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APEX > Unit 11 - Obstetrics > Flashcards

Unit 11 - Obstetrics Flashcards

1
Q

factors that make airway management more complicated in pregnant patients

A
  • increased Mallampati score
  • upper airway vascular engorgement
  • narrowing of glottic opening
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2
Q

why should a smaller ETT be used in pregnant patients

A

narrowed glottic opening

use 6.0-7.0

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3
Q

3 factors that make airway edema worse in pregnant women

A
  • preeclampsia
  • tocolytics
  • prolonged Trendelenburg
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4
Q

function of hormone relaxin in early pregnancy

A

relaxes the ligaments in the ribcage, allowing the ribs to assume a more horizontal position

Increases the AP diameter of the chest, which gives the lungs more space

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5
Q

what hormones contribute to vascular engorgement and hyperemia in pregnancy

A
  • progesterone
  • estrogen
  • relaxin
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6
Q

laryngoscope handle recommended for large-breasted women

A

Data handle (short handle)

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7
Q

why should nasal intubation be avoided in full term mothers

A

tissue in the nasopharynx is particularly friable d/t hormonal changes and local edema

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8
Q

why are pregnant women at increased risk of rapid hypoxemia during periods of apnea

A

increased O2 consumption + decreased FRC

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9
Q

why do pregnant women experience airway closure during tidal breathing

A

FRC falls below closing capacity

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10
Q

Vm in pregnancy

A

increased up to 50%

progesterone is a respiratory stimulant

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11
Q

why do pregnant women have a respiratory alkalosis

A

Progesterone is a respiratory stimulant = increased Vm by up to 50% =mom’s PaCO2 falls

Compensatory respiratory alkalosis develops

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12
Q

how does a pregnant woman’s body normalize blood pH despite increased Vm

A

renal compensation eliminates bicarbonate to normalize blood pH

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13
Q

what explains a pregnant mom’s mild increase in PaO2

A

small reduction in physiologic shunt

increases the driving pressure of oxygen across the fetoplacental interface and improves fetal gas exchange

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14
Q

what explains a pregnant mom’s mild increase in PaO2

A

small reduction in physiologic shunt

increases the driving pressure of oxygen across the fetoplacental interface and improves fetal gas exchange

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15
Q

ABG changes in pregnancy:
pH
PaO2
PaCO2
HCO3-

A
  • pH: no change
  • PaO2: increased
  • PaCO2: decreased
  • HCO3-: decreased
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16
Q

normal PaO2 in pregnancy

A

104-108 mmHg

d/t hyperventilation

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17
Q

normal PaCO2 in pregnancy

A

28-32 mmHg

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18
Q

normal HCO3- in pregnancy

A

20 mmol/L

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19
Q

changes in oxyhgb dissociation curve in pregnancy

A

↑ P50
Facilitates O2 transfer to fetus

right shift of curve

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19
Q

changes in Vm in pregnancy

A

Vm increases up to 50%
Vt ↑ 40%
RR ↑ 10%

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20
Q

changes in lung volumes and capacities in pregnancy
* TLC
* VC
* FRC
* ERV
* RV
* Closing capacity

A
  • TLC = ↓ 5%
  • VC = no change
  • FRC = ↓ 20%
  • ERV = ↓ 20-25%
  • RV = ↓ 15-20%
  • closing capacity = no change
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21
Q

why is there no change in closing capacity in pregnant patients

A

↑ CV + ↓ RV = no change in closing capacity

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22
Q

oxygen consumption in pregnancy:
* term
* 1st stage of labor
* 2nd stage of labor

A
  • Term = ↑ 20%
  • 1st stage of labor = ↑ 40%
  • 2nd stage of labor = ↑ 75%
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23
Q

