Hypertension in pregnancy

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Chapter 45 Hypertension in pregnancy

Cardiovascular changes in pregnancy

There are significant physiological adaptations of the cardiovascular system to pregnancy. Blood volume rises from an average non-pregnant 2600 mL to 3800 mL at about 32 weeks gestation. The total red cell volume grows constantly until term from 1400 mL to 1700 mL, so there is a fall in haemoglobin concentration as gestation progresses. Cardiac output rises from 5 L/minute to 7.5 L/minute, mostly during the first trimester, and the heart rate rises by 10% with an average resting rate of 88 beats/minute. The peripheral resistance is lowered by a combination of increased vasodilatory substances during pregnancy and decreased sensitivity to vasopressor substances.

Blood pressure falls in the first trimester and is at its lowest in the second trimester. The reduction in diastolic blood pressure is about 10 mmHg by mid-pregnancy. Blood pressure rises to non-pregnant levels towards the end of the third trimester.

Uterine blood flow increases steeply from 24 weeks gestation.

Other factors affecting blood pressure in pregnancy include posture (via the supine hypotension syndrome) and uterine contractions, which raise blood pressure.

Definitions. Hypertension in pregnancy is defined as:

• systolic blood pressure ≥140 mmHg, and/or

• diastolic blood pressure ≥90 mmHg (Korotkoff 5)

These measurements should be confirmed by repeated readings over several hours. Elevations of both systolic and diastolic blood pressure have both been associated with adverse fetal outcome and therefore both are important.

Severe hypertension in pregnancy is defined as:

• a systolic blood pressure ≥170 mmHg, and/or

• diastolic blood pressure ≥110 mmHg

This represents a level of blood pressure above which cerebral autoregulation is overcome in normotensive individuals. It is generally acknowledged that severe hypertension should be lowered promptly, albeit carefully, to avoid cerebral haemorrhage and hypertensive encephalopathy.

Pre-eclampsia

Incidence. While 20% of women are hypertensive at some stage of their pregnancy (blood pressure ≥140/90 mmHg), about 5%–10% of primigravid women and 2% of multiparous women fulfil a diagnosis of pre-eclampsia.

Definition. Pre-eclampsia is a multisystem disorder unique to human pregnancy, characterised by hypertension and involvement of one or more other organ systems and/or the fetus. Proteinuria is the most commonly recognised additional feature after hypertension, but should not be considered mandatory to make the diagnosis.

A diagnosis of pre-eclampsia can be made when hypertension arises after 20 weeks gestation and is accompanied by one or more of the following:

• renal involvement

• significant proteinuria: dipstick proteinuria, subsequently confirmed by spot urine protein/creatinine ratio ≥30 mg/mmol

• serum or plasma creatinine >90 μmol/L

• haematological involvement

• thrombocytopaenia

• disseminated intravascular coagulation

• liver involvement

• raised serum transaminases

• severe epigastric or right upper quadrant pain

• neurological involvement

• convulsions (eclampsia)

• hyperreflexia with sustained clonus

• severe headache

• persistent visual disturbances (photopsia, scotomata, cortical blindness, retinal vasospasm)

• pulmonary oedema

• intrauterine growth restriction

• placental abruption

Pathophysiology

Two placental conditions predispose to the development of pre-eclampsia. Ischaemia results from the failure of the normal development of the uteroplacental circulation with the presence of small defective spiral arteries, which then may become blocked by acute atherosis or thrombosis. Excessive placental size also predisposes to pre-eclampsia, as seen in multiple pregnancy, hydatidiform mole, fetal triploidy and placental hydrops.

Maternal contribution to pre-eclampsia occurs when endothelial activation results in acceleration of the normal systemic inflammatory response, which is present in all pregnancies. Activation of leucocytes and the coagulation process, and subsequent metabolic changes, result in the clinical features which are typically seen in pre-eclampsia: hypertension, oedema, proteinuria, platelet dysfunction, clotting derangements and possibly eclampsia.

The specific placental factor or factors that generate the systemic inflammatory response of pre-eclampsia remain unknown, but recent research has highlighted the contribution of three circulating placental products: soluble fms-like tyrosine kinase 1 (sFlt-1), endoglin and placental growth factor.

Placentation also depends on the invasion of the placental bed by cytotrophoblasts. Immune tolerance must occur in this setting to allow a continued relationship between the mother and the fetus.

Hence, at least four factors are likely to contribute to the development of pre-eclampsia: placental, endothelial, inflammatory and immunological.

Risk factors associated with pre-eclampsia

Risk factors are listed in Table 45.1. Other factors associated with pre-eclampsia include chronic hypertension, preexisting renal disease, autoimmune disease, more than 10 years since a previous pregnancy, a short sexual relationship prior to conception, and other thrombophilias (e.g. Factor V Leiden and possibly periodontal disease).

Table 45.1 Pre-eclampsia risk factors

Risk factor	Relative risk
Previous history of pre-eclampsia	7.19
Antiphospholipid antibodies	9.72
Preexisting diabetes	3.56
Multiple pregnancy	2.91
Nulliparity	2.90
Family history of pre-eclampsia	2.90
Elevated body mass index (BMI) >25	2.47
Maternal age >40	1.96
Diastolic blood pressure >80 mmHg at first antenatal visit	1.38

Recurrence risk

Studies of the risk of recurrent pre-eclampsia in women with a history of a hypertensive disorder in a prior pregnancy show variable results. Recurrence rates vary from 6%–55%, with the greatest risk in women with early-onset pre-eclampsia and chronic hypertension. An Australian study suggests a 14% risk of developing pre-eclampsia, and also a 14% risk of developing gestational hypertension in their next pregnancy.

Clinical spectrum

Pre-eclampsia is a multisystem disorder with both maternal and fetal consequences.

Hypertension

Hypertension may be labile, often with flattened or the reverse of normal diurnal rhythm. This is thought to be due to decreased responsiveness to angiotensin II. Many of the complications of pre-eclampsia are due to arterial damage and loss of vascular autoregulation.

Renal system

Glomerular swelling of endothelial cells and intracapillary cells known as endotheliosis is the main response to pre-eclampsia. This causes a reduced glomerular filtration rate, which slows urate clearance and raises serum creatinine levels. In uncomplicated pregnancy, glomerular filtration normally increases. A serum creatinine level of 0.09 μmol/L in pregnancy may predict renal involvement.

Proteinuria is often a late sign of pre-eclampsia and indicates poorer prognosis for the mother and fetus.

The commonest cause of nephrotic syndrome in pregnancy is pre-eclampsia. There is a reduced maternal plasma volume due to increased leakiness of capillaries, and hypoalbuminaemia predisposing to reduction in colloid oncotic pressure and raised fluid in interstitial spaces. The complications of fluid changes include pulmonary and laryngeal oedema, and acute renal failure.

Platelets

The reduction of platelets in pre-eclampsia is due to increased consumption and lowered platelet lifespan. However, this is an inconsistent feature of pre-eclampsia.

Coagulation

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