Gestational and chronic hypertension in pregnancy

• Gestational and chronic hypertension in pregnancy are two of the four hypertensive disorders of pregnancy, alongside pre-eclampsia and eclampsia. They are defined by a blood pressure of 140 mmHg systolic or 90 mmHg diastolic, confirmed on two occasions at least four hours apart, with chronic hypertension present before 20 weeks and gestational hypertension arising at or after 20 weeks.^{[2] [7]}
• Chronic hypertension affects roughly 0.9 to 1.5% of pregnant women and carries a 25% risk of superimposed pre-eclampsia, while all hypertensive disorders of pregnancy together complicate about 5 to 10% of pregnancies and cause roughly 14% of maternal deaths worldwide.^{[3][7][5] [2][8]}
• The safe antihypertensives in pregnancy are labetalol, nifedipine and methyldopa, plus hydralazine for acute severe rises; ACE inhibitors, angiotensin receptor blockers and thiazide-like diuretics are avoided. ^[1][7]
• Targets differ by guideline: NICE aims for 135/85 mmHg or lower on treatment, ISSHP 110 to 140/under 85 mmHg, while ACOG uses 120 to 160/80 to 110 mmHg. Say which protocol your unit uses.^[1][2]
• The treatment threshold for chronic hypertension changed after the CHAP study: 140/90 mmHg, rather than waiting for 160/110 mmHg, improves outcomes without increasing small babies.^{[4] [1][7] [2]}
• Distinguishing these from pre-eclampsia is the daily clinical question: pre-eclampsia is new hypertension after 20 weeks with proteinuria or other evidence of maternal organ or uteroplacental dysfunction.^[2][7]

By the end of this page you should be able to:

1. Define chronic and gestational hypertension in pregnancy and classify them against the other hypertensive disorders of pregnancy.
2. Describe the pathophysiology that links abnormal placentation, chronic hypertension and pre-eclampsia, and why pregnancy is a vascular stress test.
3. Take and record a blood pressure properly in pregnancy and apply the cut-offs for hypertension, severe hypertension and proteinuria.
4. Choose and dose the safe antihypertensive drugs, avoiding those contraindicated in pregnancy.
5. Apply NICE, ACOG, RCOG and WHO guidance to targets, monitoring, timing of birth and postnatal care, and explain where they disagree.
6. Separate gestational or chronic hypertension from pre-eclampsia, and state the first-line and escalation steps when pre-eclampsia appears. ^[1]

The four disorders overlap in blood pressure but differ in when they appear and what else is wrong.

• Chronic hypertension. Blood pressure that is present before pregnancy, first diagnosed before 20 weeks of gestation, or detected for the first time in pregnancy but not resolved after birth. It may be primary (most common) or secondary to renal, endocrine or vascular disease.^[7][2]
• Gestational hypertension. New hypertension at or after 20 weeks in a woman previously normotensive, with no proteinuria or other feature of pre-eclampsia. It resolves within about 12 weeks of birth in most women.^{[7] [2]}
• Pre-eclampsia. New hypertension at or after 20 weeks with at least one of: proteinuria of 300 mg per 24 hours or a protein:creatinine ratio of 30 mg/mmol; renal insufficiency (creatinine above 1.1 mg/dL or doubling); thrombocytopenia under 100,000 per microlitre; impaired liver function (ALT or AST of two times the normal ceiling or more); pulmonary oedema; or new-onset headache or visual disturbance.^{[2] [7]}
• Pre-eclampsia superimposed on chronic hypertension. Chronic hypertension with a sudden change in any of the pre-eclampsia parameters.
• White-coat hypertension. Clinic blood pressure 140/90 mmHg or above with normal blood pressure outside the clinic, confirmed by home or ambulatory monitoring. It is not harmless and carries an 8% risk of pre-eclampsia, so it needs follow-up. Treatment is usually withheld if clinic pressure stays below 160/110 mmHg and out-of-office pressure is normal.^[7]
• Antenatally unclassified hypertension. Blood pressure first measured after 20 weeks without a baseline: the European Society of Cardiology labels this "antenatally unclassified" until the postnatal course clarifies it. ^[2]

Chronic hypertension is associated with substantial morbidity: in one large review 25% of women with chronic hypertension developed superimposed pre-eclampsia, 28% delivered preterm, 17% had a growth-restricted baby and 4% had a perinatal death.^[7]

Hypertensive disorders of pregnancy as a group complicate about 5 to 10% of all pregnancies and are the second leading direct cause of maternal death worldwide, accounting for roughly 14% of maternal deaths. ^[8][5] Losses are heavily concentrated in low and middle income countries.