CO received by uterus

A

10%

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24
Q

hemodynamic variables that increase in pregnancy

A

HR
Stroke volume

CO increased 40%

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25
Q

CO during labor

A
  • 1st stage: CO ↑ 20%
  • 2nd stage: CO ↑ 50%
  • 3rd stage: CO ↑ 80%
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26
Q

when does CO return to pre-labor values

A

24-48 hours

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27
Q

when does CO return to pre-pregnancy values

A

~2 weeks

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28
Q

how do twins affect CO

A

↑ 20% above single fetus

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29
Q

changes in MAP, SBP, and DBP in pregnancy

A

MAP & SBP remain stable
DBP ↓ 15%

↑ blood volume + ↓ SVR = net even effect on MAP

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30
Q

changes in MAP, SBP, and DBP in pregnancy

A

MAP & SBP remain stable
DBP ↓ 15%

↑ blood volume + ↓ SVR = net even effect on MAP

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31
Q

changes in vascular resistance in pregnancy

A

SVR = ↓ 15%
PVR = ↓ 30%

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32
Q

how does progesterone affect vascular resistance in pregnancy

A
  • ↑ nitric oxide = vasodilation (↓ SVR)
  • ↓ response to angiotensin & NE (↓ PVR)
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33
Q

how are CVP and PAOP affected by pregnancy

A

Pregnancy by itself doesn’t alter filling pressure, however autotransfusion during uterine contraction increases filling pressure

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34
Q

cardiac axis in pregnancy

A

left axis deviation

Gravid uterus pushes diaphragm cephalad = heart pushed up and left

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35
Q

cardiac axis in pregnancy

A

left axis deviation

Gravid uterus pushes diaphragm cephalad = heart pushed up and left

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36
Q

what causes aortocaval compression in pregnant women

A

gravid uterus compresses both the vena cava and the aorta = ↓venous return to the heart as well as arterial flow to the uterus and lower extremities

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37
Q

how can aortocaval compression be reduced

A

elevating the mother’s right torso 15 degrees
(left uterine displacement)

displaces the uterus away from the vena cava and aorta

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38
Q

when should LUD be used for pregnant women

A

starting in 2nd trimester

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39
Q

changes in intravascular fluid volume in pregnancy

A

↑ 35%

prepares mom for hemorrhage w/ labor

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40
Q

changes in intravascular fluid volume in pregnancy

A

↑ 35%

prepares mom for hemorrhage w/ labor

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41
Q

what causes dilutional anemia in pregnant women

A

increased intravascular fluid volue, plasma vol, and erythrocyte volume

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42
Q

clotting factors increased in pregnancy

A

↑ 1, 7, 8, 9, 10, 12

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43
Q

protein S in pregnancy

A

decreased

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44
Q

protein C in pregnancy

A
  • no change in protein C
  • resistance to activated protein C
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45
Q

how is hypercoagulability counteracted in pregnancy

A

increased fibrin breakdown

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46
Q

why do pregnant moms have a tendency to develop consumption coagulopathy

A

mom makes more clots but also breaks them down faster

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47
Q

changes in PT, PTT and plt count in pregnancy

A
  • PT & PTT = ↓ up to 20%
  • Plt = unchanged or ↓ 10% d/t hemodilution & comsumption
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48
Q

Most common cause of thrombocytopenia during pregnancy

A

gestational thrombocytopenia
(does not increase rate of complications)

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49
Q

etiologies of thrombocytopenia in pregnancy

A
  • gestational (most common)
  • hypertensive disorders
  • idiopathic
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50
Q

how does pregnancy affect MAC

A

↓ 30-40% from baseline due to ↑ progesterone

(begins at 8-12 weeks)

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50
Q

how does pregnancy affect MAC

A

↓ 30-40% from baseline due to ↑ progesterone

(begins at 8-12 weeks)

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51
Q

why are pregnant women more sensitive to LAs

A

↑ progesterone

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52
Q

why is a decreased epidural LA dose given to pregnant women

A

Epidural vein volume increases = decreased volume of subarachnoid & epidural spaces (compression)

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53
Q

effects of increased gastrin in pregnancy

A

↑ gastric volume
↓ gastric pH

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54
Q

how does gastric emtpying change in pregnancy

A

↓ after labor begins
no change before

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55
Q

LES sphincter tone in pregnancy

A

decreased

d/t ↑ progesterone, ↑ estrogen, cephalad displacement of diaphragm

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56
Q

LES sphincter tone in pregnancy

A

decreased

d/t ↑ progesterone, ↑ estrogen, cephalad displacement of diaphragm

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57
Q

CrCl in pregnancy

A

increased

↑ blood volume = ↑ Cr delivered to kidney per unit time

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58
Q

CrCl in pregnancy

A

increased

↑ blood volume = ↑ Cr delivered to kidney per unit time

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59
Q

GFR in pregnancy

A

increased

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60
Q

Cr and BUN in pregnancy

A

decreased

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61
Q

uterine blood flow in pregnancy

A

↑ up to 700-900 mL/min

accounts for 10% of CO

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62
Q

uterine blood flow in pregnancy

A

↑ up to 700-900 mL/min

accounts for 10% of CO

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63
Q

serum albumin in pregnancy

A

↓ = increased free fraction of highly protein bound drugs

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64
Q

pseudocholinesterase in pregnancy

A

↓
no meaningful effect on succs metabolism

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65
Q

urine glucose in pregnancy

A

increased as a result of ↑ GFR and reduced reabsorption in peritubular capillaries

