Figure 2.1
Differential diagnosis of dyspnoea. SOB shortness of breath
Definition of Heart Failure
Heart failure (HF) is a common clinical syndrome whereby the heart fails to meet the metabolic demands of the body. Heart failure represents the end-stage of a number of structural and functional cardiac disorders that impair the ability of the ventricle to fill with (diastolic dysfunction) or eject (systolic dysfunction) blood. The clinical diagnosis of heart failure is based on the presence of a triad of typical symptoms, signs and objective evidence of a structural or functional cardiac abnormality (as assessed by an imaging modality or serum natriuretic peptides). The clinical features of heart failure are attributed predominantly to a reduction in cardiac output (fatigue, weakness) and to increased pulmonary or systemic venous congestion and fluid accumulation (dyspnoea, oedema, hepatic congestion and ascites).
Epidemiology
Heart failure has reached epidemic proportions worldwide, affecting approximately 2–3 % of the world’s population. Despite treatment advances within the past few decades patient outcome is still poor, with a 5 year survival <50 %, which represent a survival time that is worse than that for most cancers. The primary causes of death are either progressive pump failure or sudden cardiac death secondary to ventricular arrhythmia. Hospitalisation figures for heart failure are also very high, which places a huge financial burden on healthcare resources.
Causes of Heart Failure
Causes of heart failure are outlined on Table 2.1
Table 2.1
Causes of heart failure
Ischaemic heart disease | Accounting for 70 % of patients with heart failure in the developed world |
Idiopathic | Sporadic Familial in up to 50 % of cases |
Valve disease | Accounting for 10 % of patients with heart failure |
Hypertension | The primary cause of heart failure in patients of African/Caribbean descent |
Alcoholic cardiomyopathy | |
Tachycardia-induced cardiomyopathy | Often atrial fibrillation or flutter but any long-standing supraventricular tachycardia High burden of ventricular ectopy/arrhythmias |
Other acquired causes | Myocarditis (usually viral, other infectious causes include HIV, Chaga’s disease, Lyme disease) Peripartum cardiomyopathy Infiltrative disease (amyloidosis, sarcoidosis, haemochromatosis) With other systemic conditions: thyroid disease, connective tissue disease Stress-induced or Takotsubo cardiomyopathy Iatrogenic (chemotherapy, radiotherapy) Nutritional (Beri-Beri) |
Other inherited cardiomyopathies | Arrhythmogenic right ventricular cardiomyopathy Left ventricular non-compaction Burnt out stage of hypertrophic cardiomyopathy |
Types of Heart Failure
Heart failure can be differentiated into systolic versus diastolic, left versus right and low versus high output heart failure. Most patients will suffer from a low output state due to structural or functional heart disease. Examples of high output heart failure include severe anaemia, thyrotoxicosis and Paget’s disease. Right and left heart failure refers to whether the patient has predominantly systemic venous congestion (swollen ankles, hepatomegaly) or pulmonary venous congestion (pulmonary oedema) and do not necessarily reflect which ventricle is affected most.
Heart Failure with Preserved Ejection Fraction
Heart failure with preserved ejection fraction, also known as diastolic heart failure refers to abnormal cardiac relaxation or filling. It is characterised by a normal or near normal ejection fraction (usually >50 %) and normal left ventricular end-diastolic volume, with echocardiographic evidence of diastolic dysfunction. It is important to note that impaired diastolic function and diastolic heart failure are not synonymous. As part of the ageing process a number of individuals develop a degree of diastolic dysfunction, but not every one with diastolic dysfunction has diastolic heart failure. The diagnosis of heart failure with preserved ejection fraction or HFpEF requires the presence of symptoms and signs of heart failure. Management of diastolic heart failure primarily requires identifying and treating the underlying cause, however a strong evidence-base is lacking for most of the treatments used currently. General management principles include meticulous blood pressure control, control of ventricular rate in arrhythmias such as atrial fibrillation and use of diuretics for symptomatic relief of fluid overload. Despite the systolic function being preserved, diastolic heart failure is not a benign condition, with diastolic heart failure having a similar prognosis to that of systolic heart failure.
How to Assess Individuals with Dyspnoea
History
A detailed history is important in investigating the cause of breathlessness, as in many cases the diagnosis or a good differential can be gained (Table 2.2). In those with established heart failure it is important to document their New York Heart Association (NYHA) class (Table 2.3), as it provides a measure of their functional capacity and forms the basis for a number of therapeutic interventions. It is also important to remember that heart failure is a multi-system disorder so patients may present with gastrointestinal, genitourinary and cerebrovascular symptoms.
