HEART FAILURE

6


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:



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:



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.





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:




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:




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



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’.



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).



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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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Jun 18, 2016 | Posted by in CARDIOLOGY | Comments Off on HEART FAILURE

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