Hypertension in pregnancy

Hypertension in pregnancy - technical

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In normal pregnancy the arterial pressure falls in the second half of the first trimester: systolic pressure then remains unchanged throughout pregnancy, with diastolic pressure tending to rise gradually towards its prepregnancy level in the later weeks.

Definitions, epidemiology and clinical features—(1) Pregnancy-induced hypertension (PIH), transient hypertension of pregnancy, or gestational hypertension describe new hypertension, defined as blood pressure equal to or in excess of 140/90 mmHg, which without proteinuria affects up to 10% of women after mid term (20 weeks) and resolves after delivery. (2) Pre-eclampsia, which affects 3 to 5% of pregnancies, is defined by the presence of PIH and pregnancy-induced proteinuria arising after 20 weeks gestation that both improve after delivery. Other features include (a) renal insufficiency; (b) hepatocellular dysfunction and/or severe epigastric/right upper quadrant pain; (c) neurological problems—convulsions (eclampsia), severe headaches, persistent scotomata; (d) haematological disturbances—thrombocytopenia, disseminated intravascular coagulation, haemolysis; (e) fetal growth restriction.

Differential diagnosis—the main differential diagnosis of pre-eclampsia is from chronic hypertension, which in its pure form does not share the renal, coagulation, hepatic and placental abnormalities of pre-eclampsia. The perinatal risks of chronic hypertension in pregnancy result from superimposed pre-eclampsia.

Aetiology—the cause of pre-eclampsia is unknown, but it depends upon the placenta and is characterized by diffuse maternal endothelial dysfunction and a systemic inflammatory response.

Management before pregnancy and prevention—women with no more than moderate chronic hypertension should stop antihypertensive treatment before conception. There is no good method of preventing pre-eclampsia, but low-dose aspirin may be effective in some women.

Management during pregnancy—extreme hypertension (≥160/110 mmHg), whatever the underlying cause, is as dangerous as it is in any other medical situation and demands treatment, but there is no clear reason for treating more moderate hypertension on either maternal or fetal grounds, although most centres will initiate treatment at less extreme levels of blood pressure. As far as it is known the progression of moderate pre-eclampsia is not delayed, nor is the later superimposition of pre-eclampsia on moderate chronic hypertension prevented. Key aspects of management include:

  • Antihypertensive agents—methyldopa is the most thoroughly tested drug for use in pregnancy: no significant adverse reactions have been observed, but because of its side effect profile labetalol and nifedipine are popular alternatives.
  • Magnesium sulphate – this should be given to prevent eclampsia (grand-mal convulsions) in women with the HELLP syndrome (haemolysis, elevated liver enzymes and low platelet counts) and those who have had one eclamptic convulsion.
  • Delivery of the baby and placenta—this is the definitive treatment for pre-eclampsia.

Cardiovascular changes in pregnancy (Bullet list 1)

Cardiac output increases during the first trimester and remains steady in the second and early third trimesters but towards full term declines in the supine but not lateral recumbent position, owing to the pressure of the gravid uterus on the inferior vena cava, which reduces venous return to the heart. In the third trimester about two-thirds of the additional cardiac output is distributed to the placental circulation and to augment renal plasma flow. The increased output results from both a greater stroke volume and a higher pulse rate. Plasma volume increases progressively during the second and third trimesters and is significantly correlated with the birthweight of the conceptus. Arterial pressure falls in the second half of the first trimester while the cardiac output is increasing because peripheral resistance decreases relatively more than the cardiac output increases. The uteroplacental circulation is too small at this time to cause these changes, which must therefore result from generalized arteriolar dilatation.

In the later weeks of pregnancy diastolic pressure tends to rise slowly towards what it was before pregnancy, the systolic pressure remaining more or less unchanged. However, in the supine position, with venocaval compression and reduced venous return, the arterial pressure may be atypically low with a narrowed pulse pressure and reflex vasoconstriction. This fall in systolic pressure may exceed 30% in 10% of cases and cause the ‘supine hypotension syndrome’—evident as restlessness, faintness, breathlessness, and pallor.

Bullet list 1 Cardiovascular changes in pregnancy

  • Increased cardiac output
  • Increased plasma volume
  • Increase heart rate
  • Increased stroke volume
  • Reduced arterial pressure, (mainly in second trimester)
  • Reduced peripheral resistance

Hypertension in pregnancy: definition, causes, and terminology

Causes and terminology

Hypertension in obstetric practice is conventionally recognized at or above an arbitrary threshold of 140/90. In the second half of pregnancy about one-quarter of all women will be, at least transiently, hypertensive by this criterion. About 2.5% have a maximum arterial pressure of 160/105 or more and about 1% of 170/110 or more.

