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
2
Q
why should a smaller ETT be used in pregnant patients
A
narrowed glottic opening
use 6.0-7.0
3
Q
3 factors that make airway edema worse in pregnant women
A
- preeclampsia
- tocolytics
- prolonged Trendelenburg
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
5
Q
what hormones contribute to vascular engorgement and hyperemia in pregnancy
A
- progesterone
- estrogen
- relaxin
6
Q
laryngoscope handle recommended for large-breasted women
A
Data handle (short handle)
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
8
Q
why are pregnant women at increased risk of rapid hypoxemia during periods of apnea
A
increased O2 consumption + decreased FRC
9
Q
why do pregnant women experience airway closure during tidal breathing
A
FRC falls below closing capacity
10
Q
Vm in pregnancy
A
increased up to 50%
progesterone is a respiratory stimulant
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
12
Q
how does a pregnant woman’s body normalize blood pH despite increased Vm
A
renal compensation eliminates bicarbonate to normalize blood pH
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
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
15
Q
ABG changes in pregnancy:
pH
PaO2
PaCO2
HCO3-
A
- pH: no change
- PaO2: increased
- PaCO2: decreased
- HCO3-: decreased
16
Q
normal PaO2 in pregnancy
A
104-108 mmHg
d/t hyperventilation
17
Q
normal PaCO2 in pregnancy
A
28-32 mmHg
18
Q
normal HCO3- in pregnancy
A
20 mmol/L
19
Q
changes in oxyhgb dissociation curve in pregnancy
A
↑ P50
Facilitates O2 transfer to fetus
right shift of curve
19
Q
changes in Vm in pregnancy
A
Vm increases up to 50%
Vt ↑ 40%
RR ↑ 10%
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
21
Q
why is there no change in closing capacity in pregnant patients
A
↑ CV + ↓ RV = no change in closing capacity
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%
23
Q
CO received by uterus
A
10%
24
hemodynamic variables that increase in pregnancy
HR
Stroke volume
| CO increased 40%
25
CO during labor
* 1st stage: CO ↑ 20%
* 2nd stage: CO ↑ 50%
* 3rd stage: CO ↑ 80%
26
when does CO return to **pre-labor** values
24-48 hours
27
when does CO return to **pre-pregnancy** values
~2 weeks
28
how do twins affect CO
↑ 20% above single fetus
29
changes in MAP, SBP, and DBP in pregnancy
MAP & SBP remain stable
DBP ↓ 15%
| ↑ blood volume + ↓ SVR = net even effect on MAP
30
changes in MAP, SBP, and DBP in pregnancy
MAP & SBP remain stable
DBP ↓ 15%
| ↑ blood volume + ↓ SVR = net even effect on MAP
31
changes in vascular resistance in pregnancy
SVR = ↓ 15%
PVR = ↓ 30%
32
how does progesterone affect vascular resistance in pregnancy
* ↑ nitric oxide = vasodilation (↓ SVR)
* ↓ response to angiotensin & NE (↓ PVR)
33
how are CVP and PAOP affected by pregnancy
Pregnancy by itself doesn’t alter filling pressure, however autotransfusion during uterine contraction increases filling pressure
34
cardiac axis in pregnancy
left axis deviation
## Footnote
Gravid uterus pushes diaphragm cephalad = heart pushed up and left
35
cardiac axis in pregnancy
left axis deviation
## Footnote
Gravid uterus pushes diaphragm cephalad = heart pushed up and left
36
what causes aortocaval compression in pregnant women
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
37
how can aortocaval compression be reduced
elevating the mother's right torso 15 degrees
(left uterine displacement)
## Footnote
displaces the uterus away from the vena cava and aorta
38
when should LUD be used for pregnant women
starting in 2nd trimester
39
changes in intravascular fluid volume in pregnancy
↑ 35%
| prepares mom for hemorrhage w/ labor
40
changes in intravascular fluid volume in pregnancy
↑ 35%
| prepares mom for hemorrhage w/ labor
41
what causes dilutional anemia in pregnant women
