OB - Nag Flashcards
Preg cardiovascular/HD changes at term
-HR
-SV
-CO
-SVR
everything increases except SVR
Preg hematologic changes at term
-total blood volume
-plasma volume
-RBC volume
-coag factors
-platelets
everything increases except platelets (no change/ - )
++ coag factors
plasma volume ~40-50% more
Preg respiratory changes at term
-MV
-Vt
-RR
-FRC
everything increases except FRC decreases
-MV increases 50%
T/F CO increases in pregnant pts mainly because of HR and to a lesser extent SV
False
SV increase > HR increase
T/F Blood volume markedly increases as the body prepares mom for blood loss at delivery
True
gross
What is the cause of dilutional anemia during pregnancy?
plasma volume increases at a larger extent than RBC volume increases
-40-50% vs 20% increase
What is the main cause of MV increasing so high (45%) during pregnancy?
Vt increases
T/F O2 consumption is markedly increased as is CO2 production during pregnancy
True
Pregnant pts have a _ (increased / decreased) sensitivity to LA and a _ (increased / decreased) MAC for all general anesthetics.
more sensitive to LA
decreased MAC for GA
T/F Pregnant pts are in a hypercoagulable state due to increased platelet count
False
they ARE in hypercoagulable state but bc of increased FIBRINOGEN and COAG FACTORS, platelet count is normal or decreased
Aortocaval compression during pregnancy causes profound HOTN and can be relieved by _ _ _
Left uterine displacement (LUD)
T/F Pregnant pts should be considered full stomach if they are 20+ wks gestation
ehhh…
Nagelhout says 12+ wks
Howie’s PPT says 20 wks, but in reality treat ALL pregnant pts as full stomachs/asp risk
T/F The need for thorough airway eval in pregnant pts is due to their propensity for chipped and damaged teeth
False
significant airway changes occur -> difficult airway risk
Pregnant pt’s HR begins increasing in the _ tri and peaks at _ wks. Tachyarrhythmias are more likely to occur in _ (early/late) pregnancy
1st tri - 32wks
tachyarrhythmia risk higher in late preg
Increased CO
-begins at: _ wks and increases over time
-ends at: _ days postpartum (returns to baseline)
-highest point during PREG: _ trimester
-highest point during LABOR: _ stage
-reaches MAX VALUE:
begins: 5wks
ends: 14 days pp
Highest point during PREG: 2nd tri
Highest point during LABOR: 2nd stage
Reaches MAX VALUE: immediately post partum (80-100% increase)
At term _ % of CO perfuses the gravid uterus
10%
Why does labor cause increases in CO for mom?
during uterine cx it autotransfuses blood to central circulation
Why does mom’s CO increase so drastically immediately pp? (2 reasons)
-uterine cx causes autotransfusion back to central circulation
-increased venous return from aortocaval decompression
Diaphragm is displaced _ during preg, heart shifts up and left causing enlarged cardiac silhouette on CXR. The ventricular walls thicken and _ (EDV / ESV) increases
cephalad
up and left
EDV
Normal or not normal: CV exam on preg pt
-grade 1/2 systolic murmur
-grade 3 systolic murmur
-3rd heart sound
-cp or syncope
-diastolic murmur
-cardiac enlargement
-SOB, edema, poor exercise tolerance
N:
-grade 1/2 systolic murmur
-3rd heart sound
-SOB, edema, exercise intol
pathologic:
-grade 3+ murmur
-diastolic murmur
-cp or syncope
-cardiac enlargement
What causes increased plasma volume in preg?
levels of progesterone and estrogen -> enhance RAAS
What causes increased RBC volume in preg?
increased erythropoietin levels in 8th wk
Normal blood loss
-vag delivery
-uncomplicated CS
vag: <500mL
uncomp CS: 500-1000mL
During labor each cx moves _ - _ mL blood from uterus to central circulation
300-500mL
When do preg pts have stronger baroreceptor reflexes for HR, 6-8wks or at term?
term
If mom has neuraxial anesthesia and cx occurs her HR will _ (increase/decrease) as preload transiently _ (increase/decreases)
HR drops as preload rises transiently during cx
Biggest hemodynamic decrease in preg is _. Why? (2 reasons)
SVR ~20-40%
-bc there is decreased resistance to uteroplacental, pulmonary, renal, and cutaneous capillary beds (more BF going deeper into other tissue)
-venous capacitance system loses tone - > blood pools
think about how mom’s skin/hair/nails are glowing during pregnancy but also her ankles are swollen
By term _ % of the CO perfuses the low resistance intervillous space in the uterus
10%
T/F Central sympathetic outflow in preg pt is double that of a nonpreg pt
True
T/F The decreased SVR in preg pts causes decreased SBP(15mmHg less), resulting in increased MAP.
FALSE
SVR decrease -> decrease in DBP -> decreased MAP
Aortocaval compression
-cause
compression of vena cava and aorta by gravid uterus in supine position
-worse if abdomen is tense or when uterus is even bigger (hydramnios, multiparous)
Aortocaval compression
-response
decreased CO and venous return -> tachycardia + vasoconstriction of LE BUT uterine BF and fetal O2 is still reduced
T/F If aortocaval compression occurs BP will be low on all parts of body
false
upper body will be normal, lower body will be low and poor perfusion to uterus
Aortocaval compression is aka
supine hypotensive syndrome
Aortocaval compression
-tx
LUD by 15 degree tilt of table or 15cm wedge under R hip
Aortocaval compression
-impact of positioning for neuraxial: lateral vs sitting
Maternal cardiac index is better in lateral(both R+L) position than flexed sitting position
-no difference in fetal BF based off positioning
Hypercoag state from preg
-factors that increase
I (fibrinogen)
VII
VIII
IX
X
XII
vWF
WBC
Hypercaog state from preg
-factors that decrease
XI
XIII
platelets (from hemodilution or accelerated platelet clearance)
Resp changes in preg
-airway
capillary engorgement -> narrow glottic opening + airway edema from nasopharynx-trachea = bleed risk
-use smaller ETT(6.5/7fr) + AVOID nasal intubation
higher MP score + breasts in the way
-use short handle blade + ramping
Increased O2 consumption can be up to _% at rest and _% during labor
33%
100%
MV in preg pt is increased up to 50%, this is mainly because of increased _ and _ to a lesser extent
MV elevated mainly from increased Vt, and a little from increased RR
T/F By 12wk gest arterial PCO2 decreases to 30-32mmHg due to increased FRC. Mom becomes kinda hypoxic from metabolic alkalosis that persists.
False
PCO2 is lower from increased MV
not hypoxic, actually has PO2 >100mmHg thru preg
No alkalosis bc compensatory serum bicarb decreases from 26->22
Upward pressure from the pregnant diaphragm results in which lung volumes and what resp pattern?
