Your browser is no longer supported

For the best possible experience using our website we recommend you upgrade to a newer version or another browser.

Your browser appears to have cookies disabled. For the best experience of this website, please enable cookies in your browser

We'll assume we have your consent to use cookies, for example so you won't need to log in each time you visit our site.
Learn more

Review

Heart failure 1: pathogenesis, presentation and diagnosis

  • Comment

Heart failure is a common cause of hospital admissions and is increasing in incidence. Part one of this three-part series sums up why it happens and how to diagnose it

Abstract

Heart failure is a common long-term condition with increasing incidence. More a syndrome than a disease, it can have many causes. The main clinical symptoms are breathlessness, fatigue and ankle swelling, but these are not specific to the condition; patients can also present with depression. This article, the first in a three-part series, describes the pathophysiology, aetiology, clinical presentation and diagnostic features of this long-term condition. Part two covers management, treatment options and the crucial role of nurses in supporting and educating patients, while part three covers the management of heart failure in frail patients.

Citation: Jarvis S, Saman S (2017) Heart failure 1: pathogenesis, presentation and diagnosis. Nursing Times [online]; 113: 9, 49-53.

Authors: Selina Jarvis is research nurse and former Mary Seacole development scholar, King’s Health Partners and Kingston and St George’s University of London; Selva Saman is consultant, Port Shepstone Regional Hospital, Port Shepstone, South Africa.

Introduction

Heart failure (HF) is a major public health problem in the developed world and one of the fastest-growing illnesses over recent decades (World Health Organization, 2011). It is associated with frequent hospital admissions, high readmission rates and high morbidity and mortality – with major costs to the NHS. This first article in a three-part series explains the underlying pathophysiology, aetiology, clinical features and diagnosis of HF.

Epidemiology and cost

Heart failure is a common long-term condition; it affects 26 million people worldwide (Bui et al, 2011), and in many countries population-based studies have shown that it affects 1-2% of the general population (Ponikowski et al, 2014). In England, around 900,000 people have a diagnosis of HF (NHS England, 2013). Incidence and prevalence increase with advancing age, and are likely to rise in the future as the UK population ages. In terms of prognosis, globally, 17-45% of patients admitted to hospital die within one year of admission and the majority die within four to five years (Ponikowski et al, 2014; López-Sendón, 2011; Hobbs et al, 2007).

Acute HF – whether new-onset in patients without known cardiac dysfunction or caused by acute decompensation in those with chronic HF – is a common cause of hospital admissions and is linked to high readmission rates in the first six months after the first admission.

In 2015-16, around 188,000 hospital inpatient admissions in the UK were attributed to HF; it remains the leading cause of hospital admissions in people aged 65 and over, accounts for 2% of total NHS expenditure, and the total global cost of HF has been reported as £108bn per year (Cook et al, 2014, Brown and Clarke, 2013).

Understanding heart failure

Definition

There are multiple definitions of HF, which indicates that it should be considered a syndrome rather than a disease (Pearse and Cowie, 2014). The 2016 European Society of Cardiology guidelines define HF as:

“[A] clinical syndrome characterized by typical symptoms (e.g. breathlessness, ankle swelling and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure, pulmonary crackles and peripheral oedema) caused by a structural and/or functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressures at rest or during stress” (Ponikowski et al, 2016).

Pathophysiology

The heart acts as the pump that, through coordinated muscle activity, supplies the organs and tissues of the body with oxygenated blood. To function properly, it must undergo proper relaxation to aid appropriate filling of blood during diastole, and have coordinated contraction dependent on a functional heart muscle (or myocardium) during systole. In HF, the heart is unable to pump enough blood to meet the body’s needs; this may be due – among other causes – to abnormalities of the heart muscle after a myocardial infarction, or problems with heart valves or heart rhythm. HF can affect the left or the right ventricle, and is consequently referred to as left or right HF.