increased intravascular fluid volue, plasma vol, and erythrocyte volume
42
clotting factors increased in pregnancy
↑ 1, 7, 8, 9, 10, 12
43
protein S in pregnancy
decreased
44
protein C in pregnancy
* no change in protein C
* resistance to activated protein C
45
how is hypercoagulability counteracted in pregnancy
increased fibrin breakdown
46
why do pregnant moms have a tendency to develop consumption coagulopathy
mom makes more clots but also breaks them down faster
47
changes in PT, PTT and plt count in pregnancy
* PT & PTT = ↓ up to 20%
* Plt = unchanged or ↓ 10% d/t hemodilution & comsumption
48
Most common cause of thrombocytopenia during pregnancy
gestational thrombocytopenia
(does not increase rate of complications)
49
etiologies of thrombocytopenia in pregnancy
* gestational (most common)
* hypertensive disorders
* idiopathic
50
how does pregnancy affect MAC
↓ 30-40% from baseline due to ↑ progesterone
| (begins at 8-12 weeks)
50
how does pregnancy affect MAC
↓ 30-40% from baseline due to ↑ progesterone
| (begins at 8-12 weeks)
51
why are pregnant women more sensitive to LAs
↑ progesterone
52
why is a decreased epidural LA dose given to pregnant women
Epidural vein volume increases = decreased volume of subarachnoid & epidural spaces (compression)
53
effects of increased gastrin in pregnancy
↑ gastric volume
↓ gastric pH
54
how does gastric emtpying change in pregnancy
↓ after labor begins
no change before
55
LES sphincter tone in pregnancy
decreased
| d/t ↑ progesterone, ↑ estrogen, cephalad displacement of diaphragm
56
LES sphincter tone in pregnancy
decreased
| d/t ↑ progesterone, ↑ estrogen, cephalad displacement of diaphragm
57
CrCl in pregnancy
increased
## Footnote
↑ blood volume = ↑ Cr delivered to kidney per unit time
58
CrCl in pregnancy
increased
## Footnote
↑ blood volume = ↑ Cr delivered to kidney per unit time
59
GFR in pregnancy
increased
60
Cr and BUN in pregnancy
decreased
61
uterine blood flow in pregnancy
↑ up to 700-900 mL/min
| accounts for 10% of CO
62
uterine blood flow in pregnancy
↑ up to 700-900 mL/min
| accounts for 10% of CO
63
serum albumin in pregnancy
↓ = increased free fraction of highly protein bound drugs
64
pseudocholinesterase in pregnancy
↓
*no meaningful effect on succs metabolism*
65
urine glucose in pregnancy
increased as a result of ↑ GFR and reduced reabsorption in peritubular capillaries
66
uterine blood flow in non-pregnant state
100 mL/min
| pregnant = up to 700 mL/min
67
uterine blood flow in non-pregnant state
100 mL/min
| pregnant = up to 700-900 mL/min
68
is uterine blood flow autoregulated
no - dependent on MAP, CO, and uterine vascular resistance
69
uterine blood flow =
(uterine artery pressure - uterine venous pressure) / uterine vascular resistance
70
2 factors that ↓ Uterine Blood Flow
* Decreased perfusion
* Increased resistance
71
what can cause decreased uterine perfusion and therefore decreased UBF
maternal hypotension (sympathectomy, hemorrhage, aortocaval compression)
72
what can cause increased resistance and therefore ↓ UBF
uterine contraction, hypertensive conditions that ↑ UVR
73
most important variables in placental drug transfer
* diffusion coefficient (drug characteristics)
* concentration gradient between maternal and fetal circulation
74
principle that describes how a drug traverses a biologic membrane
Fick principle
75
4 drug characteristics that favor placental transfer:
* Low molecular weight (< 500 Daltons)
* High lipid solubility
* Non-ionized
* Non-polar
| (most anesthetic drugs are smaller than 500 daltons)
76
meds that do NOT undergo placental transfer
* NMBs
* glycopyrrolate
* heparin
* insulin
77
Do LAs undergo placental transfer
yes **except** chloroprocaine (rapid ester metabolism)
78
stage 1 of labor
Beginning of regular contractions to full cervical dilation (10 cm)
79
stage 2 of labor