Decreased FRC, ERV, and RV
(FRC=ERV+RV)
restrictive breathing pattern
Decreased FRC and increased O2 consumption in preg pt = _ (increased / decreased) apneic reserve
decreased
If FRC is decreased and there is no change to closing capacity in pregnant pts, will small airway closure increase or decrease?
increase
-FRC/CC ratio will decrease and cause small airway closure before full exhale of Vt -> desat when sleeping (sometimes <90%)
In preg pt is DO2 increased or decreased?
increased
-small airway closure occurs more but the increased CO and RIGHTWARD shift in O2Hgb curve = more O2 delivered to tissue
MV can increase by _ % during maternal cx, potentially causing mom’s PaCO2 to drop to < _ mmHg (alkalemia). This causes her to _ (increase / decreased) RR between cx and eventually become _
increase 300%
PaCO2 <15mmHg
decreased RR
hypoxemic
-increased RR causing PaCO2 of ~20 is ok for fetus per scalp blood sample (won’t cause acidosis / hypoxia) unless complicated labor or fetal issues already exist
Increased sensitivity to LA and GA begins in the _ tri
1st
-increased nerve sensitivity + engorged epidural veins
Mechanical changes like _ _ veins are responsible for increased block height in pregnancy
engorged epidural veins
-from increased intraabdominal pressure, can decrease volume of epidural and SA space
Increased levels of gastrin in preg _ (inc / dec) gastric volume and _ (inc / dec) gastric pH
increase
decrease
Meds to tx asp risk in pregnant pt (4)
Nonparticulate antacids (Bicitra)
-reduce pH
H2 receptor antagonists (Pepcid)
-reduce pH
Metoclopramide
-increase gastric emptying, decrease N/V, increase LES tone
consider Zofran for HOTN prophylaxis for spinals
-blunts BEZOLD JARISH reflex
What causes mechanical obstruction to outflow thru pylorus, decreased gastric emptying, and increased intragastric pressure in preg pts?
upward shift of stomach
Increased levels of the hormone, _, during preg can decrease gastric motility and decrease LES tone -> GERD
progesterone
Going into labor _ (inc / dec) gastric emptying due to pain and IV pain meds
decreases
GA on preg pt
-technique for induction:
RSI + cricoid pressure + preox for 3 min!
Liver enzymes elevated in preg pt:
ALT, AST, ALP, LDH
-albumin is DECREASED
Serum cholinesterase activity in preg pt is _ (inc / dec), however they _ (will / will not) have prolonged drug effects
decreased
will not
Increased CO in preg pt -> _ (inc/dec) renal plasma flow and _ (inc/dec) GFR
increased
increased
-peeing a lot
Increased GFR in preg pt will cause Creatinine clearance to increase to 140 - 160 mL/min - > BUN _ (inc/dec) and Creatinine level will _ (inc/dec) as well
BUN decreases
Creatinine decreases
T/F Increased GFR and decreased renal absorption cause preg pt to have glucosuria and proteinuria
true
Uterine BF is supplied by 2 _ arteries
uterine
Placental BF on the uterine sd is supplied by which 3 type of arteries? Which one supplies the intervillous space?
maternal arcuate artery
radial artery
spiral arteries <- supply intervillous space
Maternal _ _ receive blood from intervillous space and send it back to central circulation
venous sinuses
Uterine BF at term = _ mL/min or ~ 10% of mom’s CO
800mL/min
Deox blood flows from the fetus to the uterus via 2 umbilical _ then into central _ on the placenta, mixing with mom’s blood to exchange nutrients and waste. sorry mom
umbilical ARTERIES (like Pulm arteries) - not veins!
central villi
O2 + CO2 are _ limited and do not rely on normal gas diffusion in the placenta
PERFUSION
-decreases in mom’s uterine BF or increased placental resistance will drop fetal O2
T/F Uteroplacental perfusion is autoregulation dependent
False, depends on mom’s uterine BF/ BP
T/F Phenylephrine is teratogenic to the fetus
false
-safe to give in standard doses
T/F Placental BF stays normal with neuraxial anesthesia and becomes impaired from inhaled agents
False
impaired from neuraxial, normal with IA
Placental transfer of free drugs (NON-protein-bound) depends on (4 items)
-magnitude of concentration gradient
-molecular wt
-lipid solubility
-state of ionization
Drugs with molecular wt < _ Da cross the placenta easily
<500 Da
Transfer of drugs from mom’s circulation to fetus is determined PRIMARILY by _
diffusion
Factors favoring diffusion of drugs into fetal circulation from maternal blood include: (4 items)
-low molecular wt
-high lipid solubility
-low degree of ionization
-low protein binding
T/F Fenanyl has high lipid solubility and easily crosses into placenta
True
T/F ionized drugs are polar and hydrophilic/ H2O soluble which prevents diffusion thru the lipid membrane to the placenta
True
LA are variably ionized _ (acidic / basic) compounds and more _ (acidic / basic) ambient pH causes a higher degree of _ (ionization/nonionization) which crosses the placenta easier
basic
more basic
nonionization
- basic + basic = less ionization = crosses easier
NDMR are large, ionized drugs that are not affected by ambient pH due to their quaternary amines and _ (do / do not) cross the placenta barrier
do not
Factors that decrease effects of maternal drugs on fetus: (3)
Dilution
-moms hepatic enzymes drop drug levels before going to uterus, diluted in intervillous spce, then bsorbed and diluted again in placenta before reaching fetus
Shunts
-1/5 of fetal CO goes back to placenta from the shunt from foramen oval and ductus arteriosus without touching fetus
Acid/base status of fetus
-protective for fetus but if more acidic = more ion trapping = more accumulation
1st stage labor pain is from _ distention, stretching of the lower _ segment and possibly myometrial _
cervical
uterine
ischemia
1st stage labor pain is from nonspecific nociceptor _ stimulation, carried by _ fibers to the cord from _ - _ segments
visceral stimulation
C fibers
T10-L1 segments
C fibers = nonlocalized aching + cramping
2nd stage of labor begins when _ _ is complete and the presenting part of the fetus _
cervical dilation
descends
2nd stage labor pain is due to compression and stretching of _ afferent fibers from the pudendal nerve entering the SC at _ - _
somatic afferent
S2-S4
Neuraxial anesthesia for labor pain in the 1st and 2nd stages should have a _ - _ sensory block
T10-S4
3 essential requirements for successful L+D:
Fetus properly positioned and right size to fit thru
Uterus cx regularly and effectively
Pelvic outlet configured for fetus to fit thru
T/F Labor begins officially when cx are regular and cause cervix to change
T
1st stage labor
-what is happening?