• Chronic hypertension is present in 0.9 to 1.5% of pregnant women. Its rate rose by 67% in the decade to 2009, fastest in Black women at 87%, driven by obesity and older age at first pregnancy. ^[3]
• Gestational hypertension is more common than chronic hypertension but exact incidence varies by setting and criteria.
• Burden of chronic hypertension in pregnancy: superimposed pre-eclampsia 25%, preterm delivery 28%, fetal growth restriction 17%, perinatal death 4%. ^[7]
• Long-term legacy: women who have had a hypertensive disorder of pregnancy carry a 2-fold to 4-fold increase in future cardiovascular disease, including hypertension, stroke and chronic kidney disease, and may develop hypertension up to ten years earlier than other women. ^[7][2]

Chronic hypertension in pregnancy is usually primary (essential) hypertension, the same condition found in non-pregnant adults, unmasked or aggravated by pregnancy. Secondary causes (renal disease, primary hyperaldosteronism, renovascular disease, phaeochromocytoma, Cushing syndrome, thyroid disease, obstructive sleep apnoea) are less common but should be sought in young women, resistant hypertension, or when there is no family history. ^[2]

Risk factors for pre-eclampsia that also colour the management of gestational and chronic hypertension include (NICE NG133, 2019, amended 2019/2023): ^[1]

• High risk (any one of): a past pregnancy complicated by hypertension, kidney disease that is chronic, an autoimmune condition (for example lupus or antiphospholipid syndrome), diabetes of either type, or hypertension that predates the pregnancy.
• Moderate risk (more than one of): first pregnancy, age 40 years or older, pregnancy interval longer than 10 years, BMI 35 kg per m2 or more at the first visit, family history of pre-eclampsia, multiple pregnancy.

A normal pregnancy is a low-resistance, high-flow state. Systemic vascular resistance falls, plasma volume and cardiac output rise by up to 40%, and renal blood flow and glomerular filtration increase. Blood pressure normally falls in the first trimester and returns toward baseline by term. ^[2]

In chronic hypertension this adaptation is impaired: the vessels are stiffer, the fall in pressure is blunted, and the kidneys and placenta see higher resistance. Chronic hypertension in pregnancy is therefore a marker of underlying vascular disease as much as a blood pressure number.

Gestational hypertension reflects a failure of the mothers vascular adaptation without (yet) the placental lesion that defines pre-eclampsia. Some 25% of women with gestational hypertension go on to develop pre-eclampsia, especially when it presents before 32 weeks.

Pre-eclampsia is a placental disease. Inadequate remodelling of the spiral arteries (their muscular walls are retained) limits uteroplacental perfusion. The hypoxic placenta releases anti-angiogenic factors (notably soluble fms-like tyrosine kinase 1, sFlt-1), which mop up the pro-angiogenic placental growth factor (PlGF). The result is widespread maternal endothelial dysfunction: vasoconstriction, leaky capillaries, platelet activation and organ ischaemia. Chronic hypertension is the second commonest risk factor for this process (relative risk 5.1) and is itself worsened by it. ^[2]

Why raised blood pressure matters in pregnancy is not abstract: severe hypertension above 160/110 mmHg damages cerebral autoregulation and is a leading cause of stroke, and women with pre-eclampsia become susceptible to intracerebral bleeding at blood pressures as low as 150 to 170 mmHg systolic. ^[2] That is why hypertensive emergencies are treated within minutes.

Most chronic hypertension is detected at booking or at a pre-conception review. Most gestational hypertension is detected on routine antenatal blood pressure measurement; women are often asymptomatic until severe.

Always ask about, and warn about, the symptoms that mark the transition to pre-eclampsia: ^[1]

• Severe headache
• Visual disturbance (blurring, flashing lights, scotomata)
• Severe pain just below the ribs or in the epigastrium
• Vomiting
• Sudden swelling of the face, hands or feet

Late presentation with one of these is the commonest way serious disease is missed. Functional symptoms of severe hypertension (breathlessness, chest pain, neurological change) and reduced fetal movement in the mother should also be sought.

