1. Hypertension in Pregnancy
Dr. MSc. Raul Hernandez Canete

2. Hypertension Sustained BP elevation of 140/90 or greater
Proper cuff size
Measurement taken while seated
Use 5th Korotkoff sound
30/15 increase in BP over baseline levels

3. Classification of Hypertension in Pregnancy
Chronic Hypertension
Pregnancy-Induced Hypertension
Preeclampsia, Eclampsia
Chronic Hypertension with superimposed preeclampsia.
HELLP syndrome

4. Pregnancy-Induced Hypertension
Suggests a disorder of blood pressure arising because of the presence of pregnancy
The condition is classified into four main groups depending on the cardiovascular, renal, cerebral and hepatic manifestations:
- Gestational Hypertension
- Pre-eclampsia
- Eclampsia
- HELLP syndrome

5. Etiology and Pathophysiology
Exact etiology and pathophysiology: unclear
The incidence of hypertensive disorder in pregnancy is 8-10%.
They are recognized predisposing factors.

6. Recognized predisposing factors:
First pregnancy
Family history
Extremes of maternal age
Medical:
- pre-existing hypertension
- congenital thrombophilia
- systemic lupus erythematosus
- diabetes mellitus
Obstetrics:
- multiple pregnancy
- hydatidiform mole
- hydrops fetalis

7. “Disease of theories”
It is likely that inadequate placental perfusion resulting from inadequate placental invasion precipitates the release of some form of chemical trigger which, in susceptible mothers, leads to endothelial damage, metabolic changes and a form of inflammatory response

8. Placental invasion: In pre-eclampsia adequate trophoblastic invasion does not seem to occur (or limited to the decidual portion of the vessels)>>> failure to convert the spiral arteries to low resistance and high flow system>>>uteroplacental hypoperfusion results in the release of a potent circulating factor>>widespread activation of endothelial cells:
- Decreased production of prostacyclin (vasodilator)
- platelet activation
- increased production of thromboxane A2 (vasoconstrictor)
- increased the sensitivity to vasoconstrictors such as angiotensin II

9. Potential secondary effects of the metabolic, inflammatory endothelial alterations in pre-eclampsia:
CVS: Increased peripheral resistance leading to hypertension. Increased vascular permeability and reduced maternal plasma volume
Lungs: Laryngeal and pulmonary oedema
Renal: Glomerular damage leading to proteinuria, hypoproteinaemia and reduce oncotic pressure which further exacerbates the hypovolaemia. May develop acute renal failure +/- cortical necrosis

10. Cont…..
Clotting: Hypercoagulability, with increased fibrin formation and increased fibrinolysis, i.e. disseminated intravascular coagulation
Liver: HELLP syndrome, Hepatic rupture
CNS: Thrombosis and fibrinoid necrosis of the cerebral arterioles. Eclampsia, cerebral hemorrhage and cerebral oedema.
Fetus: Impaired uteroplacental circulation, potentially leading to FGR, hypoxemia and IUFD, Placentae abruption.

11. Chronic Hypertension Pre-existing hypertension
Hypertension before 20 weeks of gestation
If hypertension persists beyond 6 weeks postpartum

12. Preeclampsia Hypertension after 20 weeks of gestation
Proteinuria- 300mg
Edema

13. Preeclampsia Hypertension after 20 weeks of gestation
Proteinuria- 300mg
Edema
BP > 160 systolic or >110 diastolic
2grams of protein in 24 hour urine
Oliguria
Cerebral of visual disturbances
Pulmonary edema or cyanosis
Epigastric or RUQ pain
Impaired liver function
Thrombocytopenia
IUGR

14. Risk Factors FACTOR RISK RATIO Nulliparity 3:1 Age > 40
African American
1.5:1
Chronic hypertension
10:1
Renal disease
20:1
Antiphospholipid syndrome

15. Risk Factors FACTOR RISK RATIO Family history of PIH 5:1
Diabetes mellitus
2:1
Twin gestation
4:1

16. Severe Preeclampsia BP > 160-180 systolic or 110 diastolic
Proteinuria > 2 g per day
Pulmonary edema
Oliguria
Elevated liver enzymes
Low platelets
Growth restriction
Decreased AFV
Headache
Epigastric pain

17. Pregnancy-Induced Hypertension
After 20 weeks of gestation
No proteinuria
Not associated with significant maternal morbidity and perinatal mortality

18. Management The ultimate cure is delivery Assess gestational age
Assess cervix
Fetal well-being
Laboratory assessment
Rule out severe disease!!