-when do latent and active phases begin + end?
events: effacement + dilation
*Latent Phase: onset of regular cx - point where cervix changes quickly
Active Phase: 2-3cm dilation - 10cm dilation
2nd stage labor
-begins
-ends
begins: 10cm or fully dilated
ends: delivery of fetus
3rd stage labor
-begins
-ends
begins: fetal delivery
ends: placental delivery
Cervical dilation progresses usually _ - _ cm/hr when in active phase for nulliparous pt
1-1.2cm/hr
If labor is dysfunctional, may require _
oxytocin
FHR monitoring options:
-intermittent w fetoscope
-continuous w doppler
-continuous w internal fetal ECG (requires slight dilation + rupture of membrane)
T/F FHR can be monitored by a tocodynameter
false
this monitors uterine cx duration
Uterine cx monitoring options:
Tocodynameter
+preserved membrane, less invasive
-lots of artifact, measures duration and not pressure
Internal pressure cath between fetus + uterine wall
+more reliable, measures pressure + duration, allows for amniotic sac infusion if meconium present
-requires partial dilation and rupture of membrane (risks involved)
Indications for internal uterine cx monitoring: (2)
-high risk pregnancy
-if oxytocin is being used
ASA recs for FHR monitoring
before and after neuraxial interventions
Fetal O2 is limited by _ _ _
maternal blood flow
Why can’t the uterus autoregulate blood flow?
Uterine arteries are maximally dilated during pregnancy
-drop in moms BP or BF = fetal hypoxia + acidosis = FHR changes
FHR
-normal
-tachy
-brady
N = 110-160 (higher if premie)
tachy = >160 (at term)
brady = <110
Causes of fetal tachycardia
asphyxia
arrhythmias
mom has fever
chorioamnionitis
mom receives terbutaline or atropine
Causes of fetal bradycardia:
drugs given to mom
compression of fetus’ head
umbilical cord compression
mom or fetal hypoxia
Single best indicator of fetal wellness:
FHR variability
-intact CNS (ANS+SNS)
-good O2 reserve
-normal cardiac function
Baseline FHR variability is when fluctuations of FHR occur _ or more cycles/min with _ (regular / irregular) amplitude and frequency
2+ cycles/min
IRREGULAR amp + freq
FHR variability is described by change in bpm
-absent
-minimal
-moderate
-marked
absent = 0
minimal <5
mod 6-25 (ideal)
marked >25
Factors that decrease FHR variability
Hypoxia -> CNS depression
Fetus sleeping
Acidosis
Anencephaly
Drugs (CNS depressants and autonomic agents) - opioids can decrease variability for 30 mins, MgSO4 can too
Defects in fetal heart function
T/F FHR variability refers to baseline and accelerations and decelerations
false
-just baselien
T/F Only way to accurately monitor FHR variability is with direct FHR monitor with a scalp electrode
T
FHR - Accelerations
-define
-causes
abrupt increase from baseline
causes:
fetal movement
signifies good O2
FHR accelerations are considered reactive if occurring _ or more times within _ mins
2+ times in 20 min
FHR - Early Decel
-define
occur w each cx
begin + end w cx
decrease in rate and return to baseline
uniform
mild drop in HR (~20)
FHR - Early Decels
-cause
compression of head -> vagal stimulation
FHR - Variable Decels
-define
vary in appearance
ABRUPT onset/recovery
maintain variability
FHR - Variable Decels
-causes
labor-related
baroreceptor-mediated response to cord compression = nonominous normally
-if delayed recovery phase could mean fetal compromise occuring
FHR - Late Decels
-define
occur w each cx
low point of decel occurs AFTER peak point of cx
decrease in rate and return to baseline
uniform
vary in depth and variability
FHR - Late Decels
-causes
uteroplacental insufficiency = NONREASSURING, needs investigation
FHR categories
-I
-II
-III
I = normal, moderate variability, NO variable or late decels
II = anything not I or III, don’t predict abnormal acid/base status but warrant continued monitoring
III = fetal brady or absent variability with variable or late decels = abnormal acid/base = need intervention
Nonreassuring FHR tracings suggest fetal _. If laboring mom wants anesthesia and FHR tracings are nonreassuring, how do we navigate this?
suggest fetal hypoxia
-weigh severity of fetal compromise w risks of worsening it from anesthesia w benefits for mom
-OB team may request anyways to prep for urgent/unplanned operative vag delivery or CS (CYA and put this in note)
Intrauterine resuscitation intervention:
change moms position
IV boluses
D/C oxytocin
IV pressors for mom
Tocolytics
O2 for mom
T/F IV analgesia > neuraxial analgesia in labor
F
-good option if neuraxial is refused, isn’t available, or CI
IV labor analgesia
-cons
poor pain mgmt
resp depression for mom/fetus
N/V
decreases LES tone
increases risk of fetal acidosis compared to neuraxial
T/F Epidurals increase the risk of CS, long term back ache, poor APGAR scores and NICU admissions
F
What allows opioids to cross placenta?
highly protein bound
lipid soluble
<500Da small
IV/IM Merperidine for labor
-dose
-1/2 life
-pain relief profile
Dose: 50-100mg IM Q 4hr PRN
1/2 life: 2-3 hr mom
METABOLITES ARE STRONG - LAST 30 HR IN MOM AND DAYS IN FETUS
pain profile: poor, like 1g tylenol
IV/IM Merperidine for labor
-fetal circulation
-reversal
fetal circ within 2 mins
Naloxone reverses it along with its metabolite
IV Fentanyl for labor
-dose
-fetal circulation
Doses:
IV bolus: 25-100mcg
IV PCA bolus: 25-50mcg 3-6min lockout time 4hr max of 1-1.5mg
Fetal circ: within 1 min, decreases FHR variability for 30min
T/F IV Morphine is appropriate for labor pain
F
-too sedating, duration too long
IV Butorphanol + Nalbuphine
-drug class
opioid agonist-antagonists
IV Butorphanol + Nalbuphine
-pros
-ceiling effect (higher doses do not increase respiratory depression)
-less N/V than pure opioid agonists
-allows mom to rest and have sedation in 1st stg labor
-BUTORPHANOL has no metabolites that last
IV Butorphanol + Nalbuphine
-cons
-Butorphanol increases PAP + myocardial work (bad for preeclampsia)
-Nalbuphine causes more drop in FHR variability than meperidine :/
Butorphanol + Nalbuphine doses
Butorphanol (5x morphine strength)
1-2 mg IV or IM ; 1/2 life 3hr
Nalbuphine (10x morphine strength)