• Blood pressure measurement. Seated, the arm supported at heart level, appropriately sized cuff, after five minutes of rest. The diagnosis requires two readings at least four hours apart (or sooner if severe). Automated devices must be validated in pregnancy. ^[2]
• Fundoscopy: papilloedema or haemorrhages suggest severe, chronic or malignant hypertension.
• Reflexes and clonus: hyperreflexia is common and not specific, but sustained clonus is a warning sign.
• Uterine and fetal examination: fundal height, fetal lie, fetal heart.
• Legs: sudden oedema of the face or hands is more worrying than ankle oedema, which is common and benign.
• Evidence of secondary causes in young or resistant patients (Table 5 concept from AHA statement): abdominal bruits, hypokalaemia, features of Cushing syndrome.

A point that causes international confusion: under NICE, ISSHP and several other guidelines, gestational or chronic hypertension plus fetal growth restriction or an abnormal umbilical artery Doppler qualifies as pre-eclampsia even without proteinuria, because uteroplacental dysfunction is treated as an end-organ feature. ACOG does not count isolated uteroplacental dysfunction as pre-eclampsia, so the same woman may be labelled "gestational hypertension with fetal growth restriction" in the United States. ^[8]

• Review medication before conception or at the first opportunity. ACE inhibitors and angiotensin receptor blockers are contraindicated in pregnancy; NICE advises stopping them within two working days of notification of pregnancy, while Australian guidance advises stopping them ideally before conception or at diagnosis of pregnancy, because of an increased risk of congenital abnormalities; switch to a pregnancy-safe agent. Women using them for renal disease need a nephrology review. ^[1][7]
• Thiazide or thiazide-like diuretics may increase the risk of congenital abnormalities and neonatal complications; discuss switching when planning a pregnancy. ^[1]
• For other agents there is no clear evidence of increased congenital malformation risk, but check each drug against local guidance. ^[1]
• All women with chronic hypertension should be referred to a specialist in hypertensive disorders of pregnancy for risk counselling. ^[1]
• Safe antihypertensive agents in pregnancy (Australian Prescriber table): ^[7]

• If already on a safe drug, continue it unless the sustained systolic pressure is below 110 mmHg, or the diastolic below 70 mmHg, or the woman has symptomatic hypotension. A first-trimester physiological fall often allows dose reduction. ^[1]
• If not on treatment, offer antihypertensive therapy when sustained blood pressure is 140/90 mmHg or higher, rather than waiting for severe hypertension. ^[1] This is the change driven by the CHAP study. ^[4]
• Treat urgently at once when pressure reaches 160/110 mmHg.
• Target while on treatment: NICE aims for 135/85 mmHg or lower; other guidelines differ (see the targets table below). ^[1][2]
• Lifestyle advice as for non-pregnant adults: weight, exercise, healthy eating and reducing salt; the NICE hypertension guideline applies in pregnancy too. ^[1]
• Aspirin (NICE: 75 to 150 mg daily from 12 weeks until birth; AHA and Australian protocols: 150 mg daily from 12 to 16 weeks until 36 weeks) reduces pre-eclampsia, preterm birth and stillbirth in women at risk; the start and stop windows differ by guideline. ^[1][7]
• PLGF-based testing between 20 and 36 weeks plus 6 days to help rule out pre-eclampsia when suspected. ^[1]

Where guidelines disagree, the disagreement is real, not semantic: lower targets protect the mother's brain and reduce severe hypertension, but older US guidance worried about uteroplacental perfusion and fetal growth. The CHAP study addressed this for chronic hypertension by showing that treating to 140/90 mmHg reduced pre-eclampsia with severe features, medically indicated preterm birth before 35 weeks, abruption and fetal or neonatal death, without increasing small babies (30.2 versus 37.0%, risk ratio 0.82). ^{[4] [8] [2]}

• Fetal surveillance: ultrasound for growth and amniotic fluid volume plus umbilical artery Doppler at 28, 32 and 36 weeks. ^[1]
• Cardiotocography only if clinically indicated. ^[1]
• Antenatal appointments: weekly if blood pressure is poorly controlled, every 2 to 4 weeks if well controlled. ^[1]
• Growth restriction triggers extra fetal testing via the local RCOG-based fetal surveillance pathway where available.

• Do not offer planned early birth before 37 weeks if the blood pressure is below 160/110 mmHg, with or without treatment, unless there are other medical indications. ^[1]
• At 37 weeks and beyond, with pressure below 160/110 mmHg, timing of birth is agreed between the woman and a senior obstetrician, weighing maternal and fetal indications. ^[1]
• If planned early birth is necessary, offer a course of antenatal corticosteroids and magnesium sulfate where indicated, as for any preterm birth. ^[1]

A pregnant woman with severe hypertension (160/110 mmHg or above) or any feature of pre-eclampsia needs secondary care assessment the same day.

