Heart Failure (chronic)
Definition and demographics
heart failure occurs when the heart function fails to perfuse the body adequately under normal physiological conditions. Heart failure can be divided into acute or chronic heart failure, may be caused by reduction of ejection fraction (systolic failure) or failure for the heart to fill (diastolic heart failure or heart failure with preserved ejection fraction), affect the left heart or the right heart, or both sides. It can also be divided into heart failure caused by an intrinsic disease of the heart(high output), or due to increased demands of the body (low output).
There is an increasing prevalence of heart failure patients due to the increase in older individuals and better outcomes for other cardiovascular diseases. The prevalence of heart failure is around 2-3% in the general population, with increasing incidence amongst older people. There is a slightly higher incidence amongst men compared to women, especially in the middle aged population.
This post deals primarily with chronic heart failure although some of the information is relevant to acute heart failure.
Causes and pathophysiology
Risk factors for heart failure include:
Coronary heart disease
Smoking
Hypertension
Obesity
Diabetes mellitus
Valvular heart disease
Heart failure can be caused by:
Valvular heart disease (aortic stenosis, aortic regurgitation, mitral regurgitation, and tricuspid disease)
Dialated cardiomyopathy
Arrhythmias - atrial fibrillation, heart block, sick sinus syndrome)
Hypertrophic/obstructive/restrictive cardiomyopathy
Congenital heart disease (atrial septal defect and ventricular septal defect)
Pericardial disease - constrictive pericarditis, pericardial effusion.
Drugs and alcohol - B blockers, calcium antagonists, anti-arrhythmics, cytotoxics)
Hyperdynamic circulation - anaemia, thyrotoxicosis, haemochromatosis, paget's disease, pregnancy.
Infections - chagas disease,
Ischaemic heart disease, dilated cardiomyopathy and hypertension are the top causes of heart failure. Heart failure may be multifactorial.
Pathophysiology
Different causes of heart failure reduces the ability of the heart to pump blood around in different ways. Cardiac output of the heart is maintained by changing stroke volume and heart rate. Stroke volume is governed by changes in preload (the stretching of the heart muscle before contraction - closely related to end diastolic volume), after load (the load the ventricles have to contract against), and the inotrophy of the heart. Many causes of heart failure affect stroke volume by affecting one of these factors.
Preload may be affected by factors including atrial contraction, venous pressure, and ventricular filling time. Initially an increase in preload leads to an increase in stroke volume, through the frank-starling mechanism. However, as the heart cells are over stretched, the muscle looses its ability to generate greater contractile forces. Factors in heart failure which affects after load includes atrial fibrillation, which reduces ventricular filling, valvular disease which increases the end systolic volume, and tachycardia caused by a compensatory response which reduces filling time.
Afterload refers to the stress in the heart wall when contracting, and is closely link to the pressure it has to pump against and the thickness of the heart wall. An increase in afterload leads to a reduction in stroke volume. Factors which increase after load in heart failure include aortic valvular disease , hypertension, and dilated cardiomyopathy, which may be caused by coronary heart disease, or alcohol. In response to increased after load, the heart muscle may respond by increasing in size, which is often seen in aortic stenosis, and hypertrophic obstructive myopathy. However, heart muscle hypertrophy also reduce end diastolic volume reducing preload.
The inotrophy of the heart is maintained by sympathetic activation. Initially this acts as a compensatory mechanism to maintain cardiac output where the other factors are affected. However prolonged sympathetic activation may have negative effects.
Arrythmias may affect the heart by affecting its ability to contract in a coordinated manner and therefore maintain stroke volume, or may directly affect the heart rate.
Where stroke volume is affected, the heart often compensates by increasing heart rate. This initially adequately maintains cardiac output, and symptoms of heart failure may only be experienced when the body's needs increase, as in the case of exertion. However, as the disease progresses, increasing heart rate often leads to reduced ventricular filling time which reduces stroke volume, worsening heart failure. The inability of the heart to maintain an adequate output causes several consequences. Firstly, there is an increase in venous pressure, which increases the leaking of fluid into the interstitial space in the tissues upstream. When the left ventricles fail, the pulmonary venous pressure is increased, which causes pulmonary oedema, which affects gas exchange and causes breathlessness. Increased venous pressure also increases the after load of the right ventricle, which predisposes the right ventricles to failing. Where the right ventricles fail, there is an increased venous pressure systemically, which causes peripheral oedema and oedema to the organs. Oedema tends to be most prominent in the ankles and sacrum due to gravity. Systemic venous hypertension may also cause hepatic congestaion, causing hepatomegaly and hepatic pain, and ascites. Reduced cardiac output also leads to reduced renal perfusion. This may lead to increase in renin release causing the retention of salt and water, usually worsening the oedema. In severe cardiac failure, blood may be redistributed to the more perfusion dependent organs such as the brains, the heart and the kidneys, causing a reduction in perfusion of the skin and muscles.