In patients with HF, cardiac output (stroke volume multiplied by the heart rate) is reduced. As a result, two tightly regulated compensatory mechanisms are activated (Fig 1):

  • Sympathetic compensatory mechanism – the baroreceptors sense a decrease in blood pressure (BP), leading to the release of catecholamine (noradrenaline), which stimulates beta-1 adrenoceptor cells in the heart. This culminates in an increased heart rate, contraction and stroke volume, which will increase the cardiac output. Although it can be helpful in the short term to maintain cardiac output, in the long term the mechanism can be damaging and actually exacerbate HF;
  • Renin-angiotensin-aldosterone (RAA) compensatory mechanism – the underperfusion due to reduced BP is detected by the kidneys. This activates the RAA pathway, which controls BP and electrolyte balance. Vasoconstriction, salt and fluid retention are some of the consequences. In the short term, this maintains organ perfusion, but in the long term, it exacerbates cardiac dysfunction and remodelling.

Some of the pharmacological treatments discussed in part two of this article target these sympathetic and RAA compensatory responses.

fig 1 pathophysiology of heart failure

Aetiology

The aetiology of HF is diverse and there is geographical variation, so the underlying cause of the cardiac dysfunction should always be determined in patients presenting with suspected HF. In the developed world, ischaemic heart disease and hypertension are the leading causes, while rheumatic heart disease leading to valvular dysfunction is more likely in developing countries (Pearse and Cowie, 2014). The main causes of HF are shown in Table 1.

table 1 aetiology of heart failure

Classifying heart failure

According to severity of symptoms

HF can be classified according to the symptoms and degree of limitation of physical activity. One classification system is that of the New York Heart Association (NYHA), which encompasses four main classes (NYHA, 1994) (Table 2). The use of the NYHA classification has been questioned in recent years, but it is still the most widely used, both in clinical practice and when deciding which treatment options are best for a particular patient. Many clinical trials recruit and report on patient outcomes according to NYHA class. The American College of Cardiology/American Heart Association has produced a staging tool for HF, which is sometimes used (Hunt et al, 2001) (Table 2).

table 2 classification of heart failure

Cardiac function or structure

Regardless of aetiology, the consequence of HF is a decline in the pump function of the heart. This may lead to the patient experiencing progressive episodes of acute decompensation, further reducing the ability of the heart to fill with or eject blood (Abraham et al, 2017). Ejection fraction (the percentage of blood ejected from the left ventricle per beat) can vary between patients, but ultimately the process culminates in similar symptoms and signs. There are different categorisations of HF based on left ventricular ejection fraction (LVEF) (Ponikowski et al, 2016) (Table 3):

  • In HF with reduced ejection fraction (HFrEF), the condition affects the contraction of the heart muscle and the systolic function of the heart is affected; in this case the LVEF is <40% (systolic HF);
  • In HF with preserved ejection fraction (HFpEF), the systolic function is preserved but there is impairment of the filling during diastole; in this case the LVEF is ≥50% (diastolic HF);
  • There are patients who have an LVEF of 40-49%: they are considered to have HF with mid-range ejection fraction (HFmrEF).

table 3 criteria for diagnosing heart failutr according to left ventricar impairment

Diagnosing heart failure

The clinical diagnosis of HF is based on thorough clinical assessment, history-taking, signs and symptoms, and selected laboratory and imaging test results (Abraham et al, 2017).

The different elements of HF diagnosis are summarised in Fig 2.

fig 2 clinical laboratory and imaging tests to diagnose heart failure

Signs and symptoms

When evaluating a patient, a detailed history and examination are required to determine whether there are symptoms and signs indicative of HF. It is prudent to consider whether these symptoms and signs occur in the context of cardiac damage – for example, in acute coronary syndrome, in which case the correction of ischaemia will take precedence (Abraham et al, 2017).

