obstetrics Flashcards
physiology of upper airway swelling in the parturient
increased progesterone, estrogen, and relaxin cause vascular engorgement and hyperemia. also larger ECF volume- all lead to upper aw swelling. this affects nasal passages, oropharynx, epiglottis, larynx, trachea
what size ett for parturient
6-7 ETT r/t narrowed glottic opening
what’s the name for a short handled laryngoscope
Datta handle
should you do an NPA in a parturient
no, try to avoid. all of her is engorged ok, including the nasal passages
aw edema is made worse by what?
pre eclampsia, tocolytics, prolonged trendelenburg
FRC in relation to closing capacity for parturient
FRC falls below closing capacity in parturient, leading to aw closure during tidal breathing
what would you expect the ABG of a parturient to look like
pH: no change
PaO2: increased to 104-108mmHg (d/t hyperventilation)
PaCO2 decreased to 28-32
HCO3- decreased to 20mmoL
P50 in a parturient shifts to
right or is increased, increased O2 to fetus this way
mom p50: 30mmHg
fetus P50: 19mmHg (left, decreased)
how much does O2 consumption increase during pregnancy
20%
changes in HR and SV for parturient
both increase, 15 and 30% respectively
percent increase in CO during labor stages
1st stage: 20%
2nd stage: 50%
3rd stage: 80%
SVR and PVR changes during pregnancy
decrease in SVR because progesterone produces NO which causes vasodilation and decrease in PVR in response to angiotensin and NE
overall effect of progesterone on parturient
cardiac axis deviation during pregnnacy
left axis deviation due to diaphragm being pushed cephalad so heard is pushed up and left
left displacement of uterus should be used during which trimesters
both second and third
clotting factors that increase in a parturient include
1, 7, 8, 9, 10, 12. (pregnancy causes hyper coagulable state- DVT is 6 times higher risk in parturients
anticoagulants that decrease during pregnancy include
antithrombin and protein s
fibrinolytic system in parturient
increase in fibrin breakdown but decrease in factors 11 and 13- mom makes more clot but also breaks it down faster
how much does PT/PTT decrease in a parturient
20%
PT: 9.6-12.9 seconds
PTT: 25-35 seconds
how does platelet count change in a parturient
remains unchanged or decreases up to 10% (due to hemodilution and consumption)
do filling pressures (CVP and PAOP) change during pregnancy?
no
why does creatinine clearance increase in a parturient
r/t increased intravascular volume and CO- more creatinine delivered to the kidney per unit of time
what happens to creatinine and BUN in parturient
decreased
why does urine glucose increase in parturient
increased GFR and reduced reabsorption in peritubular capillaries
why are parturients sensitive to LA’s
increased progesterone
what is progesterone responsible for
lower esophageal sphincter tone
reduced MAC
reduced PaCO2 d/t increased MV
increased RAAS
decreased SVR and PVR
how much does MAC get reduced in a parturient
30-40%
GI changes in a parturient:
gastric volume
gastric pH
LES sphincter tone
gastric emptying
gastric volume: increased r/t gastrin
gastric pH: decreased r/t gastrin
LES sphincter tone: decreased r/t increased progesterone and estrogen
gastric emptying: no change until labor begins (then decreased)
how many mL/min is uterine BF in parturient at term
700-900mL/min (accounts for 10% of CO)
what happens to serum albumin in parturients
decrease
what happens to pseudocholinesterase in parturients
decreases but not enough for an aggressive effect when administering drugs like succ.
how does ICP change in a parturient
it doesnt
what is uterine blood flow dependent upon
MAP, uterine blood flow, and uterine vascular resistance, since it’s a low resistance system, its primarily dependent on MAP and CO
2 causes of reduced uterine BF include
decreased perfusion (maternal HoTN from sympathectomy, hemorrhage, or aortocaval compression)
increased resistance (uterine contraction, hypertensive conditions)
which principal describes how drugs traverse placenta and what is the equation
ficks principle
2 most important variables for a drug crossing to the placenta include
diffusion coefficient (drug characteristics) and concentration gradient between maternal and fetal circulation
drug characteristics that favor placental transfer include
LMW (<500 daltons)
high lipid solubility
non ionized
non polar
drugs that have significant placental transfer include
LA’s (except chlorprocaine d/t rapid metabolism)
IV anesthetics
volatiles
opioids
benzos
atropine
BB’s
mag (not lipophilic but it is small)
drugs that do NOT have significant placental transfer include
glyco
heparin
insulin
NMB’s
describe the 3 stages of labor
stage 1: beginning of regular contractions to full cervical dilation (10cm)
stage 2: full cervical dilation to delivery of the fetus (pain in perineum begins during this stage)
stage 3: delivery of placenta
describe the friedman curve
NPO guidelines for mom
can drink clears through labor and eat solids until block is placed
when does the latent phase of labor end?
