Chapter Thirty-Two. Cardiac and hypertensive disorders
Introduction
Heart disease in pregnancy is a serious medical condition; there were 44 indirect deaths in 2000–2002 (Drife 2005). This has risen since the last Confidential Enquiry due to deaths from cardiomyopathy and myocardial infarction; these are both acquired problems and this may in part be due to women being older when becoming pregnant. However, there are younger women also embarking on a pregnancy who have undergone corrective surgery from heart disease in childhood where in the past they would not have survived heart surgery (Clarke & Butt 2005). This has implications within the maternity service for those women of childbearing years. The most dangerous cardiac lesions are those that involve pulmonary hypertension such as primary pulmonary hypertension and Eisenmenger’s syndrome, and Marfan’s syndrome, an autosomal dominant disorder of connective tissue which may result in aortic dilatation and rupture late in pregnancy or in labour.
Rheumatic heart disease is still fairly common despite the reduction in rheumatic fever in the British population. The most common lesion is rheumatic mitral stenosis with the most common complication being pulmonary oedema occurring in late pregnancy or immediately after delivery. It is important to consider that, although the indigenous population may have a changing pattern of heart disease, we see many immigrants who may have not been diagnosed with a condition.
Cardiac disorders in pregnancy
The incidence of heart disease in the pregnant population is about 1% (Lupton et al 2002). It is important to understand the physiological adaptation of the heart and circulation in pregnancy in order to understand the detrimental effects in pregnancy on the health of a woman with diagnosed heart disease. The changes in the cardiovascular system begin early, reach their maximum at about 30 weeks and are maintained until term. They include:
• An increase in cardiac output by 50%.
• A heart rate increase of 10–20 beats/min (bpm).
• A decrease in total peripheral resistance.
• A lowering of blood pressure in the first and second trimesters with a rise at 34 weeks, myocardial hypertrophy and heart chamber enlargement in the third trimester.
The changes in cardiac output in normal pregnancy without pre-existing cardiac problems may produce signs and symptoms of cardiac disease: for example, dyspnoea, orthopnoea, breathlessness on exertion, oedema and occasional palpitations (Lupton et al 2002). Heart sounds may change and confuse diagnosis (Prasad & Ventura 2001).
Risk factors
In some women the adaptive changes may exceed the ability of the heart to function, and congestive cardiac failure with pulmonary oedema may occur. More rarely, sudden death may be the outcome. There are times during pregnancy when cardiac decompensation is higher:
• At 12 and 32 weeks when the haemodynamic changes are increasing towards their maximum, with the most critical time between 28 and 32 weeks.
• The second dangerous period is during labour and delivery. During labour every uterine contraction injects blood from the uteroplacental circulation into the maternal bloodstream, which temporarily increases the cardiac output by 15–20%. The continuous demand on the heart may precipitate heart failure. Pushing during the second stage of labour increases the risk further by reducing venous return. Intravenous fluids should be accurately calculated, as overperfusion will be increased by the sudden injection of 300–500 ml of blood into the maternal circulation at delivery of the placenta. Congestive heart failure is frequent at this time (Lupton et al 2002).
• Finally, 4–5 days following delivery is a danger period, with thrombus formation and pulmonary embolism being a problem as blood constituents rapidly return to normal levels.
Main types of cardiac disorder
Rheumatic heart disease
The main effect of this disease is to cause valvular lesions. Mitral and aortic incompetence may be improved during pregnancy because of the lower pressure within the arterial tree. However, there is a risk of endocarditis. Mitral stenosis requires an increase in left atrial pressure to push blood into the left ventricle and will require an even greater effort in pregnancy. Women with mitral stenosis may develop increasing breathlessness. The heart rate increases which decreases diastolic filling time and there is a rise in left atrial pressure which causes pulmonary oedema, hence the breathlessness (Lupton et al 2002).
To prevent pulmonary oedema diuretics should be given with β-blockers to aid diastolic filling (Prasad & Ventura 2001, Ray et al 2004, Sawhney et al 2003). Anticoagulation is important: warfarin crosses the placenta and causes embryopathy; heparin is safe for the fetus but the mother may develop thrombocytopenia and it affects bone density. Low-molecular-weight heparin may be used and is safer for the mother but may cause bleeding in the fetus (RCOG 2007, Uebing et al 2006). Most regimens use heparin for the first trimester, changing to warfarin until 2 weeks before the due date, when heparin is recommenced. This prevents the warfarin affecting fetal blood clotting time. Prophylactic antibiotics should be routine for operative or normal delivery to prevent infective endocarditis (Uebing et al 2006).
Congenital heart disease
A review of the literature by Drentham et al (2007) looking at 2491 pregnancies found that 11% exhibited cardiac complications, with a high incidence of preterm birth and consequent mortality and recurrence of heart defects in the babies was high.
