INTRODUCTION

Chronic heart failure (CHF) is a growing public health problem, both in Australia and New Zealand, and globally. This condition is associated with significant morbidity, mortality and economic burden, particularly among those aged 65 years and older (Australian Institute of Health and Welfare, 2004; Stewart et al, 2003). Epidemiological data estimates the lifetime risk of developing CHF as 1 in 5 (Stewart & Horowitz, 2002). The prevalence of CHF is predicted to increase with the ageing of the population and the continuing decrease in fatal coronary heart disease (Lloyd-Jones et al, 2003). The current burden of CHF is a measure of both the success of treating conditions such as acute myocardial infarction, allowing people to live longer, and the failure to avoid deleterious conditions that contribute to developing cardiovascular disease, such as inactivity, smoking, hypertension, diabetes and obesity. As you work through this chapter, it is important that you recognise that nurses and other health professionals play a critical role in preventing, treating and managing CHF. Nurses have key roles in independent practice, such as engaging in patient counselling, through to collaborative practice, where they work with physician and pharmacy colleagues in undertaking medication titration. Several key principles underpin the structure of this chapter. Firstly, it is important to appreciate the pathophysiological and epidemiological basis of CHF to undertake informed clinical practice; secondly, the role of the nurses in promoting evidence-based practice strategies to prevent and manage CHF is underscored; and thirdly, the process of reflection in developing clinical practice from prevention to palliation of CHF is emphasised. CHF is a complex condition and it will be difficult to assimilate all the information at once. As you encounter patients with CHF in your clinical practice, take the time to reflect on their treatment regimen and, importantly, talk to the patient and their family on what it is like to live with this chronic condition.

There are no definitive data on the incidence and prevalence of CHF in Australia and available information is largely modelled from clinical trials and international data sets. It was estimated that in the year 2000, 325,000 Australians had symptomatic heart failure and another 214,000 Australians had asymptomatic left-ventricular dysfunction (2.8% of the population) (Clark et al, 2004). A survey of randomly selected residents in Canberra, aged between 60 and 86 years, was conducted between February 2002 and June 2003 (Abhayaratna et al, 2006). Participants enrolled in the study had a comprehensive clinical history, were examined by a cardiologist and received an echocardiogram. Consistent with other data sets, the incidence of CHF in the Canberra Heart Study increased with age (4.4 times increase from the 60–64 years group to the 80–86 years group). These figures are significant given the changing demographics of the Australian population. The ageing of the Australian population, which is consistent with other Western societies, will see a three-to four-times increase in the number of Australians over the age of 65 years (Australian Bureau of Statistics, 2005). This predicted increase will also be seen in those over the age of 85 years. Given that CHF is a condition that is predominately a disease of the elderly, these trends and predictions give cause for concern.

Although you will encounter patients with CHF across the life span from paediatrics to gerontology, the majority of people you will deal with in your clinical practice are likely to be older and suffering from multiple, concurrent conditions, such as diabetes, depression, arthritis and chronic obstructive pulmonary disease. It is therefore important that you approach the person with CHF from a position that considers the range of physical, social, cultural, psychological and spiritual factors affecting the life of a person with a chronic condition, and do not merely focus on the biomedical dimensions of CHF management (Davidson et al, 2007). Managing CHF often includes considering the therapeutic implications of a range of conditions also considered in this text, in particular diabetes and respiratory conditions. Over the past decade, there has been an increasing focus on managing CHF because of the high costs to the individual and the healthcare system, primarily stemming from frequent hospitalisations, many of which are avoidable.

DEFINITION OF CHRONIC HEART FAILURE

In spite of the burden and prevalence of CHF, there is no international consensus on the definition of this condition. The National Heart Foundation and the Cardiac Society of Australia and New Zealand define CHF as:

… a complex clinical syndrome with typical symptoms (e.g. dyspnoea, fatigue) that can occur at rest or on effort, and is characterised by objective evidence of an underlying structural abnormality or cardiac dysfunction that impairs the ability of the ventricle to fill with or eject blood (particularly during physical activity). A diagnosis of CHF may be further strengthened by improvement in symptoms in response to treatment (National Heart Foundation of Australia & Cardiac Society of Australia & New Zealand, 2006).

CAUSES OF HEART FAILURE

CHF is a complex clinical syndrome characterised by evidence of an underlying structural abnormality or cardiac dysfunction that impairs the ability of the ventricle to either fill with or eject blood. The most common cause of CHF is ischaemic heart disease, which is present in over 50% of newly diagnosed patients. Hypertension is present in approximately two-thirds of people with CHF. Less common is idiopathic dilated cardiomyopathy, representing 5–10% of the cases of CHF. Left-ventricular hypertrophy contributes to the development of CHF, due to changes in the heart muscle caused by the stress of pressure and volume overload. Remodelling is characterised by a change in the dimensions of the left ventricle and the ventricular wall, causing myocardial fibrosis, myocyte hypertrophy and hypertrophy of the coronary artery smooth muscle cells. The causes of CHF are broadly attributed to ventricular function and the capacity of the ventricles to contract and relax.

