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Obestetrics > Apex- OB > Flashcards

Apex- OB Flashcards

1
Q

Q: how does the upper airway change during pregnancy
A: everything becomes swollen and engorged
Q: Why though?

A

Progesterone, estrogen and relaxin combined with an increased in ECF volume

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2
Q

Diffult intubation is __x more likely in full term patients?

A

8

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3
Q

How do the lungs change in pregnancy. Early vs later

A

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

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4
Q

Why are pregnant patients more likely to desat faster during apnea?

due

A

due to decreased FRC and increased O2 consumption

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5
Q

How does the acoid/base balance change during pregnancy?

generally speaking

A

progesterone = respiratory stimulant
→ increases mV up to 50%
→ moms PaCO2 decreases → Resp alkalosis (fully compensated)
→ renal compensation lowers bicarb to normalize pH.

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6
Q

P50 of pregnant patient

A

increased/right

right = release, release more o2 to baby

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7
Q

%change in Vt/RR of pregnant patient

A

40% increase in Vt
10% increase in RR

equaling a 50% increase in MV (proegesterone = resp stimulant)

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8
Q

Lung volume changes in pregnant pt
TLC
VC
FRC
ERV
RV
CC

increase/decrease by what % or no change

A

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

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9
Q

VO2 (oxygen consumption) increases by what% when mom is:
Term:
1st stage labor:
2nd stage labor:

A

Term- 20% (25)
1st stage labor- 40% over pre-labor (50)
2nd stage labor - 75% over pre-labor (75)

Relate to CO

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10
Q

What % of cardiac output does the uterus recieve?

A

10%

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11
Q

CO = HR x SV

how much does each variable increase and why?

A

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”)

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12
Q

Compard to pre-labor values, CO during labor increases how much during:
1st stage labor-
2nd stage labor-
3rd stage labor-

A

1st stage labor - 20% (25%)
2nd stage labor - 50%
3rd stage labor - 80% (75%)

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13
Q

When does CO return to pre-labor values?

When does it return to pre-pregnancy values?

A

returns to pre-labor values in 24-48 hours
returns to pre-pregnancy values in ~ 2 weeks

2 days/2 weeks

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14
Q

Pregnancy effects on:
MAP
SBP
DBP

A

MAP - no change
SBP- no change
*DBP decreases 15%

MAP = [(SVR x CO/80)] + CVP or SBP + 2(DBP) / 3 (70-110)

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15
Q

Pregnancy effects on SVR and PVR and why?

A

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

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16
Q

Why doesn’t a pregnant moms MAP increase with all that extra blood volume?

A

bc progesterone increases nitric oxide release from VSM → vasodilation

increased blood volume + decreased SVR = net effect on MAP

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17
Q

True/False: CVP and PAOP are increased with pregnancy

A

False- pregnancy iteself does not alter filling pressures; however, uterine contraction induced autotransfusion does increase filling pressure.

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18
Q

What kind of axis deviation would you expect to see on EKG

A

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

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19
Q

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

A. Decreased ERV

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20
Q

Why do pregnant patients have a dilutional anemia?

A

Bc plasma volume expands faster than RBC production can keep up

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21
Q

LUD should be used when?

A

starting in the 2nd trimester

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22
Q

3 pathways in which progesterone works

A
  1. increased RAAS activity → increased blood volume → increased CO
  2. VSM relaxation (from nitric oxide release) → decreased SVR and PVR → increased blood flow
  3. increased minute ventilation (Vt 40%, RR 10%) → decreased PaCO2 → kidneys eliminate HCO3 to preserve pH
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23
Q

what does aortocaval compression result in?

A

compression of both the vena cava and the aorta
→decreased venous return to heart
→ AND decreased arterial flow to the uterus and lower extermities

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24
Q

LUD elevates the moms (right/left) torso by how many degrees?

A

elevates right torso by 15 degrees

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25
Q

Why does moms intravascular volume increase anyway? and to what % does it increase?