5-10mg IV, IM, or SC
T/F IV Remi has highest drop in pain scores but still less than epidural analgesia
T
Remifentanil
-class
-metabolism
-fetal impact
Class: ultra SA opioid agonist
Metabolism: rapid, plasma/tissue esterase
Fetus: crosses to them but rapid distribution and metabolism bc esterases = SAFE
IV Remifentanil for labor
-dose
PCA bolus: 0.25mcg/kg w 2 min lockout
PCA background infusion: 0.025-0.05mcg/kg/min
IV Ketamine for labor
-pros
profound analgesia in subhypnotic doses
preserves airway reflexes
somatic analgesia + sedation
sympathomimetic (good if hypovolemic)
no drop in uterine BF
safe for fetus in doses up to 1mg/kg
IV Ketamine for labor
-cons
short duration
increased amnesia
sympathomimetic (bad for preeclampsia/HTN)
doses >1mg/kg = increased uterine cx -> acidosis + poor APGAR scores
Agent of choice for induction for pt with acute asthma needing GA for urgent CS =
ketamine
IV Ketamine for labor
-dose
IV infusion: 0.2mg/kg/hr
IV boluses: 0.2-0.5mg/kg -if neuraxial is inadequate
duration: 5-15mins
Requirements for neuraxial anesthesia in OB:
must be in LABOR
-regular cx + dilation + effacement
Early start of neuraxial during labor is a good option for:
morbid obese
severe scoliosis
known difficult airway
multiple gest pregnancy
preeclampsia
T/F Epidurals can decrease need for GA if emergent CS needed
T
indwelling cath can be dosed for L+D pain but also dosed for different blockade for surgical deliveries
Absolute CI for neuraxial:
pt refuse
can’t cooperate
severe uncorrected hypovolemia
uncorrected coag issue/ on ACs
increased ICP from a mass
infection at site
Platelets <80-100k
Relative CI for neuraxial:
stable presenting CNS dz
chronic severe HA or backache
severe stenotic valve lesions
untreated bacteremia
-with proper optimization can prolly get neuraxial
Platelets must be _ - _ k + for safe neuraxial anesthesia
75-80k
more like 100k tho
Conditions requiring AC in preg pts:
DVT
Antiphospholipid antibody syndrome
Factor V leiden mutations
Proteins C + S deficiency
Major concern with ACs and epidurals
epidural hematoma
-from uncontrolled bleeding in nondistendable epidural space -> ischemia to SC + neuro issues
T/F Need platelet count right before doing neuraxial
f
T/F If mom is HTN or has known coag issue, elective neuraxial should be delayed until labs are ready (coags, etC)
T
T/F If mom didn’t get good prenatal care, baseline labs are indicated
T
Neuraxial analgesia for labor
-emergency drugs you want nearby
Propofol (to stop LAST sX)
Sux
Ephedrine
Epi
Phenyl
Naloxone
Atropine
CaCl (for MgSO4 tox)
Bicarb
Crash + airway cart with ACLS + Intralipid!
Bupivacaine
-pros
long duration
differential block (sensory>motor)
less tachyphylaxis than Lido
Bupivacaine
-cons
refractory cardiac arrest if given IV accidentally
-harder to resusc than other LAs
Bupivacaine _ % is banned from OB anesthesia bc high risk tox
Bupi 0.75%
Bupivacaine safe doses
low conc for continuous epidural
spinal <15mg
-give in fractions at a time w freq asp + test dose
Lidocaine
-pros
rapid onset
intermed duration
great for CS anesthesia
better motor block with Epi
Lido
-cons
dense motor block too strong for labor analgesia
neurotox if in SA space - risk for cauda equina syndrome from maldistribution
2-chloroprocaine
pros
rapid onset
brief duration
good for emergent CS with existing epidural
metabolized by ester hydrolysis
2-chloroprocaine
cons
brief duration
rapid metabolism by ester hydrolysis
neurotox if given in SA space
Ropivacaine
pros
cons
pro: less tox than bupi
con: less potent than bupi w less motor blk
Order of strength of LA: Bupivacaine, Ropivacaine, Levobupivacaine
Bupi > Levobupi > Ropi
Opioids increase the potency of _ LAs
amide
-sufenta extends analgesia
Labor duration after epidural is shorter with _ - sufentanil combo
bupi + sufenta
Antiseptic of choice before neuraxial:
CHG in alcohol solution
Monitoring for placing neuraxial
Baseline BP + pulseox
Q2min for 15 min then Q5min for another 15 mins
Neuraxial placement
Sitting pros and cons
+:
Easiest for pt
Allows max interspace width for CRNA
-:
Can’t use with fetal head entrapment, prolapse umbilical cord, or breech
Neuraxial placement:
Lateral pros and cons
+:
Lower rates of IV placement
Limits mom moving too much
-:
Harder to find midline w scapula shifting anterior
T/F Higher risk of failure of neuraxial placement if obese mom
T
-skin to epidural space is further
Why is neuraxial best for laboring obese pt?
They have higher rates of CS and potentially diff airway
Neuraxial placement tips for obese patient
Make sure right size equiptment
Consider early placement
Bring US to help
Epidural test dose purpose
Identify epidural caths inserted into SA or epidural vein
T/F must aspirate for CSF or blood after placing epidural in before each administration of medication
T
T/F negative aspiration of CSF or blood from epidural cath means it’s definitely not in IV or SA space
False but ok for labor epidurals honestly
Do a test dose to be positive
T/F an epidural test is the minimum amount of a drug needed to cause moderate detectable effect when given in subarachnoid space or IV
T
Epidural test dose
Actual dose of Lido +epi
3mL of 1.5% Lido + Epi 1:200,000
Or
45mg Lido and 15mcg Epi in 3mL
Test dose
Lido effects
IV: early s/s tox (numbness, lightheaded, audio changes)
SA: noticeable spinal block in 3-5 min
When is Epi useful for test doses in L+D?
Before giving larger volumes+conc of LA for CS deliveries
Why is Epi not ideal for epidural test doses for labor?
HR increasing is unreliable bc moms HR will increase with cx anyways
Also Epi can vasoconstrict uterine artery and decrease BF to fetus
Alt techniques for a normal test dose for epidurals for labor:
Multi orifice cath incremental admin of small dose of diluted LA
Careful asp for CSF or blood Q injection
T/F if laboring mom has epidural and continuous infusion of dilute LA and is comfortable, Cath must be in epidural space
T
If laboring mom is receiving continuous epidural infusion of dilute LA and develops a dense motor block, where is the cath?
