HEART FAILURE

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HEART FAILURE

Chapter objectives

After studying this chapter you should be able to:

1. Describe the gross changes in cardiac function which may lead to the syndrome of heart failure.

2. Explain the differences between systolic and diastolic heart failure.

3. Discuss the concept of compensated cardiac failure and explain the pathophysiological changes by which compensation is achieved.

4. Describe the key metabolic changes within the myocytes of a failing heart.

5. Identify the changes in neurohormonal mechanisms which accompany heart failure often initially as a positive adaptive contribution but subsequently as a source of further decay in cardiac performance.

6. Explain the actions, advantages and limitations of the groups of drugs used therapeutically for the management of heart failure.

The typical ‘textbook person’ at rest has a cardiac output of about 5 L/min (see Chapter 4). The key physiological variables determining cardiac output are grouped as follows:

• preload events (filling pressure of the ventricle)

• contractility events (events inside the myocyte particularly associated with [Ca⁺⁺] and [H⁺])

• afterload events (the resistance to blood leaving the heart)

• heart rate regulation.

The first three items on this list determine the stroke volume of each ventricle and the heart rate is primarily regulated by the baroreceptor reflex which keeps arterial blood pressure quite constant (see Chapter 9).

Heart failure is a complex syndrome and may be the main manifestation of practically any form of heart disorder. Many definitions of the term have been proposed and one of the most popular is as follows:

A pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues

(Braunwald 1986)

The clinical presentation of heart failure often involves a rather vague collection of symptoms, exercise intolerance, breathlessness (particularly when supine), tiredness and ankle swelling, although not all patients necessarily have all of these symptoms. Pulmonary congestion and breathlessness will not necessarily occur unless the underlying defect is fairly substantial and/or long lasting. Ankle swelling is specifically a characteristic of right heart failure. The prevalence of heart failure in the community is age related, increasing from about 1% at age 50 to 9% at age 80. In the UK it has been reported to be responsible for about 5% of hospital medical admissions.

In Case 6.1:1 the history is outlined of a 37-year-old man who finds that his exercise capacity is becoming limited.

Case 6.1 Heart failure: 1

A builder with increasing exercise intolerance

Steven is a 37-year-old builder. Though active in his job he has noticed that over the last year he has found himself increasingly tired at the end of the day. His ability to carry heavy weights appeared to have declined substantially and occasionally he had chest pain whilst exerting himself. He sought the advice of his GP. Physical examination was largely normal apart from a high resting heart rate of 98 bpm and a loud ejection systolic murmur heard at the left sternal edge and at the apex but radiating to the neck. Steven’s GP also elicited a history of unexpected death at a young age in his father’s family. Two of Steven’s paternal uncles had died suddenly at less than 30 years of age. The GP was concerned that there may be a familial cardiomyopathy of the obstructive type and referred him for urgent cardiology investigations. This history raises some fundamental questions:

1. Which aspects of this history might be consistent with a diagnosis of heart failure?

2. Which valves are likely to be associated with the systolic murmur and is it an indication of stenosis or regurgitation (or both)?

3. What investigations would you expect the cardiologist to carry out initially?

Answers to these questions can be found in the text of this chapter and in Chapter 3.

Interesting facts

Reduced performance of the heart muscle in systole is the most common form of heart failure but impaired diastolic function is also a common scenario.

Systolic vs diastolic failure

Impaired systolic function is the commonest cause of heart failure. However in 30–40% of all patients diastolic dysfunction is a major contributor and sometimes the primary cause of congestive cardiac failure.

In general the causes of heart failure can be attributed to one or more of the following:

• decreased myocyte contractility

• inappropriate workload due to pressure overload (e.g. hypertension causing increased afterload) or volume overload (increased preload)

• restricted filling of the ventricles (e.g. valve stenosis)

• myocyte loss.

These changes may represent either myocyte-related failure as in ischaemic heart disease or problems such as valve disease in a heart which may have normal myocyte function.