A

to prepare mom for hemorrhage with labor

increases 35%

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26
Q

How much doe Plasma and RBC volume increase

A

Plasma - 45%
RBC 20%

*creates dilutional anemia

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27
Q

What clotting factors are increased during pregnancy?

A

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?

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28
Q

How are anticoagulants affected with pregnancy?

A

decreased antithrombin and protein S
(no change in protein C)

*DVT is 6x higher in pregnant women

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29
Q

Risk for DVT in pregnant women is how many times greater?

A

6x

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30
Q

Is fibrin breakdown increased or decreased in preganancy?

A

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)

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31
Q

How is moms anti-fibrinolytic system affected?

A

decreased factors 11 and 13
→ reduces fibrin polymerization

whatever the fuck that means

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32
Q

How are PT/PTT affected in pregnancy?

A

both decrease by 20%

normal PT = 9-12; normal PTT 25-35

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33
Q

How is platelet count affected by pregnancy?

A

unchanged or decreases up to 10% due to hemodilution and consumption

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34
Q

what is the most common cause of thrombocytopenia? does it increase the rate of complications?

A

gestational thrombocytopenia and no

is this whats from hemodilution and consumption?

other causes may be hypertensive disorders of pregnancy and idopathic

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35
Q

Pregnancy causes MAC to decrease by _____ %

this process begins when?

what is is caused by?

A

decreased mac 30-40%
starts at 8-12 weeks (first T)
caused by increase in progesterone

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36
Q

How is gastric emptying time affected before the onset of labor and after labor begins?

A

unchanged before onset of labor
slows after labor begins

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37
Q

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

A

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

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38
Q

How are the following GI paramaters affected during pregnancy and why:

-Gastric volume
-Gastric pH
-LES sphincter tone
-Gastric emptying

A

-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

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39
Q

How are the following renal parmaters affecting during pregnancy and why?

-GFR
-Creat clearence
-Urine glucose
-BUN and creat

A
  • 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)
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40
Q

urterine blood flow in ml/min

A

700-900ml/min

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41
Q

what is the effect of pregnancy on serum albumin

A

decreased → free fraction of highly protein bound drugs increase

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42
Q

how is pseudocholinesterase affected by pregnancy?

A

it’s decreased but there is no meaningful effect on sux metabolism

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43
Q

T/F - urterine blood flow is autoregulated

A

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

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44
Q

3 drug properties that favor placental transfer:

A
  1. low molecular weight (< 500 daltons)
  2. high lipid solubility
  3. non-ionized
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45
Q

2 causes of reduced uterine blood flow + examples of each

A
  1. Decreased perfusion: Maternal hypotension (sympathectomy, hemorrhage, aortocaval compression)
  2. Increased resistance: uterine contraction, HTN conditions
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46
Q

Neo vs Ephedrine - why one over the other

A

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

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47
Q

What are the 5 drugs that don’t cross the placenta

A

CHING

Chloroprocaine (rapidly metabolized)
Heparin
Insuilin
NMBs
Glycoopyrrolate

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48
Q

Magnesium is not lipophillic but still crosses the placenta - why?

A

low molecular weight

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49
Q

Which stage of labor begins with the onset of perineal pain?

A. Latent
B. Active
C. First
D. Second

A

D. Second

begins with full cervical dilation > delivery of newborn

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50
Q

How many stages of labor and what do each begin/end with?

A

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

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51
Q

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

A

moderate clears throoughout labor
solid food up until neuraxial block is placed

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52
Q

T/F- epidural can prolong the first stage of labor

does it increase the need for a c/s?

A

false

no

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53
Q

What can stage 1 labor be divided into?

A

Latent: onset of regular contractions > cervical dilation of 2-3cm

Active: cervical dilation 3cm > 10cm

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54
Q

Why don’t you have to ask when mom last ate or drank?

A

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

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55
Q

When should moms get an epidural?

A

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.