An acute injury to the heart, such as ischaemic heart disease, and prolonged overload of the ventricles often leads to changes in the cardiac muscle (remodelling) which often worsens heart failure.
Presentation:
Left heart failure tends to present with: Breathlessness which is usually initially worse with exertion.
Orthopnoea, Paroxysmal nocturnal dyspnoea and a nocturnal cough or wheeze, usually due to the pooling of fluids in the lungs in the evening.
Right heart failure may present with peripheral oedema, hepatomegaly and liver capsule pain. Patient may also present with nocturia due to the return of fluid from oedema when the patient lies flat. Patient may also present with nausea and anorexia.
In addition the patient may feel fatigued, have cool peripheries and muscle wasting.
Left and right heart failure may occur together.
Heart failure may present acutely as a new presentation, be chronic and stable, chronic and worsening gradually or present as an acute decompensation of existing heart failure.
Examination:
Patient may look ill or exhausted, they may be obviously oedematous. They may be cyanosed.
On examination of the heart, the patient may be tachycardic, hypotensive, have a displaced apex beat (caused by left sided dilation or hypertrophy) , or have a right ventricular heave (caused by pulmonary hypertension). The patient may have a raised JVP, and may have a gallop rhythm (S3 heart sound - sounding like 'ken-tucky'). Patients may also have murmurs from associated valvular disease.
On respiratory examination, the patient may have bibasal crackles and/or wheezes in their chest. They may in addition present with pleural effusions.
The patient may in addition have extensive peripheral oedema worse in the ankles or the sacrum, and hepatomegaly, or may present with ascities.
The new york heart association classification may help stage the severity of heart failure:
Class 1 - no limitation with normal activity
Class II - normal physical activities causes dysnpnoea
Class III - mild activities causes dyspnoea
Class IV - dysnoeic at rest.
Differential diagnosis
Conditions causing shortness of breath:
Oliguric renal failure
Acute respiratory distress syndrome
Lymphatic insufficiency following lung transplant or lymphangitic carcionomatosis.
Iatrogenic fluid overload
COPD
Pulmonary embolism
Anaemia
Conditions causing peripheral oedema:
Immobility
Reduced oncotic pressure in cirrhosis/hypoalbuminaemia
Renal disease causing protein loss and increased sodium and water retention
Some drugs
Varicose veins
Obesity
Reduced oncotic pressure from starvation, malabsorption or diseases causing protein loss.
Pregnancy
post thrombotic syndrome.
Investigations and management
Diagnosis of heart failure according to the european society of cardiology is based on both clinical history and examination, and evidence of cardiac dysfunctions.
Investigations
Initial investigations in suspected heart failure include:
ECG - may show ischaemia, arrthymia or signs of ventricular hypertrophy. Heart failure is unlikely with a normal ECG.
Bloods: B Naturiuretic peptides and NPproBNP are released with increased cardiac stress, and has a high sensitivity for cardiac failure. Where the diagnosis of heart failure is not certain, these should be measured to rule out heart failure. In addition a full blood count, Liver function tests, urea and electrolytes, cardiac enzymes and thyroid function tests may be performed.
Chest x ray- may show signs of pulmonary oedema, cardiomegaly may be present, with upper lobe diversion (larger blood vessel in the upper lobes due to blood diversion), Kerly B lines (fluid between the lobules of the lungs), and increased opacity in the hilar region causing a bat wing like appearance.
Echocardiography - Is used to assess LV systolic function, diastolic function, wall thickness, wall motion, and any valvular disease.
Other tests may include urinalysis, lung function tests (may be slightly reduced or normal in heart failure, suspect COPD or asthma if low), stress echocardiography, radionuclide imaging to assess ventricular function when echocardiography is not available. Cardiac MRI is the gold standard study for assessing cardiac function, however it is often expensive and therefore isn't used. Cardiac biopsy can be performed where cardiomyopathy is suspected. Additional tests such as an angiogram may be done depending on the underlying cause of the heart failure.
