Chronic Hypertension in Pregnancy

• Impaired endothelial function and vasodilatory capacity: Endothelial dysfunction in chronic hypertensive patients impairs synthesis and action of nitric oxide (NO) and prostacyclin, critical vasodilators essential for pregnancy-mediated vascular adaptation. This prevents the normal second and third trimester BP reduction, leaving baseline hypertension unchanged or worsening.

• Placental ischemia and abnormal trophoblastic invasion: Chronic hypertension is associated with inadequate remodeling of spiral arteries by cytotrophoblasts. The placenta develops in a relatively hypoxic, high-resistance state. This predisposes to superimposed preeclampsia when additional placental insufficiency develops, triggering release of soluble fms-like tyrosine kinase-1 (sFlt-1) and other antiangiogenic factors that amplify endothelial dysfunction and proteinuria.

• Increased cardiovascular reactivity and sympathetic tone: Chronic hypertensive patients demonstrate heightened response to vasoconstrictive stimuli (angiotensin II, norepinephrine) and impaired baroreceptor sensitivity. Pregnancy-associated expansion of plasma volume may trigger compensatory sympathetic activation and renin-angiotensin-aldosterone system (RAAS) engagement, paradoxically increasing BP despite normal pregnancy-related vasodilation in other vascular beds.

• Primary (essential) hypertension: Accounts for 80-90% of chronic hypertension in pregnancy; typically develops gradually over decades with multifactorial inheritance involving gene-environment interactions affecting sodium handling, RAAS, and vascular tone regulation.

• Secondary hypertension:
• Chronic kidney disease (most common secondary cause in pregnancy; diabetes, glomerulonephritis, polycystic kidney disease)
• Primary aldosteronism (hypokalemia, metabolic alkalosis; screening with aldosterone-to-renin ratio)
• Renovascular disease (fibromuscular dysplasia in younger women; atherosclerotic disease in older women)
• Pheochromocytoma (paroxysmal hypertension, palpitations, diaphoresis; plasma metanephrines, imaging)
• Hyperthyroidism (tachycardia, heat intolerance, thyroid peroxidase antibodies)
• Obstructive sleep apnea (daytime somnolence, witnessed apneas, Epworth scale)

• Risk factors for adverse pregnancy outcomes:
• Maternal age >35 years
• Preexisting target organ damage (left ventricular hypertrophy on ECG/echo, proteinuria, elevated creatinine)
• Poorly controlled BP at conception or early pregnancy (SBP >160 mmHg)
• Prior hypertensive complication or cardiovascular event
• African American ethnicity (higher baseline risk)
• Multiparity (paradoxically increases risk in hypertensive women)

• Asymptomatic (most common): Normal prenatal visits with elevated BP readings; discovered incidentally during routine care.

• Symptomatic from sustained hypertension:
• Headache (occipital or frontal; persistent quality)
• Visual disturbances (scotomata, photopsia, blurred vision)
• Dyspnea on exertion or orthopnea (if left ventricular dysfunction present)
• Chest discomfort or palpitations
• Nausea (may herald progression to preeclampsia)

• Physical examination findings:
• Elevated BP (≥140/90 mmHg documented on ≥2 separate occasions, ≥4 hours apart); compare to baseline measurements if available
• Left ventricular heave (sustained apical impulse, indicator of LVH)
• S4 gallop (atrial kick against stiff ventricle; sign of LV diastolic dysfunction)
• Retinal changes on fundoscopy (flame hemorrhages, cotton-wool spots, papilledema indicate hypertensive retinopathy; presence confirms target organ damage)
• Edema (peripheral or facial; must distinguish from preeclampsia-associated edema)
• Abdominal tenderness or right upper quadrant pain (if hepatic involvement or HELLP syndrome develops)

• Symptoms concerning for superimposed preeclampsia (requires urgent evaluation):
• Severe persistent headache unresponsive to acetaminophen
• Epigastric or right upper quadrant pain
• Visual disturbances appearing acutely
• Sudden-onset dyspnea
• Altered mental status or confusion

