Apex- OB Flashcards
Q: how does the upper airway change during pregnancy
A: everything becomes swollen and engorged
Q: Why though?
Progesterone, estrogen and relaxin combined with an increased in ECF volume
Diffult intubation is __x more likely in full term patients?
8
How do the lungs change in pregnancy. Early vs later
Early → relaxin relaxes the ligaments in the ribcage, increasing the A-P diameter, giving lungs more space
As the gravid uterus grows, diaphragm shifts cephelad
→ decreased FRC (due to decreased ERV and RV)
→ increased o2 consumption + decreased FRC = faster onset of hypoxemia during apnea
Why are pregnant patients more likely to desat faster during apnea?
due
due to decreased FRC and increased O2 consumption
How does the acoid/base balance change during pregnancy?
generally speaking
progesterone = respiratory stimulant
→ increases mV up to 50%
→ moms PaCO2 decreases → Resp alkalosis (fully compensated)
→ renal compensation lowers bicarb to normalize pH.
P50 of pregnant patient
increased/right
right = release, release more o2 to baby
%change in Vt/RR of pregnant patient
40% increase in Vt
10% increase in RR
equaling a 50% increase in MV (proegesterone = resp stimulant)
Lung volume changes in pregnant pt
TLC
VC
FRC
ERV
RV
CC
increase/decrease by what % or no change
TLC - decrease 5%
VC- no change (it’s vital that moms VC stays normal)
FRC- decrease 20%
→ERV- decrase 20-25% (diaphragm compresses lungs)
→RV- decrease 15-20% (diaphram compression of lungs)
CC- no change → increased CV + decreased RV= no change in closing capacity
VO2 (oxygen consumption) increases by what% when mom is:
Term:
1st stage labor:
2nd stage labor:
Term- 20% (25)
1st stage labor- 40% over pre-labor (50)
2nd stage labor - 75% over pre-labor (75)
Relate to CO
What % of cardiac output does the uterus recieve?
10%
CO = HR x SV
how much does each variable increase and why?
CO increases 40%
SV increases 30% (intravascular volume increase)
HR increases 10-15% (to satisfy metabolic demand)
normal CO = 4-6L
normal SV = 60-90mls (“69 strokes”)
Compard to pre-labor values, CO during labor increases how much during:
1st stage labor-
2nd stage labor-
3rd stage labor-
1st stage labor - 20% (25%)
2nd stage labor - 50%
3rd stage labor - 80% (75%)
When does CO return to pre-labor values?
When does it return to pre-pregnancy values?
returns to pre-labor values in 24-48 hours
returns to pre-pregnancy values in ~ 2 weeks
2 days/2 weeks
Pregnancy effects on:
MAP
SBP
DBP
MAP - no change
SBP- no change
*DBP decreases 15%
MAP = [(SVR x CO/80)] + CVP or SBP + 2(DBP) / 3 (70-110)
Pregnancy effects on SVR and PVR and why?
SVR- decreases 15% → progesterone increases nitric oxide release from VSM → vasodilation
PVR- decreases 30%! decrease response to angiotension and NE
SVR (900-1500); MAP-CVP/CO x80
PVR (150-250); mean PAP- PAOP/CO x80
Why doesn’t a pregnant moms MAP increase with all that extra blood volume?
bc progesterone increases nitric oxide release from VSM → vasodilation
increased blood volume + decreased SVR = net effect on MAP
True/False: CVP and PAOP are increased with pregnancy
False- pregnancy iteself does not alter filling pressures; however, uterine contraction induced autotransfusion does increase filling pressure.
What kind of axis deviation would you expect to see on EKG
Left axis devation
→gravid uterus pushes diaphragm cephalad → pushes heart up and left
axis deviations are monitored with leads I & AVF
Normal axis = both leads positive
left axis = lead I positive deflection, AVF negative deflection
right axis = lead 1 negative deflection, AVF postive deflection
A patient requires an emergency C/S. Which of the following is MOST likely the cause for a rapid arterial oxygen desaturation during intubation?
