Introduction
There is an increasing prevalence of cardiovascular disease (CVD) in women of child bearing age. It is estimated that about 0.2–4% of all pregnancies in the developed world have cardiovascular complications despite no known prior disease. CVD is a major cause of non-obstetric death amongst expectant and new mothers in the UK. Hypertensive disorders are the most frequent CVD during pregnancy, occurring in 6–8% of all pregnancies.
The improved longevity following successful medical and surgical treatment of congenital heart diseases has led to an increased number of women becoming pregnant with treated congenital heart disease, with an increased predominance of shunt lesions.
In the developing world the burden of valvular heart disease among pregnant women persists, but these issues are also seen in the developing world amongst immigrant populations.
Increased prevalence of risk factors for atherosclerotic disease along with an increased maternal age has led to an increased incidence of coronary artery disease.
Cardiomyopathies, though rare, cause significant morbidity. Peripartum cardiomyopathy (PPCM) is the most common cause of severe complications.
CVD in pregnancy poses a challenging scenario due to changes in the maternal physiology adversely affecting the suboptimal cardiovascular system. The responsibility of the treating physician in these cases ranges from prenatal counselling, antenatal and postnatal care of the mother and also potentially extends to the care of the unborn foetus. Considering the difficulties of conducting research in this area, it is not surprising that robust prospective randomised studies are lacking.
Cardiovascular Physiological Changes in Pregnancy
Though there are widespread metabolic changes in the pregnant female, for the purposes of this chapter we will confine our discussion to the cardiovascular changes that occur during pregnancy
Pregnancy has a profound effect on the circulatory system to meet the additional metabolic demands of the mother and the foetus.
The placenta invades maternal uterine tissue early in pregnancy and releases an array of hormones and other factors. These hormones create physiological changes in the mother, which favour nutrient and oxygen delivery to the growing foetus.
There is an increase in red cell mass and increase in blood volume, causing increased preload. However, there is dilutional anaemia due to a disproportionate increase of the plasma component of blood as compared to its cellular component.
Further increases in cardiac output by about 20–50% are achieved by an increase in stroke volume of about 15–30% in early pregnancy and an increase of heart rate by about 15–30%, mainly towards the latter stages as caval compression prevents further increases in stroke volume.
There is a decrease in total vascular resistance by about 30% due to increased flow into the uteroplacental circulation, coupled with secretion of vasodilatory substances from the placenta such as nitric oxide and prostaglandins. The systolic blood pressure for the most part remains unchanged but the mean arterial pressure is reduced initially but increases towards the end of pregnancy.
The cardiac performance improves with progressive LV remodelling during pregnancy. There is dilatation of the heart by about 30% with eccentric hypertrophy. These changes tend to resolve within 2 weeks of postpartum state.
By the second trimester the enlarging uterus will cause a degree of aortocaval compression, reducing the amount of venous return in the supine position.
A series of haemostatic changes, such as increased platelet adhesiveness and increased concentration of coagulation factors, leads to a hypercoaguable state; this, coupled with stasis due to caval compression described above, can increase the risk of deep vein thrombosis.
Further during labour, pain, anxiety and uterine contractions cause increased cardiovascular stress. Efforts to mitigate pain with neuraxial anaesthesia or intercurrent haemorrhage during delivery affect cardiovascular performance.
Post delivery, the phenomenon of autotransfusion, resorption of oedema and uterine involution places a significant stress on the cardiovascular system.
There is a reduction in cardiac output in the postpartum period.
Diagnosis of Cardiovascular Diseases
History and Clinical Examination
A thorough history, specifically looking to elicit familial history of cardiomyopathies, Marfan syndrome, long QT syndromes and sudden deaths, should be sought. Assessment of progression of ongoing breathlessness is a good prognostic tool to predict heart failure. History should include baseline functional status and previous cardiac events as these are strong predictors of peripartum cardiac events.
The strongest predictors are:
Any prior cardiac event;
Cyanosis or poor functional status;
Left sided obstruction;
Ventricular dysfunction.
Examination is directed towards looking for signs of heart failure; if new signs or murmurs are found, this mandates further investigations. Blood pressure is measured either at home or in the clinic in the left lateral recumbent position.
Urinalysis for glucose and proteinuria should be performed.
Electrocardiography
A standard 12 lead ECG, which is a safe and inexpensive screening tool, should be used. The normal ECG of pregnancy sometimes manifests as left axis deviation, increased R wave amplitude in V1 and V2, T wave inversion in V2, small Q wave in lead II, III and aVF, and inverted T wave in lead III, V1–V3.
There is an increase in the rate of maternal arrhythmias during pregnancy.
Further analysis of rhythm disturbances may warrant exercise ECG, tilt table testing and electrophysiological studies.
