Ross & Wilson Anatomy and Physiology in Health and Illness (55 page)

describe rheumatic heart disease and its effects on cardiac function

explain the underlying pathophysiology of pericarditis

describe, with reference to standard ECG trace, the main cardiac arrhythmias

describe the principal congenital cardiac abnormalities.

Heart (cardiac) failure

The heart is described as
failing
when the cardiac output is unable to maintain the circulation of sufficient blood to meet the needs of the body. In mild cases, cardiac output is adequate at rest and becomes inadequate only when increased cardiac output is required, e.g. in exercise. Heart failure may affect either side of the heart, but since both sides of the heart are part of one circuit, when one half of the pump begins to fail it frequently leads to increased strain on, and eventual failure of, the other side. The main clinical manifestations depend on which side of the heart is most affected. Left ventricular failure is more common than right, because of the greater workload of the left ventricle.

Compensatory mechanisms in heart failure

When heart failure happens acutely, the body has little time to make compensatory changes, but if the heart fails over a period of time the following changes are likely to occur in an attempt to maintain cardiac output and tissue perfusion, especially of vital organs:

•
the cardiac muscle fibres enlarge and increase in number, which makes the walls of the chambers thicker

•
the heart chambers enlarge

•
decreased renal blood flow activates the renin–angiotensin–aldosterone system (
p. 338
), which leads to salt and water retention. This increases blood volume and cardiac workload. The direct vasoconstrictor action of angiotensin 2 increases peripheral resistance and puts further strain on the failing heart.

Acute heart failure

A sudden decrease in output of blood from both ventricles causes acute reduction in the oxygen supply to the tissues. Recovery from the acute phase may be followed by chronic failure, or death may occur due to anoxia of vital centres in the brain. Effects on body systems are described below. The commonest causes are:

•
myocardial infarction (
p. 121
)

•
pulmonary embolism, blocking blood flow through the pulmonary circulation – the heart fails if it cannot pump hard enough to overcome the obstruction

•
severe cardiac arrhythmia, when the pumping action of the heart is badly impaired or stopped

•
rupture of a heart chamber or valve cusp; both greatly increase the cardiac effort required to maintain adequate output

•
severe malignant hypertension, which greatly increases resistance to blood flow.

Chronic heart failure

This develops gradually and in the early stages there may be no symptoms because compensatory changes occur as described above. When further compensation is not possible there is a gradual decline in myocardial efficiency. Underlying causes include degenerative heart changes with advancing age, and many chronic conditions, e.g. anaemia, lung disease, hypertension or cardiac disease.

Right-sided (congestive cardiac) failure

The right ventricle fails when the pressure developed within it by the contracting myocardium is not enough to push blood through the lungs.

When compensation has reached its limit, and the ventricle can no longer empty completely, the right atrium and venae cavae become congested with blood and this is followed by congestion throughout the venous system. The organs affected first are the liver, spleen and kidneys.
Oedema
(
p. 117
) of the limbs and
ascites
(excess fluid in the peritoneal cavity) usually follow.

This problem may be caused by increased vascular resistance in the lungs or weakness of the myocardium.

Resistance to blood flow through the lungs

When this is increased the right ventricle has more work to do. It may be caused by:

•
pulmonary embolism

•
left ventricular failure, when the pulmonary circulation is congested because the left ventricle is not clearing all the blood flowing into it

•
narrowing (stenosis) of the pulmonary valve.

Weakness of the myocardium

This may be caused by ischaemia following infarction.

Left-sided (left ventricular) failure

This occurs when the pressure developed in the left ventricle by the contracting myocardium is not enough to force blood into the aorta and the ventricle cannot then pump out all the blood it receives. Causes include ischaemic heart disease, which reduces the efficiency of the myocardium, and hypertension, when the heart’s workload is increased because of raised systemic resistance. Disease of the mitral and/or aortic valves may prevent efficient emptying of the heart chambers, so that myocardial workload is increased.

Failure of the left ventricle leads to dilation of the atrium and an increase in pulmonary blood pressure. This is followed by a rise in the blood pressure in the right side of the heart and eventually systemic venous congestion.

Exercise tolerance is progressively reduced as the condition worsens and is accompanied by cough caused by pulmonary oedema. The sufferer is easily tired and is likely to have poorly perfused peripheral tissues and low blood pressure.

Congestion in the lungs leads to pulmonary oedema and dyspnoea, often most severe at night. This paroxysmal
nocturnal dyspnoea
may be due to raised blood volume as fluid from peripheral oedema is reabsorbed when the patient slips down in bed during sleep.

Disorders of heart valves

The heart valves prevent backflow of blood in the heart during the cardiac cycle. The left atrioventricular and aortic valves are subject to greater pressures than those on the right side and are therefore more susceptible to damage.

Distinctive heart sounds arise when the valves close during the cardiac cycle (
p. 84
). Damaged valves generate abnormal heart sounds called
murmurs
. A severe valve disorder causes heart failure. The most common causes of valve defects are rheumatic fever, fibrosis following inflammation and congenital abnormalities.

Stenosis

This is the narrowing of a valve opening, impeding blood flow through the valve. It occurs when inflammation and encrustations roughen the edges of the cusps so that they stick together, narrowing the valve opening. When healing occurs, fibrous tissue is formed which shrinks as it ages, increasing the stenosis and leading to incompetence.

Incompetence

Sometimes called
regurgitation
, this is a functional defect caused by failure of a valve to close completely, allowing blood to flow back into the ventricle when it relaxes.

Ischaemic heart disease

Ischaemia is due to the effects of atheroma, causing narrowing or occlusion of one or more branches of the coronary arteries. Atheromatous plaques (
p. 113
) cause narrowing. Occlusion may be by plaques alone, or plaques complicated by thrombosis. The overall effect depends on the size of the coronary artery involved and whether it is only narrowed or completely blocked. Narrowing of an artery leads to
angina pectoris
, and occlusion to myocardial infarction.

When atheroma develops slowly, a
collateral arterial blood supply
may have time to develop and effectively supplement or replace the original. This consists of the dilation of normally occurring anastomotic arteries joining adjacent arteries. When sudden severe narrowing or occlusion of an artery occurs, the anastomotic arteries dilate but may not be able to supply enough blood to meet myocardial needs.

Angina pectoris

This is sometimes called
angina of effort
because the increased cardiac output required during extra physical effort causes severe chest pain, which may also radiate to the arms, neck and jaw. Other factors that may precipitate angina include cold weather and emotional states.