A. decreased ERV
B. increased IRC
C. increased RV
D. Decreased VC
A. Decreased ERV
Why do pregnant patients have a dilutional anemia?
Bc plasma volume expands faster than RBC production can keep up
LUD should be used when?
starting in the 2nd trimester
3 pathways in which progesterone works
- increased RAAS activity → increased blood volume → increased CO
- VSM relaxation (from nitric oxide release) → decreased SVR and PVR → increased blood flow
- increased minute ventilation (Vt 40%, RR 10%) → decreased PaCO2 → kidneys eliminate HCO3 to preserve pH
what does aortocaval compression result in?
compression of both the vena cava and the aorta
→decreased venous return to heart
→ AND decreased arterial flow to the uterus and lower extermities
LUD elevates the moms (right/left) torso by how many degrees?
elevates right torso by 15 degrees
Why does moms intravascular volume increase anyway? and to what % does it increase?
to prepare mom for hemorrhage with labor
increases 35%
How much doe Plasma and RBC volume increase
Plasma - 45%
RBC 20%
*creates dilutional anemia
What clotting factors are increased during pregnancy?
1, 7, 8, 9, 10, 12
(think 7-12 but 11 is just a 1)
*pregnancy creates a hypercoagulable state
maybe to prepare for hemorrage with labor?
How are anticoagulants affected with pregnancy?
decreased antithrombin and protein S
(no change in protein C)
*DVT is 6x higher in pregnant women
Risk for DVT in pregnant women is how many times greater?
6x
Is fibrin breakdown increased or decreased in preganancy?
increased fibrin breakdown
→in attempt to counteract a state of hypercoagulability
bottom line- mom makes more clot, but she breakds it down faster (consumptive coagulopathy)
How is moms anti-fibrinolytic system affected?
decreased factors 11 and 13
→ reduces fibrin polymerization
whatever the fuck that means
How are PT/PTT affected in pregnancy?
both decrease by 20%
normal PT = 9-12; normal PTT 25-35
How is platelet count affected by pregnancy?
unchanged or decreases up to 10% due to hemodilution and consumption
what is the most common cause of thrombocytopenia? does it increase the rate of complications?
gestational thrombocytopenia and no
is this whats from hemodilution and consumption?
other causes may be hypertensive disorders of pregnancy and idopathic
Pregnancy causes MAC to decrease by _____ %
this process begins when?
what is is caused by?
decreased mac 30-40%
starts at 8-12 weeks (first T)
caused by increase in progesterone
How is gastric emptying time affected before the onset of labor and after labor begins?
unchanged before onset of labor
slows after labor begins
Are the following neurologic changes increased/decreased/or unaffected by pregnancy (and why)
-MAC (and by how much)
-Sensitivity to local anesthetics
-epidural vein volume
-ICP
MAC - decreased 30-40% (progesterone)
Sensitivty to LAs - increased (progesterone) (need less)
Epidural vein volume- increased → decreased volume of subarachnoid and epidural spaces from compression)
ICP- no change
How are the following GI paramaters affected during pregnancy and why:
-Gastric volume
-Gastric pH
-LES sphincter tone
-Gastric emptying
-Gastric volume: INCREASED → gastrin
-Gastric pH: DECREASED → gastrin
-LES tone: DECREASED → progesterone, estrogen, & cephalad displacement of the diaphragm
-Gastric emptying: no change before labor onset/ decreased after labor begins
*gastrin increases gastric volume and reduces gastric pH
How are the following renal parmaters affecting during pregnancy and why?
