Chapter 3 Cardiac conditions

INTRODUCTION

It is rare in industrialized countries to see young people debilitated by a cardiac problem. Those who have a congenital defect at birth will in most cases have had surgery to correct the problem. Rheumatic fever which damages the heart in children and adults is virtually unheard of. However, there remains a small proportion of women of childbearing age who have a known defect that has caused no problems to date and has not required treatment. There are also some women in whom a defect has been corrected and some in whom one has not been diagnosed. For these women, pregnancy and childbirth can be dangerous depending on how well the damaged heart can deal with the extra workload.

Although cardiac disease in pregnancy complicates few pregnancies, it continues to contribute significantly to maternal and fetal mortality and morbidity. Some 10–25% of all maternal deaths are due to cardiac disease (Avila et al 2003). The main causes of maternal mortality are: pulmonary hypertension, endocarditis, cardiomyopathy, myocarditis, coronary artery disease and sudden lethal cardiac arrhythmia. Medical advances have increased the number of women who survive to adulthood and successfully achieve pregnancy. The midwife must therefore have a good understanding of these disorders in order to care for them appropriately.

RELEVANT ANATOMY AND PHYSIOLOGY

The heart is a cone-shaped muscular hollow organ situated in a space between the lungs – the mediastinum (Fig. 3.1). The muscular wall is composed of an outer protective layer, the pericardium, a middle muscular layer, the myocardium and an innermost layer – the endocardium. The pericardium is a double outermost layer which surrounds the heart preventing overfilling and also allowing free movement within the mediastinum. The muscular myocardium varies in thickness reflecting the work required by the underlying chamber of the heart. The endothelial endocardium lines the heart, the valves and the blood vessels leaving the heart and provides a smooth surface reducing friction between blood and the walls of the heart.

Figure 3.1 Internal structureof the heart.

The four chambers of the heart: the right and left atria (singular atrium) and right and left ventricles, are separated by valves which prevent the blood flowing backwards into the heart. With each contraction of the heart, all four valves open and allow blood to pass through. As the heart relaxes, these valves close and it is the sounds of the valves closing that create the familiar ‘lub-dup’ heart sounds heard through a stethoscope.

The four valves of the heart are:

1. The tricuspid valve, situated between the right atrium and ventricle, composed of three flaps or cusps

2. The mitral valve, between the left atrium and ventricle. This valve is also known as the bicuspid valve as it is composed of two cusps

3.&4. Two semilunar valves which are situated in the pulmonary artery and aorta as they leave the heart. These valves consist of three semicircular cusps attached to the inner surface of the heart.

The mitral and tricuspid valves are prevented from opening backwards into the atria by fibres–the chordae tendineae, attached to the walls of the ventricles.

Deoxygenated blood from the body enters the right atrium of the heart via the vena cava (Fig. 3.2). Once the atrium is filled, the tricuspid valve opens and, assisted by contraction of the atria, the blood is moved into the right ventricle. Once this has filled, the ventricle contracts and pushes the blood into the pulmonary arteries. Blood is carried to the lungs where it is oxygenated and then returned to the left side of the heart. In synchrony with the right side, oxygenated blood pours into the left atrium, is moved into the left ventricle and then into the aorta, the largest artery in the body. The heart then rests for a brief moment of time. The entire cycle – the cardiac cycle – takes 0.8 s and is controlled by the pacemaker of the heart.

Figure 3.2 Direction of blood flow through the heart.

PHYSIOLOGICAL CHANGES IN PREGNANCY

Prenatally cardiac output increases from the first trimester until it reaches a plateau at 28–34 weeks. This is due to the increase in blood volume, the effects of the hormones of pregnancy and the increase in vasculature through the uterus. These alterations increase the workload of the heart considerably but healthy women are able to adjust to these physiological changes with ease (see also Ch. 2). However, the changes provoke symptoms similar to mild cardiac disease such as dyspnoea, especially with exercise, fatigue and oedema. Additionally, the above changes may provoke the occasional dysrhythmia or episode of palpitations (Jordan 2002). There is also an increased risk of thromboembolism during pregnancy with the risk being highest after birth (Lee 2005).

During labour there is a significant increase in cardiac output as a result of uterine contractionsand following birth blood returning from the uterine circulation increases blood volume dramatically until a brisk diuresis corrects fluid balance.

CARDIAC DISEASE IN PREGNANCY

The presence of heart disease although rare, is associated with a significant risk to mother and fetus. In the most recent Confidential Enquiry into Maternal and Child Health (CEMACH) 2000–2002, cardiac disease was the leading cause of indirect death with 44 mortalities in the 3 years (Lewis & Drife 2004). Cardiac disease was the second most common cause of maternal death overall, second only to psychiatric causes and more frequent than thromboembolic disease. In women with congenital heart disease, the presence of pulmonary hypertension was the crucial factor. In acquired disorders, the main causes were cardiomyopathy, myocardial infarction, aneurysm and dissection of the aorta. Eisenmenger’s syndrome, although rare, is a life-threatening condition in pregnancy, carrying a 40% mortality rate with each pregnancy

Cardiac disorders are classified as congenital or acquired. In women of childbearing age, acquired disorders are rare. The most common cause of an acquired cardiac disorder in fertile women is rheumatic heart disease as a complication of rheumatic fever as a child. Congenital heart disease is more common in the UK (Iserin 2001) and occurs in 0.5–2% of the population (Gilbert & Harmon 1998).

