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APEX-across the lifespan > LIFESPAN-obstetrics 9--18 > Flashcards

LIFESPAN-obstetrics 9--18 Flashcards

1
Q

2 things fetal heart rate indirectly measures

A
  1. Fetal hypoxia

2. Fetal acidosis

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2
Q

Fetal oxygenations is a function of what 2 things

A
  1. uterine bf

2. placental bf

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3
Q

What are 3 fetal responses to decreased oxygenation

A
  1. peripheral vasoconstriction
  2. HTN
  3. baroreceptor-mediated reduction in HR
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4
Q

What are the parameters for the following fetal heart rates:
Normal=
Bradycardia=
Tachycardia=

A 
Normal= 110-160
Bradycardia= <110
Tachycardia= >160
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5
Q

What are 2 causes of fetal bradycardia

A
  1. asphyxia

2. acidosis

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6
Q

What are 2 causes of fetal tachycardia

A
  1. hypoxemia

2. arrythmias

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7
Q

What are 2 maternal causes of fetal bradycardia

A
  1. hypoxemia

2. drugs that decrease uteroplacental perfusion

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8
Q

What are 5 maternal causes of fetal tachycardia

A
  1. fever
  2. chorioamnionitis
  3. atropine
  4. ephedrine
  5. terbutaline
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9
Q

Is fetal HR variability normal?

A

Yes

It should have a variability of 6-25 bpm

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10
Q

What are the 4 classes of fetal HR variability

A
  1. minimal <5 bpm
  2. moderate 6-25 bpm
  3. marked >25 bpm
  4. absent = worrisome
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11
Q

What are 6 factors that reduce fetal HR variability

A
  1. CNS depressant drugs
  2. Hypoxemia
  3. Fetal sleeps
  4. Acidosis
  5. Anencephaly
  6. Cardiac anomalies
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12
Q

What are the 3 types of fetal decelerations

A
  1. early
  2. late
  3. variable
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13
Q

What is a cause of early decelerations

Is there a risk of hypoxemia

A 
Cause = head compression that increases vagal tone (HR <20 bpm from baseline)
Hypoxemia = NO risk
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14
Q

How do early decelerations correlate with uterine contraction

A

Onset and offset parallel uterine contraction

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15
Q

What is a cause of late decelerations

Is there a risk of fetal hypoxemia

A

Cause = uteroplacental insufficiency

Hypoxemia = high risk, requires urgent fetal assessment

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16
Q

How do late decelerations correlate with uterine contraction

A

FHR falls after peak of contraction then returns to baseline after contraction

Occurs with each contraction

Gradual reduction of FHR

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17
Q

What are 4 maternal causes of late deceleration

A
  1. HoTN
  2. Hypovolemia
  3. acidosis
  4. preE
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18
Q

What is a cause of variable deceleration

Is there a risk of fetal hypoxemia

A

Cause = umbilical cord compression causing baroreceptor mediated reduction in FHR

hypoxemia = high risk, requires urgent fetal assessment

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19
Q

How do variable decelerations correlate with uterine contractions

A

No consistent pattern between FHR and contraction

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20
Q

How does fetal health affect recovery from variable decelerations

A

fetal compromise prolongs FHR recovery time

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21
Q

Mnemonic for fetal decelerations

A 
VEAL CHOP
Variable decels = Cord compression
Early decels = Head compression
Accelerations = Ok or give O2
Late decels = Placental insufficiency
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22
Q

What are 5 findings of Category 3 evaluation of FHR

A
  1. bradycardia
  2. absent baseline variability
  3. recurrent late decels
  4. recurrent variables decels
  5. sinusoidal pattern
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23
Q

What does category 3 evaluation of FHR suggest

A

abnormal fetal acid-base status with significant threat to fetal oxygenation

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24
Q

What does category 2 evaluation of FHR suggest

A

It cannot predict a normal or abnormal acid-base status

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25
Q

What are 5 findings associated with category 2 evaluation of FHR

A
  1. bradycardia w/o the absence of baseline FHR variability
  2. Tachycardia
  3. Variable variability
  4. Absent or minimal acceleration with fetal stimulation
  5. recurrent variable decels
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26
Q