when the cervix dilates to 2-3cm
when does the active stage of labor occur?
during stage 1 when cervix is dilating from 3-10cm
which nerve roots are affected by pain during the first stage of labor
T10-L1 posterior nerve roots
which nerve roots are affected during the second stage of labor
S2-S4 (vagina, perineum, pelvic floor)
afferent pathway for uterus and cervix is
(and quality of pain)
visceral C fibers in hypogastric plexus
dull, diffuse, cramping pain
regional technique for uterus and cervix is
neuraxial (epidural, spinal, CSE)
paravertebral lumbar sympathetic block
paracervical block (comes with high risk of fetal bradycardia)
afferent pathway for perineum is
(and quality of pain)
pudendal nerve
sharp, well localized
regional techniques for perineum include
neuraxial
pudendal nerve block
consequences of uncontrolled pain in parturient include
increased catecholamines- HTN and reduced uterine BF
hyperventilation and left shift of HGB dissociation curve- less O2 to fetus
when doing CSE, do you put LA in intrathecal space
yes then you thread the wire
describe the epidural expansion technique and why its performed
saline into epidural space immediately after LA is placed in intrathecal space. increases rostral spread of LA to achieve higher level via compression of subarachnoid space
which LA reduces the efficacy of morphine and why?
2-chlorprocaine (antagonizes mu and kappa in sc)
bupivicaine key facts
racemic mixture
minimal tachyphylaxis
low placental transfer due to increased protein binding and increased ionization
greater sensory block relative to other LA’s
cardiac toxicity more common with R enantiomer
cardiac toxicity occurs before seizures
.75% contraindicated d/t risk during IV injection
ropivicaine chemical makeup
S enantiomer or bupivicaine + substitution of propyl group
when compared to bupivicaine, ropiv has decreased
risk of CV toxicity, potency, and motor block
key facts of levobupiviaine
pure S enantiomer of bupiv
less CV toxicity compared to bupiv
not avail in US
lidocaine key facts
not popular for labor analgesia due to strong motor block
risk of neuro toxicity if given in subarachnoid space
2 chlorprocaine key facts
fast onset so useful in c/s
minimal placental transfer (metabolized via pseudocholinesterase)
antagonizes mu and kappa
risk of arachnoiditis when used for spinal anesthesia d/t preservatives
solutions without methylparaben and methyl sulfite do not cause neuro toxicity
benefits of opioids in neuraxial block (when administered alone) include
no loss of sensation or proprioception
no sympathectomy (superior hemodynamic stability)
do not impair moms ability to push
spinal bolus of bupivicaine
% for epidural bolus
% for continuous epidural infusion
1.5-2.5mg
.0625-.125%
.05-.215%
spinal bolus of ropivicaine
% for epidural bolus
% for continuous epidural infusion
2-3.5mg
.08-.2%
.08-.2%
spinal bolus of levobupivicaine
% for epidural bolus
% for continuous epidural infusion
2-3.5mg
.0625-.125%
.05-.125%
spinal bolus of lidocaine
% for epidural bolus
% for continuous epidural infusion
no no no spinal boluses of lido
.75-1%
.5-1%
spinal bolus of fentanyl
epidural bolus
continuous infusion rate
15-25mcg
50-100mcg
1.5-3mcg/mL
spinal bolus of sufentanil
epidural bolus
continuous infusion rate
1.5-5mcg
5-10mcg
.2-.4mcg/mL
spinal bolus of morphine
epidural bolus
continuous infusion rate
125-250mcg
NA
NA
spinal bolus of meperidine
epidural bolus
continuous infusion rate
10-20mg
NA
NA
spinal bolus of epi
epidural bolus
continuous infusion rate
2.25-200mcg
25-75mcg
25-50mcg/h
spinal bolus of clonidine
epidural bolus
continuous infusion rate
15-30mcg
25-75mcg
25-50mcg/h
spinal bolus of neostigmine
epidural bolus
continuous infusion rate
NA
500-750mcg
25-75mcg/h
3 ways a patient can develop a total spinal
- epidural dose injected into subarachnoid space
- epidural dose injected into subdural space (neither catheter aspiration nor test dose will be able to rule this out. will see a high spinal in 20-25min)
