1.1 Hypertensive Disorders of Pregnancy

Classification and Diagnostic Criteria

Hypertensive disorders complicate approximately 10% of all pregnancies worldwide and remain a leading direct cause of maternal and perinatal morbidity and mortality. In accordance with American College of Obstetricians and Gynecologists (ACOG) and Association of Women's Health, Obstetric and Neonatal Nurses (AWHONN) standards, hypertensive disorders of pregnancy are classified into six distinct clinical categories:

1. Chronic Hypertension: Systolic blood pressure (SBP) ≥140 mmHg or diastolic blood pressure (DBP) ≥90 mmHg that predates pregnancy or is diagnosed before 20 weeks of gestation, or persists longer than 12 weeks postpartum.
2. Gestational Hypertension: New-onset SBP ≥140 mmHg or DBP ≥90 mmHg on two occasions at least 4 hours apart after 20 weeks of gestation in a previously normotensive woman, without proteinuria and without any systemic severe features. Blood pressure normalizes by 12 weeks postpartum.
3. Preeclampsia without Severe Features: New-onset hypertension (SBP ≥140 mmHg or DBP ≥90 mmHg on two occasions at least 4 hours apart after 20 weeks of gestation) combined with proteinuria (≥300 mg per 24-hour urine collection, urine protein-to-creatinine [UPC] ratio ≥0.3 mg/mg, or dipstick reading of 2+ if quantitative methods are unavailable).
4. Preeclampsia with Severe Features: Preeclampsia presenting with severe-range blood pressures (SBP ≥160 mmHg or DBP ≥110 mmHg on two occasions at least 15 minutes apart) OR new-onset hypertension accompanied by any of the following systemic end-organ dysfunctions, regardless of proteinuria status:
   • Thrombocytopenia: Platelet count <100,000/μL
   • Renal Insufficiency: Serum creatinine >1.1 mg/dL or a doubling of serum creatinine in the absence of underlying renal disease
   • Impaired Liver Function: Serum transaminases (AST or ALT) elevated to twice the upper limit of normal, or severe persistent right upper quadrant (RUQ) or epigastric pain unresponsive to medication and not accounted for by alternative diagnoses
   • Pulmonary Edema: Acute fluid extravasation into alveolar spaces resulting in dyspnea, tachypnea, rales, and oxygen desaturation
   • New-Onset Cerebral or Visual Disturbances: Intractable, throbbing frontal/occipital headache unresponsive to acetaminophen, photopsia, scotomata, cortical blindness, retinal vasospasm, or altered mental status
5. Eclampsia: The occurrence of new-onset grand mal (generalized tonic-clonic) seizures or coma in a patient with preeclampsia, unexplained by other neurologic pathology such as epilepsy, intracranial hemorrhage, or metabolic derangements.
6. Chronic Hypertension with Superimposed Preeclampsia: Development of new-onset proteinuria (≥300 mg/24h or UPC ≥0.3) after 20 weeks in a woman with chronic hypertension, or a sudden, severe escalation in baseline blood pressures, thrombocytopenia (<100,000/μL), transaminitis, or other end-organ features in a patient with pre-existing hypertension.

+-------------------------------------------------------------------------------------------------------------------+
|                                 DIAGNOSTIC ALGORITHM: HYPERTENSION AFTER 20 WEEKS                                 |
+-------------------------------------------------------------------------------------------------------------------+
                                                         |
                                         [ BP ≥140/90 mmHg after 20 weeks ]
                                                         |
                         +-------------------------------+-------------------------------+
                         |                                                               |
                [ Proteinuria Present ]                                        [ Proteinuria Absent ]
             (≥300mg/24h, UPC ≥0.3, or 2+)                                               |
                         |                                           +-------------------+-------------------+
                         |                                           |                                       |
       +-----------------+-----------------+               [ Any Severe Feature? ]            [ No Severe Features ]
       |                                   |               (Platelets <100k, Cr >1.1,                 |
[ BP <160/110 & ]                  [ BP ≥160/110 or ]       AST/ALT 2x, Pulm Edema,          [ Gestational HTN ]
[ No Severe Feat ]                 [ Any Severe Feat]       Cerebral/Visual symptoms)        (Deliver at 37 0/7 wk)
       |                                   |                         |                                       |
[ Preeclampsia ]                   [ Preeclampsia w/ ]               +-------------------+                   |
[ w/o Severe Feat]                 [ Severe Features ]                                   |                   |
(Deliver at 37 0/7)                (Deliver at 34 0/7)                         [ Preeclampsia w/ ]           |
                                                                               [ Severe Features ]           |

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Pathophysiology of Preeclampsia

The fundamental etiology of preeclampsia originates in abnormal placental development during early gestation. In normal placentation, invasive extravillous cytotrophoblasts remodel the maternal uterine spiral arteries, transforming narrow, muscular, high-resistance vessels into wide, non-muscular, low-resistance conduits capable of accommodating a 10-fold increase in uteroplacental blood flow.