• Acute severe hypertension: treat immediately with one of labetalol (oral or intravenous), oral nifedipine or intravenous hydralazine. ^[1][7]
• Urgent (AHA/Australian dosing examples): ^[7]
  • Hydralazine 5 to 10 mg intravenously, repeat after 20 minutes if blood pressure remains above 160/110 mmHg.
  • Labetalol 20 to 80 mg intravenously over 2 minutes, repeat after 10 minutes if needed; 200 mg orally is an alternative.
  • Nifedipine 10 mg orally; a 30 to 45 minute onset.
• Magnesium sulfate reduces eclampsia by about half. Give it if there is a fit, severe pre-eclampsia, or birth is planned within 24 hours, using the Collaborative Eclampsia Trial regimen: loading dose 4 g intravenously over 5 to 15 minutes, then 1 g per hour for 24 hours, continued for 24 hours after the last fit; recurrent fits take a further 2 to 4 g over 5 to 15 minutes. ^{[1][7] [2]}
• Only magnesium sulphate for seizure prophylaxis, not diazepam or phenytoin. ^[1]
• Fluid balance: do not use volume expansion in severe pre-eclampsia unless hydralazine is the antihypertensive; restrict maintenance fluids to 80 mL per hour unless there are other losses; consider up to 500 mL of crystalloid before or with the first dose of intravenous hydralazine. ^[1]
• HELLP syndrome: do not use dexamethasone or betamethasone to treat it. ^[1]
• Threshold for escalating medical therapy in critical care: severe hypertension, severe pre-eclampsia or eclampsia. ^[1]

NICE gives bandwidths driven by gestation at diagnosis: ^[1]

Planned early birth before 37 weeks is considered when there is any threshold feature of severe pre-eclampsia: inability to control blood pressure despite three or more drug classes in appropriate doses, maternal oxygen saturation below 90%, progressive deterioration in liver or renal function or platelets, ongoing neurological features, placental abruption, reversed end-diastolic flow in the umbilical artery, a non-reassuring fetal heart tracing or stillbirth. ^[1]

Bed rest in hospital is not used to treat gestational hypertension. ^[1]

Blood pressure falls then often rises again in the first week after birth, and hypertensive women need structured review.

• Chronic hypertension: measure blood pressure daily for the first 2 days, at least once between days 3 and 5, and as clinically indicated if treatment changes. Aim to keep it below 140/90 mmHg, continue treatment if required, stop methyldopa within 2 days of birth and switch to an alternative, and offer a specialist review at 6 to 8 weeks. ^{[1] [2]}
• Gestational hypertension: daily for 2 days, then at least once days 3 to 5; continue or start treatment as required; if methyldopa was used stop it within 2 days; if she was never treated, start treatment if blood pressure is 150/100 mmHg or higher; a written care plan covers who monitors, thresholds for reducing or stopping treatment and when to refer. Offer a medical review at 2 weeks after transfer to community care if she remains treated, and at 6 to 8 weeks for all women. ^[1]
• Pre-eclampsia postpartum: blood pressure at least 4 times a day as an inpatient; daily or every 1 to 2 days for up to 2 weeks in the community if treated; full blood count, liver and kidney tests at 48 to 72 hours after birth or step down and not repeat if normal; urinary dipstick at 6 to 8 weeks and, if proteinuria persists, a kidney function review at 3 months. ^{[1] [2]}
• Breastfeeding and medicines: the drugs safe in pregnancy are generally safe in breastfeeding, though methyldopa carries a 30% risk of depression and is usually stopped postpartum; ACE inhibitors, particularly enalapril, have very low concentrations in breast milk and are often introduced after birth. ^[7]
• Gestational hypertension resolves within 12 weeks of delivery in most women; if it does not, investigate primary or secondary hypertension. ^[7]
• Chronic hypertension does not resolve: the woman returns to her usual treatment (if compatible with feeding and future pregnancy) after a pre-conception review. ^[7]

Both maternal and fetal outcomes worsen as blood pressure rises and as pre-eclampsia develops.