Pregnancy-induced hypertension (PIH), transient hypertension of pregnancy, or gestational hypertension are terms used to describe new hypertension that appears after mid term (20 weeks) and resolves after delivery (Bullet list 2). This is one of the components of pre-eclampsia, which is a syndrome comprising PIH and pregnancy-induced proteinuria. Pre-eclampsia (previously called pre-eclamptic toxaemia, PET) is so called because it may precede eclampsia, which is one of a number of possible crises of the condition. Eclampsia is characterized by grand-mal convulsions, but other crises (described below) may be as dangerous and occur more commonly. Not all cases of eclampsia are preceded by a prodromal illness of pre-eclampsia, so the terminology is simplistic. Toxaemia is an obsolete expression, previously used to describe any hypertension or proteinuria in pregnancy, whether pregnancy-induced or not.

Bullet list 2 Terminology

  • Pregnancy-induced hypertension (PIH), also gestational hypertension: new hypertension after 20 weeks, regressing after delivery
  • Pre-eclampsia (pre-eclamptic toxaemia or PET): a multisystem syndrome, defined by the presence of PIH combined with pregnancy-induced proteinuria, regressing after delivery
  • Superimposed pre-eclampsia: pre-eclampsia occurring in association with chronic hypertension or renal disease or both
  • Eclampsia: Grand-mal convulsions associated with pre-eclampsia. The risk of convulsions quickly recedes after delivery

Pregnancy-induced hypertension (PIH) on its own (a relatively common clinical presentation) is not pre-eclampsia; at least one more sign is required. The clusters of clinical features that comprise any syndrome are chosen for convenience; they describe outward appearances and embody no special truth about the underlying disease or diseases. When a syndrome such as pre-eclampsia is ‘defined’, rules are set that bring consistency to what is being discussed. The validity of the rules cannot be tested because there is no standard to which to refer. All the definitions of pre-eclampsia suffer from these limitations and none can be said to be the best. The conventional components of the cluster are PIH combined with new proteinuria that regress after delivery.

Almost all hypertension presenting before mid term (gestational age of 20 weeks) indicates pre-existing or chronic hypertension; the exceptions are women with rare very early-onset pre-eclampsia. However, normotension in the first half of pregnancy does not necessarily mean long-term normotension because the fall in blood pressure induced in early pregnancy may be exaggerated in some women. Many with relatively severe hypertension may have normal blood pressures by 12 weeks, without treatment; in one study as many as 60% of women with chronic hypertension defined before pregnancy were normotensive by the end of the first trimester. In other words, some women enjoy the benefits of pregnancy-induced normotension just as others suffer the disadvantages of PIH. Pregnancy-induced normotension tends to be lost in the third trimester. If the prepregnancy blood pressures are unknown then this may be misinterpreted as PIH rather than recognized for what it is, namely re-establishment of the normal, long-term blood pressure.

Pregnancy-induced hypertension thus represents at least two clinical situations: early pre-eclampsia or occult chronic hypertension. In many cases the signs of pre-eclampsia are not confirmed but nevertheless the blood pressure reverts to normal after delivery. It is possible that these are early unconfirmed stages of pre-eclampsia; an alternative is that an innate tendency to hypertension has been revealed in pregnancy but will become overt only many years later. The studies have not been done to confirm or refute this suggestion.

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Hypertension in the puerperium

In relation to both chronic hypertension and pre-eclampsia the highest blood pressures are often recorded in the puerperium, typically peaking at about 5–7 days after delivery. Antihypertensive treatment has to be continued, in some women for 3–6 weeks or even longer after delivery. It is preferable to stop methyl dopa which causes depression and substitute other preparations which may include ACE inhibitors. There is no clear evidence that treatment interferes with breastfeeding (Table 1).

Table 1 Antihypertensive drugs and breastfeeding
Drug Secretion in breast milk
Methyldopa Minimal secretion; too small to be harmful
Labetalol Secreted in breast milk in small amounts
Atenolol Secreted in breast milk in small amounts
Nifedipine Secreted in breast milk
ACE inhibitors Secreted in breast milk but in small amounts that are unlikely to be harmful

Long-term sequelae of hypertension in pregnancy

Women who have had pre-eclampsia have an increased risk in later life of sustained hypertension, ischaemic heart disease, and stroke. Although it is inappropriate to immediately place this burden of knowledge on women who already have had the troubled experience of pre-eclampsia, organization of low-key community follow-up is likely to be helpful.