Table 2.2
Questions you must ask patients presenting with dyspnoea and the potential differential diagnosis
Question | Interpretation |
|---|---|
Duration/pattern of breathlessness | This helps determine the chronicity of the condition. |
Exercise tolerance | Quantify degree of breathlessness with regards to exercise tolerance using NYHA class. |
Symptoms related to reduced cardiac output | Fatigue |
Symptoms related to fluid overload | Orthopnoea, breathlessness that is worse on lying flat. Paroxysmal nocturnal dyspnoea Peripheral oedema and ascites Polyphonic wheeze: usually in keeping with obstructive airways disease such as COPD and asthma although can occur in heart failure, so-called ‘cardiac asthma’. Sputum: white in keeping with COPD, white-pink usually in keeping with pulmonary oedema, yellow-green usually in keeping with infection or suppurative lung disease. |
Gastrointestinal symptoms | Abdominal distension and pain, anorexia, bloating, nausea, constipation and jaundice secondary to congestive hepatomegaly, ascites, reduced bowel perfusion and oedema |
Genitourinary symptoms | Oliguria/anuria, urinary frequency, nocturia secondary to impaired renal perfusion |
Cerebrovascular symptoms | Confusion, memory impairment, anxiety, headaches, insomnia, bad dreams or nightmares, psychosis with disorientation, delirium, or hallucinations secondary to cerebral hypoperfusion and associated electrolyte abnormalities |
Musculoskeletal symptoms | Gout, carpal tunnel syndrome, muscle cramps |
Past cardiac history | Ischaemic heart disease, hypertension or valvular heart disease are risk factors for heart failure. Cardiac arrhythmias especially atrial fibrillation with a fast ventricular response, can present with breathlessness |
Past respiratory history | Do they have established pulmonary pathology such as obstructive airways disease, previous pulmonary embolism, bronchiectasis or pulmonary fibrosis. |
Other past medical history | Do they have a known history of diabetes, thyroid disease or HIV? These can be risk factors for heart failure. Do they have a history of allergic rhinitis or atopic eczema? These may predispose to asthma. Any history of bleeding disorders or anaemia?Anaemia itself may cause shortness of breath. Are they deconditioned or obese? Being overweight itself can lead to a subjective feeling of shortness of breath Do they have a history of autoimmune disease or a rheumatological condition? This may predispose them to pulmonary fibrosis. Any history of neuromuscular disorders e.g. motor neurone disease which can lead to respiratory muscle weakness and breathlessness. Any past psychiatric history? As there may be a psychogenic component to the breathlessness. |
Social history | There may be several environmental factors which could predispose or exacerbate symptoms. Smoking history: this could predispose to COPD or ischaemic heart disease or exacerbate asthma. Does the patient have any pets? Pets may predispose to extrinsic allergic alveolitis or asthma. What is the patient’s occupation? In certain jobs the patient may be exposed to chemicals or toxins which can cause or aggravate certain conditions. Exposure to carcinogens could lead to lung cancer or asbestos exposure could lead to asbestosis or predispose to lung cancer. Asthma can be exacerbated by several chemicals and therefore is not uncommon among painters, hairdressers and domestic staff. A characteristic feature of this type of asthma is amelioration of the symptoms when away from work or on holiday. |
Drug history | Have they started any new medications which could induce breathlessness? Are they on any long term drugs e.g. amiodarone or methotrexate which predispose to lung fibrosis? Have they had previous chemotherapy? Certain chemotherapeutic agents can cause a dilated cardiomyopathy. If they are on long-term pharmacological therapy do they comply with their medications? |
Table 2.3
NYHA Classification of heart failure
Class I | No limitation of physical activity |
Class II | Slight limitation of physical activity. Comfortable at rest, but normal daily activities cause breathlessness |
Class III | Marked limitation of physical activity. Comfortable at rest, but less than normal activity results in breathlessness |
Class IV | Severe limitation. Breathless may be present at rest |
Clinical Examination
General Inspection
It is important to establish the patient’s vital signs including blood pressure (to ensure haemodynamic stability and exclude hypertension), oxygen saturations, pulse (rate and whether regular or irregular).
Is there pallor suggestive of anaemia or cyanosis suggestive of hypoxia?
Is there nicotine staining on the fingers, suggestive of smoking history?
Assess for finger clubbing which can occur in lung cancer, suppurative lung disease, congenital cyanotic heart disease and endocarditis.
Cardiovascular System
Begin by assessing the radial and carotid pulse. Document the rate, rhythm and character.
Measure the jugular venous pressure (JVP), to check for fluid overload.
Palpate the apex beat. Is it displaced? Lateral displacement can occur in patients with left ventricular enlargement.
Are the heart sounds normal and regular? Are there any added sounds for example, a third heart sound (S3) in left ventricular failure or a fourth heart sound (S4) suggestive of a stiffened left ventricle, or murmurs to suggest valvular heart disease.
Listen for pericardial rub which could be a sign of pericardial inflammation.
Is there peripheral oedema (pitting), if so how high does it extend? (this may be indicative of right or biventricular failure).
Respiratory System
Are there abnormalities of the chest wall e.g. a barrel shaped chest which may be in-keeping with longstanding chronic obstructive pulmonary disease (COPD).