• Pre-eclampsia superimposed on chronic hypertension: about 1 in 4 women with chronic hypertension. ^[7]
• Preterm delivery (28% in chronic hypertension) and fetal growth restriction (17%) (we monitor for these specifically at 28, 32 and 36 weeks in chronic hypertension). ^{[7][1] [2]}
• Severe hypertension, stroke, pulmonary oedema, acute kidney injury, liver rupture, placental abruption and disseminated intravascular coagulation as end-organ events. ^[2][1]
• Small for gestational age when blood pressure is uncontrolled or when high-dose antihypertensives are overused, which balances the need to treat. ^[2]
• Postpartum hypertension can appear or worsen in the first weeks after birth, including de novo postpartum pre-eclampsia, and is a major cause of postpartum stroke. ^[2]
• Long-term cardiovascular disease risk 2-fold to 4-fold after any hypertensive disorder of pregnancy. ^[7]

For gestational hypertension blood pressure normalises within 12 weeks in most women; if not, look for chronic or secondary hypertension. ^[7] For chronic hypertension the outlook is that of the underlying vascular disease, modified by pregnancy events: women who have had superimposed pre-eclampsia, early-onset disease, or growth restriction are at the highest future risk and need annual review of blood pressure, lipids and glucose with lifestyle support. ^[7] More severe pre-eclampsia and delivery before 34 weeks carry still higher long-term cardiovascular risk. ^[2]

Women who have had pre-eclampsia need particular follow-up: all women are reviewed at 6 to 8 weeks postpartum, and in primary care indefinitely, since roughly 15% of maternal deaths occur postpartum. ^[2][7]

• First-trimester risk assessment for pre-eclampsia using maternal factors, blood pressure and, where available, PlGF and uterine artery Doppler. ^[2][7]
• Low-dose aspirin (NICE: 75 to 150 mg daily from 12 weeks until birth; AHA and Australian: 150 mg daily from 12 to 16 weeks until 36 weeks) cuts preterm pre-eclampsia risk by around 60% in high-risk women and is recommended by NICE for all women with chronic hypertension and for women with more than one moderate risk factor. ^[1][7]
• Calcium supplementation to reach about 1000 mg daily through diet or supplements in women with inadequate intake reduces hypertensive disorders. ^[7]
• Exercise may reduce gestational hypertension risk by roughly 30% and pre-eclampsia by about 40%; pre-pregnancy body mass index is the strongest modifiable risk. ^[2]
• Not recommended for prevention: salt restriction alone, diuretics, antioxidants, fish oil, garlic, magnesium, folic acid alone, nitric oxide donors, progesterone or low molecular weight heparin. ^[1]
• Low-risk pregnancies should not be screened with antihypertensive or fetal testing beyond routine antenatal care; testing low-risk women produces false positives. ^[8]

• Pregnancy: all of the above. This topic is itself the pregnancy-specific management.
• Children: primary hypertension is rare in pregnancy; true hypertension before 20 weeks or resistant pressure needs assessment for secondary causes, and women with repaired congenital or acquired heart disease need multidisciplinary care. ^[2]
• Older women and women with chronic disease: in women with pre-existing renal, cardiac or autoimmune disease the treatment threshold may be lower and specialist teams (nephrology, cardiology, rheumatology) should be involved; NICE advises considering individual risk and referring on. ^[1][2]
• Breastfeeding: most pregnancy-safe antihypertensives are compatible with breastfeeding; angiotensin-converting enzyme inhibitors such as enalapril are commonly introduced postpartum, and methyldopa is usually withdrawn because of depression risk. ^[7]
• Women with a history of pre-eclampsia: offer early pre-conception review before the next pregnancy; optimise blood pressure and weight; counsel on recurrence risk and on the 2-fold to 4-fold rise in lifetime cardiovascular risk. ^[7][2]

• Protocols must be one. The international review shows that low and middle income countries often use a 150/100 mmHg threshold to start treatment and to define severe disease, while high-income guidelines use 160/110 mmHg. Whichever protocol a unit adopts should be written down and audited; mixing them is where harm occurs. ^[8]
• Oral and inexpensive drugs work. Labetalol, nifedipine, methyldopa and hydralazine given orally can control acute severe hypertension in resource-poor settings, though supplies and cold chains must be secured. ^{[2] [1]}
• Magnesium sulfate is the priority drug for seizure prevention (4 g intravenously or 10 g intramuscularly total 5 g into each buttock with 1 mL lignocaine, then 5 g intramuscularly alternate buttocks every 4 hours) and should be stocked before advanced blood pressure monitors. ^[1]
• Fetal surveillance can be basic: symphysis-fundal height, fetal movement awareness, handheld Doppler and, where available, ultrasound at 28, 32 and 36 weeks in chronic hypertension; all are better than nothing if tied to a clear referral rule. ^[8][1]
• Measure blood pressure properly: an appropriately sized cuff, correct technique and twice-daily rechecking of unexpected values prevent more harm than any guideline nuance.
• Postpartum vigilance matters most where monitoring is limited: women should be told to return urgently for severe headache, visual change, epigastric pain, vomiting or sudden swelling in the 6 weeks after birth. ^[1][2]