SA space
T/F pain is a marker for increased risk of CS
T
Which is false about epidurals:
-increase risk CS
-increase risk forceps delivery
-increase risk prolonged labor
Increase risk of CS
T/F spinals allow for segmental blks
F epidurals
Benefits of adding opioids to epidurals for labor
reduced conc of LA required
good analgesia
preserved motor function
reduces risk of both drugs since smaller doses of each
Epidural for 1st stage labor optimally inserted at the interspaces between _ - _ and the sensory block should extend from _ - _ dermatomes
Epidural inserted at L2-L4
1st stg labor dermatome coverage: T10-L1
Epidural for 2nd stage labor optimally inserted at _ - _ and the sensory block should extend from _ - _ dermatomes
Epidural placed at L2-L4
2nd stg labor dermatome coverage: T10-S4
T/F Epi in LA can increase depth of motor blk
T
Pt should not be left unattended for 1st _ min after initial or following doses of epidural
20 mins
Benefits of continuous epidurals
less change to level of blk
less total drug given
better pain control
less work for staff
What happens if continuous epidural migrates
-SA space
-IV
SA: gradual increase in motor block easily noticeable
IV: loss of pain relief, no s/s of tox (bc usually diluted)
Concentrations of LA for continuous epidurals
-Bupi
-Ropi
-fentanyl + sufentanil
Bupi: 0.0635%-0.125%
Ropi: 0.1-0.2%
Fentanyl: 1-3mcg/mL
Sufentanil: 0.3-0.5mcg/mL
@ rates 8-10mL/hr
Describe ideal epidural block for L+D:
effective pain relief for cx
dense pain relief at perineum at delivery
minor motor blk
If pt needs to have an instrumented vag delivery, make blk denser with:
2% Lido + Epi 1:200,000 +/- Fentanyl 50-100mcg
Concentration of LA for PCEA epidurals
Bupi 0.125%
Ropi 0.2%
2-10mL/hr
boluses of 5mL
Combined Spinal Epidural (CSE) for labor
-2 methods
Needle thru Needle
-larger epidural inserted to epidural space then thinner spinal inserted within it, check for CSF + dose spinal + remove it, leave epidural in; confirms epidural placement
Dural Puncture Epidural
-dura punctured with Touhy needle with spinal, spinal confirmed, dosed, then removed, epidural inserted thru touhy
Why are spinals not generally great for labor? When are they particularly useful during labor?
finite duration, less flexible
Spinals work for:
multips
imminent delivery in 2nd stg
pts who labor w/o anesthesia and need it for surgical vag delivery or extensive peri repair
pt w spinal surgery hx w obliterated epidural space
T/F Spinal anesthesia for labor is not 1st choice bc associated w high risk post dural puncture HA
T
CSE has the spinal component consisting of:
narcotic (fentanyl 15-25mcg or sufenta 10mcg)
or
isobaric bupi
Early 1st stg labor spinal option =
Narcotics alone
fentanyl 15-25mcg
sufenta 10mcg
Late 1st stg labor spinal option =
narcotic + LA
fast onset + minimal motor blk
There is an increased risk for cauda equina syndrome with _
macrocatheters (27-32G)
LA work at nerve _ whereas neuraxial opioids bind to R in the substancia _ in the _ horn of the SC
axon
substancia gelatinosa
dorsal horn
Epidural opioids are absorbed in the _ and eventually the SC where they act on SC opioid R
CSF
Ceiling effect of opioids in the SA or epidural space:
-inc dose doesnt inc analgesia or duration
- will inc s/e tho
T/F Naloxone or Nalbuphine can reduce undesirable effects of neuraxial opioids without removing analgesia
T
-better to relieve itch than antihistamines
Neuraxial Fentanyl add ins for LABOR
-doses
-onset
-DOA
Epidural: 50-100mcg Q 90 min
Epidural continuous: 1-2.5mcg/mL
Spinal: 10-25mcg Q 90 min
onset: 10 min
DOA: 60-140 min
T/F Epidural fentanyl will enter breast milk in standard doses ~100mcg or less
F
Neuraxial Sufentanil add ins for LABOR
-doses
-caution
Epidural:5-10mcg
Continuous Epidural: 0.3-0.5mcg/mL
caution: sufentanil is prepped often in 50mcg/mL vials - triple check dosing!
Why is morphine not good for LABOR?
slow onset in spinal or epidural
T/F Morphine has no purpose in L+D anesthesia
F
-good for CS
Neuraxial Morphine for CS
-spinal dose
spinal: 0.15mg or 150mcg
Common indications for CS:
Poor head/pelvic proportions
Nonreassuring fetal state
Labor arrest after dilation
Malpresentation (breech)
Premie (VLBW <1500g)
Prior CS
Prior uterine sx
Why is neuraxial better for CS?
Decreased risk mortality from failed intubation or asp of gastric content
Better neonate outcomes from less respiratory depression
Mom is awake for birth
T/F LUD should be done for GA CS only
F
should be done for ALL CS
-less rates of fetal CNS depress and acidosis than supine
The _ (upper/lower) extremities should be strapped in for CS
lower
CS EBL is _ - _mL
500-1000mL
Factors surrounding CS EBL:
surg time
technique
mom’s BP
fetal lie
fetal size
placental implantation
coag status
whether or not uterus cx after placenta is delivered
Amniotic fluid volume is _ mL and should be accounted for during EBL measurement
700mL
CS requires dermatome coverage up to _
T4
A T4 blk for CS can cause profound _ from sympathectomy
HOTN
-risk for fetal compromise
Ways to minimize HOTN from T4 blk for CS:
LUD!
Fluids and pressors
Asp risk proph for CS:
Nonparticulate antacid (Bicitra)
H2R antagonist
+/- Metoclopramide
+/- Zofran to prevent N/V + HOTN from neuraxial
increase gastric pH and emptying
Hold abx in CS until after:
cord clamping
Important way to prevent HOTN and preserve CO in CS:
LUD!
Most commonly used anesthetic in CS:
spinal
pros: rapid and dense blk, requires less drug
cons: fixed duration, rapid onset sympathectomy -> HOTN
Good spinal dose for CS
HYPERBARIC Bupi 0.75% 13 mg
-gives 90-120 min of surgical level anesthesia
T/F Hyperbaric LA doesn’t spread high w spinals due to compound curvature of spine
T
Spinal blk for CS results in _ 80% of time regardless of LUD
HOTN
Risks of HOTN from spinal for CS for mom:
N/V
passing out
reduced uteroplacental BF
CV collapse
Ways to prevent HOTN during spinal for CS:
fluids (pre or coloading)
proph pressors (ephedrine/phenyl)
Drawbacks of Ephedrine for maternal HOTN
tachyphylaxis
effects last 5 min
can cross to fetus and risk acidosis
MOA for ephedrine
Direct beta stim and Indirect alpha stim
1st line pressor for maternal HOTN is _. Why?
Phenylephrine
safe for baby
Choose pressor for mom if HOTN based on _.
HR
-ephedrine if HR low
-phenyl if HR high/normal
T/F If adding opioids to a Bupi spinal for CS, it will increase analgesia without impacting blk height
T
Options for opioid add ins for Bupi spinal for CS
-fentanyl
-sufentanil
-morphine
Fentanyl: 10-20mcg O: 5-10min DOA: 60-90min
Sufentanil: 2.5-5mcg O: 5-10min DOA: 60-90 min
Morphine: 0.15mg O: 60-90min DOA: 12-18hr
When to start oxytocin during a CS?