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66
Q

uterine blood flow in non-pregnant state

A

100 mL/min

pregnant = up to 700 mL/min

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67
Q

uterine blood flow in non-pregnant state

A

100 mL/min

pregnant = up to 700-900 mL/min

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68
Q

is uterine blood flow autoregulated

A

no - dependent on MAP, CO, and uterine vascular resistance

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69
Q

uterine blood flow =

A

(uterine artery pressure - uterine venous pressure) / uterine vascular resistance

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70
Q

2 factors that ↓ Uterine Blood Flow

A
  • Decreased perfusion
  • Increased resistance
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71
Q

what can cause decreased uterine perfusion and therefore decreased UBF

A

maternal hypotension (sympathectomy, hemorrhage, aortocaval compression)

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72
Q

what can cause increased resistance and therefore ↓ UBF

A

uterine contraction, hypertensive conditions that ↑ UVR

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73
Q

most important variables in placental drug transfer

A
  • diffusion coefficient (drug characteristics)
  • concentration gradient between maternal and fetal circulation
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74
Q

principle that describes how a drug traverses a biologic membrane

A

Fick principle

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75
Q

4 drug characteristics that favor placental transfer:

A
  • Low molecular weight (< 500 Daltons)
  • High lipid solubility
  • Non-ionized
  • Non-polar

(most anesthetic drugs are smaller than 500 daltons)

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76
Q

meds that do NOT undergo placental transfer

A
  • NMBs
  • glycopyrrolate
  • heparin
  • insulin
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77
Q

Do LAs undergo placental transfer

A

yes except chloroprocaine (rapid ester metabolism)

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78
Q

stage 1 of labor

A

Beginning of regular contractions to full cervical dilation (10 cm)

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79
Q

stage 2 of labor

A

Full cervical dilation to delivery of fetus

Perineal pain begins

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80
Q

illustrates normal progress of labor

A

Friedman curve

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81
Q

stage 3 of labor

A

delivery of placenta

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82
Q

what is dysfunctional labor

A

doesn’t follow expected pattern of Friedman curve

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83
Q

Friedman curve - Latent phase

A

1-8 hours
Cervical dilation: 2-3 cm

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84
Q

Friedman curve - active phase

A

hours 8-13
Full cervical dilation

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85
Q

Friedman curve - fetal delivery

A

hours 14-16

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86
Q

NPO ASA Practice Guidelines for Obstetric Analgesia

A

a healthy laboring mother may:
* Drink moderate amount of clear liquids throughout labor
* Eat solid food up to the point the neuraxial block is placed

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87
Q

when does the latent phase of labor end

A

when the cervix dilates to 2-3 cm

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88
Q

when does the active phase of labor occur

A

in stage 1 when cervix is 3-10 cm dilated

after latent phase

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89
Q

when does the active phase of labor occur

A

in stage 1 when cervix is 3-10 cm dilated

after latent phase

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90
Q

how does epidural analgesia affect the progress of labor

A

it does NOT prolong the first stage of labor

91
Q

where does pain begin in 1st stage of labor

A

lower uterine segment and cervix

92
Q

where does pain originate in 1st stage of labor

A

T10-L1 posterior nerve roots

93
Q

pain impulses in 2nd stage of labor

A

adds in pain impulse from vagina, perineum, and pelvic floor

94
Q

where do pain impulses travel from in 2nd stage of labor

A

from perineum to S2-S4 posterior nerve roots

95
Q

innervates the perineum

A

pudendal n.

derives from S2-S4

pudendal n. block is not useful in 1st stage of labor

96
Q

innervates the perineum

A

pudendal n.

derives from S2-S4

pudendal n. block is not useful in 1st stage of labor

97
Q

analgesic options that target 1st stage labor pain

A
  • Neuraxial (spinal, epidural, CSE)
  • Paravertebral lumbar block
  • Paracervical block
98
Q

analgesic options that target 2nd stage labor pain

A
  • Neuraxial (spinal, epidural, CSE)
  • Pudendal nerve block
99
Q

afferent pathway assoc. with first stage of labor

A

Visceral C fibers hypogastric plexus

100
Q

afferent pathway assoc. with 2nd stage of labor

A

pudednal n.