• Hypertension in pregnancy is 140/90 mmHg or above on two occasions at least four hours apart, and severe hypertension is 160/110 mmHg or above; the condition is present before 20 weeks in chronic hypertension and arises at or after 20 weeks in gestational hypertension. ^[2]
• Hypertensive disorders of pregnancy complicate 5 to 10% of pregnancies and cause about 14% of maternal deaths; chronic hypertension affects 0.9 to 1.5% of pregnant women. ^[8][3]
• Chronic hypertension carries roughly 25% superimposed pre-eclampsia, 28% preterm delivery, 17% fetal growth restriction and 4% perinatal death. ^[7]
• Safe drugs: labetalol, nifedipine, methyldopa, hydralazine (acute), prazosin; avoid ACE inhibitors, angiotensin receptor blockers and thiazide diuretics; stop ACE inhibitors and ARBs promptly in pregnancy. ^[1][7]
• Start or continue treatment when blood pressure is 140/90 mmHg or higher, unless sustained pressure is below 110/70 mmHg or there is symptomatic hypotension, and treat severe pressure as an emergency. ^[1]
• Targets differ by guideline: NICE 135/85 mmHg or lower; ISSHP 110 to 140/under 85 mmHg; ACOG 120 to 160/80 to 110 mmHg; WHO above the lower limit of normal. ^[1][2][5]
• CHAP supports treating chronic hypertension at 140/90 mmHg instead of waiting for 160/110 mmHg. ^[4]
• Pre-eclampsia is hypertension after 20 weeks plus proteinuria or other maternal or uteroplacental end-organ evidence; NICE and ISSHP also count fetal growth restriction or abnormal umbilical Doppler, but ACOG does not. ^[2][8]
• Chronic hypertension fetal scans at 28, 32 and 36 weeks; gestational hypertension scans at diagnosis and every 2 to 4 weeks. ^[1]
• Birth is not brought forward before 37 weeks unless severe features or uncontrolled hypertension at 160/110 mmHg or above; from 37 weeks birth is initiated within 24 to 48 hours in pre-eclampsia. ^[1]
• Postpartum monitoring is as important as antenatal monitoring: daily for 2 days then days 3 to 5, with a 6 to 8 week review and long-term cardiovascular follow-up. ^[1][7]
• Aspirin (75 to 150 mg from 12 weeks per NICE; 150 mg from 12 to 16 weeks per AHA/Australian) reduces pre-eclampsia in high-risk women, but diuretics, antioxidants and salt restriction alone do not. ^[1][7]
• In low-resource settings the priorities are one written protocol, oral antihypertensives, magnesium sulfate, basic blood pressure technique and postpartum danger-symptom education. ^[8][2]

Gestational and chronic hypertension in pregnancy; hypertensive disorders of pregnancy; pre-eclampsia and eclampsia; antepartum fetal surveillance; hypertension; stroke in pregnancy; HELLP syndrome (all as MedGrasp obstetrics and cardiology topics, linked as plain text when their verified pages are available).

• If already on a safe drug, continue it unless the sustained systolic pressure is below 110 mmHg, or the diastolic below 70 mmHg, or the woman has symptomatic hypotension. A first-trimester physiological fall often allows dose reduction. ^[1]
• If not on treatment, offer antihypertensive therapy when sustained blood pressure is 140/90 mmHg or higher, rather than waiting for severe hypertension. ^[1] This is the change driven by the CHAP study. ^[4]
• Treat urgently at once when pressure reaches 160/110 mmHg.
• Target while on treatment: NICE aims for 135/85 mmHg or lower; other guidelines differ (see the targets table below). ^[1][2]
• Lifestyle advice as for non-pregnant adults: weight, exercise, healthy eating and reducing salt; the NICE hypertension guideline applies in pregnancy too. ^[1]
• Aspirin (NICE: 75 to 150 mg daily from 12 weeks until birth; AHA and Australian protocols: 150 mg daily from 12 to 16 weeks until 36 weeks) reduces pre-eclampsia, preterm birth and stillbirth in women at risk; the start and stop windows differ by guideline. ^[1][7]
• PLGF-based testing between 20 and 36 weeks plus 6 days to help rule out pre-eclampsia when suspected. ^[1]