-GFR
-Creat clearence
-Urine glucose
-BUN and creat
- GFR - increased (increased BV & CO)
- Creat clearance- increased (increase BV & CO)
- urinary glucose - increased (increased GFR and decreased renal absorpiton)
- BUN/Crt - DECREASED (due to increased creat clearence)
urterine blood flow in ml/min
700-900ml/min
what is the effect of pregnancy on serum albumin
decreased → free fraction of highly protein bound drugs increase
how is pseudocholinesterase affected by pregnancy?
it’s decreased but there is no meaningful effect on sux metabolism
T/F - urterine blood flow is autoregulated
FALSE
→ therefore it’s dependent on MAP, CO, and Uterine vascular resistance
& since it’s a low resistance system, uterine blood flow is primarily dependent on CO (HR x SV) and MAP
3 drug properties that favor placental transfer:
- low molecular weight (< 500 daltons)
- high lipid solubility
- non-ionized
2 causes of reduced uterine blood flow + examples of each
- Decreased perfusion: Maternal hypotension (sympathectomy, hemorrhage, aortocaval compression)
- Increased resistance: uterine contraction, HTN conditions
Neo vs Ephedrine - why one over the other
neo was often avoided bc it was thought to increase uterine vascualr resistance and reduce placental perfusion.
most recent evidence shows neo is just as efficent in preventing hypotension and causes no fetal depression & actually moms that got neo had higher fental pH values (less fetal acidosis)
-neo might be superior for this reason, but avoid if HR is already low to avoid reducions in CO if reflex bradycardia occurs
What are the 5 drugs that don’t cross the placenta
CHING
Chloroprocaine (rapidly metabolized)
Heparin
Insuilin
NMBs
Glycoopyrrolate
Magnesium is not lipophillic but still crosses the placenta - why?
low molecular weight
Which stage of labor begins with the onset of perineal pain?
A. Latent
B. Active
C. First
D. Second
D. Second
begins with full cervical dilation > delivery of newborn
How many stages of labor and what do each begin/end with?
Stage 1: beginning of REGULAR contractions → full cervical dilation (10cm)
Stage 2: Full cervical dilation → delivery of the fetus
Stage 3: Delivery of the placenta
According to the ASA practice Guidelines for OB Analgesia, the laboring mother who is healthhy may:
Drink a moderate amount of clear liquids up until when
Eat solid food up until when
moderate clears throoughout labor
solid food up until neuraxial block is placed
T/F- epidural can prolong the first stage of labor
does it increase the need for a c/s?
false
no
What can stage 1 labor be divided into?
Latent: onset of regular contractions > cervical dilation of 2-3cm
Active: cervical dilation 3cm > 10cm
Why don’t you have to ask when mom last ate or drank?
bc a laboring mom is always considered a full stomach
then why do they postpone c/s sometimes based on when they eat?
-says they should remain NPO if there is a high probability of a surgical intervention requiring GA
When should moms get an epidural?
whenever she wants. AOCG guidelines recommend the timing should be individualized to each patient and the patient should NOT have to wait until they achieve a predetermined cervical dilation before receiving analagesia.
Stage 1 of labor
beginning of regular contractions until cervix is fully dilated (10cm)
Stage 2 labor
full cervical dilation (10cm) to delivery of fetus
Stage 3 labor
delivery of the placenta
When does the latent phase of labor end?
When the cervix dilates 2-3cm
When does the active phase of labor begin?
in phase 1 when the cervix is 3-10cm dilated (after the latent phase)
Why is a pudendal block inappropriate for stage 1 labor pain?
bc stage 1 labor pain begins in the lower urerine segment and the cervix
-pain signals travel from posterior nerve roots of T10-L1
- the pudendal nerve is derived from S2-S4 and innervates the perineum & perineal pain does not occur until stage 2 labor
First stage labor pain vs second stage
generally speaking
1st stage pain - lower uterine segment and cervix
2nd stage pain - adds in vagina, perineum and pelvic floor
Which block is associated with a high risk of fetal bradycardia?
paracervical block
1st stage labor
2 consequences of uncontrolled pain
- increase in maternal catecholamines → HTN → decreased uterine blood flow
- Maternal hyperventilation → left shift in oxyhemoglobin curve → decreased delivery of o2 to the fetus
fill in the blanks
If administering nitrous oxide to the pregnant patient, how should it be administered and what does it actually do?
