Heart Failure Diagnosis and Investigation

See also: Management of heart failure.

The European Society of Cardiology's guidelines require there to be both symptoms of heart failure (for example, breathlessness, fatigue, ankle swelling) and objective evidence of cardiac dysfunction (systolic or diastolic, at rest) before the diagnosis is made.⁴ Heart failure may have a number of different aetiologies (see below) – always try and determine the cause. Left ventricular failure (LVF) and right ventricular failure (RVF) may occur independently, or together as congestive cardiac failure (CCF). Heart failure should never be the only diagnosis, as it is a syndrome occurring as a result of other diagnostic entities.⁴

• A recent UK survey of heart failure management in general practice found an average prevalence of 8.3 per 1,000 population.
• Prevalence was heavily age-dependent, ranging from 0.2 per 1,000 in those aged under 35, to 125 per 1,000 in those aged over 85.⁵
• Prevalence from Framingham data also shows dramatic increases with age:
  • 8 per 1,000 aged 50–59
  • 66–79 per 1,000 aged 80–89
• Prevalence approximately doubles for each decade of ageing.⁶
• The prevalence of asymptomatic LVSD in the general population appears to be ~3%.⁷

Coronary artery disease and/or hypertension were implicated as the cause of heart failure in over 90% of cases in the Framingham study.⁸ In UK general practice population, about 47% of men have coronary artery disease causing their heart failure, and in 46% of women hypertension is the cause.⁵

In general the heart fails as a whole, but sometimes a disproportionate burden falls on one ventricle, and this influences the pattern of symptoms and signs.

Cardinal symptoms

• Dyspnoea and fatigue (may limit exercise tolerance).
• Fluid retention (may cause pulmonary or peripheral oedema).
• Patients do not necessarily have both, and either may dominate at any one time. In addition, patients may be depressed or complain of drug-related side-effects.
• When the left ventricle is failing (LVF): dyspnoea, poor exercise tolerance, fatigue, orthopnoea, paroxysmal nocturnal dyspnoea (PND), nocturnal cough (± pink frothy sputum) or wheeze, nocturia, cold peripheries, weight loss and muscle wasting.
• Right ventricular failure: (RVF) peripheral oedema (up to thighs, sacrum, abdominal wall), abdominal distension (ascites), nausea, anorexia, facial engorgement, pulsation in neck and face (tricuspid regurgitation), epistaxis.

Signs

• The patient may look ill and exhausted, with tachypnoea, cool peripheries, peripheral ± central cyanosis.
• There may be a tachycardia at rest, low systolic BP, a displaced apex (LV dilatation) or RV heave (pulmonary hypertension), a narrow pulse pressure or pulsus alternans (alternating large and small pulse pressures)⁹ and a raised JVP.
• On auscultation there may be a gallop rhythm due to presence of S₃ (see heart sounds) or murmurs of mitral or aortic valve disease; bilateral basal end-inspiratory crackles ± wheeze ("cardiac asthma"), pleural effusions, tender hepatomegaly – pulsatile in tricuspid regurgitation, with ascites and often extensive peripheral oedema.¹⁰
• The peak expiratory flow rate may be reduced, but if it is <150 litres/min suspect COPD or asthma.

• FBC, U&E and creatinine, LFT's, glucose, fasting lipids, thyroid function tests; consider cardiac enzymes if an MI is possible in the last few days.
• 12-lead-ECG: This may elucidate the cause of heart failure (e.g. SVT/AF, Q-waves suggesting previous MI; also look for ischaemic ST changes, bundle branch block, atrial fibrillation, left axis deviation, and ventricular hypertrophy). A normal ECG makes LVSD unlikely (negative predictive value of 98%).¹¹
• Echocardiography is the key test to provide a semi-objective assessment of cardiac function.
• It is increasingly available "open access" to GPs and should be performed in almost all patients with symptoms or signs of heart failure (SIGN guidelines state that all patients with suspected heart failure should have an echo 'if at all possible'). Those with murmurs, atrial fibrillation, at "high risk" for LVSD (post MI, arrhythmias or poorly controlled hypertension), or where the diagnosis/cause of heart failure is uncertain, are prime candidates for echocardiography.
• CXR: Cardiomegaly (cardiothoracic ratio >50%), prominent upper lobe veins (upper lobe diversion), peribronchial cuffing, diffuse interstitial or alveolar shadowing, fluid in the fissures, pleural effusions, Kerley B lines. The pulmonary shadowing may be classical perihilar "bat's wings" or occasionally unilateral (if nursed on one side), or nodular (especially with pre-existing COPD).
• Additional Tests:
  • Consider 24 hr ECG to detect paroxysmal arrhythmias.
  • Measurement of N-Terminal pro-brain natriuretic peptide (NT-pro-BNP) has been shown to be consistently elevated in heart failure. It is a good predictor of death and cardiovascular events in acute and chronic heart failure patients. It has been demonstrated that its use improves diagnostic accuracy in a community setting. It is also very useful as a guide to optimisation of therapy.¹²
  • B-Type (or brain) natriuretic peptide (BNP) is useful to exclude LVF as cause of dyspnoea – if a patient presents with breathlessness and has a low BNP, a cardiac cause is unlikely. The use of BNP tests to rule out heart failure in primary care has the potential to reduce demand for echocardiography.¹³ BNP may also have a role in management; recent studies which adjusted therapy to BNP levels have shown improved outcomes.¹⁴
  • Provision of primary care BNP testing is patchy and results may take a significant time to return, so in the UK it is not widely used in this setting currently.
  • Radionuclide imaging may be helpful to assess global ventricular function when echocardiography is not possible.
  • Endomyocardial biopsy is rarely needed.

This may be assessed using a standardised exercise test or the six minute walk test (which strongly and independently predicts morbidity and mortality in patients with left ventricular dysfunction).¹⁵ Remember most patients do not show a linear deterioration, but may fluctuate even in the absence of treatment changes, and changes in treatment may make things better, or worse, in the absence of measurable changes in ventricular function. Some still use the New York Heart Association Classification of Heart Failure, outlined below:

Prognosis is poor on the whole, with 5 year mortality varying from 26–75%.¹⁶ Heart failure accounts for at least 5% of medical hospital admissions in the UK and up to 16% of patients are back in hospital within 6 months of their first admission. When patients present with acute pulmonary oedema their prognosis is poorer; survival rates are predicted by severity. In those presenting with cardiogenic shock (hypotension with systolic BP <90mmHg, oliguria and low cardiac output), hospital mortality can be as high as 90%.

As the term heart failure can bring ideas of inescapable catastrophe to some patients, it may best be avoided. Use of the term congestion is an alternative, but some patients may feel patronised if they are more fully aware of the nature of their condition, along with the fact that fluid overload is not always a given in heart failure. Explaining that the heart is not pumping as strongly as it should be is understood by nearly all patients, and is a good starting point from which to elaborate and give them further information if necessary. As ever, know your patient and communicate accordingly.