Pathophysiology of cardiac disease

Acquired cardiac disorders

Acquired cardiac disorders occur as a complication of another disease process. In women of childbearing age, the cause of the damage may be scarring left after an inflammatory response to an infection. Although this is uncommon in the UK today, the most likely disease process is rheumatic fever. Other inflammatory conditions that rarely occur are infective endocarditis and pericarditis. Ischaemic heart disease in pregnancy is increasing, especially in women over the age of 34 years.

Rheumatic heart disease

Rheumatic heart disease is the result of an acute inflammatory complication of a group A streptococcus infection. This initial infection may present as a respiratory infection or scarlet fever. In people thought to be susceptible to the antibodies produced in the initial infection, rheumatic fever commonly manifests as fever and joint pain. The intensity of the fever can vary considerably however, from a mild condition that goes unnoticed to an acute illness with a mortality rate of 2–3%. A common complication of rheumatic fever is cardiac disease which may not show any symptoms for many years. Other organs that may be affected are the joints, skin and brain.

In those individuals with rheumatic heart disease, the endocardium becomes inflamed and subsequently scarred. This is found most commonly on the valves of the heart, particularly the mitral valve and to a lesser extent, the tricuspid valve. The valves become distorted and dysfunctional. The ends of the cusps of the valves become roughened, fuse together and the opening narrowed, a condition known asmitral or atrial (relating to the tricuspid valve) stenosis. Further, the damage may prevent the cusps of the valves from closing fully allowing backflow of blood in the heart, mitral/atrial incompetence. The result of these changes is a damaged heart in which circulation of blood is impaired (Box 3.1). The heart has to work harder to pump sufficient blood around the body. Over time, the heart increases in size, a condition known as hypertrophy. This weakens the heart and any further strain, such as pregnancy, may lead to heart failure.

Box 3.1 Artificial valves

Surgery can significantly enlarge the size of an orifice bordered by an damaged heart valve. Some individuals however have too great a damage to the valve and require its replacement with an artificial valve. Artificial valves can be mechanical or tissue. Mechanical valves normally last for as long as required but the patient must take thromboprophylaxis for the rest of her life to prevent clots forming on the valve. A tissue valve does not require anticoagulants but does not last as long. Tissue valves, made traditionally from pig heart valves, are considered to last approximately 15 years.

Other conditions that have a similar effect are:

• Infective endocarditis: This is an inflammation of the endocardium of the heart particularly of the valves but from other infective disorders. Factors that predispose an individual to developing this condition include intravenous drug abuse, damaged valves (as described above), minor infections, dental treatment and cardiac surgery. In this condition, the infective organism grows on the valves scarring the tissue with similar results to rheumatic heart disease

• Pericarditis: This is inflammation of the pericardium as a result of infection, cardiac injury or an autoimmune response. This may result in pericardial infusion preventing the heart from expanding sufficiently, or scarring of the pericardium preventing stretch. The patient finds it painful to breathe and experiences chest pain.

Ischaemic heart disease and myocardial infarction

With increasing dietary and obesity problems in the industrialized world, it is becoming increasingly common to meet women who have the early signs of ischaemic heart disease. Blood vessels are damaged by a high level of circulating fats and plaques of atherosclerosis (Box 3.2) begin to narrow the lumen of the blood vessels (Foxton 2003). Where this happens in the coronary arteries surrounding and nourishing the tissues of the heart, the heart becomes ischaemic and is unable to continue functioning properly. Women are increasingly leaving pregnancy until they are olderwith the added risk that ischaemic heart disease may be well advanced. The added workload to the heart, of pregnancy and childbirth, may result in angina or rarely a heart attack – myocardial infarction (MI). Acute myocardial infarction during childbirth is very rare, occurring in1 in 10 000–30 000 women (Baird & Kennedy 2006). However, maternal mortality from an MI may be up to 40%. Permanent changes to the heart due to chronic hypertension may also complicate pregnancy.

Box 3.2 Atherosclerosis

Atherosclerosis is a disease affecting the arteries of the body. Commonly it is referred to as ‘hardening’ or ‘furring’ of the arteries, caused by the formation of multiple fatty plaques. Hardening refers to the changes in the blood vessel wall as a result ofthe presence of the plaques. Furring refers to thenarrowing of the blood vessel preventing adequate blood supply to the organ it feeds.

Over a long period of time, the artery becomes more damaged until the vessel becomes completely occluded either by the plaques or by rupture of the plaque and the formation of a thrombus. This will often cause pain or dysfunction of the associated organ, such as a myocardial infarction if a coronary artery is involved, a cerebrovascular accident, ‘stroke’ if a cerebral artery is involved or other problems such as intermittent claudication, if one of the arteries of the legs is involved. Atherosclerosis is a bodywide process and can cause similar events anywhere in the body.

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