- single shot spinal after failed epidural block (possible the LA from the failed epidural can go into intrathecal space)
anesthetic management of total spinal
vasopressors, IVF, left uterine displacement, leg elevation
fetal bradycardia and causes
<110
fetal: asphyxia, acidosis
maternal: hypoxemia, drugs that decrease ureteroplacental perfusion
fetal tachycardia and causes
> 160
fetal: hypoxemia, arrhythmias
maternal: fever, choramnionitis, atropine, ephedrine, terbutaline
FHR categorizations
minimal
moderate
marked
absent
minimal <5BPM
moderate 6-25BPM (normal, healthy SNS/PSNS)
marked >25BPM
absent
things that reduce FHR variability
CNS depressants
hypoxemia
fetal sleep
acidosis
ancephaly
cardiac anomalies
describe early decelerations and causes
describe late decelerations and causes
describe variable decelerations and causes
VEAL CHOP pneumonic
variable decels: cord compression
early decels: head compression
accelerations: ok or give O2
late decels: placental insufficiency
category 1 for FHR
normal acid base status with no threats to fetal O2
baseline HR 110-160
moderate variability
accelerations absent or present
early decels absent or present
no late or variable decels
category 2 for FHR
cannot predict a normal acid base status
bradycardia without absence of baseline FHR variability
tachycardia
variable variability
absent or minimal acceleration with fetal stimulation
recurrent or variable decels
category 3 for FHR
strongly suggests abnormal acid base status with significant threat to fetal O2
bradycardia
absent baseline variability
recurrent late decels
recurrent variable decels
sinusoidal pattern
premature delivery is defined as
<37w or <259d from last menstrual cycle
incidence of prematurity rises with
multiple gestations and PROM
complications of premature delivery include (5)
respiratory distress syndrome
intraventricular hemorrhage
NEC
Hoglycemia
hyperbilirubinemia
which steroid is given to increase fetal lung maturity in the setting of preterm labor
betamethasone, take effect in 18h and peak effect in 48h
MOA of magnesium as it relates to parturient
relaxes smooth muscle by turning off myosin light chain kinase in smooth muscle including uterus. hyper polarizes membranes in excitable tissues
first sign of magnesium toxicity
diminished DTR’s
s/sx of hypomagnesemia <1.2mg/dL
tetany
seiures
dysrhythmias
s/sx of hypomagnesemia 1.2-1.8mg/dL
neuromuscular irritability
hypokalemia
s/sx of hypermagnesemia 2.5-5mg/dL
no s/sx typically
s/sx of hypermagnesemia 5-7mg/dL
diminished DTR’s
lethargy/drowsiness
flushing
n/v
s/sx of hypernagnesemia 7-12mg/dL
loss of DTR’s
HoTN
EKG changes
somnolence
s/sx of hypermagnesemia >12mg/dL
respiratory depression- apnea
complete heart block
cardiac arrest
coma
paralysis
(p.edema can be an issue as mag increases as well)
tx of hypermagnesemia
diuretics
IV calcium gluconate 1g over 10m
supportive measures
endogenous oxytocin is released following stimulation of
cervix, vagina, breasts
SE of oxytocin admin include
water retention (structurally similar to vasopressin), hyponatremia, hypotension, reflex tachycardia, and coronary vasoconstriction
half life of oxytocin
4-17m
methergine
drug class
dose
route of admin
metabolism
half life
uterotonic (second line)
.2mg IM
(IV can cause vasoconstriction, HTN, cerebral hemorrhage)
hepatic metabolism
half life 2h
hemabate
drug class
dose
SE
third line uterotonic
250mcg IM
n/v, HTN, HoTN, diarrhea, bronchospasm
when is a GA appropriate?
maternal hemorrhage
fetal distress
coagulopathy
patient refusal of regional
contraindication to regional
triple prophylaxis for aspiration during GA includes
sodium citrate to neutralize gastric acid (15-30mL within 15-30min of induction)
H2 receptor antagonist (ranitidine) to reduce gastric acid secretion 1 hour before induction
gastrokinetic agent (metaclopromide) to hasten gastric emptying and increase LES tone- 1 hour before induction
pre oxygenate mom for how long before induction?