Full cervical dilation to delivery of fetus
| Perineal pain begins
80
illustrates normal progress of labor
Friedman curve
81
stage 3 of labor
delivery of placenta
82
what is dysfunctional labor
doesn't follow expected pattern of Friedman curve
83
Friedman curve - Latent phase
1-8 hours
Cervical dilation: 2-3 cm
84
Friedman curve - active phase
hours 8-13
Full cervical dilation
85
Friedman curve - fetal delivery
hours 14-16
86
NPO ASA Practice Guidelines for Obstetric Analgesia
**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
87
when does the latent phase of labor end
when the cervix dilates to 2-3 cm
88
when does the active phase of labor occur
in stage 1 when cervix is 3-10 cm dilated
| after latent phase
89
when does the active phase of labor occur
in stage 1 when cervix is 3-10 cm dilated
| after latent phase
90
how does epidural analgesia affect the progress of labor
it does NOT prolong the first stage of labor
91
where does pain begin in 1st stage of labor
lower uterine segment and cervix
92
where does pain originate in 1st stage of labor
T10-L1 posterior nerve roots
93
pain impulses in 2nd stage of labor
adds in pain impulse from vagina, perineum, and pelvic floor
94
where do pain impulses travel from in 2nd stage of labor
from perineum to S2-S4 posterior nerve roots
95
innervates the perineum
pudendal n.
| derives from S2-S4
## Footnote
pudendal n. block is not useful in 1st stage of labor
96
innervates the perineum
pudendal n.
| derives from S2-S4
## Footnote
pudendal n. block is not useful in 1st stage of labor
97
analgesic options that target 1st stage labor pain
* Neuraxial (spinal, epidural, CSE)
* Paravertebral lumbar block
* Paracervical block
98
analgesic options that target 2nd stage labor pain
* Neuraxial (spinal, epidural, CSE)
* Pudendal nerve block
99
afferent pathway assoc. with first stage of labor
Visceral C fibers hypogastric plexus
100
afferent pathway assoc. with 2nd stage of labor
pudednal n.
101
quality of pain in 1st stage of labor
Dull
Diffuse
Cramping
102
quality of pain in 2nd stage of labor
Sharp
Well localized
103
regional technique in 1st stage of labor assoc with high risk of fetal bradycardia
paracervical block
104
dual benefit of CSE
rapid onset of spinal anesthesia and ability to prolong duration of anesthesia with indwelling epidural catheter
105
"needle through needle" technique for CSE
* 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
Epidural volume extension technique for CSE
* 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
total neuraxial coverage needed for 2nd stage of labor
T10-S4
108
how does the maternal breathing pattern affect fetal oxygenation
maternal hyperventilation = L shift of oxyhgb curve = decreased O2 delivery to fetus
109
which LA reduces the efficacy of epidural morphine
2-chloroprocaine
## Footnote
Antagonizes opioid receptors (mu & kappa) and reduces efficacy of epidural morphine
110
LAs commonly used in OB
* bupivacaine
* ropivacaine
* lidocaine
* 2-chloroprocaine
111
concentration of bupivacaine contraindicated via epidural
0.75%
| risk toxicity with IV injection
112
concentration of bupivacaine contraindicated via epidural
0.75%
| risk toxicity with IV injection
113
placental transfer of bupivacaine
low d/t ↑ protein binding and ↑ ionization
114
LA used in OB with greater sensory block relative to other LAs
bupivacaine
115
benefits of neuraxial opioids when used **alone**
* no loss of sensation or proprioception
* no sympathectomy
* do not impair mom’s ability to push
116
neuraxial opioid with LA properties
meperidine
117
LA useful for emergency C/S when epidural is already in place
2-Chloroprocaine
| very fast onset
118
LA useful for emergency C/S when epidural is already in place
2-Chloroprocaine
| very fast onset
119
receptors antagonized by neuraxial 2-chloroprocaine
mu & kappa opioid receptors