In preeclampsia, this trophoblastic invasion is shallow and incomplete, leaving the spiral arteries narrow, hyper-reactive, and with high vascular resistance. As pregnancy progresses, the increased metabolic demand of the growing fetus creates localized placental ischemia and hypoxia. In response, the underperfused placenta releases excess anti-angiogenic factors into maternal circulation, primarily:

• Soluble fms-like tyrosine kinase-1 (sFlt-1): Antagonizes Vascular Endothelial Growth Factor (VEGF) and Placental Growth Factor (PlGF).
• Soluble Endoglin (sEng): Inhibits Transforming Growth Factor-beta (TGF-β).

These circulating anti-angiogenic factors cause widespread maternal vascular endothelial cell dysfunction, triggering systemic vasospasm, capillary leakage, loss of vascular tone, activation of the coagulation cascade, and intravascular volume contraction. End-organ perfusion drops across every major organ system: cerebral edema/ischemia causes headaches and hyperreflexia; renal endotheliosis impairs glomerular filtration rate (GFR); hepatic sinusoidal fibrin deposition causes transaminitis and stretch of Glisson's capsule; and microvascular pulmonary capillary leak leads to acute pulmonary edema.

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Emergency Management of Acute Severe Hypertension

Acute onset of severe hypertension—defined as SBP ≥160 mmHg or DBP ≥110 mmHg confirmed on repeat measurement within 15 minutes—is an obstetric hypertensive emergency. Sustained severe-range blood pressures dramatically increase the risk of maternal hemorrhagic stroke, intracranial hemorrhage, placental abruption, and congestive heart failure. Treatment must be initiated within 30 to 60 minutes of confirmation.

The therapeutic target is NOT a normotensive blood pressure, but rather reduction to a safe range (SBP 140–150 mmHg and DBP 90–100 mmHg). Rapid over-correction below this range causes acute uteroplacental hypoperfusion, compromising fetal oxygenation and inducing severe fetal heart rate decelerations.

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|                         FIRST-LINE ANTIHYPERTENSIVE PROTOCOL FOR ACUTE SEVERE HYPERTENSION                        |
+-------------------------------------------------------------------------------------------------------------------+
                                                         |
                                       [ Severe BP Confirmed (≥160/110 mmHg) ]
                                                         |
                 +---------------------------------------+---------------------------------------+
                 |                                       |                                       |
       [ IV LABETALOL ALGORITHM ]              [ IV HYDRALAZINE ALGORITHM ]            [ ORAL NIFEDIPINE ALGORITHM ]
                 |                                       |                                       |
       Initial: 20 mg IV over 2 min            Initial: 5 or 10 mg IV over 2 min       Initial: 10 or 20 mg PO
       Recheck BP in 10 min                    Recheck BP in 20 min                    (Immediate release; swallow intact)
                 |                                       |                             Recheck BP in 20 min
       If BP ≥160/110 at 10 min:               If BP ≥160/110 at 20 min:                 |
       Give 40 mg IV over 2 min                Give 10 mg IV over 2 min                If BP ≥160/110 at 20 min:
       Recheck BP in 10 min                    Recheck BP in 20 min                    Give 20 mg PO
                 |                                       |                             Recheck BP in 20 min
       If BP ≥160/110 at 10 min:               If BP ≥160/110 at 20 min:                 |
       Give 80 mg IV over 2 min                Give 20 mg IV (or switch agent)         If BP ≥160/110 at 20 min:
       (Max cumulative dose: 220-300 mg)       (Max cumulative IV dose: 20-30 mg)      Give 20 mg PO
                 |                                       |                                       |
                 +---------------------------------------+---------------------------------------+
                                                         |
                                 [ If BP Remains Severe: Switch to Secondary Agent ]
                                 [ (e.g., Nicardipine IV infusion: 5 mg/hr, max 15 mg/hr) ]

