Clinical Obstetrics: HTN Flashcards
Plasma volume / Blood volume
Normal CV Changes in Pregnancy
Increase w/ weeks gestation
Blood volume increases ~60%
Red cell mass
Normal CV Changes in Pregnancy
Increases w/ weeks gestation
Hematocrit
Normal CV Changes in Pregnancy
Decreases w/ weeks gestation
* Physiological anemia
Greater increase in plasma volume than red cell mass
Heart rate
Normal Physiological Changes in Pregnancy
Increases w/ weeks gestation
HR increases 10-15 bpm
Stroke volume
Normal Physiological Changes in Pregnancy
Increases w/ weeks gestation
Cardiac output
* Undetected heart problems may present during pregnancy due to increased demand on heart
Normal Physiological Changes in Pregnancy
Increases w/ weeks gestation
Normal CO = 5 L/min; at 20 weeks gestation = 7 L/min
Blood pressure
Normal Physiological Changes in Pregnancy
Decreases w/ weeks gestation
Systemic vascular resistance (SVR)
Normal Physiological Changes in Pregnancy
Decreases w/ week gestation
* Vasopressor (Ang II) resistance during pregnancy
* Increased endothelium-dependent factors: NO
* Upregulated by estradiol & vasodilatory prostaglandins (PGI2)
Peripheral vasodilation leads to 25-30% decrease in SVR
Hypertensive disorders of pregnancy
- Gestational HTN
- Preeclampsia
- Eclampsia
- Chronic HTN
SBP >140 or DBP >90 mm Hg
* >20 weeks gestation
* Absence of proteinuria, systemic signs/symptoms
Gestational HTN
- SBP >140 or DBP >90 mm Hg
- > 20 weeks gestation
- Proteinuria with or without signs/symptos
- Preeclampsia signs/Sx/labs w/o proteinuria
Preeclampsia
- SBP > 140 or DBP > 90
- Pregestational or <20 wks gestation
Chronic HTN
Physiological changes of pregnancy should resolve by 6 weeks postpartum
Blood Pressure
* SBP >140 mm Hg OR DBP >90 mm Hg on 2 occasions at least 4 hrs apart after 20 wks gestation in woman w/ previously normal BP
OR
* SBP >160 mm Hg OR DBP >110 mm Hg confirmed within short interval (15 min)
Proteinuria
* >300 mg per 24-hour urine collection
OR
* Protein/creatinine ratio >0.3
OR
* Dipstick reading of 2+ (used only if other quantitative methods not available)
Preeclampsia
- Nulliparity
- Multifetal gestations (i.e., twins)
- Chronic HTN
- Pregestational / gestational diabetes
- SLE
- Pregestational BMI >30
- Antiphospholipid antibody syndrome
- Maternal age >35 years
- Kidney disease
- Thrombophilia
- Assisted reproductive technology
- Obstructive sleep apnea
Risk Factors
Preeclampsia
Two-stage theory of pre-eclampsia
Etiology
- Lack of remodeling of spiral arteriole intima by cytotrophoblasts leading to less capacitance, decreased blood flow, and hypoxia
* Remodeling normally dilates spiral arterioles, results in lower resistance, greater capacitance, increased blood flow - Placental hypoxia damages syncytium
* Increased maternal oxidative stress and endothelial & immunological dysfunction leading to maternal end-organ damage
Mediators of preeclampsia
- Hypoxia results in upregulation of sFlt1
- Increased sFlt1 reduces free VEGF & PIGF
- Decreased free VEGF & PIGF results in endothelial dysfunction of maternal blood vessel
sFlt1: soluble EGF transporter
Maternal end-organ damage in preeclampsia
- HTN
- Glomerular dysfunction
- Proteinuria
- Brain & liver edema
- Coagulation abnormalities
Preeclampsia
Etiology
Vasospasm
* Uterine vessels (two-stage theory)
* Inadequate maternal vascular response to trophoblast-mediated vascular changes
* Endothelial damage
* Hemostasis
* Prostanoid balance
* PGI2:TXA2 balance shifted to favor TXA2
* TXA2 promotes: vasoconstriction; platelet aggregation
* Endothelium-derived factors
* Decreased NO in pts w/ preeclampsia resulting in vasoconstriction
* Lipid peroxide, free radicals & antioxidants
* Increase in preeclampsia resulting in vascular injury
Preeclampsia
Pathophysiology
Mediated by systemic vasospasm
* Cardiovascular effects
* Hematologic effects
* Neurologic effects
* Pulmonary effects
* Renal effects
* Fetal effects