htn disorders of pregancy Flashcards
htn impact
maternal mobility and mortality
earlier = higher risk for severe preE
gestation htn = increased r/o chronic htn later
obesity link
r/o placental abruption, preterm, IUGR
gestational htn
3BP >/= 140 or 90, after 20 wk, no proteinuria, chronic if persist 6+ week after delivery
preeclampsia
20 wk with proteinuria, mild or severe
rf: chronic htn, renal disease, DM, Rh incomp, primigravidity (1st pregnancy), fam hx, <20 yo or >40 yo, multiple gestation, IVF, new paternity
preeclampsia patho
unknown etiology
prostacyclin is a vasodilator that is decreased in preeclampsia allowing for vasoconstriction and reduces renal perfusion. decreased placental perfusion results in hypoxia
htn -> decreased placental perfusion
cell damage causes: vasoconstriction, activation of coag cascae, IV fluid redistribution
end result is decreased organ perfusion
start lowdose aspirin if at risk
preeclampsia patho - normal pregnancy
increase blood plasma volume -> vasodilation -> decreased systemic vascular resistance -> increased CO -> decreased colloid osmotic P
preeclampsia cm - maternal
BP: normal, mild, severe
s/s: epigastric pain (liver), CNS (blurred vision, HA), bleeding, n/v, visual disturbances, HA, irritable/hyperreflexia, retinal edema, retinal arteriolar narrowing (decreased retinal perfusion)
fibrinolysis hemolysis: HELLP, renal fail, DIC
capillary leak: proteinuria, facial edema, pulmonary edema, ascites, pleural effusions
preeclampsia cm - fetal
vascular stillbirth, abruption, IUGR, abnormal UA doppler, oligohydraminos
preeclampsia labs
CBC, liver enzymes (LDH, AST, ALT), chm pannel (BUN, creatinine, glucose, uric acid), type and screen and/or crossmatch
24 hr collection for protein and creatinine clearance (show how much is being lost)
protein dipsticks or protein/creatinine clearance ratio
preeclampsia cm - mild
> /= 140 OR 90 on 2 occasions at least 4 hrs apart with previously normal BP
proteinuria >300mg/24hr
protein/creatinine ratio >/= 0.3
1+ urine dipstick (if only method available)
edema/weight gain (not diagnostic)
OR
increase BP with any of the following w/o proteinuria: plt <100,000, cerebral or vision changes, serum creatinine [] >1.1 or doubling of serum creatinine [] in absence of renal disease, pulmonary edema, or liver enzymes >twice upper limit of normal
preeclampsia cm - severe
> /= 160 OR 110 on 2 occasions at least. 4 hrs apart with pt on bedrest (unless on antihypertensives)
proteinuria >/= 300mg/24hr
plt <100,000
pulmonary edema
new cerebral or vision changes
liver enzymes >twice upper limit of normal
severe, persistent epigastric pain
preeclampsia tm - home
mild
educate on worsening
rest, lateral positioning, daily BP, weight, and fetal movement counts
preeclampsia tm - hospital
mild
bedrest (side), weigh, S worse, BP q6, mod-high protein diet, mod Na
fetal movement record, biophysical profile, doppler velocimetry, serial US
dont need to check for proteinuria, more freq NST and AFI
preeclampsia tm - severe
complete bed rest, decreased env stimuli, anticonvulsant therapy (mgso4), F+E replace, corticosteroids (fetal lungs), antihypertensives (labetalol and hydralazine; procardia good for postpartum period)
acute control of severe htn
persistant >15 min, >160 or >105
IV labetalol (CI = asthma), IV hydralazine (CI = tachy), oral nifedipine (CI = tachy)
prevent convulsions
IV mgso4 - dont leave pt during bolus, will feel hot
loading dose and maintenance
if convulsion: bolus
treat: eclampsia, severe preE, HELLP
mgso4
SE: HA, n/v, hot, flushed, sedation, muscle weak
toxicity: decreased or absent reflexes, decreased RR, change in LOC, therapeutic level (4-7), IV Ca gluconate readily available
eclampsia cm
grand mal seizure
coma
eclampsia tm
obstetircal emergency
dont stop seizure, prevent recurrence
airway!, pt on side, assess fetus, proceed with emergent delivery if hypoxia or abruption
note time of onset, body involvement, duration
avoid aspiration and prevent injury, suction prn
mgso4 bolus
seizure assessment
fetal status, S of labor
S of placental abruption (vaginal bleeding, uterine rigidity)
consider induction of labor if delivery delayed
eclampsia tm - intrapartal
may require induction with oxytocin or c/s
S of worsening preE assessed
EFM
pain relief
eclampsia tm - postpartum
monitor vaginal bleeding, S of shock, regularly assess BP and pulse, S of preE assessed - seizures may occur first week PP, mgso4 continued at least 24 hrs post delivery
HELLP syndrome
hemolysis, elevated liver enzymes, low plt
associated with severe preE
rbc fragmented as they pass through damaged blood vessels d/t vasospasm and plt aggregate at sites of damage which cause low plt count (<100,000)
elevated liver enzymes d/t obstructed blood flow
liver distension causes epigastric pain and possible liver rupture, DIC
HELLP syndrome cm
n/v, flulike symptoms and epigastric pain
HELLP syndrome tm
attempt to stabilize
deliver fetus regardless of gestation (after 48 hr of steroid benefit if <34 wk)
chronic htn
> 140 OR 90 before pregnancy, or before 20th wk, or persist 6 wk PP
watch for development of superimposed preE, evaluate growth of fetus q4 wk by US
chronic htn tm
home if possible
bedrest, L side lying, diet, nifedipine and labetalol, 24 hr urine studies as baseline, preE panel labs, regular NST and BPPs
chronic htn with superimposed preE
cm: sudden increase in previously well controlled BP of if more antihtn meds needed, new proteinuria or escalation of previous renal issue, edema (upper body), rise in serum uric acid
tm: as with chronic htn initially, treat as preE if conditions worsen
developing/worsening s of preE
HA, epigastric pain, visual disturbances, hyperreflexia (and clonus), pulmonary edema, seizure (eclampsia), sudden weight gain
mgso4 assessment
vs, loc, lung/resp assess (pulmonary edema, resp depression), CNS changes (HA, visual change, reflexes, clonus), I+O, r upper quad pain, continuous FM, s of toxicity, foley (want 30 mL/hr
