Module 5 Flashcards
Hypertensive disorders of pregnancy
pre-existing HTN (essential vs. secondary)
gestational HTN
pre-eclampsia
severe pre-eclampsia
eclampsia
HELLP
gestational HTN
occurs after 20 weeks
1) with proteinuria (with or without adverse conditions)
2) without proteinuria (with or without adverse conditions)
pre-eclampsia
HTN + proteinuria (+1 or greater) OR end-organ dysfunction OR severe consequences (eclampsia)
RF for HTN in pregnancy
family hx
extremes of reproductive age (<20 or >35)
primigravida
multiple gestation
diabetes, renal dx, prior HTN
collagen vascular dx
no mid-trimester fall in BPO
excessive weight gain (>2 lb/week)
finger/facial edema
Patho of pre-eclampsia
poor placentation
first stage: cytotrophoblast invades endometrium & remodels spiral arteries
second stage: cytotrophoblast invades myometrium & remodels arteries –> wider, low pressure system
pre-eclampsia occurs when this remodeling does not occur. placental ischemia –> release of inflammatory cytokines/factors that get released into maternal circulation and cause endothelial dysfunction
Adverse outcomes of pre-eclampsia
vascular remodeling/endothelial vasospasm = HTN
kidney damage = proteinuria, liver damage = elevated enzymes
RBC traveling through damaged blood vessels sheared = hemolysis
clotting activated by endothelial injury/turbulent blood flow thrombocytopenia s/t systemic clotting –> DIC edema (increased capillary permeability)
eclampsia/headache/hemiplegia/visual disturbance (cerebral vasospasm)
cardiomyopathy
ARDS
Nursing mgmt of pre-eclampsia
bed rest
fetal assessment (ultrasound/nonstress test)
weight gain
blood pressure measurements
proteinuria
fetal movement
general symptoms
Severe pre-eclampsia
gestational HTN with or without proteinuria with 1+ adverse conditions
Severe pre-eclampsia adverse conditions
severe N/V
frontal headache
visual disturbance
epigastric/RUQ pain
chest pain
SOB
leukocytosis
abnormal coagulation
thrombocytopenia
increased creatinine/uric aid
increased liver enzymes (AST, ALT, LDH, bili)
decreased albumin
fetoplacental (abnormal FHR, IUGR, oligohydramnios, absent/reversed end-diastolic flow)
Maternal signs of severe pre-clampsia
DBP > 110
oliguria <500/day
pulmonary edema
suspected abruptio placenta
Maternal labs for severe pre-eclampsia
platelets <100
elevated liver enzymes (AST/ALT)
plasma albumin <18
heavy proteinuria 3+ or greater
Fetal signs of severe pre-eclampsia
IUGR
oligohydramnios
absent/reversed end diastolic flow of doppler
S/S of eclampsia
**often not observed prior to seizures
severe headache/occipital headache
brisk reflexes
visual disturbances
Severe pre-eclampsia treatment
1:1 nursing
calm, quiet environment
transfer to specialized unit
increased monitoring (HR/BP Q15min/4 hours until stabilized –> Q30min)
oral HTN medication
IV insertion
indwelling catheter (monitor output)
proteinuria testing
I&O documentation
O2 supplementation
VTE prophylaxis
seizure precautions (padded rails)
ensue calcium gluconate/maternal resuscitation equipment ready
Pharmacologic management of severe pre-eclampsia
nifedipine (CCB)
labetolol (beta blocker)
hydralazine (vasodilator)
methyldopa
Magnesium sulfate
seizure prophylaxis
Magnesium sulfate MOA
decreases CNS irritability
blocks Ach release –> blocking neuromuscular conduction
relaxes smooth muscle of uterus (competes w/ calcium)
peripheral vasodilation
increased uterine/renal perfusion
increased prostacyclin from endothelial cells (vasodilation)
reduced platelet aggregation
inhibits RAAS
Magnesium sulfate antidote
calcium gluconate IV
Magnesium sulfate side effects
flushing of skin
hypotension
metallic taste
N/V
palpitations
sweating
Magnesium sulfate toxicity
absent deep tendon reflexes
cardiac arrhythmia
CNS depression
excessive drowsiness
muscle weakness, ataxia
respiraotry depression (<12)
slurred speech
hypocalcemia + tetany (competes with calcium which is needed for muscle contraction)
Eclampsia
new onset generalized tonic-clonic seizures assoc w/ pre-eclampsia
can occur up to 24 hours postpartum
Gestational diabetes
insulin resistance –> diabetes after 20 weeks
Human placental lactogen
produced ~6-30 weeks
antagonist to insulin
increases insulin resistance
GDM & fetal development
macrosomia (>90th percentile)
hyperinsulinemia = decreased surfactant production
increased fetal BMR = fetal hypoxemia = metabolic acidosis
increased erythropoiesis = polycythemia = decreased iron for developing organs = cardiomyopathy, altered neurodevelopment, cardiac remodeling