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56
Q

Stage 1 of labor

A

beginning of regular contractions until cervix is fully dilated (10cm)

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57
Q

Stage 2 labor

A

full cervical dilation (10cm) to delivery of fetus

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58
Q

Stage 3 labor

A

delivery of the placenta

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59
Q

When does the latent phase of labor end?

A

When the cervix dilates 2-3cm

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60
Q

When does the active phase of labor begin?

A

in phase 1 when the cervix is 3-10cm dilated (after the latent phase)

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61
Q

Why is a pudendal block inappropriate for stage 1 labor pain?

A

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
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62
Q

First stage labor pain vs second stage

generally speaking

A

1st stage pain - lower uterine segment and cervix
2nd stage pain - adds in vagina, perineum and pelvic floor

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63
Q

Which block is associated with a high risk of fetal bradycardia?

A

paracervical block

1st stage labor

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64
Q

2 consequences of uncontrolled pain

A
  1. increase in maternal catecholamines → HTN → decreased uterine blood flow
  2. Maternal hyperventilation → left shift in oxyhemoglobin curve → decreased delivery of o2 to the fetus
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65
Q

fill in the blanks

A
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66
Q

If administering nitrous oxide to the pregnant patient, how should it be administered and what does it actually do?

A

50% nitrous and 50% o2 self administered by the patient via facemask

-provides a non-invasive alternative for labor analgesia

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67
Q

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

A

False

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68
Q

T/F- N20 can decrease uterine contractility

A

false - it preserves it

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69
Q

T/F- n20 can cause neonatal depression

A

false

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70
Q

Why do some providers like to do a combined spinal/epidural technique? (CSE)

A

dual benifit of rapid onset of spinal anesthesia and the ability to prolong the duration of anesthesia with an indwelling epidural cath

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71
Q

What is the most common appraoch to CSE?

4 steps

A
  1. epidural needle into epidural space
  2. spinal needle placed through the epidural needle → LA and opioid injected into intrathecal space
  3. Spinal needle removed
  4. Epidural cath is threaded through the epidural needle

“Needle through needle” technique

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72
Q

When doing a CSE, what does the epidural volume extension technique invole and what puprose does it serve?

A

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

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73
Q

Which local anesthetic reduces the efficacy of epdirual morophine?

why?

A

2-Chloroprocaine

it antagonizes mu and kappa receptors in the spinal cord, reducign the efficacy of epdiural morphine

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74
Q

What are the 4 most common local anesthetics used in OB?

A

BPV, Ropi (Long acting)
, Lido (intermediate)
, Chlorprocaine (short acting)

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75
Q

What local anesthetic is contraindicated and epidurals and why?

A

0.75% BPV

-risk of toxicity with IV injection and epidural veins are engorged with pregnancy

76
Q

4 side effects of neuraxial opioids - which is most common

if there are all these side effects, why would you use it?

A
  1. pruritis (most common)
  2. N/V
  3. Sedation
  4. Respiratory depression

  • no loss of sensation or proprioception
  • no sympathectomy (supierior hemodynamic stability)
  • doesnt interfere with moms ability to push
77
Q

Do neuraxial opioids depress the fetus?

A

not meaningfully

78
Q

Why is lidocaine not used for labor analgesia but used if a C/S is needed

A

bc of it’s strong motor block

79
Q

Why shouldnt you give lidocaine in a spinal?

A

can cause neurotoxicity

80
Q

Which opioid possesses local anesthetic properties?

A

Meperidine

81
Q

Why isn’t lidocaine typically used for continuous epidural infusion?

A

tachyphylaxis + it crosses the placenta to a greater degree than the alternatives
+ strong motor block

82
Q

Why dont we just amdminister neuraxial opioids alone instead of with LAs?

A

bc they dont relax the perineum and provide less analgesia compared to locals

83
Q

Dosing of Fentanyl/Su/Morphine/Meperdidne for Spinals

A

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)

84
Q

What 2 opioids can be used for bolus’ing epidurals - dosing?