50% nitrous and 50% o2 self administered by the patient via facemask
-provides a non-invasive alternative for labor analgesia
t/f - when nitrous is administered alone (not with opioids), a 50/50 mixture can be associated with hypoxia, loss of airway reflexes, and/or unconsciouness
False
T/F- N20 can decrease uterine contractility
false - it preserves it
T/F- n20 can cause neonatal depression
false
Why do some providers like to do a combined spinal/epidural technique? (CSE)
dual benifit of rapid onset of spinal anesthesia and the ability to prolong the duration of anesthesia with an indwelling epidural cath
What is the most common appraoch to CSE?
4 steps
- epidural needle into epidural space
- spinal needle placed through the epidural needle → LA and opioid injected into intrathecal space
- Spinal needle removed
- Epidural cath is threaded through the epidural needle
“Needle through needle” technique
When doing a CSE, what does the epidural volume extension technique invole and what puprose does it serve?
Immediately after LA is administered into subarachnoid space and spinal needle is removed, saline is injected into the epidural space
→ this added volume into the epidural space compresses the subarachnoid space, enhancing rostral spread of the LA (pushes the LA towards the brai nto achieve a higher level for a given dose)
*administering a smaller dose of LA in the subarachnoid space and compressing it provides more stable hemodynamics
Which local anesthetic reduces the efficacy of epdirual morophine?
why?
2-Chloroprocaine
it antagonizes mu and kappa receptors in the spinal cord, reducign the efficacy of epdiural morphine
What are the 4 most common local anesthetics used in OB?
BPV, Ropi (Long acting)
, Lido (intermediate)
, Chlorprocaine (short acting)
What local anesthetic is contraindicated and epidurals and why?
0.75% BPV
-risk of toxicity with IV injection and epidural veins are engorged with pregnancy
4 side effects of neuraxial opioids - which is most common
if there are all these side effects, why would you use it?
- pruritis (most common)
- N/V
- Sedation
- Respiratory depression
- no loss of sensation or proprioception
- no sympathectomy (supierior hemodynamic stability)
- doesnt interfere with moms ability to push
Do neuraxial opioids depress the fetus?
not meaningfully
Why is lidocaine not used for labor analgesia but used if a C/S is needed
bc of it’s strong motor block
Why shouldnt you give lidocaine in a spinal?
can cause neurotoxicity
Which opioid possesses local anesthetic properties?
Meperidine
Why isn’t lidocaine typically used for continuous epidural infusion?
tachyphylaxis + it crosses the placenta to a greater degree than the alternatives
+ strong motor block
Why dont we just amdminister neuraxial opioids alone instead of with LAs?
bc they dont relax the perineum and provide less analgesia compared to locals
Dosing of Fentanyl/Su/Morphine/Meperdidne for Spinals
Meperidine = most (least potent) → 10-20mg
Moprhine → 150-250mcg (0.1-0.2mg)
Fentanyl → 15mcg - 25mcg (100x more potent than mso4)
Sufent → 1.5-5mcg (1000x more potent thant mso4)
What 2 opioids can be used for bolus’ing epidurals - dosing?
fentanyl 50-100mcg (spinal 15-25)
sufent - 5-10mcg (spinal 1.5-5mcg)
*sufent 10x more potent than fent
15 mins after a patient’s epidural was dosed, the patient becomes hypotensive and experiences respiratory arrest. What is the MOST likley etiology?