Clinical Pharmacology of First-Line Agents

• Labetalol (Trandate): Combined non-selective beta-blocker and selective alpha-1 blocker (3:1 ratio IV). Decreases systemic vascular resistance without reducing maternal cardiac output or uteroplacental blood flow.
  • Dosing: 20 mg IV over 2 minutes. If severe BP persists at 10 minutes, administer 40 mg IV; if still severe at 10 minutes, administer 80 mg IV; if still severe, administer an additional 80 mg IV (maximum single dose 80 mg, maximum cumulative dose 220–300 mg).
  • Contraindications & Cautions: Avoid in patients with active asthma, reactive airway disease, severe bradycardia (maternal HR <60 bpm), second- or third-degree heart block, or uncompensated congestive heart failure.
• Hydralazine (Apresoline): Direct peripheral arteriolar vasodilator. Reduces afterload by relaxing vascular smooth muscle.
  • Dosing: 5 mg or 10 mg IV over 2 minutes. If severe BP persists at 20 minutes, administer 10 mg IV. If still severe at 20 minutes, switch to labetalol or oral nifedipine.
  • Clinical Considerations: Slower onset of action (10–20 minutes) compared to labetalol. Associated with reflex maternal tachycardia, headaches, flushing, and unpredictable precipitous maternal hypotension.
• Nifedipine (Procardia): Dihydropyridine calcium channel blocker that inhibits calcium influx into vascular smooth muscle, causing peripheral vasodilation.
  • Dosing: 10 mg or 20 mg oral capsule swallowed whole (never punctured, crushed, or administered sublingually due to risk of sudden severe hypotension). If severe BP persists at 20 minutes, administer 20 mg oral; if still severe at 20 minutes, administer 20 mg oral.
  • Clinical Considerations: Excellent first-line option when IV access is not yet established. Rapid gastrointestinal absorption produces BP reduction within 15–20 minutes.

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Magnesium Sulfate Seizure Prophylaxis and Toxicity Management

Magnesium sulfate ($MgSO_4$) is the international standard of care and primary pharmacologic agent for the prevention and treatment of eclamptic seizures. It acts as a central nervous system depressant, blocks peripheral neuromuscular transmission by reducing acetylcholine release at the motor endplate, and promotes cerebral vasodilation by blocking voltage-gated calcium channels.

Critical Principle: Magnesium sulfate is an anticonvulsant and neuroprotective agent; it is NOT an antihypertensive drug. It must never be used to lower blood pressure, and antihypertensive agents must never be withheld in the expectation that magnesium will correct severe hypertension.

Administration Protocols

• Intravenous Loading Dose: 4 to 6 g of magnesium sulfate diluted in 100 mL of 5% Dextrose in Water ($D_5W$) or 0.9% Normal Saline administered via an automated smart pump piggybacked into the primary line over 20 to 30 minutes.
• Intravenous Maintenance Infusion: Continuous infusion of 1 to 2 g/hour (prepared as 20 g in 500 mL or 40 g in 1000 mL crystalloid, running at 25–50 mL/hr) continued throughout labor and for at least 24 hours postpartum (or 24 hours after the last convulsion in eclampsia).
• Intramuscular Regimen (Z-track in transport or resource-limited settings): 10 g loading dose administered as two 5 g deep IM injections (50% solution) into each upper outer buttock quadrant, followed by 5 g IM every 4 hours.

Therapeutic Monitoring and Inpatient Nursing Protocols

Because magnesium is excreted exclusively by the kidneys, any reduction in renal perfusion rapidly leads to drug accumulation and life-threatening toxicity. The inpatient obstetric nurse must maintain rigorous, time-sensitive bedside assessments:

1. Deep Tendon Reflexes (DTRs): Assessed every 1 hour during active titration, and at least every 2 hours during stable maintenance. Patellar reflexes (or biceps reflexes if epidural is dense) must be present (≥1+).
2. Respiratory Rate: Monitored continuously with pulse oximetry and manual counting every 1 hour. Must remain ≥12 breaths per minute with depth and symmetry.
3. Urine Output: Measured hourly via an indwelling Foley catheter with an attached urometer. Minimum safe threshold is ≥30 mL/hour (or ≥0.5 mL/kg/hour). If output drops below 30 mL/hr for 2 consecutive hours, notify the provider immediately and obtain a stat serum magnesium level.
4. Total Fluid Restriction: To prevent iatrogenic pulmonary edema in the presence of capillary leak, total maternal fluid intake (including all IV piggybacks, maintenance fluids, and oral sips) must be restricted to 80 to 125 mL/hour (or a strict maximum of 2,000 mL per 24 hours).
5. Therapeutic Serum Levels: Routine serum blood draws are not necessary in clinically stable patients with normal renal function and brisk reflexes. Serum magnesium levels should be drawn in patients with renal impairment (creatinine >1.1 mg/dL), oliguria (<30 mL/hr), absent DTRs, or worsening clinical status. Therapeutic range: 4.8 to 8.4 mg/dL (4.0 to 7.0 mEq/L or 2.0 to 3.5 mmol/L).