• BP measurement and timing:
• Confirmed elevation ≥140/90 mmHg documented on ≥2 separate occasions, ≥4 hours apart
• Documented before 20 weeks' gestation (or ideally before pregnancy)
• OR persisting >12 weeks postpartum (distinguishes from gestational hypertension, which resolves within 12 weeks postpartum)
• Proper technique: seated, feet flat, arm at heart level after 5 minutes rest; use appropriate cuff size

• Baseline evaluation and risk stratification (recommended at first prenatal visit):
• Serum creatinine and electrolytes: Assess renal function baseline; elevated creatinine (>1.1 mg/dL) indicates preexisting renal disease and increases preeclampsia risk
• Urinalysis and 24-hour urine protein (or urine protein-to-creatinine ratio): Baseline proteinuria—if present, increases risk of superimposed preeclampsia; repeat at each trimester and when superimposed preeclampsia suspected
• Complete blood count: Baseline hemoglobin/hematocrit; platelet count important for HELLP diagnosis if complications develop
• Liver function tests: Baseline AST/ALT; marked elevation suggests hepatic involvement in preeclampsia
• ECG and/or echocardiography: Document presence/absence of left ventricular hypertrophy (LVH), which indicates target organ damage and higher maternal risk; LVH defined as LV mass index >110 g/m² (women) on echo

• Additional testing for secondary hypertension (if clinical suspicion):
• Renal artery duplex ultrasonography or MR angiography for renovascular disease (not CT angiography due to radiation; MRA preferred in pregnancy)
• Plasma metanephrines or 24-hour urine catecholamines if pheochromocytoma suspected (paroxysmal symptoms, severe hypertension)
• Thyroid-stimulating hormone (TSH): Screen for hyperthyroidism
• Plasma renin activity and aldosterone for primary aldosteronism (if compatible presentation)

• Fetal assessment:
• Ultrasound dating at first trimester visit (critical for distinguishing <20 vs ≥20 week onset)
• Serial growth ultrasounds (every 4 weeks starting at 24-26 weeks if risk factors present) to assess for intrauterine growth restriction (IUGR)
• Doppler studies (umbilical artery, middle cerebral artery) if IUGR suspected or in women with severe hypertension

• Diagnostic criteria summary:
• Chronic hypertension: BP ≥140/90 mmHg documented before 20 weeks OR prepregnancy
• Gestational hypertension: BP ≥140/90 mmHg first detected at ≥20 weeks, normalization within 12 weeks postpartum
• Preeclampsia superimposed on chronic hypertension: New-onset proteinuria (≥0.3 g/24h) after 20 weeks in previously non-proteinuric woman, OR sudden worsening of existing proteinuria, OR new-onset hypertensive symptoms/severe features after 20 weeks

First-Line Pharmacologic Therapy

• Methyldopa: Gold-standard agent with longest safety record; mechanism of action involves α-2 adrenergic agonism in central nervous system, reducing sympathetic outflow; dose 250-500 mg BID-TID; slower onset (4-6 hours); minimal placental transfer; no adverse fetal effects in large registries; downside is patient intolerance (sedation, fatigue, depression in some women).

• Labetalol: Preferred initial agent in modern practice; combined α and β-adrenergic antagonist (β:α blockade ratio 7:1) providing both heart rate and BP reduction; dose 200-400 mg BID-TID; rapid onset (2-4 hours); effective for both chronic control and acute BP reduction; excellent placental safety profile; minimal fetal effects; well-tolerated; becoming first-line choice at many centers.

• Nifedipine (extended-release): Long-acting calcium channel blocker; blocks L-type calcium channels in vascular smooth muscle, causing vasodilation; dose 30-60 mg daily in divided doses; effective for chronic control; no fetal adverse effects; useful for those with contraindications to β-blockers (asthma, bradycardia); avoid short-acting immediate-release formulation (risk of unpredictable absorption, reflex tachycardia).

