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%