Heart failure may result from functional changes affecting either systole or diastole or both. Table 6.1 summarizes some of the key differences between systolic and diastolic heart failure. Examples of these different forms of cardiac failure are:

Table 6.1

Some characteristic differences between systolic and diastolic heart failure

	Systolic heart failure	Diastolic heart failure
Systolic BP	Low normal; hypertension	Low normal; hypertension
End-diastolic volume	↑↑	Normal or ↓
End-systolic volume	↑↑	↓
Stroke volume	Normal or ↓	Normal or ↓
Ejection fraction	↓↓	Normal
Myocardial hypertrophy	Eccentric	Concentric
LV wall thickness	↓	↑↑
Extracellular matrix	↓	↑↑

It is widely thought that cardiac myocytes cannot proliferate, only change size and shape. Some recent reports however suggest limited myocyte division is possible after myocardial infarction. In eccentric hypertrophy extra sarcomeres (see Fig. 2.1) are added in series and so myocyte length increases leading to a dilated heart. In concentric hypertrophy extra sarcomeres are added in parallel and so myocyte diameter increases.

• Mainly systolic dysfunction:

ischaemic heart disease

dilated cardiomyopathy

decreased myocyte contractility.

• Mainly diastolic dysfunction:

impaired relaxation due to fibrosis (e.g. amyloidosis)

mitral or tricuspid valve stenosis

constrictive pericarditis.

• Mixed systolic/diastolic dysfunction:

aortic valve stenosis

cardiac hypertrophy.

Primary left heart failure is more common than primary right heart failure and systolic failure is more common than diastolic failure. Left-sided failure is the commonest cause of right heart failure.

In order to understand the fundamental mechanisms involved we need to consider a range of topics which can be grouped under the following subheadings:

• haemodynamic events

• metabolic events

• neurohormonal aspects.

Haemodynamic events

Haemodynamic events in systolic heart failure

If the degree of functional impairment of the heart is relatively small then at rest the ventricle may be able to maintain a normal stroke volume and hence a normal cardiac output. This is achieved by an increase in filling pressure of the ventricle and hence an increase in end-diastolic volume. This increase in ‘preload’ causes the impaired ventricular function to move up a Starling curve (see Chapter 4) to reach a normal stroke volume (Fig. 6.1). There is however a limitation on the ability to increase stroke volume above the resting levels. This manifests itself as part of the exercise limitation experienced by heart failure patients. The increase in preload to restore resting stroke volume for a damaged heart to normal levels is referred to as ‘compensation’.

Fig. 6.1 Compensatory mechanisms in a failing ventricle. A compensatory increase in filling pressure allows a failing ventricle to achieve a normal resting stroke volume. The scope for increasing stroke volume in response to increased workload in exercise is limited. This diagram does not have numerical values on the horizontal axis and so could refer to either the right or left ventricle.

The extent to which compensation can occur is limited by the shape of the cardiac function curve. If end-diastolic volume increases too much then a plateau is reached when further increases in end-diastolic volume do not produce a corresponding increase in the force of contraction of the ventricle. If the cardiac output is still inadequate when this plateau region is reached then end-diastolic volume may continue to increase and this will eventually cause the force of contraction to decrease. This is the region of ‘decompensation’ on the Starling curve and may rapidly lead to death (Fig. 6.2).

Fig. 6.2 Decompensated cardiac failure. In compensated cardiac failure the resting stroke volume and therefore resting cardiac output can reach normal levels by virtue of an increase in filling pressure (preload) for the ventricle (see Fig. 6.1). In decompensated failure increases in preload fail to achieve a satisfactory cardiac output and further increases may lead to a decline in stroke volume.

The commonest form of heart failure is left ventricle systolic failure. It has an annual mortality rate of 15–30% depending on disease severity. In pure left heart failure, the healthy right ventricle will continue to pump blood into the lungs until left ventricular preload is increased enough to restore ventricular balance, i.e. the same output from the two sides of the heart. This ventricular balance will be achieved at the price of raised left atrial, pulmonary capillary and pulmonary artery pressures. The raised pulmonary capillary pressure may result in pulmonary oedema (see Chapter 11) and this will cause the lungs to become ‘stiff’. There will be an increased resistance to inflation of the lungs (a decreased compliance) and this will produce a sensation of breathlessness (dyspnoea). The pulmonary oedema may also upset the balance between the distribution of lung ventilation and pulmonary blood flow causing a ‘ventilation-perfusion mismatch’ which will result in arterial hypoxaemia. This in turn will further reduce the delivery of oxygen to the heart and potentially exacerbate heart failure, producing a vicious circle of events.

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