A

fentanyl 50-100mcg (spinal 15-25)
sufent - 5-10mcg (spinal 1.5-5mcg)

*sufent 10x more potent than fent

85
Q

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

A

C. Subdural injection

the symptoms describe a total spinal & due to the time course ,the most likely explaination is a subdural injection

86
Q

3 ways a patient can develpo a total spinal

A
  1. epidural dose injected into the SA space
    → bad day: get ready to intubate and stablize
  2. epidural dose injected into the subdural space (s/sx may be delayed)
  3. 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
87
Q

s/s of a total spinal (4)

A

rapid progression of sensory and motor block
dyspnea, difficulty speaking, hypotension

88
Q

T/F- loss of consciousness from a total spinal occurs from the brain being anesthetized

A

false - result of cerebra lhypoperfusion from severe hypotension

89
Q

initial treatment for a total spinal (4)

A
  1. vasopressors
  2. IVF fluid
  3. LUD
  4. leg elevation

*if pt loses consciousness or is unable to protect airway- intubate

90
Q

3 differential diagnoses of a total spinal

A
  1. amniotic fluid embolism
  2. anaphylactic shock
  3. eclampsia?
91
Q

see image

A

maternal acidosis and preeclampsia

VEAL CHOP
Variable = cord compression
Early = Head compression
Accelerations = Ok or give O2
Late = Placental insuffiency

92
Q

Normal fetal HR

A

110-160

93
Q

Fetal causes (2) and maternal causes (2) of fetal bradycardia

what is fetal bradycardia

A

Fetal asphyxia and acidosis
Maternal hypoxemia or drugs tat reduce uteroplacental perfusion

HR <110

94
Q

Fetal causes (2) and maternal causes (2) of fetal bradycardia

what is fetal bradycardia

A

Fetal asphyxia and acidosis
Maternal hypoxemia or drugs tat reduce uteroplacental perfusion

HR <110

95
Q

Fetal causes (2) and Maternal Causes (5) of fetal tachycardia

what is defined as fetal tachycardia

A

fetal hypoxemia/arrythmias
maternal causes:
Fever
Atropine
Choriomnionitis
Ephedrine
Terbutaline

HR > 160

96
Q

What does normal fetal HR variability suggest

what is normal HR variability?

A

suggests intact CNS + normal oxygenation and acid-base blance

6-25bpm

97
Q

What does lack of fetal HR variability suggest?

A

fetal distress

causes: CNS depressants, hypoxemia, acidoisis

98
Q

Between early, late, and variable decels - which ones put the fetus at risk?

A

late and variable

Variable → Cord compression*
Early → Head compression
Accelerations → Ok/give O2
Late → Placental insuffiency (perfusion)
L

99
Q

What kind of deceleartions are caused by pre-eclampsia?

A

Late

add it o the list of P’s - placental insuffiency, pefusion decrease, pre-eclampsia

100
Q

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

A

sinusodial pattern & absent baseline variability

101
Q

The American College of OBGYNS recommends the 3 teir system for evaluation of fetal HR; categories are 1-3, what does each category suggest

A

1- normal acid-base with no threat
2- cannot predict
3- strongly suggests acid-base abnormailty with a significant threat to fetal oxygenation

102
Q

Premature delivery is defined as delivery before how many weeks gestation?

A

Premie = before 37 weeks

103
Q

What is the leading cause of perinatal M&M

what is this risk even higher for?

A

premature delivery (before 37 weeks)

newborns weighing < 1500g

104
Q

In the setting of preterm labor, what is given to hasten fetal lung maturity?

When does it begin to take effect?

peak effect?

A

Corticosteroids (Betamethasone)

begins to work in 18hrs

peak effect 48hrs

105
Q

What are tocolytic drugs and when are they used?