Echocardiography
This is the preferred mode of cardiac imaging due to its non-invasive nature, safety profile and reproducibility. The transthoracic route is preferred to the trans‑ oesophageal (TOE) route.
In cases where TOE is used, care must be taken regarding aspects such as gastric stasis, reflux and sedation needs, which might impact on foetal well being, necessitating foetal monitoring.
Exercise Testing
This provides an objective quantification of cardiopulmonary function especially in patients being followed up for grown-up congenital heart disease (GUCH) and valvular heart disease. It should preferably be performed in the prenatal period to help with risk assessment and prenatal counseling.
The European Society of Cardiology (ESC) recommends that in asymptomatic patients it is advisable to use exercise testing to attain 80% of maximal capacity during pregnancy. The safety of exercise testing during pregnancy has not been established, but there is no evidence that it increases the risk of spontaneous abortion.
Magnetic Resonance Imaging
This is a useful modality that will provide information for diagnosis and therapy. It is probably safe in the second and third trimesters. It can also be used to diagnose foetal neurological defects identified by ultrasound.
Gadolinium ions are known to cross the placental barrier; the safety of gadolinium is not known in a developing foetus and should be avoided.
Cardiac Catheterisation
If needed in a pregnant patient, this should preferably be undertaken by the radial route, limiting the radiation exposure time and shielding the foetus from direct radiation.
Electrophysiological studies or ablation if needed should use an electroanatomical mapping system in conjunction with MRI to reduce radiation dose.
Chest X-rays and CT Scans
A single diagnostic investigation requiring radiation exposure is not sufficient to threaten the well being of the developing foetus. However, frequency of exposure, and accumulated dose of radiation, do result in adverse foetal effects such as foetal cell death, teratogenesis, carcinogenesis and mutations in germ cells in the foetus.
A radiation dose below 50 mGy to the pregnant mother is the accepted level of radiation below which there is no evidence of increased foetal risk.
If ionising radiation is used, its dose should be documented in the record and the principle of ALARA ‘as low as reasonably achievable’ should be used.
The foetus as a rule is protected by the mother’s abdomen and the exposure to radiation is far below the level of exposure of the mother.
Table 49.1 gives the amount of radiation exposure for common radiological procedures.
Table 49.1 Estimated foetal and maternal effective doses for various diagnostic and interventional radiology procedures
| Procedure | Foetal exposure | Risk of childhood cancer |
|---|---|---|
| Chest radiograph (PA and lateral) | 0.001–0.01 mGy | <1:100,000 |
| CT chest (including CTPA) | 0.01–0.1 mGy | <1:100,000 |
| Lung perfusion scan | 0.1–1 mGy | 1:100,000 to 1:10,000 |
| CT chest abdomen pelvis | 10 mGy | 1:10,000 to 1:1000 |
| Coronary angiography | 1.5 mGy | 1:10,000 to 1:1000 |
| PCI or radiofrequency catheter ablation | 3 mGy | 1:10,000 to 1:1000 |
CT computed tomography; PCI percutaneous coronary intervention; PA posteroanterior.
Natural childhood cancer risk 1:500.
Common Cardiovascular Disorders
Hypertensive Disorders of Pregnancy
Definitions
Gestational hypertension is a clinical diagnosis defined by the new onset of hypertension (systolic blood pressure ≥140mmHg and/or diastolic blood pressure ≥90 mmHg) at ≥20 weeks of gestation in the absence of proteinuria or new signs of end-organ dysfunction. The blood pressure readings should be documented on at least two occasions at least 4 hours apart. Gestational hypertension is severe when systolic blood pressure is ≥160 mmHg and/or diastolic blood pressure is ≥110 mmHg on two consecutive blood pressure measurements at least 4 hours apart.
Gestational hypertension is a temporary diagnosis for hypertensive pregnant women who do not meet the criteria for pre-eclampsia (see Table 49.2) or chronic hypertension (hypertension first detected before the twentieth week of pregnancy). The diagnosis is changed to:
Pre-eclampsia, if proteinuria or new signs of end-organ dysfunction develop;
Chronic (primary or secondary) hypertension, if blood pressure elevation persists ≥12 weeks post partum;
Transient hypertension of pregnancy, if blood pressure returns to normal by 12 weeks post partum.
Thus, reassessment up to 12 weeks post partum is necessary to establish a final diagnosis.
Table 49.2 Diagnosis of pre-eclampsia
| Systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg on two occasions at least 4 hours apart after 20 weeks of gestation in a previously normotensive patient. If systolic blood pressure is ≥160 mmHg or diastolic blood pressure is ≥110 mmHg, confirmation within minutes is sufficient | |
| AND | |
| Proteinuria ≥0.3 g in a 24-hour urine specimen or protein (mg/dl)/creatinine (mg/dl) ratio ≥0.3 | |
| Dipstick ≥1+ if a quantitative measurement is unavailable | |
| In patients with new-onset hypertension without proteinuria, the new onset of any of the following is diagnostic of pre-eclampsia: | |
| Platelet count <100,000/µl | Liver transaminases raised to twice normal limits |
| Serum creatinine > 100 µmol/l OR doubling of serum creatinine in the absence of renal disease | |
| Cerebral or visual symptoms | Pulmonary oedema |
Gestational hypertension occurs in 6–17% of healthy nulliparous women and 2–4% of multiparous women. Previous history of pre-eclampsia, multifoetal pregnancies and raised body mass index are the significant risk factors.