120
neuraxial LA with risk of arachnoiditis when used for spinal anesthesia
2-chloroprocaine
| due to preservatives
120
neuraxial LA with risk of arachnoiditis when used for spinal anesthesia
2-chloroprocaine
| due to preservatives
121
SEs of neuraxial opioids
* pruritis (most common)
* N/V
* sedation
* respiratory depression
122
LA that is not popular for labor analgesia
lidocaine
| strong motor block (good for c section)
123
spinal dose of bupivacaine
1.5-5 mg
124
epidural bupivacaine
bolus: 0.0625 – 0.125%
infusion: 0.5 – 0.125%
125
spinal ropivacaine dose
2 – 3.5 mg
126
epidural ropivacaine
bolus & infusion: 0.08 – 0.2%
127
why is lidocaine typically not used for continuous epidural infusion
* tachyphylaxis is more likely to develop
* crosses placenta to greater degree than others
128
mL/hr for lumbar epidural infusion
8-15 mL/hr
129
spinal bolus of fentanyl
15-25 mcg
130
epidural fentanyl dosing
bolus: 50-100 mcg
epidural: 1.5-3 mcg/mL
131
spinal bolus of sufentanil
1.5-5 mcg
132
sufentanil epidural dosing
bolus: 5-10 mcg
infusion: 0.2-0.4 mcg/mL
133
spinal dose of morphine
125-250 mg
134
epi dosing as a spinal adjuvant
2.25-200 mcg
135
epidural dosing of epi
| as an adjuvant
bolus: 25 – 75 mcg
infusion: 20 – 50 mcg/hr
136
spinal dose of clonidine
15-30 mcg
137
epidural dosing of clonidine
bolus: 75-100 mcg
infusion: 10-30 mcg/hr
138
epidural dosing of neostigmine
bolus = 500-100 mcg
infusion = 25-75 mcg/hr
139
3 ways an OB patient can develop a high spinal
* Epidural dose injected into subarachnoid space
* Epidural dose injected into subdural space
* Single shot spinal after a failed epidural block
140
treatment of a total spinal
**supportive**
airway management
IVF
vasopressors
LUD
leg elevation
141
typical presentation of total spinal caused by epidural dose injected in subdural space
s/s excessive cephalad spread **10-15 minutes** after epidural dosed
142
can a subdural injection be ruled out
Neither catheter aspiration nor a test dose will rule out subdural placement
143
how can a single-shot spinal after a failed epidural lead to a high/total spinal
* 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
presentation of total spinal
* typically rapid progression of sensory and motor block
* Dyspnea, difficulty phonating, hypotension
* hypotension = cerebral hypoperfusion = LOC
145
differential diagnosis when OB pt presents with s/s total spinal
* anaphylactic shock
* eclampsia
* amniotic fluid embolism
146
surrogate measure of overall fetal wellbeing
| Provides indirect method to assess fetal hypoxia & acidosis
FHR
147
fetal oxygenation is a function of what 2 things
uterine blood flow
placental blood flow
148
how does the fetus respond to stress
* peripheral vasoconstriction
* HTN
* baroreceptor-mediated reduced HR
149
normal FHR
110-160
150
fetal causes of fetal bradycardia
Asphyxia
Acidosis
| FHR < 110
151
maternal causes of fetal bradycardia
* Hypoxemia
* Drugs that ↓ uteroplacental perfusion
152
fetal causes of fetal tachycardia
Hypoxemia
Arrhythmias
153
maternal causes of fetal tachycardia
Fever
Chorioamnionitis
Atropine
Ephedrine
Terbutaline
154
normal FHR variability
6-25 bpm
155
what does FHR variability suggest
* 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
FHR variability:
* minimal
* moderate
* marked
* absent
* Minimal: < 5 bpm
* Moderate: 6 - 25 bpm
* Marked: > 25 bpm
* Absent: a worrisome finding
157
things that decrease FHR variability
* **CNS depressants** (opioids, sedatives
anesthetics, barbiturates, magnesium sulfate)
* **hypoxemia**
* fetal sleep
* **acidosis**
* anencephaly
* cardiac anomalies
158
what causes early decels
Uterine contractions compress fetal head
159
FHR with early decels
HR < 20 from baseline
160
change in HR with early decels
< 20 from baseline
161
onset & offset of early decels compared to contractions