3-5 min. just do as theyre prepping and draping her since you cant induce until that has been done anyway
what to do for maintenance with these patients?
low concentration of volatile (.8 MAC) and 50% N2O
what is normal amniotic fluid volume
~700mL
after the first trimester, avoid this group of drugs
NSAIDS- they can close the ductus arteriosis!
in an ideal world, surgery is delayed until how many weeks until after delivery
2-6w
best trimester for surgery in a pregnant patient if you HAVE to
second trimester
when is risk for teratogenicity highest
13-60 days
when should you avoid N2O
first two trimesters. loosely linked to congenital disabilities
at how many weeks is a parturient a full stomach
~18 weeks
define chronic HTN in parturient
occurs before 20w gestation. does not return to normal after delivery
define gestational HTN in parturient
develops after 20w gestation
does not create proteinuria
the only thing to do is if it goes back to normal after delivery you can dx it against chronic HTN
define pre eclampsia in parturient
includes HTN (mild 140/90, severe 160/110) that develops after 20w gestation. proteinuria is typically present
when can preeclampsia be present without proteinuria
persistent RUQ or epigastric pain
persistent CNS or visual sx
fetal growth restriction
thrombocytopenia
elevated serum liver enzymes
define severe pre eclampsia in parturient
BP >160/110
includes seizures
plt count <100,000
HELLP syndrome
pulmonary edema
cyanosis, HA, visual impairment, epigastric pain
the patient with pre eclampsia produces up to 7 times this hormone than normal
thromboxane (vasoconstriction, platelet aggregation, reduced placental BF)
key complications of pre eclampsia include
HF, pulmonary edema, ICH, cerebral edema, DIC, proteinuria
tx for acute HTN (BP >160/110)
labetalol 20mg followed by 40-80mg q10m up to 220mg
hydralazine 5mg IV up to 20mg
nifedipine 10mg PO q20min to a max dose of 50mg
nicardipine infusion starting at 5mg/h and titrated by 2.5mg/h q5m up to a max of 15mg/h
pre eclamptic patients and sympathomimetics/methergine
exaggerated response
anesthetic management for eclampsia
load 4g mag over 10 min
1-2mg/h infusion
HELLP syndrome and overview
hemolysis, elevated liver enzymes, low platelet count
definitive tx is placental delivery
patients are at higher risk of DIC and intra abdominal bleeding
assess for thrombocytopenia before placing block
OB risks of cocaine use include
spontaneous abortion
premature labor
placental abruption
low APGAR
which BB to use if patient uses/is on coke
labetalol (try to avoid B1/B2 otherwise is SVR is high asf)
compare and contrast placenta accreta, increta, precreta
accreta: attaches to surface of myometrium
increta: invades myometrium
precreta: extends beyond uterus
define placenta previa
attaches to lower uterine segment
partially or completely covering cervical os
associated with painless vaginal bleeding
potential for hemorrhage
often requires c/s
risk factors: previous c/s, multiple births
risk factors for placental abruption (partial or complete) includes
PIH
pre eclampsia
chronic HTN
cocaine use
smoking
excessive ETOH use
s/sx placental abruption
maternal pain, vaginal hemorrhage, fetal hypoxia
risk of AFE leading to DIC
vaginal delivery possible if fetus is stable
(obtain large bore IV’s and prepare for c/s)
MOST common cause of PPH
uterine atony
risk of uterine atony increased by
multiparty
multiple gestations
polyhydraminos
prolonged oxytocin infusion before surgery
describe the APGAAR score (5 categories)
normal: 8-10
moderate distress: 4-7
impending demise: 0-3
RR/breathing for new born
RR 30-60BPM
breathing takes 30s, normal RR takes 90s
immediately after delivery, what is neonatal SpO2? what does it rise to after 10 minutes?
60%
rises to 90% after 10m
a mom is requiring a forceps delivery with a .125% bupiv epidural infusion already running. what is the best plan of action
bolus 3% chlorprocaine or a pudendal nerve block if there was no epidural