Second-Line Agents

• Hydralazine: Direct-acting vasodilator (mechanism: increased cGMP via guanylate cyclase activation); potent agent typically reserved for acute BP reduction in labor/delivery or preeclampsia; dose 50 mg IM/IV every 4-6 hours; use caution chronically due to reflex tachycardia and potential for lupus-like syndrome with prolonged use; preferred in acute settings rather than chronic monotherapy.

• Atenolol: β-blocker with selective β1 adrenergic antagonism; reduces heart rate and contractility; dose 50-100 mg daily; some observational data suggesting possible association with IUGR (though controversial and not definitively established); generally reserved for women with specific indications (prior myocardial infarction, arrhythmias) rather than first-line chronic therapy.

• Chlorthalidone or hydrochlorothiazide: Thiazide diuretics affecting sodium reabsorption in distal convoluted tubule; less ideal in pregnancy due to volume depletion concerns and metabolic effects (hypokalemia, hyponatremia, hyperglycemia); reserve for women already on these agents prepregnancy with good prior tolerance.

Absolute Contraindications (Teratogenic)

• ACE inhibitors (e.g., lisinopril, enalapril) and angiotensin II receptor blockers (ARBs) (e.g., losartan, valsartan): Absolutely contraindicated, particularly in first trimester (association with fetal renal dysgenesis, oligohydramnios, IUGR, fetal death); if woman on these agents prepregnancy, switch immediately upon conception or positive pregnancy test.

• Atenolol: Increasingly considered relatively contraindicated in early pregnancy due to potential IUGR risk; if used, restrict to later pregnancy or specific indications with careful monitoring.

• Diuretics (chronic use): Generally avoided as monotherapy; may reduce placental perfusion via intravascular volume depletion; acceptable only if prior diuretic-dependent (e.g., systolic heart failure).

BP Targets

• Goal BP: 140-150/90-100 mmHg (less aggressive than non-pregnant hypertension targets); rationale is to reduce severe hypertension-related maternal complications while avoiding excessive lowering that compromises placental perfusion and fetal growth.

• Severe hypertension (≥160/110 mmHg): Requires acute treatment with goal to lower by no more than 10-15% in first 60 minutes; higher risk of maternal stroke, abruption, myocardial infarction, and acute kidney injury if untreated; treatment options include IV hydralazine (5 mg bolus, repeat every 20 minutes to max 20 mg), IV labetalol (10-20 mg bolus over 2 minutes, repeat every 10 minutes to max 80 mg), or oral immediate-release nifedipine (10-20 mg).

Non-Pharmacological Measures

• Lifestyle modification: Sodium restriction to 2-3 g/day, adequate hydration (2-3 L fluid daily to maintain intravascular volume), regular aerobic exercise (30 minutes most days) as tolerated in pregnancy, stress reduction, adequate sleep.

• Monitoring frequency:
• Baseline: Establish baseline BP, creatinine, proteinuria, platelet count, liver enzymes before initiating/modifying therapy
• Monthly until 28 weeks: Routine prenatal visits with BP checks
• Biweekly 28-36 weeks: Increased frequency to detect superimposed preeclampsia earlier
• Weekly ≥36 weeks: Weekly assessment until delivery; can be transitioned to twice-weekly or delivery as clinically indicated

• Patient education: Importance of medication adherence, symptoms requiring urgent evaluation (severe headache, visual changes, epigastric pain), home BP monitoring if available, dietary sodium restriction.

Delivery Planning

• Timing: Most women with well-controlled chronic hypertension can proceed with expectant management to 39 weeks; indications for earlier delivery (37-38 weeks) include poorly controlled hypertension despite medications, superimposed preeclampsia, IUGR, or other obstetric indication.

• Anesthesia considerations: Regional anesthesia (epidural) generally preferred for labor/delivery; requires platelet count ≥70,000/μL if preeclampsia concern; avoid NSAIDs postpartum.