Onset and offset parallels uterine contraction
| Loses variability with each deceleration
162
onset & offset of early decels compared to contractions
Onset and offset parallels uterine contraction
| Loses variability with each deceleration
163
risk to baby with early decels
no risk of fetal hypoxia
164
condition that may cause this FHR pattern
head compression
| early decels
165
conditions that contribute to this FHR pattern
* maternal hypotension
* hypovolemia
* acidosis
* preeclampsia
| late decels
166
conditions that contribute to this FHR pattern
maternal:
* hypotension
* hypovolemia
* acidosis
* preeclampsia
| late decels
167
what causes late decels
Uteroplacental insufficiency
| Decreased uteroplacental perfusion leads to fetal compromise
168
FHR pattern in late decels
* FHR falls after peak of contraction and then returns to baseline after contraction
* Occurs with **each** contraction
* **Gradual** (not abrupt) reduction in FHR
169
what causes this FHR pattern
umbilical cord compression
| Umbilical compression causes baroreceptor-mediated reduced FHR
170
FHR pattern assoc with variable decels
* No consistent pattern between FHR and uterine contraction
* Maintains variability during deceleration
171
evaluating FHR - category 1
* Baseline HR 110-160
* Moderate variability
* Accelerations absent or present
* Early decelerations absent or present
* No late or variable decelerations
## Footnote
**strongly suggests normal acid-base status with no threat to fetal oxygenation **
172
evaluating FHR - category 1
* Baseline HR 110-160
* Moderate variability
* Accelerations absent or present
* Early decelerations absent or present
* No late or variable decelerations
## Footnote
**strongly suggests normal acid-base status with no threat to fetal oxygenation **
173
evaluating FHR - category 2
**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
evaluating FHR - category 3
**strongly suggests abnormal acid-base status with significant threat to fetal oxygenation**
* Bradycardia
* Absent baseline variability
* Recurrent late deceleration
* Sinusoidal pattern
175
conditions assoc. with sinusoidal pattern
* alone, considered abnormal and strongly indicates fetal asphyxia
* also assoc with maternal opioids, fetal anemia
176
definition of premature delivery
before 37 weeks gestation or less than 259 days from last menstrual cycle
177
Leading cause of perinatal morbidity & mortality
prematurity
178
2 things that increase incidence of premature delivery
multiple gestations and premature rupture of membranes
179
complications of prematuriy
* resp distress syndrome
* IVH
* NEC
* hypoglycemia
* hypocalcemia
* hyperbilirubinemia
180
given in the setting of preterm labor to hasten fetal lung development
corticosteroids (betamethasone)
181
when do corticosteroids take effect & peak to hasten fetal lung developent
* Take effect within 18 hours
* Peak benefit at 48 hours
182
use of tocolytic agents in premature labor
used to delay labor by suppressing uterine contractions (up to 24-48 hours)
| Provide a bridge that allow corticosteroids to work
183
use of tocolytic agents in premature labor
used to delay labor by suppressing uterine contractions (up to 24-48 hours)
| Provide a bridge that allow corticosteroids to work
184
Tocolytic agents or corticosteroids are seldom given after ____ wga
33
185
how do beta 2 agonists affect the uterus
Beta-2 stimulation = increased intracellular cAMP
* turns on protein kinase
* turns off MLCK
* ultimately **relaxes** uterus
186
SEs of beta 2 agonists in labor
* hyperglycemia
* newborn at risk of hypoglycemia
* hypokalemia
* increased FHR (crosses placenta)
187
why are newborns of hyperglycemic mothers at risk of hypoglycemia after delivery
Mother’s glucose supply is gone, but insulin in neonatal circulation remains
188
MOA of magnesium sulfate in OB population