101
Q

quality of pain in 1st stage of labor

A

Dull
Diffuse
Cramping

102
Q

quality of pain in 2nd stage of labor

A

Sharp
Well localized

103
Q

regional technique in 1st stage of labor assoc with high risk of fetal bradycardia

A

paracervical block

104
Q

dual benefit of CSE

A

rapid onset of spinal anesthesia and ability to prolong duration of anesthesia with indwelling epidural catheter

105
Q

“needle through needle” technique for CSE

A
  • Epidural space identified with epidural needle
  • spinal needle placed through epidural needle
  • LA and opioid injected in intrathecal space
  • spinal needle removed
  • epidural catheter threaded through epidural needle
106
Q

Epidural volume extension technique for CSE

A
  • involves injecting saline into epidural space immediately after LA injected into subarachnoid space
  • compresses subarachnoid space & enhances rostral spread of LA (achieve higher level for given dose)
107
Q

total neuraxial coverage needed for 2nd stage of labor

A

T10-S4

108
Q

how does the maternal breathing pattern affect fetal oxygenation

A

maternal hyperventilation = L shift of oxyhgb curve = decreased O2 delivery to fetus

109
Q

which LA reduces the efficacy of epidural morphine

A

2-chloroprocaine

Antagonizes opioid receptors (mu & kappa) and reduces efficacy of epidural morphine

110
Q

LAs commonly used in OB

A
  • bupivacaine
  • ropivacaine
  • lidocaine
  • 2-chloroprocaine
111
Q

concentration of bupivacaine contraindicated via epidural

A

0.75%

risk toxicity with IV injection

112
Q

concentration of bupivacaine contraindicated via epidural

A

0.75%

risk toxicity with IV injection

113
Q

placental transfer of bupivacaine

A

low d/t ↑ protein binding and ↑ ionization

114
Q

LA used in OB with greater sensory block relative to other LAs

A

bupivacaine

115
Q

benefits of neuraxial opioids when used alone

A
  • no loss of sensation or proprioception
  • no sympathectomy
  • do not impair mom’s ability to push
116
Q

neuraxial opioid with LA properties

A

meperidine

117
Q

LA useful for emergency C/S when epidural is already in place

A

2-Chloroprocaine

very fast onset

118
Q

LA useful for emergency C/S when epidural is already in place

A

2-Chloroprocaine

very fast onset

119
Q

receptors antagonized by neuraxial 2-chloroprocaine

A

mu & kappa opioid receptors

120
Q

neuraxial LA with risk of arachnoiditis when used for spinal anesthesia

A

2-chloroprocaine

due to preservatives

120
Q

neuraxial LA with risk of arachnoiditis when used for spinal anesthesia

A

2-chloroprocaine

due to preservatives

121
Q

SEs of neuraxial opioids

A
  • pruritis (most common)
  • N/V
  • sedation
  • respiratory depression
122
Q

LA that is not popular for labor analgesia

A

lidocaine

strong motor block (good for c section)

123
Q

spinal dose of bupivacaine

A

1.5-5 mg

124
Q

epidural bupivacaine

A

bolus: 0.0625 – 0.125%
infusion: 0.5 – 0.125%

125
Q

spinal ropivacaine dose

A

2 – 3.5 mg

126
Q

epidural ropivacaine

A

bolus & infusion: 0.08 – 0.2%

127
Q

why is lidocaine typically not used for continuous epidural infusion

A
  • tachyphylaxis is more likely to develop
  • crosses placenta to greater degree than others
128
Q