A. Epidural catheter migration
B. Loss of accessory muscle strength
C. Subdural injection
D. Eclampsia
C. Subdural injection
the symptoms describe a total spinal & due to the time course ,the most likely explaination is a subdural injection
3 ways a patient can develpo a total spinal
- epidural dose injected into the SA space
→ bad day: get ready to intubate and stablize - epidural dose injected into the subdural space (s/sx may be delayed)
- single-shot spinal after a failed epdiural block
→ volume given during the epidural had to go somewhere- can compress the subarachnoid space and lead to a higher than expected spread with a given spinal dose OR it can leak through the hole and enter the SA space
s/s of a total spinal (4)
rapid progression of sensory and motor block
dyspnea, difficulty speaking, hypotension
T/F- loss of consciousness from a total spinal occurs from the brain being anesthetized
false - result of cerebra lhypoperfusion from severe hypotension
initial treatment for a total spinal (4)
- vasopressors
- IVF fluid
- LUD
- leg elevation
*if pt loses consciousness or is unable to protect airway- intubate
3 differential diagnoses of a total spinal
- amniotic fluid embolism
- anaphylactic shock
- eclampsia?
see image
maternal acidosis and preeclampsia
VEAL CHOP
Variable = cord compression
Early = Head compression
Accelerations = Ok or give O2
Late = Placental insuffiency
Normal fetal HR
110-160
Fetal causes (2) and maternal causes (2) of fetal bradycardia
what is fetal bradycardia
Fetal asphyxia and acidosis
Maternal hypoxemia or drugs tat reduce uteroplacental perfusion
HR <110
Fetal causes (2) and maternal causes (2) of fetal bradycardia
what is fetal bradycardia
Fetal asphyxia and acidosis
Maternal hypoxemia or drugs tat reduce uteroplacental perfusion
HR <110
Fetal causes (2) and Maternal Causes (5) of fetal tachycardia
what is defined as fetal tachycardia
fetal hypoxemia/arrythmias
maternal causes:
Fever
Atropine
Choriomnionitis
Ephedrine
Terbutaline
HR > 160
What does normal fetal HR variability suggest
what is normal HR variability?
suggests intact CNS + normal oxygenation and acid-base blance
6-25bpm
What does lack of fetal HR variability suggest?
fetal distress
causes: CNS depressants, hypoxemia, acidoisis
Between early, late, and variable decels - which ones put the fetus at risk?
late and variable
Variable → Cord compression*
Early → Head compression
Accelerations → Ok/give O2
Late → Placental insuffiency (perfusion)
L
What kind of deceleartions are caused by pre-eclampsia?
Late
add it o the list of P’s - placental insuffiency, pefusion decrease, pre-eclampsia
According to the American College of OBGYNs, which findings are predictive of poor fetal status (select 2):
-sinusoidal pattern
-no late or variable decelerations
-bradycardia without absence of baseline variability
-absent baseline variability
sinusodial pattern & absent baseline variability
The American College of OBGYNS recommends the 3 teir system for evaluation of fetal HR; categories are 1-3, what does each category suggest
1- normal acid-base with no threat
2- cannot predict
3- strongly suggests acid-base abnormailty with a significant threat to fetal oxygenation
Premature delivery is defined as delivery before how many weeks gestation?
Premie = before 37 weeks
What is the leading cause of perinatal M&M
what is this risk even higher for?
premature delivery (before 37 weeks)
newborns weighing < 1500g
In the setting of preterm labor, what is given to hasten fetal lung maturity?
When does it begin to take effect?
peak effect?
Corticosteroids (Betamethasone)
begins to work in 18hrs
peak effect 48hrs
What are tocolytic drugs and when are they used?