• Postpartum BP management: Continue or reinstitute antihypertensive agents postpartum; most women require continued therapy; breastfeeding-compatible agents include methyldopa, labetalol, nifedipine (minimal passage into breast milk); coordinate with pediatrician if high-risk agents considered.

Maternal Complications

• Superimposed preeclampsia: Most common and serious complication, occurring in 25-30% of women with chronic hypertension; characterized by new-onset or worsening proteinuria after 20 weeks, new hypertensive symptoms, or laboratory/clinical severe features; managed with delivery timing based on gestational age and maternal/fetal condition; diagnosis criteria include any one of: (1) new-onset proteinuria ≥0.3 g/24h after 20 weeks in previously non-proteinuric woman, (2) sudden increase in proteinuria if preexisting kidney disease, (3) appearance of severe features (severe range BP ≥160/110, severe headache, visual disturbances, epigastric pain, pulmonary edema, oliguria, thrombocytopenia <100K, hepatic transaminase elevation ≥2× upper limit normal).

• Maternal cerebrovascular accident (stroke): Hypertensive emergencies and

What exam stems hinge on

• Treat at ≥140/90 mmHg, target <140/90 mmHg: Following the CHAP trial (2022), ACOG's 2022 practice advisory supports initiating or titrating antihypertensive therapy for chronic hypertension in pregnancy when BP is ≥140/90 mmHg, with a goal below 140/90 mmHg. Treating to this target reduced adverse pregnancy outcomes without a demonstrated increase in small-for-gestational-age birth. The older "permissive" 150/100 mmHg threshold is outdated and should not be selected on current exams.
• Low-dose aspirin is the most-tested "next best step": ACOG and the USPSTF recommend aspirin 81 mg daily, started between 12 and 28 weeks (ideally before 16 weeks) and continued to delivery. Chronic hypertension is by itself a high-risk factor — one high-risk factor is enough. Mechanism: irreversible platelet COX-1 inhibition shifts the thromboxane A2/prostacyclin balance in the underperfused placental bed.
• The teratogen question: ACE inhibitors and ARBs cause fetal renopathy — oligohydramnios, renal tubular dysgenesis, anuria, skull hypoplasia, limb contractures (Potter sequence physiology). Stop the drug and substitute labetalol, nifedipine XL, or methyldopa. Common distractor: captopril is not "safe because it is short-acting" — every ACE inhibitor is contraindicated in pregnancy; the short half-life is useful only for rapid titration in nonpregnant patients.
• Severe-range BP (≥160/110 mmHg) is an obstetric emergency: ACOG directs treatment within roughly 30–60 minutes using IV labetalol, IV hydralazine, or oral immediate-release nifedipine. Distractor to avoid: magnesium sulfate is seizure prophylaxis for preeclampsia with severe features and eclampsia — it does not lower blood pressure.
• The 20-week rule decides the diagnosis: hypertension documented before 20 weeks is chronic; new hypertension after 20 weeks is gestational. Proteinuria before 20 weeks is not a criterion for chronic hypertension — it signals baseline renal disease, which raises superimposed preeclampsia risk and makes that diagnosis harder to establish. Because the mid-pregnancy vasodilatory nadir can normalize BP in an untreated chronic hypertensive, a woman "first diagnosed" at 30 weeks who remains hypertensive beyond 12 weeks postpartum had chronic hypertension all along.
• Drug-specific buzzwords: methyldopa → positive direct Coombs test (usually without overt hemolysis), sedation, hepatitis; labetalol → avoid in asthma/heart block, watch neonatal bradycardia and hypoglycemia; atenolol → association with fetal growth restriction; hydralazine → reflex tachycardia and drug-induced lupus with chronic use.
• The association examiners love: superimposed preeclampsia complicates roughly a quarter to a third of these pregnancies, and abruptio placentae, growth restriction, and preterm delivery cluster with it.