In chronic heart failure, echocardiography with additional investigations including ECG and chest X-ray is usually recommended where heart failure is suspected and likely. patients should be referred to secondary care services within 2 weeks where there is a high risk of heart failure, especially in patients who have had a recent MI. Where the diagnosis is more doubtful, serum natriuretic peptides should be measured.
Management
management of heart failure often includes lifestyle advice, medical treatment to relieve symptoms, to improve outcomes, and treating any underlying causes appropriately,.
General measures:
Lifestyle factors which may improve heart failure includes managing obesity, dietary changes where large meals should be avoided and salt should be restricted. Fluid restriction may be necessary in severe heart failure. Patients with heart failure should quit smoking . Rest may often improve acute exacerbations of heart failure, but may increase the risk of DVTs. Low impact exercise including walking and low intensity cycling should be encouraged to maintain peripheral muscle function. Patients should also be given flu vaccinations. Patients may have questions about travel, driving or sexual health. In general, patients with stage III and IV heart failure may need oxygen during air travel and should be discouraged from travel to hot and humid areas or high altitude as they are less able to adapt to these conditions. Commercial drivers may need to stop driving, although private drivers do not need to notify the DVLA. Symptoms may be experienced during intercourse if the patient becomes symptomatic with light/moderate exertion. Sexual intercourse after sleep, with the partner doing most of the work can minimise symptoms. Patients should be supported with adequate education and counselling. A multidisciplinary approach should be taken in the management of these patients.
Medical management:
Diuretics
Loop diuretics, potassium sparing diuretics and thiazide diuretics reduce sodium resorption increasing renal excretion of water. This provides symptomatic relief to patients with fluid overload reducing breathlessness and increasing exercise tolerance levels.
Loop diuretics are initially used, with a potassium sparing diuretic given in addition. Thiazide diuretics are added where theres are not adequate. Serum electrolytes should be monitored regularly as diuretics could cause hypokalaemia and hypomagnesia.
ACE inhibitors
Ace inhibitors reduce water retention and blood pressure by inhibiting the conversion of angiotensin I to angiotensin II. ACEI both improves symptoms and survival, and it is therefore recommended that all patients are put on ACE inhibitors. They may cause a dry cough, hypotension, and hyperkalaemia, so patients on existing potassium sparing diuretics should be stopped initially. ACEI should be introduced gradually with regular blood pressure monitoring and monitoring of serum creatinine.
Angiotensin II receptor antagonists:
should be used as second line if the patient is not tolerant of ACE inhibitors. It is shown to reduce hospitalisation.
B Blockers
B blocker improves the functional status of patients and reduce mortality and morbidity. All patients with heart failure should therefore be put on b blockers. Appropriate B Blockers include Bisoprolol, Carvedilol, and Nebivolol in patients over 70 with mild to moderate heart failure.
Aldosterone antagonists
Spironolactone and eplerenone have been shown to improve survival in heart failure. These should therefore be added where the patient can tolerate these.
Vasodialators
Vasodialators (hydrazine and nitrates) should be used in patients who are intolerant of both ACEI and AIIRAs. They reduce preload and after load of the heart and lead to improved survival rates.
Cardiac glycosides
Digioxin can be used in patients with heart failure, and reduces hospital admissions. It is recommended in patients with atrial fibrillation, or where patient is symptomatic despite the use of ACE inhibitors, b blocker and diuretics.
In later stages of heart failure, inotropes and vasopressors may be considered. Patients may additionally need anticoagulants as heart failure increases the risk of stroke. In younger patients with heart failure, cardiac transplant may be considered.
In additional to medical treatment of heart failure, any underlying disease should be treated. For example, underlying hypertension, and hyperlipidaemia should be monitored. Patients with SA nodal or AV node disease may benefit from pacing.
Prognosis:
Prognosis of heart failure is poor, however survival is improving. 50% of patients with heart failure will die within 4 years, and prognosis is generally worse than some cancers such as breast cancer.
http://images.radiopaedia.org/images/357/e5025b1e2c3276e28c815b93207000_big_gallery.jpg
http://www.slideshare.net/cardiacinfo/stages-of-heart-failure-and-treatment-options-for-systolic
Kumar P, Clark M, Kumar and Clark's Clinical Medicine, 7th ed. Edinburgh, Saunders Elseviers, 2009.
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