4 examples
they delay labor by supressing uterine contractions for up to 24-48 hours providing a bridge that allows exogenous corticosteroids time to hasten fetal lung maturity
Mag sulfate, Beta-agonists, CCBs, Nitric oxide donors
Fetal complications associated with prematurity (3 major ones + 3 others)
- Respiratory distress syndrome
- intraventricular hemorrhage
- necrotizing enterocolitis
hypoglycemia, hypocalcemia
hyperbilirubinemia
What’s the first sign of magnesium toxicity?
diminished DTRs
Beta-2 agonists such as ritodrine and terbutaline arent used today as tocolytic agents but how would they work in supressing uterine contractions?
sciency stuff
Beta 2 stimulation → ↑cAMP → turns on protein kinases and turns off mysoin light-chain kinases → relaxation
How does mag sulfate relax the uterus?
what else does it relax?
why would it be used to treat pts with pre-eclampsia?
mag antagonizes calcium and relaxes smooth muscle by turning off myosin light-chain in the uterus
vasculature and airway
it hyperpolarizes membranes in excitable tissues (seizure prophylaxis)
How is magnesium elminated?
the kidneys - so moms with renal insuffiency should be closely monitored
Normal mag level
1.8-2.5mg/dL
Hypomagnesia symptoms for a mag < 1.2 vs 1.2-1.8 (3 each)
Mag < 1.2: tetany, seizures, dysrhythmias
1.2-1.8: hypoK, hypoCA, & neuromusuclar irritability
Mag symptoms with a level of 2.5-5
none
Diminished DTRs + mild symptoms = mag:
Loss of DTRs + moderate symptoms= mag:
Resp depression> CHG > Coma = mag:
5-7
7-12
>12 +
treatment for hypermagnesemia? (3)
- supportive measures
- diuretics to facilitate mag excretion
- 1g Calcium gluconate over 10 minutes (to antagonize Mag++)
How do CCBs work as a tocolytic?
what’s the first-line agent
they block the influx of calcium into the uterine muscle, which reduces calcium release from the SR which turns off myosin light-chain kinases and relaxes uterine muscle
PO nifedipine
The incidence of prematurity rises with what 2 things?
multiple gestations & premature rupture of membranes
Anesthetic considerations for the use of methergine include:
A. IV administration is safe
B. Tocolysis
C. Administration of 0.2mg
D. Risk of water intoxication
Dose is 0.2mg IM
Medication given for inducing labor
Oxytocin - stimulates contractions
Where is oxytocin primarily synthesized?
where is it stored and released ?
Synthetic equivilent
synthesized → paraventricular nuclei of the hypothalamus
stored in and released from → posterior pituitary
Pitocin
Truth or myth: having sex can help induce labor
True - stimulation of the cervix, vagina, and breasts releases oxytocin which stimulates uterine contraction
During C/S, when should pitocin be administered?
after delivery of the placenta
What is pitocin structurally similar to?
side effects? (5)
water retention, hyponatremia, coronary vasoconstriction
hypotension and reflex tachycardia (don’t geet this- would think it would cause the opposite)
how is oxytocin metabolized?
1/2 life?
by the liver
4-17 minutes (5-15)
What’s the ergot alkaloid?
dose?
Methergine
-second-line uterotonic
0.2mg IM!!!!
What happens if you give methergin IV?
significant vasoconstriction, HTN, and cerebral hemorrhage
how is methergine metabolized?
half life?
liver
(Compared to 5-15min w pitocin)
2 hours
3rd line uterotonic agent
dose
prostaglandin F2 (Hemabate/Carboprost)
250mcg IM or intrauterine
which uterotonic needs to be avodied with pre-eclamptic patients vs asthmatics
no methergine to preeclamptic patients
no hemabate to asthmatics (bronchospasm)
s/e of hemabate/carboprost/prostaglandin F2
N/V/D
hypo,hypertension
bronchospasm
dose for methergine vs hemabate
methergine - 0.2mg IM
hemabate - 250mcg IM
How much higher is mortality in the pregnant population with a general anesthetic?
17x more higher
(4) scenarios where you might opt for general anesthesia over regional for c/s
- maternal hemorrhage
- fetal distress
- contraindications to regional (coagulopathy)
- pt refusal of regional
What is the triple prophylaxis agaisnt aspiration cocktail moms undergoing G/A for a C/S should have? & when?