After delivery of placenta and OB tells you to
Oxytocin is normally made in the
hypothalamus
Purpose of oxytocin in OB?
increase freq + strength of cx
-induce labor or increase uterine tone/cx after delivery
Oxytocin half life + risks with high dose or fast infusion:
1/2 life: 4-17 min
risks when given too fast or too much: tachycardia, flushing HOTN from preservative
-start 2nd IV line if bolusing pt with fluids to avoid rapid bolus oxytocin
Alt neuraxial options for postop pain mgmt after CS:
TAP blk
Quadratus lumborum blk
-blk sensory impulses from anterior abdomen + relieve pain from Pfannenstiel incision
Spinal Anesthesia Mgmt for CS BOX 51.2
-preop nonpart antacid, H2R antagonist, metoclopramide
-IV preload or coload
-monitors on, FHR / tones
-consider O2
-Lumbar puncture @ L3-L4 in sitting or lateral position
-small 24 or 25G spinal needle (NONCUTTING-Sprotte, Whitacre, Pencan)
-HYPERBARIC Bupi 15mg in 8.25% Dextrose (12-15mg)
-add fentanyl 10-20mcg for intraop pain mgmt
-add morphine 150 mcg for postop pain mgmt
-supine + LUD
-check BP Q 1 min until birth
-confirm blk level (T4)
-tx HOTN (pressors)
-give oxytocin per OB after placenta out
Why is placing an epidural in the OR for a CS not ideal?
slower onset/takes longer, everyone waiting for you, need larger LA dose
Benefits of epidural for CS
extended duration for a longer surgery
slower onset = less drastic HOTN changes are easier to manage
if already in from labor, easy to convert to surgical anesthesia
T/F Aspirating to check for CSF or blood and giving a test dose is required for an epidural for CS
T
Good epidural CS dose for a T4 blk
Lido 2% + Epi 1:200,000 in 3-5mL increments up to 15-20mL
Selection of LA for CS epidural is based on _
urgency
Add _ to Lido + Epi for epidural to make its onset faster
Bicarb
-increases amount of nonionized drug
Bicarb dose for add in to epidural
1mEq/10mL
DOA: 90-120min
Bicarb CANNOT be added to which LA?
Bupivacaine
-causes precipitate
2-chloroprocaine pros and cons for epidural for CS
pros: low tox risk from ester metabolism, good to rapidly convert to CS from labor
cons: duration is 45 min, prolly need to redose, reduced efficacy of morphine when added
How to increase block from labor epidural to CS epidural level
10-15mL more LA to increase blk from T10 - T4
Convert Epidural for labor to CS BOX 51.3
-preop nonpart antacid, H2R antagonist, metoclopramide
-DC continuous epidural infusion
-give coload (crystalloid)
-monitors on + FHR or tones
-consider O2
-supine + LUD
-asp for blood and CSF, give 2% Lido + Epi 1:200,000 + Bicarb 1mEq/10mL ~10-15mL total dose
-give in 3-5mL increments watch VS and levels of blk
-tx HOTN (pressors)
-check blk level (T4)
-once cord is clamped give 150mcg (3mL) morphine for postop pain
-give oxytocin per OB once placenta out
What should you do if after changing an epidural cath and double checking placement and blk not happening properly?
give blk more time to work before trying spinal
T/F Presence of dense spinal blk can make test dose less reliable
T
When is GA useful for CS?
-cases of existing or expected severe hypovolemic shock
-maternal heart dz
-failed neuraxial
NECESSARY when:
-neuraxial isn’t in place and surgical delivery is too urgent to wait
-if pt refuses
-pt has coag issues
Ways to decrease use of GA for CS
optimize high risk moms
early neuraxial
quickly rreplace unreliable epidurals
Difficult airway options for GA CS
ramping
short handle blade
awake intubation
LMAs, bougie, fiberoptic, follow algorithm, etc
NO NASAL (BLOODY MESS)
Induction technique for GA + CS
RSI + cricoid pressure + at least 3 min preO2
Induction meds for GA CS
Propofol 2-2.5mg/kg
-some neonate depression but quickly cleared
Etomidate 0.3mg/kg
-good for HD instability
Ketamine 1mg/kg
-good for HD unstablity or airway dz, supports BP if hypovolemic, decreased pain med requirement for 24hr postop
Sux 1-1.5mg/kg
-DOC for MR, no defasc dose of NDMR needed
Roc 0.6-1.2mg/kr
-if sux is CI, no defasc dose needed w sux
Maintenance of GA for CS
-predelivery MAC goal?
0.8 MAC w VA +/- N2O
-keep FiO2 50-100%
When to raise FiO2 during GA CS?
if fetus in distress or mom’s SpO2 < 97%
Goal PaCO2 for mom during GA CS
30-32mmHg
-<20mmHg = reduced uterine BF + L shift on O2Hgb curve —- AVOID HIGH RR/PAIN
T/F VA can increase post delivery blood loss
T
-VA is tocolytic so decreased uterine cx
Uterus will continue cx from oxytocin if MAC from GA is < _
<1.0 MAC will not interfere with oxytocin
T/F MR is required for GA + CS
False
-easier to adjust anesthetic without it
Why delay induction of GA for CS?
wait until EVERYONE is ready to go to reduce time of fetal drug exposure
Surgeon should delay incision for GA CS until:
CONFIRMATION of ETT placement
-+BS, + BL chest rise, + EtCO2
T/F Infants delivered via CS w GA are more likely to be depressed and need resusc
T
Infants delivered later than _ min after incision during GA CS are more likely to be depressed
> 3 min = increased risk
Deep or awake extubation from GA for CS?
AWAKE
GA for CS Delivery BOX 51.4
-communicate
-preanesthetic assessment + obtain consents
-prep ALL equipment
-supine w LUD
-16 or 18G IV, get baseline labs + T/S or T/C if high risk for PPH
-preop proph asp risk meds: Bicitra, Pepcid, Metoclopramide
-proph abx if needed 60 mins prior to incision
-monitors on + time out
-100% FiO2 preox for 3+ min or 4-8 VS breaths
-make sure EVERYONE is ready
-RSI + cricoid pressure (10->30N)
-Prop 2-2.5mg/kg + Sux 1-1.5mg/kg, wait 30-40s to fasc then intubate + confirm placment
-maintain w VA +/- N2O 50-100FiO2
-tx HOTN (pressors)
-redose NMBD per TOF
-watch for infant delivery
-start oxytocin per OB after placenta out
-monitor blood loss and communicate concern for more meds if needed
-bring MAC to 0.5-0.7, consider IV benzos/opioids or N2O while closing
-reverse pt + extubate AWAKE when safe
-check and treat PONV/pain
HOTN for mom manifests often as
N/V
Maternal HOTN is defined as:
20% drop from baseline or SBP <100mmHg
BP checked Q _ min from initiation of neuraxial until stable
2min
How does zofran help prevent HOTN from spinals?
reduced occurrence of BEZOLD JARISH reflex (HOTN + brady)
T/F Aggressive tx of HOTN can prevvent N/V
T
Dose of metoclopramide and when to give to mom?
