Pregnancy Associated Hypertension

Incidence and Definitions

Occurs in ~ 10% of pregnancies and is a major cause of maternal mortality. PIH includes gestational hypertension, preeclampsia, and eclampsia (preeclampsia + seizures). Characterized by BP > 140/90, and proteinuria (> 0.3 g/day). An associated condition is HELLP syndrome (hemolysis, elevated liver enzymes, low platelets). Death, if it occurs, is due to CHF, MI, coagulopathies, or cerebral hemorrhage. There is a bi-modal age distribution, with the disease occuring primarily in younger and older parturients.

All that is needed to diagnose preeclampsia is HTN and proteinuria. “Severe” preeclampsia occurs if BP > 160/110, proteinuria > 5 g/day, or there is evidence of end organ failure (oliguria, cerebral/visual disturbances, pulmonary edema, abdominal pain, IUGR, seizures, etc.).

The exact disease mechanism is unknown, though it is thought to be caused by excessive placental thromboxane production (in normal pregnancies, thromboxane:prostacyclin are 1:1, whereas in Preeclampsia the ratio is 7:1 [Wang Y et al. Am J Obstet Gynecol 167: 946, 1992]). Intense CNS vasoconstriction may be a common underlying pathophysiological aberration in these patients – postmortem exams have revealed areas of hemorrhagic necrosis.

Pregnancy Induced Hypertension

  • Pre-Eclampsia
    • BP > 140/90
    • Proteinuria (> 0.3 g/day)
    • Edema
    • Headache
  • HELLP syndrome
    • Hemolysis
    • Elevated liver enzymes
    • Low platelets
  • Eclampsia
    • Seizures

Causes of death in PIH

  • CHF
  • MI
  • Coagulopathies
  • Cerebral hemorrhage
  • Seizures

Pathophysiological Derangements

Volume Status

Preeclamptic women are hypovolemic, and there is an inverse relationship between MAP and CVP [Joyce TH et al. Anesthesiology 51: S297, 1979]. Preeclamptic women seem to respond well to volume expansion, with ~ 30% increase in CI reported by Groenendijk’s study of 10 preeclamptic non-laboring women. [Groenendijk R et al. Am J Obstet Gynecol 150: 232, 1984]


Platelets usually fall under 150,000/mm3, although the use of steroids to prevent fetal lung immaturity has been shown to increase platelet counts by ~ 25,000/mm3. [O’Brien JM et al. Am J Obstet Gynecol 183: 921, 2000]



Definitive treatment is delivery. Magnesium and antihypertensives are also used.


Magnesium can decrease CNS irritability (raises seizure threshold), decrease activity at the neuromuscular junction (weakness), and relax uterine and vascular smooth muscle (increased uterine blood flow). Usually given as 4g load over 5 minutes, followed by 1-2 g/hr. Note that magnesium crosses the placenta, however there is minimal correlation between umbilical cord magnesium levels and the incidence of low APGAR scores.

Therapeutic range is 4-6 mEq/L – in excess, one finds loss of DTRs, skeletal weakness, hypoventilation, and cardiac arrest (IV calcium is the antidote). Because Mg inhibits ACh release and many preeclamptics have decreased plasma cholinesterase levels, NMBDs must be used very carefully in these patients. Sedatives and opiates must also be decreased.

A Cochrane database review of magnesium sulfate and/or anticonvulsants for the prevention of eclampsia found six trials including 11,444 women which compared magnesium sulphate to placebo or to no anticonvulsant. Magnesium sulfate reduced the risk of eclampsia (RR 0.41, 95% CI 0.29 to 0.58) and Risk of placental abruption (RR 0.64, 95% CI 0.50 to 0.83), however there was no statistically-significant effect on maternal death (RR 0.54, 95% CI 0.26 to 1.10), serious maternal morbidity (RR 1.08, 95% CI 0.89 to 1.32), or risk of stillbirth or neonatal death (RR 1.04, 95% CI 0.93 to 1.15) [Duley L et al. Cochrane Database Syst Rev. 2003;(2):CD000025]. The most recent randomized controlled trial on the subject (post-Cochrane) compared 3375 women and found a non-significant change in the risk of maternal death (RR 0.84, 95% CI 0.60-1.18) [Magpie Trial Follow-Up Study Collaborative Group. BJOG 114: 300, 2007], as well as a non-significant difference in death/disability of the child (RR 1.06, 95% CI 0.90-1.25). [Magpie Trial Follow-Up Study Collaborative Group. BJOG 114: 289, 2007]


  • Goal = 4-6 mEq/L (1-2 g/h maintenance)
  • Excess:
    • Decreased DTR
    • Weakness
    • Hypoventilation
    • Cardiac Arrest
  • Antidote: IV calcium
  • Anesthetic Issues:
    • Use NMBD sparingly
    • Exaggerated hypotensive response to regional
    • Reduce doses of sedatives and opiates


Antihypertensives are normally started when DBP exceeds 110 mm Hg. Hydralazine and labetalol are the most commonly used – hydralazine, a vasodilator, is alleged to increase uterine placental flow [Stoelting RK. Basics of Anesthesia, 5th ed. Elsevier (China), p. 494, 2007], although there is disagreement about this – some sources suggest that as the placenta is maximally dilated, any changes in MAP will reduce blood flow [Lumbers ER. Clin Exp Pharmacol Physiol 24: 864, 1997]. Animal data (ewes) suggests that even when hydralazine lowers blood pressure by 31%, placental blood flow can be maintained (and total uteroplacental blood flow can actually increase by 24%) [Pedron SL et al. Am J Obstet Gynecol 167: 1672, 1992]. Two separate human Doppler studies have suggested that hydralazine has no effect on placental blood flow velocities [Gudmundsson S et al. Acta Obstet Gynecol Scand 74: 415, 1995; Duggan PM et al. Aust N Z J Obstet Gynaecol 32: 335, 1992]. Animal studies (baboons) suggest that labetalol at doses of 1 mg/kg or more reduces uterine blood flow, although 0.5 mg/kg did not. [Morgan MA et al. Am J Obstet Gynecol 168: 1574, 1993]

Anesthetic/Analgesic Management

Prior to placing an epidural in severely pre-eclamptic patient (which is otherwise an appropriate modality), consider performing coagulation studies. Additionally, titrate carefully the dose of EPH of PHE, as these women may be hypersensitive to adrenergic agents.

If general anesthesia and endotracheal intubation are required, keep in mind that difficult airways are more common in the preeclamptic patient due to increased airway edema and also due to coexisting conditions that can be associated with preeclampsia, e.g., obesity [Stoelting RK. Basics of Anesthesia, 5th ed. Elsevier (China), p. 495, 2007]. Also keep in mind that sympathetic responses to DL will be exaggerated (consider 1-2 ucg/kg nitroglycerin prophylactically), and that magnesium prolongs the effect of NMBDs and potential for respiratory depression.