4 examples

A

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

106
Q

Fetal complications associated with prematurity (3 major ones + 3 others)

A
  1. Respiratory distress syndrome
  2. intraventricular hemorrhage
  3. necrotizing enterocolitis

hypoglycemia, hypocalcemia
hyperbilirubinemia

107
Q

What’s the first sign of magnesium toxicity?

A

diminished DTRs

108
Q

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

A

Beta 2 stimulation → ↑cAMP → turns on protein kinases and turns off mysoin light-chain kinases → relaxation

109
Q

How does mag sulfate relax the uterus?

what else does it relax?

why would it be used to treat pts with pre-eclampsia?

A

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)

110
Q

How is magnesium elminated?

A

the kidneys - so moms with renal insuffiency should be closely monitored

111
Q

Normal mag level

A

1.8-2.5mg/dL

112
Q

Hypomagnesia symptoms for a mag < 1.2 vs 1.2-1.8 (3 each)

A

Mag < 1.2: tetany, seizures, dysrhythmias
1.2-1.8: hypoK, hypoCA, & neuromusuclar irritability

113
Q

Mag symptoms with a level of 2.5-5

A

none

114
Q

Diminished DTRs + mild symptoms = mag:
Loss of DTRs + moderate symptoms= mag:
Resp depression> CHG > Coma = mag:

A

5-7
7-12
>12 +

115
Q

treatment for hypermagnesemia? (3)

A
  1. supportive measures
  2. diuretics to facilitate mag excretion
  3. 1g Calcium gluconate over 10 minutes (to antagonize Mag++)
116
Q

How do CCBs work as a tocolytic?

what’s the first-line agent

A

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

117
Q

The incidence of prematurity rises with what 2 things?

A

multiple gestations & premature rupture of membranes

118
Q

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

A

Dose is 0.2mg IM

119
Q

Medication given for inducing labor

A

Oxytocin - stimulates contractions

120
Q

Where is oxytocin primarily synthesized?

where is it stored and released ?

Synthetic equivilent

A

synthesized → paraventricular nuclei of the hypothalamus

stored in and released from → posterior pituitary

Pitocin

121
Q

Truth or myth: having sex can help induce labor

A

True - stimulation of the cervix, vagina, and breasts releases oxytocin which stimulates uterine contraction

122
Q

During C/S, when should pitocin be administered?

A

after delivery of the placenta

123
Q

What is pitocin structurally similar to?

side effects? (5)

A

water retention, hyponatremia, coronary vasoconstriction

hypotension and reflex tachycardia (don’t geet this- would think it would cause the opposite)

124
Q

how is oxytocin metabolized?

1/2 life?

A

by the liver

4-17 minutes (5-15)

125
Q

What’s the ergot alkaloid?

dose?

A

Methergine
-second-line uterotonic

0.2mg IM!!!!

126
Q

What happens if you give methergin IV?

A

significant vasoconstriction, HTN, and cerebral hemorrhage

127
Q

how is methergine metabolized?

half life?

A

liver

(Compared to 5-15min w pitocin)

2 hours

128
Q

3rd line uterotonic agent

dose

A

prostaglandin F2 (Hemabate/Carboprost)

250mcg IM or intrauterine

129
Q

which uterotonic needs to be avodied with pre-eclamptic patients vs asthmatics

A

no methergine to preeclamptic patients
no hemabate to asthmatics (bronchospasm)

130
Q

s/e of hemabate/carboprost/prostaglandin F2

A

N/V/D
hypo,hypertension
bronchospasm

131
Q

dose for methergine vs hemabate

A

methergine - 0.2mg IM
hemabate - 250mcg IM

132
Q

How much higher is mortality in the pregnant population with a general anesthetic?

A

17x more higher

133
Q

(4) scenarios where you might opt for general anesthesia over regional for c/s

A
  1. maternal hemorrhage
  2. fetal distress
  3. contraindications to regional (coagulopathy)
  4. pt refusal of regional
134
Q

What is the triple prophylaxis agaisnt aspiration cocktail moms undergoing G/A for a C/S should have? & when?