10mg IV
give preop or at cord clamp
Multimodal options for N/V after neuraxial:
tx HOTN
Metoclopramide 10mg IV
Granisetron 1mg IV
Scop patch 2-4hr before
PDPH is most commonly from ADP with large bore epidural needle _ - _ G
16-18G
-other risks: women, pregnant, old
PDPH patho
CSF leak from SA space into epidural space -> reduces ICP -> caudal movement of cranial contents + meningeal traction when in head up position
PDPH hallmark complaint
HA in head up positions, relieved when supine
PDPH s/s
HA worse sitting/standing, better when supine
frontal + occipital pain rad to neck + shoulders
nausea, vertigo, low back pain, double vision
Which spinal needles reduce risk of PDPH?
pencil point needles (Whitacre, Pencan, Sprotte)
AVOID CUTTING - QUINCKE
Tx for PDPH
-conservative/mild
conservative/mild:
rest, caffeine (cerebral vasoconstrictor), po pain meds or topical sphenopalative ganglion blk (SPGB)
Tx for PDPH
-severe/persistent
epidural blood patch
-20mL of blood from IV obtained w sterile technique injected into epidural space in small increments
LAST
-early s/s
circumoral numbness
lightheaded
vision or audio changes
LAST
-late s/s
changed LOC, sx, CV depression
LAST
-prevention
asp for blood/CSF Q injection
test dose
intermittent/gradual dosing
monitoring
LAST
-tx
stop LA
benzos/prop for sx
airway mgmt
follow ACLS
Interlipid 20%
T/F Total spinal only happens with spinal anesthesia
F
-could be from SA migration of epidural cath or from spinal done right after a failed epidural
Total Spinal
-s/s
rapid onset;
dyspnea
slurring
HOTN
brady
If high spinal occurs and pt very bradycardic, block could have gone as high as:
T1-T4
-cardiac accelerator fibers = sympathectomy
Diff Dx for high spinal s/s
anaphylaxis
eclampsia
amniotic fluid embolism
Accidental subdural injection
-main issue
HOTN from excess sympathetic blk
-fix w pressors
Accidental subdural injection
-s/s
higher sensory blk of greater magnitude, UL, onset in 10 min
-HOTN, delayed resp compromise is possible
Cardiac arrest and pregnancy:
In _ tri, move hand s2-3cm higher during compressions
3rd
T/F During cardiac arrest in preg pt, LUD is necessary
T
Perimortem CS delivery should occur within _ min of arrest as compression and ACLs are ongoing
5min
OB related n injures involve pressure + stretch of _ nerves - > _ _ neuropathy
peripheral nerves
single periph neuropathy
Neuraxial related n injuries involve a spinal nerve _ and follow a _ distriubtion
spinal nerve root
dermatome
PPH has few definitions but roughly:
500-999mL = high susp PPH
500mL+ for vag, 1000mL+ for CS
1000mL+ loss or symptomatic hypovolemia in 1st 24hr of vag or CS birth
Most freq cause of PPH
uterine atony
Causes of PPH:
uterine atony (most common)
retained placenta
uterine abnormalities (previa, accreta, etc)
lacerated cervix or vag wall
uterine inversion
coag issues
Uterine atony is associated with(risks):
multiparous
prolonged oxytocin infusion
polyhydramnios
mult gestation preg
PPH
-prevention/tx
oxytocin, methergine, prostaglandins (hemabate), misoprostol
TXA if trad tx fail, massive transfusion, cell salvage after placenta, low dose NTG to pull out retained placenta, surgical tx (ablations), balloon tamponade
PPH tx
-doses
Methergine IM 0.2mg Q 2-4hr
Carboprost (Hemabate) 0.25mcg IM or IU Q 15-90 min x 8 total doses
Misoprostol 600-1000mg rectal/vaginal/oral x1
TXA 1g Q 30 min
CI for methergine
HTN, preeclampsia, cv dz, hypersensitivity to ergot alkaloids
-will increase BP, PAWP, and MUST GIVE IM, too potent IV
T/F Carboprost/Hemabate is a prostaglandin
T
Carboprost/Hemabate
CI + s/e
CI: asthma
S/E: bspasm, nausea, increased pulm VR
Misoprostol
-A/E
transient hyperthemic response
Intraop options to relax uterus for a surgical uterine exploration
GA + VA
Terbutaline
NTG (40mcg IV or SL)
Preeclampsia criteria for dx
-SBP 140+ or DBP 90+ 2 or more times, more than 4 hr apart after 20wk gest in normotensive pt
PLUS EITHER
-proteinuria (300mg+ in 24hr urine, protein/creat ratio 0.3+, dipstick 2+)
OR
-if no proteinuria, evidence of organ impairment (renal insuff, impaired liver, new onset persistent HA, pulm edema, or thrombocytopenia (plt<100))
Primary cause of HTN related maternal mortality:
cerebral hemorrhage
Organ dysfunction assoc w preeclampsiae
pulm edema
renal fail
hepatic rupture
cerebral edema
DIC
Eclampsia =
preeclampsia + new onset sx
Preeclampsia
-patho
failure of normal placental angiogenesis -> reduced placental perfusion worsening over time -> release factors that harm maternal organs -> MODS like picture
T/F More airway edema with preeclamptic pt
T
What 2 factors cause pulm edema in preeclampsia?
reduced colloid osmotic pressure from protein loss in pee
increased vascular permeability
CNS effects of preeclampsia:
HA
hyperreflexia
hyperexcitability
Proteinuria in preeclampsia is from _ capillary endothelial destruction
glomerular capillary endothelial destruction
T/F Pt who has been preeclamptic during preg has increased risk for CV dz later in life
T
Only definitive tx for preeclampsia
deliver fetus + placenta
OB decision to deliver based on complications:
uncontrolled HTN
eclampsia (sx)
pulm edema
placental abruption
nonreassuring fetal status
Mode of deliverying for preeclampsia is based on
fetal gest age
presentatin
cervical status
maternal and fetal VS
If severe features are absent in preeclampsia a _ - _hr trial of corticosteroids are given to speed fetal lung development
24-48hr
DOC for preeclampsia or eclampsia is
MgSO4
Therapeutic range for MgSO4 for preeclampsia is
5-9mg/dL
MgSO4 dosing for preeclampsia
loading: 4-6g/30 min
infusion: 1-2g/hr
When giving MgSO4 must monitor these in preeclamptic pt (4 items)
UO
resp status
DTR
routine labs
Mag tox levels
Mag >9 loss of patellar reflex
Mag >12 resp paralysis
Mag >30 cardiac arrest
Alt effects from MgSO4 in tx of preeclampsia
CNS depress
reduced hepatic fibrin deposition = less liver pain
decreased uterine tone
Preferred anesthetic for preeclamptic pt having vag or CS delivery
regional
-early epidural = best, spinal is ok
Uncontrolled HTN in response to _ is a major cause of hemorrhagic stroke in preeclamptic pts
laryngoscopy
Tx preeclamptic SBP > _ with _ (DOC) to avoid intracranial bleed.