19. Gestational HTN at Term
Delivery is always a reasonable option if term
If cervix is unfavorable and maternal disease is mild, expectant management with close observation is possible

20. Mild Gestational HTN not at Term
Rule out severe disease
Conservative management
Serial labs
Antenatal fetal surveillance
Outpatient versus inpatient

21. Indications for Delivery
Worsening BP
Nonreassuring fetal condition
Development of severe PIH
Fetal lung maturity
Favorable cervix

22. Unfavorable Cervix No contraindication to prostaglandin agents
If < 32 weeks, consider cesarean
When favorable, oxytocin

23. Hypertensive Emergencies
Fetal monitoring
IV access
IV hydration
The reason to treat is maternal, not fetal
May require ICU

24. Criteria for Treatment
Diastolic BP >
Systolic BP > 200
Avoid rapid reduction in BP
Do not attempt to normalize BP
Goal is DBP < 105 not < 90
May precipitate fetal distress

25. Key Steps Using Vasodilators
Avoid multiple doses in rapid succession
Allow time for drug to work
Maintain LLD position
Avoid over treatment

26. Acute Medical Therapy Hydralazine Labetalol Nifedipine Nitroprusside
Diazoxide
Clonidine

27. Hydralazine Dose: 5-10 mg every 20 minutes Onset: 10-20 minutes
Duration: 3-8 hours
Side effects: headache, flushing, tachycardia, lupus like symptoms
Mechanism: peripheral vasodilator

28. Labetalol
Dose: 20mg, then 40, then 80 every 20 minutes, for a total of 220mg
Onset: 1-2 minutes
Duration: 6-16 hours
Side effects: hypotension
Mechanism: Alpha and Beta block

29. Nifedipine Dose: 10 mg po, not sublingual Onset: 5-10 minutes
Duration: 4-8 hours
Side effects: chest pain, headache, tachycardia
Mechanism: CA channel block

30. Seizure Prophylaxis Magnesium sulfate 4-6 g bolus 1-2 g/hour
Monitor urine output, respiratory rate and reflex
With renal dysfunction, may require a lower dose

31. Magnesium Sulfate Is not a hypotensive agent
Works as a centrally acting anticonvulsant
Also blocks neuromuscular conduction
Serum levels: 6-8 mg/dL

32. Toxicity Respiratory rate < 12 Hyporeflex Altered sensorium
Urine output < cc/hour
Antidote: 10 ml of 10% solution of calcium gluconate 1 v over 3 minutes

33. Treatment of Eclampsia
Few people die of seizures
Protect patient
Avoid insertion of airways and padded tongue blades
IV access
MGSO4 4-6 bolus, if not effective, give another 2 g

34. Alternate Anticonvulsants
Diazepam 5-10 mg IV
Sodium Amytal 100 mg IV
Pentobarbital 125 mg IV
Dilantin mg IV infusion

35. After the Seizure Assess maternal labs Fetal well-being
Effect delivery
Transport when indicated
No need for immediate cesarean delivery

36. Other Complications Pulmonary edema Oliguria Persistent hypertension
DIC

37. Pulmonary Edema Fluid overload Reduced colloid osmotic pressure
Occurs more commonly following delivery as colloid oncotic pressure drops further and fluid is mobilized

38. Treatment of Pulmonary Edema
Avoid over-hydration
Restrict fluids
Lasix mg IV
Usually no need for albumin or Hetastarch (Hespan)

39. HELLP Syndrome
He-hemolysis
EL-elevated liver enzymes
LP-low platelets

40. HELLP Syndrome Is a variant of severe preeclampsia
Platelets < 100,000
LFT’s x normal
May occur against a background of what appears to be mild disease

41. Conservative Management
Controversial
Steroids
Requires tertiary care
Must have stable labs and reassuring fetal status
May use antihypertensives

42. SUMMARY Criteria for diagnosis Laboratory and fetal assessment
Magnesium sulfate seizure prophylaxis
Timing and place of delivery