mL/hr for lumbar epidural infusion

A

8-15 mL/hr

129
Q

spinal bolus of fentanyl

A

15-25 mcg

130
Q

epidural fentanyl dosing

A

bolus: 50-100 mcg
epidural: 1.5-3 mcg/mL

131
Q

spinal bolus of sufentanil

A

1.5-5 mcg

132
Q

sufentanil epidural dosing

A

bolus: 5-10 mcg
infusion: 0.2-0.4 mcg/mL

133
Q

spinal dose of morphine

A

125-250 mg

134
Q

epi dosing as a spinal adjuvant

A

2.25-200 mcg

135
Q

epidural dosing of epi

as an adjuvant

A

bolus: 25 – 75 mcg
infusion: 20 – 50 mcg/hr

136
Q

spinal dose of clonidine

A

15-30 mcg

137
Q

epidural dosing of clonidine

A

bolus: 75-100 mcg
infusion: 10-30 mcg/hr

138
Q

epidural dosing of neostigmine

A

bolus = 500-100 mcg
infusion = 25-75 mcg/hr

139
Q

3 ways an OB patient can develop a high spinal

A
  • Epidural dose injected into subarachnoid space
  • Epidural dose injected into subdural space
  • Single shot spinal after a failed epidural block
140
Q

treatment of a total spinal

A

supportive
airway management
IVF
vasopressors
LUD
leg elevation

141
Q

typical presentation of total spinal caused by epidural dose injected in subdural space

A

s/s excessive cephalad spread 10-15 minutes after epidural dosed

142
Q

can a subdural injection be ruled out

A

Neither catheter aspiration nor a test dose will rule out subdural placement

143
Q

how can a single-shot spinal after a failed epidural lead to a high/total spinal

A
  • Volume given during epidural can compress subarachnoid space. If single-shot spinal admin in this situation, you might get a higher-than-expected spread with a given dose
  • Will puncture dura during single-shot spinal - possible LA from failed epidural leaks through hole to enter subarachnoid space
144
Q

presentation of total spinal

A
  • typically rapid progression of sensory and motor block
  • Dyspnea, difficulty phonating, hypotension
  • hypotension = cerebral hypoperfusion = LOC
145
Q

differential diagnosis when OB pt presents with s/s total spinal

A
  • anaphylactic shock
  • eclampsia
  • amniotic fluid embolism
146
Q

surrogate measure of overall fetal wellbeing

Provides indirect method to assess fetal hypoxia & acidosis

A

FHR

147
Q

fetal oxygenation is a function of what 2 things

A

uterine blood flow
placental blood flow

148
Q

how does the fetus respond to stress

A
  • peripheral vasoconstriction
  • HTN
  • baroreceptor-mediated reduced HR
149
Q

normal FHR

A

110-160

150
Q

fetal causes of fetal bradycardia

A

Asphyxia
Acidosis

FHR < 110

151
Q

maternal causes of fetal bradycardia

A
  • Hypoxemia
  • Drugs that ↓ uteroplacental perfusion
152
Q

fetal causes of fetal tachycardia

A

Hypoxemia
Arrhythmias

153
Q

maternal causes of fetal tachycardia

A

Fever
Chorioamnionitis
Atropine
Ephedrine
Terbutaline

154
Q

normal FHR variability

A

6-25 bpm

155
Q

what does FHR variability suggest

A
  • intact central nervous system
  • SNS and PNS are functioning in a healthy manner
  • Also an indicator of oxygenation and a normal acid-base status
156
Q

FHR variability:
* minimal
* moderate
* marked
* absent

A
  • Minimal: < 5 bpm
  • Moderate: 6 - 25 bpm
  • Marked: > 25 bpm
  • Absent: a worrisome finding
157
Q

things that decrease FHR variability

A
  • CNS depressants (opioids, sedatives
    anesthetics, barbiturates, magnesium sulfate)
  • hypoxemia
  • fetal sleep
  • acidosis
  • anencephaly
  • cardiac anomalies
158
Q

what causes early decels

A

Uterine contractions compress fetal head

159
Q

FHR with early decels

A

HR < 20 from baseline

160
Q

change in HR with early decels

A

< 20 from baseline

161
Q

onset & offset of early decels compared to contractions

A

Onset and offset parallels uterine contraction

Loses variability with each deceleration

162
Q

onset & offset of early decels compared to contractions

A

Onset and offset parallels uterine contraction

Loses variability with each deceleration

163
Q

risk to baby with early decels

A

no risk of fetal hypoxia

164
Q

condition that may cause this FHR pattern

A

head compression

early decels

165
Q

conditions that contribute to this FHR pattern

A
  • maternal hypotension
  • hypovolemia
  • acidosis
  • preeclampsia

late decels

166
Q

conditions that contribute to this FHR pattern

A

maternal:
* hypotension
* hypovolemia
* acidosis
* preeclampsia

late decels

167
Q

what causes late decels

A

Uteroplacental insufficiency

Decreased uteroplacental perfusion leads to fetal compromise

168
Q

FHR pattern in late decels

A
  • FHR falls after peak of contraction and then returns to baseline after contraction
  • Occurs with each contraction
  • Gradual (not abrupt) reduction in FHR
169
Q