Chronic HF is characterised by multiple symptoms that are not specific to the condition. The main clinical symptoms are breathlessness (dyspnoea), fatigue and ankle swelling (Ponikowski et al, 2016). Although suggestive of HF, these are not diagnostic symptoms, as they can occur in many other medical conditions including chronic obstructive pulmonary disease. Other symptoms described in HF include orthopnoea (breathless when lying flat), paroxysmal nocturnal dyspnoea (sudden breathlessness awakening patient at night), reduced exercise tolerance and cough, but overall there is a lower sensitivity for these symptoms (Peacock and Soto, 2010).

HF may also associated with mood disturbances, which can occur acutely (National Institute for Health and Care Excellence, 2017). Depression, and to a lesser extent anxiety, are described in HF; this is common and often underappreciated, and needs to be identified since it can contribute to the negative outcomes of the condition (Moser et al, 2016).

Attention must also be paid to vital signs: BP, heart rate, oxygen saturations, respiratory rate and temperature. Chest assessment can identify bi-basal crackles suggestive of fluid overload. A shift in the placement of the apex of the heart suggests dilatation; the presence of extra heart sounds (a third heart sound or gallop rhythm) on cardiac examination is more specific to HF. Close attention is required to the patient’s fluid status through an assessment of the distension of the neck veins (a raised internal jugular venous pressure indicates fluid overload) and identification of any peripheral or ankle oedema (Fig 2). Alongside these, a review of daily weight records can show changes in fluid status, which could have culminated in weight gain.

Laboratory and imaging tests

An electrocardiogram (ECG) is an important bedside investigation to help delineate the underlying cause of HF; a comparison with previous ECGs may reveal new changes related to myocardial infarction or identify any arrhythmias. A chest X-ray can identify radiological features suggesting fluid overload and the heart may appear enlarged. Blood tests – including a full blood count to look for anaemia, and renal and liver function tests to exclude renal or liver failure as a cause of peripheral oedema – should be undertaken. Screening for cardiovascular risk factors (for example, lipid profile and fasting glucose of HBA1c) as well as thyroid function tests are often performed (NICE, 2017). Cardiac troponin tests may be undertaken in the acute setting if acute coronary syndrome is suspected to be the cause of HF.

In terms of laboratory tests that help diagnose HF, serum natriuretics have proved helpful, and brain natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) are regularly used. BNP is a neuro-hormone that is biologically active and formed from a pre-hormone, NT-proBNP. Ordinarily it is stored as granules within the cells in the ventricles, and to a lesser extent in the atria. When cardiac muscle cells (myocytes) undergo stress, NT-proBNP is released and converted to BNP. Measuring NT-proBNP or BNP levels can be particularly useful when acute HF is suspected and echocardiography is not readily available. Normal results should rule out a diagnosis of HF, whereas higher levels of these markers are often associated with a poorer prognosis. Patients with a BNP level >400 pg/ml (116pmol/L) or NT-proBNP level >2,000pg/ml (236pmol/L) should be referred for urgent transthoracic Doppler 2D echocardiography and see a specialist within two weeks (NICE, 2017).

Transthoracic Doppler 2D echocardiography is the most widely used imaging technique as it can add structural information about the heart, help exclude cardiac valvular disease and quantify ejection fraction. It can be used diagnostically and is performed in the vast majority of patients presenting with an acute exacerbation of HF (National Institute for Cardiovascular Outcomes Research, 2015).

Conclusion

Once a diagnosis of HF has been made, patients should be seen by the HF specialist team. How the disease is managed will depend on the underlying aetiology, precipitating factors, type of cardiac dysfunction and NYHA status (NICE, 2017). Nurses have a vital role in caring for patients with HF and helping them understand their condition. 

Key points

  • Heart failure should be considered a syndrome rather than a disease
  • The condition means the heart is unable to pump enough blood to meet the needs of the body
  • The leading causes in the developed world are ischaemic heart disease and hypertension
  • The clinical diagnosis is based on clinical assessment, history taking, signs and symptoms, laboratory and imaging tests
  • Comment

Have your say

You must sign in to make a comment

Please remember that the submission of any material is governed by our Terms and Conditions and by submitting material you confirm your agreement to these Terms and Conditions. Links may be included in your comments but HTML is not permitted.