Calcium antagonist
* relaxes smooth muscle by turning off myosin light chain kinase in vasculature, airway, and uterus
* hyperpolarizes membranes in excitable tissue
189
used for seizure prophylaxis and treatment in preeclampsia)
mag sulfate
| hyperpolarizes membranes in excitable tissues
190
used for seizure prophylaxis and treatment in preeclampsia
mag sulfate
hyperpolarizes membranes in excitable tissues
191
clinical assessment for presence of hypermagnesemia
DTRs
* If DTRs are present, risk of more serious side effects is low
* Diminished DTRs are the first sign of magnesium toxicity
192
how do beta 2 agonists contribute to myometrial relaxation
increased progesterone release
193
how is magnesium sulfate eliminated
via kidneys
194
1st sign of magnesium toxicity
diminished DTRs
195
normal Mg level:
* mg/dL
* mEq/L
* mmol/L
* *** 1.8-2.5mg/dL**
* 1.5-2.1 mEq/L
* 0.75- 1.05 mmol/L
196
s/s assoc with magnesium level < 1.2 mg/dL
* tetany
* seizures
* dysrhythmias
197
s/s assoc with magnesium level 1.2-1.8 mg/dL
* neuromuscular irritability
* hypokalemia
* hypocalcemia
198
symptoms assoc with magnesium level of 2.5-5 mg/dL
typically no symptoms
199
symptoms assoc with magnesium level of 5-7 mg/dL
* Diminished DTRs
* Lethargy/drowsiness
* Flushing
* N/V
200
s/s assoc with magnesium level of 7-12 mg/dL
* Loss of DTRs
* Hypotension
* EKG changes
* Somnolence
201
s/s assoc with magnesium level > 12 mg/dL
* Resp depression - apnea
* Complete heart block
* Cardiac arrest
* Coma
* Paralysis
202
4 tocolytic agents used to delay labor by suppressing uterine contractions (up to 24-48 hours)
* beta agonists
* mag sulfate
* calcium channel blockers
* nitric oxide donors
203
treatment of hypermagnesemia
* Supportive measures
* Diuretics (facilitate excretion)
* IV calcium gluconate 1 g over 10 minutes (antagonize Mg2+)
204
how do calcium channel blockers affect uterine tone
* Block influx of Ca2+ into uterine muscle = reduces Ca2+ release from SR
* Turns off myosin light-chain kinases and relaxes uterine muscle
205
first line CCB as a tocolytic in OB patients
PO nifedipine
206
potential consequence of co-administering CCB and mag sulfate
skeletal muscle weakness
207
where is oxytocin primarily synthesized
paraventricular nuclei of the hypothalamus
208
when is exogenous oxytocin released
following stimulation of the cervix, vagina, and breasts
209
oxytocin indications
* induction or augmentation of labor
* stimulating uterine contraction
* combating uterine hypotonia and hemorrhage
210
when is oxytocin given after c section
administered after the delivery of the placenta
211
SEs of oxytocin
* water retention (it's structurally similar to vasopressin)
* hyponatremia
* hypotension
* reflex tachycardia
* coronary vasoconstriction
212
AE of rapid oxytocin admin
CV collapse
213
metabolism of oxytocin
hepatic
214
half life of oxytocin
4-17 minutes
215
1st line uterotonic agent
Pitocin (oxytocin)
216
2nd line uterotonic agent
Methergine
217
dose of methergine
0.2 mg IM
218
AEs of IV Methergine admin
* significant vasoconstriction
* HTN
* cerebral hemorrhage
219
half life of methergine
2 hrs
220
3rd line uterotonic agent
Prostaglandin F2 (Hemabate or Carboprost)
221
dose of prostaglandin F2
| Hemabate or Carboprost
250 mcg IM or injected into uterus
222
SEs of prostaglandin F2
| Hemabate or Carboprost
* N/V/D
* hypotension
* HTN
* bronchospasm
223
most common cause of maternal death in OB patient under GA
failure to secure airway
224
most common cause of maternal death in OB patient under GA
failure to secure airway
225
aspiration prophylaxis for OB patient needing GA
* **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
changes in P50 in pregnancy
increases in mother, decreases in fetus
## Footnote
oxygen concentration gradient from mom-fetus ensures fetal oxygenation