what causes this FHR pattern

A

umbilical cord compression

Umbilical compression causes baroreceptor-mediated reduced FHR

170
Q

FHR pattern assoc with variable decels

A
  • No consistent pattern between FHR and uterine contraction
  • Maintains variability during deceleration
171
Q

evaluating FHR - category 1

A
  • Baseline HR 110-160
  • Moderate variability
  • Accelerations absent or present
  • Early decelerations absent or present
  • No late or variable decelerations

**strongly suggests normal acid-base status with no threat to fetal oxygenation **

172
Q

evaluating FHR - category 1

A
  • Baseline HR 110-160
  • Moderate variability
  • Accelerations absent or present
  • Early decelerations absent or present
  • No late or variable decelerations

**strongly suggests normal acid-base status with no threat to fetal oxygenation **

173
Q

evaluating FHR - category 2

A

can’t predict normal or abnormal acid-base status
* Bradycardia without absence of baseline FHR variability
* Tachycardia
* Variable variability
* Absent or minimal acceleration with fetal stimulation
* Recurrent variable decelerations

174
Q

evaluating FHR - category 3

A

strongly suggests abnormal acid-base status with significant threat to fetal oxygenation
* Bradycardia
* Absent baseline variability
* Recurrent late deceleration
* Sinusoidal pattern

175
Q

conditions assoc. with sinusoidal pattern

A
  • alone, considered abnormal and strongly indicates fetal asphyxia
  • also assoc with maternal opioids, fetal anemia
176
Q

definition of premature delivery

A

before 37 weeks gestation or less than 259 days from last menstrual cycle

177
Q

Leading cause of perinatal morbidity & mortality

A

prematurity

178
Q

2 things that increase incidence of premature delivery

A

multiple gestations and premature rupture of membranes

179
Q

complications of prematuriy

A
  • resp distress syndrome
  • IVH
  • NEC
  • hypoglycemia
  • hypocalcemia
  • hyperbilirubinemia
180
Q

given in the setting of preterm labor to hasten fetal lung development

A

corticosteroids (betamethasone)

181
Q

when do corticosteroids take effect & peak to hasten fetal lung developent

A
  • Take effect within 18 hours
  • Peak benefit at 48 hours
182
Q

use of tocolytic agents in premature labor

A

used to delay labor by suppressing uterine contractions (up to 24-48 hours)

Provide a bridge that allow corticosteroids to work

183
Q

use of tocolytic agents in premature labor

A

used to delay labor by suppressing uterine contractions (up to 24-48 hours)

Provide a bridge that allow corticosteroids to work

184
Q

Tocolytic agents or corticosteroids are seldom given after ____ wga

A

33

185
Q

how do beta 2 agonists affect the uterus

A

Beta-2 stimulation = increased intracellular cAMP
* turns on protein kinase
* turns off MLCK
* ultimately relaxes uterus

186
Q

SEs of beta 2 agonists in labor

A
  • hyperglycemia
  • newborn at risk of hypoglycemia
  • hypokalemia
  • increased FHR (crosses placenta)
187
Q

why are newborns of hyperglycemic mothers at risk of hypoglycemia after delivery

A

Mother’s glucose supply is gone, but insulin in neonatal circulation remains

188
Q

MOA of magnesium sulfate in OB population

A

Calcium antagonist
* relaxes smooth muscle by turning off myosin light chain kinase in vasculature, airway, and uterus
* hyperpolarizes membranes in excitable tissue

189
Q

used for seizure prophylaxis and treatment in preeclampsia)

A

mag sulfate

hyperpolarizes membranes in excitable tissues

190
Q

used for seizure prophylaxis and treatment in preeclampsia

A

mag sulfate

hyperpolarizes membranes in excitable tissues

191
Q

clinical assessment for presence of hypermagnesemia

A

DTRs
* If DTRs are present, risk of more serious side effects is low
* Diminished DTRs are the first sign of magnesium toxicity