SBP>160
labetalol
T/F can give opioids to blunt the SNS response from intubation for L+D pts during CS
false
bad for babay
A _ (inc / dec) dose of MR should be used for pts on MgSO4 tx for preeclampsia during GA
decreased
-prolongs effects by 25%, slows onset too
What causes thrombocytopenia in preeclamptic pts
endothelial dysfunction -> stim platelet activation + consumption
Which additional coag labs should you get on preeclamptic pt with thrombocytopenia before neuraxial anesthesia
PT and PTT
HELPP is a complication of which OB dz?
preeclampsia
HELLP stands for
Hemolysis
Elevated Liver enzymes
Low Platelets
HELLP
-s/s
epigastric or RUQ pain, upper abdominal tenderness, proteinuria, HTN, jaundice, N/V
T/F HELLP is an indication for immediate delivery in preeclampsia
T
HELLP can cause hepatic _
rupture
Common labor complication in obese pts
difficult placement for neuraxial anesthesia
fetal macrosomia
prolonged labor
failed induction and risk for asp
increased rates CS and high risk of prolonged CS, infection, and thromboembolic events
3 variations of placenta PREVIA
-marginal, partial, total
marginal: in lower uterus but >3cm from cervical os
partial: in lower uterus within 3 cm of cervical os-partly covered
total: placenta completely covers cervical os
Placenta PREVIA
-risk factors
uterine scars
prior uterine sx
prior placenta previa
adv maternal age
Placenta PREVIA
-dx
US
T/F Pt w placenta PREVIA can have vag delivery
false :(
What increases risk of bleeding w placenta PREVIA in laboring mom
manual pelvic exams
Placenta PREVIA
-risks for mom
painless bleeding prior to labor - > HD significant blood loss, increased PP bleeding b/c lower uterine segment doesn’t cx as well as rest of uterus
3 variations of placenta ACCRETA
-accreta
-increta
-percreta
Accreta: abnormal growth ONTO myometrium - most common
Increta: abnormal growth INTO myometrium
Percreta: abnormal growth THRU myometrium (onto bowels/bladder/ovary) :’(
Most common complication w placenta ACCRETA
PPH
T/F Placenta ACCRETA requires a CS
T
Placenta ACCRETA
-tx at time of delivery
uterine artery embolization/ablation
possible CS + hysterectomy combo
What is placental abruption
placenta separates from uterine wall before delivery
Placental Abruption
-big contributing risk factor (2)
HTN + preeclampsia
Placental Abruption
-risks for mom
bleed/hemorrhage
uterine irritability
poor uterine BF
DIC from amniotic fluid entering open venous sinus
T/F Placental Abruption requires a CS
F
can have vag delivery only if no fetal distress
-be ready for emergent CS anyways
Amniotic fluid embolism
-s/s triad + others
triad: acute resp distress, CV collapse, coag issues in labs
-acute HOTN, fetal distress, frothing from mouth, uterine atony, passing out, convulsions/sx
Amniotic fluid embolism
-tx
supportve
atropine 1mg(vagolytic) + zofran 8mg(antiserotonin) + ketorolac 30mg (antiTXA)
Premature L+D occurs before the _ wk
37th
Biggest risk of complications to premie newborn comes when they are VLBW (< _ g)
<1500g
Risks for newborn if premature
resp distress
intracranial hemorrhage
hyperbilirubinemia
Tocolytic drug classes:
MgSO4
CCB
-Nicardipine, Nifedipine
Beta sympathomimetic
-Terbutaline, Albuterol, Fenoterol
Prostaglandin Inhibitors
-Indomethicin
Can dx preterm labor from measuring _ protein which is normally seen at _ wks
fibronectin
35wk
Delaying a premature delivery by 24-48 hr to give _ and _ to allow fetal lung development and tx of chorioamnionitis shows good results
corticosteroids
abx
-bacteria and inflammation in fetal membranes and amniotic fluid can cause inflammatory response resulting in labor (meconium?)
Best analgesia for planned premature vag or CS delivery is
neruaxial
Can VLBW (<1500g) fetus or fetus in breech be birthed vaginally?
no
need a CS
Most common nonOB surgeries done on pregnant pts
appendectomy, chole, ovary cyst removal, trauma surgery, cervical cerclage
Goals for nonOB surgery for anesthesia standpoint
keep O2 stable for mom
avoid increased RR (pain!) + HOTN
-pain shift O2hgb curve left = less DO2 to baby
-HOTN decreases BF to baby
T/F All top drawer anesthesia drugs cross placenta and affect baby
F
-not muscle relaxants
NonOB surgery on preg pt
-reversing MR preferred method
Neostigmine + Glycopyrrolate
-sugammadex may compete for binding to progesterone, don’t know what this does to lactation and fetal health but fine if an absolute emergency
FHR monitoring for nonOB surgery occurs:
start doing this at 20wk
previable (<24wks): ok just to doppler before + after
viable (24wks+): electronic FHR + cx monitor before + after
Best time for nonOB surgery in preg pt
2nd tri
-1st tri risks damage to developing fetal organs
-3rd tri risks inducing premature labor
FHR monitor for non OB surgery
-decreased variability vs decreased HR, which is worse?
decreased variability = expected, not ominous
decreased HR (<110) = ominous, investigate further
Why is regional anesthesia preferred for nonOB surgery in preg pt
airway changes pregnany causes = risk diff airways
Cervical cerclage prevents fetal loss in the _ tri from incompetent cervix and is normally done in the _ - _ wk with _ anesthesiA
Prevents fetal loss in 2nd tri
done 12-26wks
with spinal
NonOB surgery and pregnancy BOX 51.5
-asp risk and difficult airway risk
-increased risk when delay in dx of abominal dz due to pregnancy
-greatest acute risk to fetus from maternal hypoxia, HOTN, and acidosis
-fetal risks: death, preterm labor, growth restriction, LBW
-hard to tell what exactly causes fetal issues (surgery, meds, anesthesia, etc)
-no anesthetics are teratogenic, but avoid N2O anyways
-AVOID: hypoxemia, HOTN, acidosis, hyperventilation (pain) fetal hypercarbia
-keep pneumo pressures low 10-15
-limit trend or reverse trend, change positions slowly
-monitor FHR before and after
-don’t need tocolytic therapy proph, only need it if preterm labor occurs
Tocolytics and anesthesia concerns:
-CCB
-Beta 2 Agonists
-MgSO4
CCB: vasodilation + myocardial depression can cause systemic HOTN and conduction issues
Beta 2 Agonists: maternal tachy + sometimes pulm edema
MgSO4: exacerbated HOTN + enhanced NM blockade