+-------------------------------------------------------------------------------------------------------------------+
|                                 MAGNESIUM SULFATE SERUM CONCENTRATIONS & TOXICITY                                 |
+-------------------------------------------------------------------------------------------------------------------+
  Serum Level (mg/dL)   Clinical Findings / Physiologic Manifestation
  -------------------   ---------------------------------------------------------------------------------------------
  1.5 - 2.5 mg/dL       Normal baseline physiological serum magnesium level in non-pregnant adult
  4.8 - 8.4 mg/dL       ★ THERAPEUTIC RANGE FOR SEIZURE PROPHYLAXIS (flushing, warmth, diaphoresis, nausea common)
  8.0 - 10.0 mg/dL      Loss of Deep Tendon Reflexes (Patellar / Brachial hypoactive to absent) [Early Warning Sign]
  10.0 - 12.0 mg/dL     Respiratory Depression (Bradypnea <12 breaths/min), somnolence, slurred speech
  12.0 - 15.0 mg/dL     Muscular Paralysis, severe respiratory arrest, marked hypoxemia
  >15.0 - 20.0 mg/dL    Cardiac Conduction Defects, prolonged PR/QRS intervals, complete asystole, cardiac arrest
+-------------------------------------------------------------------------------------------------------------------+

Emergency Management of Magnesium Toxicity

If magnesium toxicity is suspected (absent DTRs, respiratory rate <12/min, profound lethargy, or acute desaturation):

1. STOP THE MAGNESIUM SULFATE INFUSION IMMEDIATELY. Disconnect the piggyback at the closest hub to prevent residual delivery.
2. Call for Immediate Emergency Assistance and notify the obstetrician, anesthesiologist, and rapid response team.
3. Administer 100% Oxygen via non-rebreather mask at 10–15 L/min; prepare for immediate bag-valve-mask ventilation or endotracheal intubation if respirations are inadequate.
4. Administer the Specific Antidote:
   • Calcium Gluconate 10% solution: Administer 10 mL (1 g) IV push over 3 to 5 minutes.
   • (Alternative: Calcium Chloride 10% solution: 5–10 mL [0.5–1 g] IV over 5 minutes; note that calcium chloride is a vesicant and requires verified central or large-bore peripheral access).
5. Obtain Stat Serum Magnesium Level, arterial blood gas, and serum electrolytes.
6. Maintain Continuous Cardiac and Fetal Monitoring until maternal cardiopulmonary stability and neuromuscular function are fully restored.

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Management of Eclamptic Seizures

Eclampsia occurs in approximately 1 in 200 preeclamptic patients and can develop antepartum (38%), intrapartum (18%), or postpartum (44%, predominantly within 48 hours). The primary nursing responsibilities during an active convulsion are maternal airway protection, prevention of injury, and rapid cessation of seizure activity:

• During the Seizure:
  • Call for help and emergency obstetric response.
  • Place patient in a lateral decubitus position to promote uteroplacental perfusion and reduce aspiration risk.
  • Protect the patient from physical trauma (raise padded side rails, do not restrain limbs, do not force any object into the mouth).
  • Suction oral secretions and vomit; apply non-rebreather oxygen mask at 10–15 L/min.
• Pharmacologic Control:
  • If the patient is NOT currently on magnesium sulfate: Administer 4 to 6 g IV loading dose over 15 to 20 minutes, followed by 2 g/hour continuous maintenance.
  • If the patient is ALREADY receiving magnesium infusion: Administer a re-bolus of 2 g IV over 3 to 5 minutes.
  • If seizures are refractory to 6 g + 2 g magnesium: Administer second-line anticonvulsants (Lorazepam 2–4 mg IV over 2 minutes, Diazepam 5–10 mg IV, or Midazolam 1–2 mg IV).
• Fetal Assessment Post-Seizure: Transient fetal bradycardia (often 60–90 bpm for 3–5 minutes) and compensatory rebound tachycardia with loss of variability or recurrent late decelerations are expected during and immediately following an eclamptic seizure due to intense uterine hypertonus and maternal hypoxia. Immediate emergency cesarean delivery is contraindicated during the seizure and immediate postictal period. Allow maternal stabilization, intrauterine resuscitation, and maternal re-oxygenation for 10–15 minutes, which will typically restore normal fetal baseline and variability.

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Delivery Timing Guidelines

Delivery is the definitive cure for preeclampsia, but must be balanced against gestational age and neonatal risks of prematurity. In accordance with current ACOG and SMFM guidelines:

• Gestational Hypertension or Preeclampsia without Severe Features: Planned delivery is recommended at 37 0/7 weeks of gestation (or upon diagnosis if diagnosed at ≥37 weeks).
• Preeclampsia with Severe Features: Planned delivery is recommended at 34 0/7 weeks of gestation after maternal stabilization and a course of antenatal corticosteroids (Betamethasone 12 mg IM q24h x 2 doses).
• Immediate Delivery Regardless of Gestational Age: Indicated when maternal or fetal stability is compromised, including: eclampsia, pulmonary edema, disseminated intravascular coagulation (DIC), refractory severe hypertension, placental abruption, non-reassuring fetal status (Category III FHR tracing), or fetal demise.
• Mode of Delivery: Vaginal delivery is preferred unless an obstetric indication for cesarean delivery exists. Induction of labor with cervical ripening agents is safe and appropriate.