192
Q

how do beta 2 agonists contribute to myometrial relaxation

A

increased progesterone release

193
Q

how is magnesium sulfate eliminated

A

via kidneys

194
Q

1st sign of magnesium toxicity

A

diminished DTRs

195
Q

normal Mg level:
* mg/dL
* mEq/L
* mmol/L

A
  • * 1.8-2.5mg/dL
  • 1.5-2.1 mEq/L
  • 0.75- 1.05 mmol/L
196
Q

s/s assoc with magnesium level < 1.2 mg/dL

A
  • tetany
  • seizures
  • dysrhythmias
197
Q

s/s assoc with magnesium level 1.2-1.8 mg/dL

A
  • neuromuscular irritability
  • hypokalemia
  • hypocalcemia
198
Q

symptoms assoc with magnesium level of 2.5-5 mg/dL

A

typically no symptoms

199
Q

symptoms assoc with magnesium level of 5-7 mg/dL

A
  • Diminished DTRs
  • Lethargy/drowsiness
  • Flushing
  • N/V
200
Q

s/s assoc with magnesium level of 7-12 mg/dL

A
  • Loss of DTRs
  • Hypotension
  • EKG changes
  • Somnolence
201
Q

s/s assoc with magnesium level > 12 mg/dL

A
  • Resp depression - apnea
  • Complete heart block
  • Cardiac arrest
  • Coma
  • Paralysis
202
Q

4 tocolytic agents used to delay labor by suppressing uterine contractions (up to 24-48 hours)

A
  • beta agonists
  • mag sulfate
  • calcium channel blockers
  • nitric oxide donors
203
Q

treatment of hypermagnesemia

A
  • Supportive measures
  • Diuretics (facilitate excretion)
  • IV calcium gluconate 1 g over 10 minutes (antagonize Mg2+)
204
Q

how do calcium channel blockers affect uterine tone

A
  • Block influx of Ca2+ into uterine muscle = reduces Ca2+ release from SR
  • Turns off myosin light-chain kinases and relaxes uterine muscle
205
Q

first line CCB as a tocolytic in OB patients

A

PO nifedipine

206
Q

potential consequence of co-administering CCB and mag sulfate

A

skeletal muscle weakness

207
Q

where is oxytocin primarily synthesized

A

paraventricular nuclei of the hypothalamus

208
Q

when is exogenous oxytocin released

A

following stimulation of the cervix, vagina, and breasts

209
Q

oxytocin indications

A
  • induction or augmentation of labor
  • stimulating uterine contraction
  • combating uterine hypotonia and hemorrhage
210
Q

when is oxytocin given after c section

A

administered after the delivery of the placenta

211
Q

SEs of oxytocin

A
  • water retention (it’s structurally similar to vasopressin)
  • hyponatremia
  • hypotension
  • reflex tachycardia
  • coronary vasoconstriction
212
Q

AE of rapid oxytocin admin

A

CV collapse

213
Q

metabolism of oxytocin

A

hepatic

214
Q

half life of oxytocin

A

4-17 minutes

215
Q

1st line uterotonic agent

A

Pitocin (oxytocin)

216
Q

2nd line uterotonic agent

A

Methergine

217
Q

dose of methergine

A

0.2 mg IM

218
Q

AEs of IV Methergine admin

A
  • significant vasoconstriction
  • HTN
  • cerebral hemorrhage
219
Q

half life of methergine

A

2 hrs

220
Q

3rd line uterotonic agent

A

Prostaglandin F2 (Hemabate or Carboprost)

221
Q

dose of prostaglandin F2

Hemabate or Carboprost

A

250 mcg IM or injected into uterus

222
Q

SEs of prostaglandin F2

Hemabate or Carboprost

A
  • N/V/D
  • hypotension
  • HTN
  • bronchospasm
223
Q

most common cause of maternal death in OB patient under GA

A

failure to secure airway

224
Q

most common cause of maternal death in OB patient under GA

A

failure to secure airway

225
Q

aspiration prophylaxis for OB patient needing GA

A
  • Sodium citrate to neutralize gastric acid
  • H2 receptor antagonist (ranitidine) to reduce gastric acid secretion
  • Gastrokinetic agent (metoclopramide) to hasten emptying and increase LES tone
226
Q

changes in P50 in pregnancy

A

increases in mother, decreases in fetus

oxygen concentration gradient from mom-fetus ensures fetal oxygenation

APEX (54 decks)

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