A
  1. sodium citrate (neutralizes gastric acid)
    → 15-30mls, 15-30 minutes before induction
  2. H2 blocker (ranitidine) - reduce gastric acid secretion
    → 1 hour before induction
  3. Gastrokinetic agent (reglan) - increase gastric empty and increase LES tone
    → 1 hour before induction
135
Q

Why is a defasciulating dose not needed for an RSI on a pregnant patient

A

bc pregnancy reduces the risk of myalgia

136
Q

Where should your gases be after confirming tube placement?

A

volatile at 0.8 MAC (ET Sevo @ 1.6) + 50% nitrous

137
Q

Normal amniotic fluid volume is ~

A

700mls

*keep in mind when assessing blood loss

138
Q

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

A. Ketorolac

  • After the first trimester (12 weeks) NSAIDS can close the ductus arteriosis
139
Q

NSAIDS should not be given to pregnant moms after what point?

why?

A

after the first trimester (12 weeks)

can close the ductus arteriosus

140
Q

2 most significant risks to mom for general surgery while pregnant

what are the risks to baby? (4)

A

difficult intubation and aspiration

baby: growth delay, low birth weight, demise, preterm labor (highest with intraabdominal and pelvic surgery)

141
Q

What is the best time for surgery on the pregnant patient?
Ideal vs reality

A

ideal = 2-6 weeks after delivery
reality = 2nd trimester

142
Q

When should N20 be avoided in mom?

why?

A

during the first 2 trimesters

congential defects in animal studies

it inhibits DNA synethesis

143
Q

At how many weeks are pregnant patients considered a full stomach, requiring RSI and aspiration prophylaxis?

A

18-20 weeks

*also applies to the immediate postpartum period

144
Q

The highest risk of teratogenicity?

A

during organogenesis

day 13-60

145
Q

When should LUD be used for non-OB surgery?

A

2nd and 3rd trimester
(>12 weeks)

146
Q

why should you avoid hyperventilating mom?

A

reduces placental blood flow (risk of fetal asphyxia)

147
Q

T/F anesthesia and surgery do not increase the incidence of congenital anomalies

A

true

148
Q

Difference between Gestational HTN and Pre-eclampsia

A

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

149
Q

Eclampsia vs pre-eclampsia

A

it becomes eclampsia when the pre-elamptic mom develops seizures

150
Q

definitive treatment for preeclampsia and eclampsia

A

delivery of the fetus and placenta

151
Q

What does HELLP syndrome stand for?

what should you immidately think of when you see ur patient has HELLP syndrome?

A

Hemolysis, Elevated Liver enzymes, & Low Platelet count

What are their platelets? No epidural/spinal if < 100,000

152
Q

What does maternal cocaine abuse increase the risk of? (4)

A

spontaneous abortion, premature labor, placental abruption, low apgar scores

153
Q

What should you look at when you have a mom with chronic cocaine abuse?

A

platelet count - check it before spinal/epidural

*chronic cocaine use is associated with thrombocytopenia

154
Q

T/F- chronic HTN is a risk factor for developing preeclampsia

A

True

155
Q

The eitology of developing pre-eclampsia is unknown, however it is more common in moms less than or older than what ages ?

A

less than 20yo
older than 35yo

156
Q

What 2 patient populations are at the highest risk for developing preeclampsia?

A
  1. pts with chronic renal disease
  2. pts homozygous for the angiotensinogen T235 allele
157
Q

The healthy placenta produces what 2 substances in equal amounts

What does the preeclamptic patient produce more of?

What does this lead to? (3)

A

thromboxane and prostacyclin

7x more THROMBOXANE

vasoconstriction, platelet aggregation, reduced placental blood flow

158
Q

T/F- up to 40% of patients with eclampsia will be normotensive wehn they ahve their first seizure

A

true - nuts (haha tree nuts)

159
Q

At what BP are antihypertensive agents needed for preeclamptic patients?

