patients with impaired ventricular function and weak cardiac muscles, this increase in preload and afterload is harmful and will set off a vicious cycle which will further deteriorate cardiac function. The diagram on the right illustrates this.
Types of heart failure:
There are many ways to classify heart failure depending on the parameters involved, but the 2 most common ones used are left/right heart failure and systolic/diastolic heart failure:
- Left heart failure – common causes are ischaemic heart disease, valvular heart disease, and hypertension. Affects the blood flow systemically to the brain and the rest of the body.
- Right ventricular heart failure – common causes are chronic left heart failure resulting in back pressure to the right side of the heart, pulmonary hypertension, chronic lung disease, infarction to the right side of the heart and adult congenital heart disease. Affects blood flow to the lungs.
- Systolic heart failure – Insufficient contraction of the heart i.e. reduced ejection fraction.
- Diastolic heart failure – Insufficient relaxation of the heart muscles during diastole and hence decreased cardiac output. Patient has signs and symptoms of heart failure but ejection fraction is normal i.e. >45-50%. Common in elderly hypertensive patients.
It is important to remember that commonly patients have overlapping symptoms as chronic left heart failure for instance, will eventually lead to right heart failure.
In terms of symptoms, the most commonly used classification is the New York Heart Association classification:
- Class I patients have no limitation of physical activity
- Class II patients have slight limitation of physical activity
- Class III patients have marked limitation of physical activity
- Class IV patients have symptoms even at rest and are unable to carry on any physical activity without discomfort
Signs & Symptoms
Left heart failure:
- Tachypnoea, orthopnoea (shortness of breath on lying flat), paroxysmal nocturnal dyspnoea i.e. PND (attacks of severe sudden shortness of breath that usually wakes the patient up at night), bibasal crepitations, laterally displaced apex beat, gallop rhythm, murmurs, cyanosis.
Right heart failure:
- Peripheral pitting oedema, hepatomegaly, increased JVP, parasternal heave, ascites.
Again, it is important to remember that most patients will have some degree of overlap in their signs and symptoms.
There are also characteristic features on a chest xray (ABCDE) that is often asked about in finals:
- Alveolar oedema (in a ‘bat’s wing’s distribution)
- Kerley B lines (short white lines that run perpendicular to the pleura and is a sign of interstitial oedema)
- Upper lobe Diversion (prominent upper lobe vessels)
- Effusion (pleural)
Chest xray findings
- FBC, LFT, U+E, cardiac enzymes (BNP or NPproBNP).
- CXR – To look for the characteristic features stated above.
- Echocardiography – Assessment of LV function, valvular problems, systolic/diastolic function etc.
ACUTE PULMONARY OEDEMA
If patient is haemodynamically stable:
- Sit patient up
- Oxygen 15 L via non-rebreathable mask. Target sats should be >95%.
- Morphine 2.5 mg to 10 mg IV 2 – 6 hourly PRN. This helps vasodilatation and slows the heart rate. Particularly useful if patient is restless and short of breath.
- Anti-emetics e.g. metoclopramide 10 mg TDS IV/PO.
- Loop diuretics if systolic BP stable e.g. furosemide 40 – 160 mg IV/PO and increase every 6 – 12 hours according to response. Patients can also be put on a continuous infusion over 24 hours, for instance 300 mg/24 hours which provides a continuous background level of diuretics.
- Vasodilators e.g. IV GTN 10-200 micrograms/min titrated upwards every 10 mins until clinical improvement. Aim for systolic BP of not less than 90 mmHg.
- Non-loop diuretics can be used if there is inadequate response to loop diuretics and BP stable >85 mmHg. E.g. spironolactone 25 – 100 mg PO once daily.
- If deteriorates and unable to maintain oxygen saturation, patients may need ventilatory support. NIPPV or CPAP should be used first prior to mechanical ventilation. Discussion with ITU may be appropriate if no improvement.
- Fluid restriction, daily U+E, catheterize to monitor urine output, daily weights, low salt diet.
If haemodynamically unstable:
- Inotropes e.g. norepinephrine, dobutamine. ITU discussion is appropriate.
- Ventilation e.g. CPAP before considering mechanical ventilation. ITU discussion is appropriate.
- Intra-aortic balloon pump.
- Left ventricular assist device (LVAD). Note: Not available in all hospitals, usually in units with cardiothoracic support.
- Diuretics (loop, thiazide, potassium-sparing) reduce sodium and water retention.
e.g. Furosemide 40 mg PO once daily, spironolactone 25 - 50 mg PO daily, eplerenone 25 mg PO daily.
- ACE-inhibitors (blocks conversion from angiotensin I to II)
e.g. Ramipril 1.25 to 10 mg PO once daily.
- Angiotensin receptor blockers (blocks receptors for angiotensin II)
e.g. Candesartan 4 – 32 mg PO once daily.
- Beta-blockers (start low, go slow)
e.g. Bisoprolol 1.25 to 10 mg PO once daily.
- Vasodilators (nitrates, hydralazine) reduce preload and afterload
e.g. Isosorbide mononitrate 10 mg PO twice daily.
- Anti-arrhythmics for people with arrhythmias.
e.g. Amiodarone 200 mg daily.
- Implantable cardiac defibrillators can improve outcomes in patients with arrhythmias and symptomatic heart failure
- Resynchronization therapy (pacing) can produce a better synchronization of the ventricles and improve cardiac function
- Ventricular assist devices (VAD)
- Heart transplantation
- Non-intentional and non-oedematous weight loss of greater than 7.5% of the premorbid weight, and takes place over a continuous period of 6 months. It is thought that this is secondary to congestive gastrointestinal oedema leading to impaired nutrient absorption and congestive hepatic enlargement causing anorexia. There have also been suggestions of increasing plasma levels of tumour necrosis factor and cytokines that increase metabolic rate of tissues, which lead to more calories being burnt. Patient will struggle to put on weight despite good appetite and a high calorie diet.
Impaired kidney function
- Reduced renal perfusion secondary to the heart’s decreasing capacity to pump blood can eventually lead to kidney failure if left untreated.
- Water retention and diuretic therapy can cause hyponatraemia, hypokalaemia, and hypomagnesaemia in heart failure patients. This is made worse by the concurrent activation of neurohormonal mechanisms that enhance the release of angiotensin and vasopressin. ACE inhibitors on the other hand can cause hyperkalaemia.
- Extensive remodelling of the myocardium occurs in heart failure as part of the disease process. Scar tissues and fibrosis are usually present. This can impair conduction pathways and increase the risk of arrhythmias, both atrial and ventricular. If left untreated, rhythms such as atrial fibrillation increases the chance of further complications, for instance stroke.
- Best Practice BMJ
- Kumar and Clark Clinical Medicine
- Davidson's Principles and Practice of Medicine