Is chest expansion equal? If it is unequal this could be a sign of pneumonia, pleural effusion or pneumothorax.
What is the character of the percussion note? A dull percussion note can be suggestive of pneumonia/collapse but a stony dull percussion note is in keeping with a pleural effusion.
Polyphonic wheeze is usually in keeping with obstructive airway disease such as asthma or COPD but can also be due left ventricular failure (so called ‘cardiac asthma’).
Is there bronchial breathing? The presence of bronchial breathing is suggestive of pneumonia but can rarely be caused by localised pulmonary fibrosis or at the air-fluid interface of a pleural effusion.
Are there any crackles and if so are they coarse or fine? Early inspiratory coarse crackles suggest pneumonia or bronchiectasis whereas both pulmonary fibrosis and pulmonary oedema cause fine inspiratory crackles. Classically pulmonary fibrosis causes late inspiratory crackles whereas pulmonary oedema causes early to mid coarse inspiratory crackles (Table 2.4).
Table 2.4
Examination findings that point towards a diagnosis of heart failure or lung disease
Heart failure
Pneumonia
Lung fibrosis
Temperature
↔
↔/↑
↔
JVP
↑
↔
↔
Peripheral oedema
Yes
No
Noa
Chest expansion
Equal
Reduced on affected side
Reduced but equal
Percussion
↔ (unless effusions)
dull
↔
Crackles
Coarse inspiratory crackles (early/mid)
Coarse inspiratory crackles (unilateral)
Fine end-inspiratory crackles
Investigation of Dyspnoea
Bloods Tests
A full blood picture is recommended to check the white cell count (and neutrophil count) which might suggest infection and haemoglobin to exclude anaemia. Anaemia in itself can cause breathlessness, and patients with heart failure and anaemia (Hb <11 g/dl) generally have poorer outcomes. Measurement of blood chemistry (including sodium, potassium, calcium, urea/blood urea and creatinine/glomerular filtration rate), liver function, thyroid function and iron studies should be performed. These baseline tests are important to detect reversible causes of heart failure e.g. thyroid dysfunction. They are also important to have as a baseline when initiating pharmacological therapies e.g. ACE-inhibitors/aldosterone antagonists. Baseline liver function should be obtained as this may be abnormal in alcoholic cardiomyopathy, α1 antrypsin deficiency, haemochromatosis and hepatic congestion which can be seen in severe heart failure. C-reactive protein (CRP) can also be done looking for infection.
The use of natriuretic peptides is largely dependent on local resources. They are particularly useful in making the diagnosis in the community. Either beta-natriuretic peptide (BNP) or NT-proBNP can be used. Normal levels have a high negative predictive value making heart failure unlikely as a cause of the patient’s breathlessness. Raised levels suggest underlying heart failure (although levels can be raised for other reasons) but very high levels are associated with adverse outcomes and therefore urgent referral to a heart failure specialist is required; the UK National Institute of Clinical Excellence (NICE) suggest within 2 weeks. Natriuretic peptide levels can also be utilised for monitoring in patients with established diagnosis of heart failure as they correlate with morbidity and prognosis.
Electrocardiogram
Electrocardiograms (ECGs) are an important initial step in the work-up of heart failure. Although there are no specific changes related to heart failure, in the vast majority of cases the resting 12 lead ECG exhibits abnormalities and therefore a normal ECG should raise the possibility of an alternative diagnosis for the breathlessness. It is useful to examine the ECG systematically as outlined below:
What is the heart rate?
Tachycardia is common in untreated heart failure.
Is it regular or irregular?
Cardiac arrhythmias especially atrial fibrillation can themselves cause breathlessness or they may be a manifestation of a secondary pathology such as heart failure.
Are the QRS voltages normal?
Voltage criteria for left ventricular hypertrophy may be in keeping with long-standing hypertension, aortic stenosis or less commonly hypertrophic cardiomyopathy.
Low QRS voltages may be in keeping with infiltrative disease such as Amyloidosis.
Are there pathological Q waves or T wave inversions?
These can be suggestive of previous myocardial infarction although non-specific T-wave inversions can be seen with underlying primary cardiomyopathies.
Are there underlying conduction system defects, for example left bundle branch block or non-specific interventricular conduction delay?
These findings may be seen in those with previous myocardial infarction, hypertensive heart disease or underlying cardiomyopathy.
Chest X-ray
Radiographic features suggestive of heart failure are discussed in Table 2.5.
Table 2.5
Chest X-ray findings to distinguish between heart failure and respiratory causes of breathlessness
Heart failure | Lung pathology |
|---|---|
Pulmonary congestion with alveolar oedema | Hyper-expansion of the lung fields (COPD or asthma) |
“Bat’s wing” shadowing < div class='tao-gold-member'>
Only gold members can continue reading. Log In or Register to continue
 Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
Get Clinical Tree app for offline access
|