What 3 things are we trying to prevent?

A

> 160/110

-CVA, myocardial ischemia, and placental abruption

160
Q

When is the preeclamptic mom at the highest risk for pulmonary HTN and stroke?

A

in the postpartum period (up to 4 weeks after delivery)

161
Q

T/F- HELLP Syndrome can present for the first time in the postpartum period

A

True

162
Q

What is cocaine and how does it work?

A

it’s a ester local anestehtic that inhibits NE reuptake into the presynamptic SNS neuron which floods the synaptic cleft with NE

163
Q

T/F- chronic cocaine abuse decreases MAC

A

True (acute intox increases mac)

*opposite ETOH

164
Q

Treatment for acute HTN in the preeclamptic patient (4 options)

A
  1. Labetalol 20mg IV bolus → 40-80mg q 10mins → max dose 220mg
  2. hydralazine 5mg IV bolus → repeat q20 mins → max 20mg
  3. nifedipine 10mg po → q20mins → max 50mg
  4. Nicardipine infusion started at 5mg/hr→ titrate by 2.5mg/hr q 5 mins up to a max of 15 mg/hr
165
Q

Difference between placenta previa, accreta, increta, and percreta

A

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)

166
Q

What is assoicated with painless vaginal bleeding?

A

placenta previa

placenta attaches to the lower uterine segment

covers the cervical os

167
Q

What is placental abruption (abruptio placentae)

what 3 things is ist associated with?

A

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]

168
Q

Where does the placenta normally implant into?

A

the decidua of the endometrium

169
Q

what is the most significant concern regarding abnormal placental implantation?

A

impaired uterine contractility and the potential for hemorrhage during L&D

170
Q

What is the MOST common cause of PPH?

A

uterine atony

171
Q

3 causes of DIC that occurs during labor and delivery

A
  1. amniotic fluid embolism
  2. placenta abruption
  3. intrauterine fetal demise
172
Q

What are 4 risk factors for uterine atony?

A
  1. multiparity
  2. multiple gestations
  3. polyhydramnios
  4. prlonged oxytocin infusion before surgery
173
Q

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?

A

6

174
Q

What does the apgar scores at 1 and 5 mins correlate with?

A

1 → acid/base balance
5 → neurologic outcome

175
Q

Normal Apgar, Moderate distress, impending demise scores

A

Normal = 8-10
Moderate = 4-7
Severe = 0-3

176
Q

Normal neonatal HR and RR

A

HR 120-160 (fetal was 110-160)
RR 30- 60

177
Q

a neonatal HR less than what significantly reduces CO and impairs tissue perfusion

A

< 100

178
Q

When does breathing begin after delivery

when is a normal pattern established?

A

beings 30 seconds after delivery

normal pattern established at 90 seconds

179
Q

When does breathing begin after delivery

when is a normal pattern established?

A

beings 30 seconds after delivery

normal pattern established at 90 seconds

180
Q

T/F- immediately after delivery, the normal SpO2 is 60%

A

true

it should rise to 90% after 10 minutes

181
Q

why should a neonate be ventilated on room air instead of 100% FIO2?

what if they are bradycardic or hypoxia persists?

A

bc supplemental o2 increases risk of an inflammatory response.

have to blance the risk

182
Q

t/f- thin or watery meconium should be removed from the airway

A

false - no clinical benefit

*but should be removed if thick (vomit)

183
Q

Where should chest compressions be for the neonate and at what depth?

A

lower 1/3 of the sternum
depth of 1/3 of the AP of the chest

184
Q

what is the best indicator of adequate ventilation in the neonate

A

resolution of bradycardia

185
Q

if ventilation does not improve neonatal cv performance, by what 3 routes can you give emergency drugs?

A

umbilical vein, ETT, IO

186
Q

at what HR should chest compressions be started in the neonate

A

<60

Obestetrics (4 decks)

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