Categorisation of congenital heart disease
• Septal defects: atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA), Eisenmenger’s syndrome (Ammash & Warns 2001).
• Obstruction defects: pulmonary stenosis, aortic stenosis, coarctation of the aorta (Brickner et al 2000a).
• Cyanotic defects: tetralogy of Fallot, transposition of great vessels (American Heart Association 2002, Brickner et al 2000b).
Some of the defects mentioned above will not be problematic in pregnancy if the woman has been treated in childhood. There is a need to prevent infective endocarditis; thus, antibiotics in labour are necessary, as even though defects are repaired, some impairment may be present following the surgery. Women with prosthetic valve replacement are at risk of thromboembolism and should be anticoagulated (RCOG 2007, Uebing et al 2006).
Eisenmenger’s syndrome
Eisenmenger’s syndrome is an end-stage syndrome with pulmonary hypertension and has a high risk of maternal mortality (between 30% and 50%), and termination of pregnancy may be suggested (Lupton et al 2002). The syndrome is a result of various congenital heart defects: VSD, ASD, PDA, AVSD, or single ventricle. This causes systemic to pulmonary shunts—when the pulmonary pressures reach systemic pressures the shunt is reversed to a right to left shunt (American Heart Association 2002, Dumitresco & Walsh 2006). Cyanosis may be marked. During the third trimester, at birth and for 2 weeks postnatally the woman is at greatest risk of death and should be observed in hospital for at least 2 weeks post delivery.
Pregnancy adaptation causes the right-to-left shunt to increase cyanosis and creates back-pressure on the pulmonary circulation. Intrauterine growth restriction is seen in 30% of cases because of poor cardiac output and thus low oxygen levels in the circulation (Dumitresco & Walsh 2006). There is a high incidence of abortion and preterm birth (Siu & Colman 2001). During labour, haemodynamic monitoring should take place; vaginal delivery is preferable to caesarean section, with a shortened second stage.
Marfan’s syndrome
Marfan’s syndrome is an inherited condition involving connective tissue which causes skeletal, eye and heart abnormalities. High oestrogen levels present in pregnancy affect the structure of the aorta, where spontaneous rupture may take place, particularly in labour, where pressures within the vascular system may be variable (American Heart Association 2002, Blackburn 2003). Again, termination of the pregnancy may be advised, but, if there has been no pre-existing heart disease, pregnancy should not pose a problem.
Assessment of mothers with heart disease
Heart disease can present itself in pregnancy for the first time, or as an ongoing problem. Assessment is made jointly by the cardiologist and obstetrician so that counselling and decision making can be considered. If a termination of pregnancy is suggested, this should take place in the first trimester as, after 16 weeks continuing with the pregnancy, it may be the safer option. To assess client condition in heart diseases the following system has been widely used.
New York Heart Association classification
It is traditional to use the New York Heart Association classification (Ray et al 2004) to describe the severity of heart disease and how it affects daily activity. In practice this has little predictive value of the effect of pregnancy on the disease process.
• Class 1: no symptoms during ordinary physical activity.
• Class 2: ordinary physical activity, some fatigue, palpitations, dyspnoea.
• Class 3: symptoms during less than normal physical activity.
• Class 4: symptoms at rest, activity increased symptoms and discomfort.
If the woman is classified higher than class 2 it would indicate a poorer outcome in pregnancy. An increased risk to the fetus would be maternal smoking, prescribed anticoagulants and maternal age under 20 and over 35 (Uebing et al 2006).
Management of women with heart disease
The major maternal complications and the treatments aimed at avoiding them are:
• Endocarditis: routine antibiotics.
• Thromboemboli: anticoagulation.
• Cyanosis: rest, hospital admission.
• Arrhythmias: β-blockers, digoxin.
• Heart failure: hospital admission, dietary restriction of salt, diuretics.
• Urinary tract infection: antibiotics.
• Respiratory infection: antibiotics.
• Hypertension.
• Anaemia.
Care should be directed towards prevention of complications rather than treating them. An assessment of risk can be made during pregnancy, by using electrocardiography (ECG), echocardiography and maternal function in everyday circumstances. Counselling is important, especially if the woman is high risk. Assessment of the heart lesion is important, by examining ventricular function, pulmonary pressure, persistence of shunts and valvular obstruction (Siu & Colman 2001, Uebing et al 2006).
Specific aspects of care
Intrapartum care
Labour should take place in a unit with full resuscitation facilities and an intensive care unit. The cardiologist, obstetrician and anaesthetist should collaborate. If possible, labour should be spontaneous in onset with a vaginal delivery. The use of intravenous fluids could increase circulating blood volume, which may result in pulmonary oedema, so accurate fluid balance is essential. Blood should be cross-matched and oxygen and adult resuscitation equipment available. The heart should be monitored by ECG and pulse oximetry with accurate blood pressure recording. During active labour, the left lateral position is advantageous to assist venous return and prevent aortocaval compression.