Diagnosis
Blood pressure monitoring is the cornerstone on which the diagnosis is made; home blood pressure monitoring is useful to differentiate white coat hypertension. It is important to differentiate gestational hypertension from pre-eclampsia and pre-eclampsia from severe pre-eclampsia.
Table 49.3 gives the diagnosis of severe pre-eclampsia.
Table 49.3 Diagnostic features of severe pre-eclampsia
| |
| |
| |
| |
| Thrombocytopenia:<100,000 platelets/µl | Pulmonary oedema |
Foetal well being should be evaluated with estimation of foetal weight; umbilical artery Doppler is helpful for foetuses with intrauterine growth restriction. An abnormal Doppler profile is highly specific for severe pre-eclampsia.
HELLP syndrome represents a severe form of preeclampsia. It is characterised by:
Haemolysis with a microangiopathic picture on blood smear;
Elevated liver enzymes; and a
Low platelet count.
Patients with HELLP have a high risk of developing serious hepatic injury due to infarction, haemorrhage and hepatic rupture.
Management
Delivery minimises the risk of development of serious maternal and foetal complications due to pre-eclampsia. The management decision is a trade-off between:
The foetal benefits from expectant management (i.e. further growth and maturation);
The maternal and foetal benefits from early intervention (i.e. avoidance of complications from progression of hypertensive disease over the remainder of pregnancy); and
The maternal and foetal risks from expectant management (i.e. progression of hypertensive disease and possible sequelae, including stillbirth or asphyxia).
An overview of management of gestational hypertension is beyond the scope of this chapter; however we will focus on the management of severe eclampsia in patients likely to need intensive care.
For the common scenarios where intensive care intervention is required, parenteral drug therapy for acute management of severe hypertension is possible.
Labetolol intravenously is recommended for first line therapy because it is effective, has a rapid onset of action and a good safety profile. Suggested regime: begin with 20 mg intravenously over 2 minutes followed at 10 minute intervals by doses of 20 to 80 mg up to a maximum total cumulative dose of 300 mg, or an intravenous infusion of 1–2 mg/minute.
Hydralazine administered intravenously is a good alternative to labetolol. Suggested regime: begin with 5mg intravenously over 1 to 2 minutes, repeat as required waiting for a response that usually takes up to 15–20 minutes to manifest. The maximum bolus dose is 20 mg. If a total dose of 30 mg does not achieve optimal blood pressure control, another agent should be used.
Calcium channel blockers, sustained release nifedipine (30 mg) and immediate release nicardipine, are other options. Nicardipine can be given intravenously. Experience with these drugs in pregnancy is limited. Immediate release oral or sublingual nifedipine is best avoided as it can cause precipitous hypotension resulting in uteroplacental insufficiency.
Nitroglycerin (glyceryl trinitrate) is a good option for treatment of hypertension associated with pulmonary oedema. It is given as an intravenous infusion of 5 μg/minute and gradually increased every 3 to 5 minutes to a maximum dose of 100 μg/minute.
Antenatal corticosteroids may also be administered. Neonatal respiratory distress is very common in premature neonates of pre-eclamptic mothers. Betamethasone should be administered to mothers <34 week’ gestation to promote foetal lung maturation as the risk of these patients developing severe pre-eclampsia is high.
A ‘restrictive’ fluid strategy is advocated as patients with severe disease can develop pulmonary oedema. Oliguria should be managed by modest trials of fluid boluses and if it does not respond it should be tolerated or renal replacement therapy considered if indicated. Pulmonary oedema might warrant use of loop diuretics.
For seizure prophylaxis, magnesium sulphate is the drug of choice and should be administered for all patients with severe pre-eclampsia. Suggested regime: a loading dose of 4 to 6 g intravenously and maintenance dose of 1 to 3g/hour. Intramuscular regimes have been described but they are associated with pain at the injection site and fluctuating drug levels. Magnesium sulphate is continued for 24 hours post partum. Therapeutic levels between 2.0 and 3.5 mmol/l are to be maintained. Dose reduction might be needed in patients with renal failure. Clinical monitoring for signs of hypermagnesaemia, such as reduced patellar reflexes and respiratory depression, should be monitored and the dose reduced if signs of toxicity appear (Table 49.4).
Table 49.4 Signs of magnesium toxicity
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