SYSTOLIC HEART FAILURE: IMPAIRED VENTRICULAR CONTRACTION

CHD, resulting in decreased perfusion of the myocardium, is the most common cause of systolic heart failure. Essential hypertension may also contribute to CHF through increasing afterload and accelerating the progression of CHD. People with non-ischaemic idiopathic dilated cardiomyopathy are often younger and there may be a familial association. Less common causes of systolic heart failure include valvular heart disease, alcoholic dilated cardiomyopathy, peripartum cardiomyopathy, myocarditis and thyroid dysfunction.

DIASTOLIC HEART FAILURE: IMPAIRED VENTRICULAR RELAXATION

The most common cause of diastolic heart failure is hypertension and is most common among elderly women. Diabetes is an important contributing factor for CHF and can also be associated with myocardial ischaemia. Diastolic heart failure can occur in conditions such as aortic stenosis, hypertrophic and restrictive cardiomyopathy.

DELETERIOUS COMPENSATORY MECHANISMS IN CHRONIC HEART FAILURE

Systolic heart failure results in a fall in cardiac output due to ventricular dysfunction. The body, in response to the reduced cardiac output, activates several neurohormonal compensatory mechanisms. While the activation of these systems is effective in the short term, in the longer term they become ineffective and even deleterious, leading to further progression of CHF. The activation of these systems stresses the failing ventricle, resulting in a further reduction in cardiac output and stroke volume. These systems result in adverse changes in the structure of myocardium, which is known as remodelling. Two of these mechanisms will now be considered. You may also find it useful to revise the anatomy and physiology of the heart at this point and also consider the interaction between the kidneys and cerebral regulation of cardiac function.

RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM

When the cardiac output falls, the kidneys respond by stimulating the renin-angiotensin-aldosterone system. This system leads to the retention of sodium and water. This system of retaining sodium and water is designed for a hypovolaemic state. In CHF the reduction in kidney perfusion is not the result of hypovolaemia; rather it is the result of reduced cardiac output caused by left ventricular dysfunction (systolic CHF) or abnormal filling (diastolic CHF). The increased volume of sodium and water results in fluid retention, which is a common sign of CHF. If left untreated, the increased fluid retention will lead to oedema often manifesting as pulmonary oedema, a life-threatening condition. The long-term activation of the renin-angiotensin-aldosterone system may also contribute to the cardiac remodelling seen in CHF (Jackson et al, 2000).

SYMPATHETIC NERVOUS SYSTEM RESPONSE

An early compensatory mechanism in CHF is the stimulation of the sympathetic nervous system. Cardiac output is initially maintained through vasoconstriction and increased heart rate. Again, while effective in the short term, the resulting increase in preload and afterload further reduces cardiac output, causing results in further ventricular dysfunction. The resulting tachycardia may increase the vulnerability of the CHF myocardium to arrhythmias.

It can be seen that while the activation of the compensatory mechanisms is effective in the short term, their continual stimulation, which occurs in CHF, actually has detrimental effects on the cardiovascular system, which worsens the CHF, resulting in a cascade of pathophysiological responses. To prevent this detrimental cyclical stimulation, these compensatory mechanisms have become the target of pharmacological management of CHF, particularly with the introduction of angiotensin-converting enzyme (ACE) inhibitors, beta blockers and aldosterone antagonists, three of the common classes of drugs prescribed in CHF (Heart Failure Society of America, 2006; Hunt et al, 2005; National Heart Foundation of Australia and Cardiac Society of Australia & New Zealand, 2006; Swedberg et al, 2005).

SIGNS AND SYMPTOMS OF CHRONIC HEART FAILURE

CHF is associated with numerous signs and symptoms, of which dyspnoea (shortness of breath) is the most common. Initially, dyspnoea occurs on exertion but as CHF worsens, it may occur with minimal activity or at rest. Breathlessness that occurs at night, waking the individual, is known as orthopnoea. It is important for the nurse to note that the elevated need to sleep may indicate fluid congestion in the lungs. Therefore, when pulmonary congestion is present patients may need to sleep on a number of pillows to decrease the sensation of dyspnoea. Other signs and symptoms associated with CHF include fatigue and cachexia. Oedema can be present and reflected in a raised jugular venous pressure, ankle and sacral oedema, ascites and hepatomegaly. Other signs include tachycardia, displaced apex beat and a third heart sound. Heart murmurs can also be present, indicating structural heart disease, such as mitral regurgitation. The New York Heart Association (NYHA) Scale (see Table 20.1) may be used to classify the severity of CHF according to the impact of symptoms on physical activity. Becoming familiar with this classification system is important for monitoring the patient’s condition over time.

Table 20.1 New York Heart Association Scale

Class I	No limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations.
Class II	Slight impairment of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations.
Class III	Marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms.
Class IV	Unable to carry out any physical activity without discomfort: symptoms of CHF are present even at rest, with increased discomfort with any physical activity.