- sodium citrate (neutralizes gastric acid)
→ 15-30mls, 15-30 minutes before induction - H2 blocker (ranitidine) - reduce gastric acid secretion
→ 1 hour before induction - Gastrokinetic agent (reglan) - increase gastric empty and increase LES tone
→ 1 hour before induction
Why is a defasciulating dose not needed for an RSI on a pregnant patient
bc pregnancy reduces the risk of myalgia
Where should your gases be after confirming tube placement?
volatile at 0.8 MAC (ET Sevo @ 1.6) + 50% nitrous
Normal amniotic fluid volume is ~
700mls
*keep in mind when assessing blood loss
An OB patient at 33-weeks gestation requires a lap appy. Which drug presents the GREATEST risk to fetal well-being:
A. Ketorolac
B. Sux
C. Propofol
D. Morphine
A. Ketorolac
- After the first trimester (12 weeks) NSAIDS can close the ductus arteriosis
NSAIDS should not be given to pregnant moms after what point?
why?
after the first trimester (12 weeks)
can close the ductus arteriosus
2 most significant risks to mom for general surgery while pregnant
what are the risks to baby? (4)
difficult intubation and aspiration
baby: growth delay, low birth weight, demise, preterm labor (highest with intraabdominal and pelvic surgery)
What is the best time for surgery on the pregnant patient?
Ideal vs reality
ideal = 2-6 weeks after delivery
reality = 2nd trimester
When should N20 be avoided in mom?
why?
during the first 2 trimesters
congential defects in animal studies
it inhibits DNA synethesis
At how many weeks are pregnant patients considered a full stomach, requiring RSI and aspiration prophylaxis?
18-20 weeks
*also applies to the immediate postpartum period
The highest risk of teratogenicity?
during organogenesis
day 13-60
When should LUD be used for non-OB surgery?
2nd and 3rd trimester
(>12 weeks)
why should you avoid hyperventilating mom?
reduces placental blood flow (risk of fetal asphyxia)
T/F anesthesia and surgery do not increase the incidence of congenital anomalies
true
Difference between Gestational HTN and Pre-eclampsia
Both occur after 20 weeks gestation, both can be mild (BP > 140/90)
Pre-Eclampsia will also have proteinuria and can be severe >160/110
*only true way to diagnose gestational htn is mom returns to a normotensive state after delivery
Eclampsia vs pre-eclampsia
it becomes eclampsia when the pre-elamptic mom develops seizures
definitive treatment for preeclampsia and eclampsia
delivery of the fetus and placenta
What does HELLP syndrome stand for?
what should you immidately think of when you see ur patient has HELLP syndrome?
Hemolysis, Elevated Liver enzymes, & Low Platelet count
What are their platelets? No epidural/spinal if < 100,000
What does maternal cocaine abuse increase the risk of? (4)
spontaneous abortion, premature labor, placental abruption, low apgar scores
What should you look at when you have a mom with chronic cocaine abuse?
platelet count - check it before spinal/epidural
*chronic cocaine use is associated with thrombocytopenia
T/F- chronic HTN is a risk factor for developing preeclampsia
True
The eitology of developing pre-eclampsia is unknown, however it is more common in moms less than or older than what ages ?
less than 20yo
older than 35yo
What 2 patient populations are at the highest risk for developing preeclampsia?
- pts with chronic renal disease
- pts homozygous for the angiotensinogen T235 allele
The healthy placenta produces what 2 substances in equal amounts
What does the preeclamptic patient produce more of?
What does this lead to? (3)
thromboxane and prostacyclin
7x more THROMBOXANE
vasoconstriction, platelet aggregation, reduced placental blood flow
T/F- up to 40% of patients with eclampsia will be normotensive wehn they ahve their first seizure
true - nuts (haha tree nuts)
At what BP are antihypertensive agents needed for preeclamptic patients?