Pain relief
Epidural is the best form of pain relief to assist women in labour, as it helps relaxation (Siu & Colman 2001).
Second stage
This stage should be kept short and without exertion; if delay occurs, forceps or vacuum extraction should be performed.
Third stage
To prevent blood loss a continuous Syntocinon (oxytocin) infusion should be used instead of intramuscular Syntocinon for the third stage. When the uterus empties and contracts, approximately 500 ml of blood is returned to the central circulation.
Postnatal care
The risk of cardiac failure with pulmonary oedema is greatest in the early puerperium. Signs include tachycardia, cyanosis, oedema and distension of the liver. If pulmonary oedema occurs, acute dyspnoea with frothy sputum and haemoptysis may occur. In most units the woman will be admitted to a high dependency unit to stabilise her condition (RCOG 2007).
Hypertension in pregnancy
Terminology
Raised blood pressure in pregnancy can be termed essential hypertension if it exists before pregnancy and is >140/90 mmHg; these women may develop pre-eclampsia (Pridjian & Puschett 2002a). Pregnancy-induced hypertension (PIH) is a condition specific to pregnancy and mainly occurs after the 20th week of gestation in some 5–10% of pregnancies (Hayman & Myers 2003, Magee et al 1999). The earlier the occurrence the greater the problems, and pre-eclampsia with raised blood pressure, proteinuria of >500 mg/L/24 h and multiorgan involvement may develop (Broughton Pipkin 1995). This has a 15–20% maternal mortality rate in developed countries (Sibai et al 2005). Eclampsia (convulsions) is caused by brain oedema, and where multiple organs are affected disseminated intravascular coagulation (DIC) defects may occur. Convulsions can occur postnatally for the first time (Zhang et al 1997) and the incidence is approximately 1:2000 pregnancies. HELLP syndrome (Nutt 1997, Sibai 2004a) is an acronym for Haemolytic anaemia, Elevated Liver enzymes and Low Platelet count. This may occur on its own or as part of pre-eclampsia.
Classification
It is generally accepted that hypertension in pregnancy may be defined as a diastolic pressure of greater than 90 mmHg. Davey & MacGillivray (1986) gave a clear definition:
The occurrence of a blood pressure of 140/90 mmHg on at least two occasions 4 hours apart after the 20th week of pregnancy. The woman is normotensive before this time.
If proteinuria of 500 mg/L or more is present, the condition is described as pre-eclampsia. Severe pre-eclampsia depends on the rise in blood pressure and the clinical or laboratory results (Chari et al 1995, Morley 2004). All or some of the following symptoms may be present:
• Blood pressure >160 mmHg systolic and >110 mmHg diastolic.
• Proteinuria >5.0 g in 24 h.
• Haemolytic anaemia, elevated liver enzymes, platelet count <100 000/ml.
• Headache.
• Epigastric pain.
Incidence
Pre-eclampsia is mainly a disorder affecting primigravidae. However, PIH may occur in a multiparous woman in a first pregnancy by another partner and who has a raised body mass index, a long pregnancy interval (>10 years) and is older than 40 (Duckitt & Harrington 2005). There is also evidence that women in a prolonged sexual relationship develop an immune response to sperm and are therefore immunologically protected in later pregnancies (Morley 2004, Ness & Grainger 2008). There is a genetic predisposition to this disease, women being more likely to develop the disorder if their mothers or sisters did (Zhang et al 1997). Multiple pregnancies and women who experience a hydatidiform mole may develop symptoms of PIH before 20 weeks due to hyperplacentation. Women who were hypertensive before pregnancy may develop pre-eclampsia superimposed on the existing condition and women who had pre-eclampsia in a previous pregnancy are more likely to have an occurrence.
A major problem is that PIH can really only be diagnosed in retrospect by a post-delivery return to normal blood pressure (Hearnshaw 1996). There is also difficulty in predicting which woman is likely to progress to a more serious condition. Severe pre-eclampsia can rapidly fulminate to eclampsia before blood pressure or proteinuria reach levels of concern (Zhang et al 1997). Blood pressure returns to normal within weeks. It is believed that there is no long-term link between hypertension in pregnancy and later onset of essential hypertension, although this may occur. Proteinuria may persist for longer than the hypertension and may indicate underlying renal disease.
Pathogenesis
The cause of PIH is still not completely understood and it has been described as a disease of theories. It is difficult to use animal models as there is no comparable process with which to make analogies. Pre-eclampsia is associated with an increase in the inflammatory response, poor placentation and poor placental blood flow to the fetus. Lockwood et al (2008) found high levels of interleukin-6, an inflammatory cytokine, in the plasma of pre-eclamptic women.
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