What 3 things are we trying to prevent?
> 160/110
-CVA, myocardial ischemia, and placental abruption
When is the preeclamptic mom at the highest risk for pulmonary HTN and stroke?
in the postpartum period (up to 4 weeks after delivery)
T/F- HELLP Syndrome can present for the first time in the postpartum period
True
What is cocaine and how does it work?
it’s a ester local anestehtic that inhibits NE reuptake into the presynamptic SNS neuron which floods the synaptic cleft with NE
T/F- chronic cocaine abuse decreases MAC
True (acute intox increases mac)
*opposite ETOH
Treatment for acute HTN in the preeclamptic patient (4 options)
- Labetalol 20mg IV bolus → 40-80mg q 10mins → max dose 220mg
- hydralazine 5mg IV bolus → repeat q20 mins → max 20mg
- nifedipine 10mg po → q20mins → max 50mg
- Nicardipine infusion started at 5mg/hr→ titrate by 2.5mg/hr q 5 mins up to a max of 15 mg/hr
Difference between placenta previa, accreta, increta, and percreta
previa → placenta covers cervical os (think your geting a preview of the placenta)
accreta → attatches t o surface of the myometrium
increta → invades the myometrium
percreta → extends beyond the uterus (per-creata per-forates)
What is assoicated with painless vaginal bleeding?
placenta previa
placenta attaches to the lower uterine segment
covers the cervical os
What is placental abruption (abruptio placentae)
what 3 things is ist associated with?
when the placenta partially or completely separates from the uterine wall before delivery
*associated with pain, vaginal hemorrhage, and fetal hypoxia [painful vaginal bleeding and fetal hypoxia]
Where does the placenta normally implant into?
the decidua of the endometrium
what is the most significant concern regarding abnormal placental implantation?
impaired uterine contractility and the potential for hemorrhage during L&D
What is the MOST common cause of PPH?
uterine atony
3 causes of DIC that occurs during labor and delivery
- amniotic fluid embolism
- placenta abruption
- intrauterine fetal demise
What are 4 risk factors for uterine atony?
- multiparity
- multiple gestations
- polyhydramnios
- prlonged oxytocin infusion before surgery
5 mins following delivery, a newborn has an irregular RR, HR 105, is gramacing, has some flexion in the extremities, and has a pink body with blue extremities. What is the apgar score?
6
What does the apgar scores at 1 and 5 mins correlate with?
1 → acid/base balance
5 → neurologic outcome
Normal Apgar, Moderate distress, impending demise scores
Normal = 8-10
Moderate = 4-7
Severe = 0-3
Normal neonatal HR and RR
HR 120-160 (fetal was 110-160)
RR 30- 60
a neonatal HR less than what significantly reduces CO and impairs tissue perfusion
< 100
When does breathing begin after delivery
when is a normal pattern established?
beings 30 seconds after delivery
normal pattern established at 90 seconds
When does breathing begin after delivery
when is a normal pattern established?
beings 30 seconds after delivery
normal pattern established at 90 seconds
T/F- immediately after delivery, the normal SpO2 is 60%
true
it should rise to 90% after 10 minutes
why should a neonate be ventilated on room air instead of 100% FIO2?
what if they are bradycardic or hypoxia persists?
bc supplemental o2 increases risk of an inflammatory response.
have to blance the risk
t/f- thin or watery meconium should be removed from the airway
false - no clinical benefit
*but should be removed if thick (vomit)
Where should chest compressions be for the neonate and at what depth?
lower 1/3 of the sternum
depth of 1/3 of the AP of the chest
what is the best indicator of adequate ventilation in the neonate
resolution of bradycardia
if ventilation does not improve neonatal cv performance, by what 3 routes can you give emergency drugs?
umbilical vein, ETT, IO
at what HR should chest compressions be started in the neonate
<60