What are fetal HR findings associated with category 1 evaluation

A
  1. baseline HR between 110-160
  2. moderate variability
  3. accelerations absent or present
  4. early decels absent or present
  5. no later or variable decels
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27
Q

What are 6 fetal complications of premature delivery

A
  1. respiratory distress syndrome
  2. intraventricular hemorrhage
  3. NEC
  4. hypoglycemia
  5. hypocalcemia
  6. hyperbilirubinemia
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28
Q

What medication hastens fetal lung development in preterm labor
when do they take effect and peak

A

Betamethasone (corticosteroids)

Take effect = 18 hrs
Peak = 48 hrs

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29
Q

What are tocolytics

A

drugs used to delay labor by suppressing uterine contraction

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30
Q

What is the goal for using tocolytics

A

allow time for corticosteroids to work for fetal lung maturity

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31
Q

What are 4 examples of tocolytic agents

A
  1. beta-agonists
  2. magnesium sulfate
  3. CCBs
  4. NO donors
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32
Q

What is the MOA of beta-agonists as tocolytics

A

They increase intracellular cAMP
Protein kinase turns off myosin light-chain kinase, relaxing uterus
Increased progesterone release

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33
Q

What are 4 side-effects of beta-agonist use as tocolytics

A
  1. hyperglycemia from liver glycogenolysis
  2. newborn at higher risk for hypoglycemia
  3. Hypokalemia from intracellular K+ shifts
  4. Beta2 agonists cross the placenta and increase FHR
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34
Q

Why is magnesium sulfate used as a tocolytic

A

It is a Ca++ antagonist which relaxes smooth muscle by turning off myosin light-chain kinase in vasculature, airway, and uterus

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35
Q

What effect does mag have on excitable tissues

A

hyperpolarizes

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36
Q

How does renal insufficiency affect mag infusion

A

Kidneys eliminate Mg2+

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37
Q

What clinical assessment is used to determine the presence of hypermagnesemia

A

Deep tendon reflexes

If they are present, more serious side effects are low

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38
Q

What assessment can be a first sign of mag toxicity

A

Diminished DTRs

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39
Q

At what magnesium level are tetany, seizures and dysrhythmias possible

A

Mg < 1.2 mg/dL

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40
Q

At what magnesium level are diminished DTRs, lethargy, drowsiness, and flushing present

A

5–7 mg/dL

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41
Q

At what magnesium level are DTRs absent, HoTN, EKG changes, and somnolence present

A

7-12 mg/dL

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42
Q

At what magnesium level are CHB, respiratory depression, cardiac arrest, and coma possible

A

> 12 mg/dL

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43
Q

What effect does magnesium infusion have on NMB

A

It can potentiate NMB especially if hypermagnesemia is present

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44
Q

What pulmonary complications are possible with hypermagnesemia

A

Pulmonary edema

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45
Q

How do pts with hypermagnesemia respond to ephedrine or phenylephrine

A

They have a reduced response

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46
Q

What are 3 treatments for hypermagnesemia

A
  1. supportive measures
  2. diuretics to facilitate excretion
  3. IV calcium gluconate 1g to antagonize Mg2+
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47
Q

How do CCB act as a tocolytic

A

They block the influx of Ca++ into the uterine muscle, reducing Ca++ release from SR, turning off myosin light-chain kinases.
Ultimately relaxes uterine muscle

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48
Q

What is the first-line CCB used as a tocolytic

A

nifedipine

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49
Q

Define premature delivery

A

delivery before 37 weeks or less than 259 days from LMP

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50
Q

The incidence of prematurity increases with what 2 factors

A
  1. multiple gestations

2. PROM

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51
Q

Coadministration of nifedipine with what drug increases the likelihood of skeletal muscle weakness in the pregnant patient

A

Magnesium

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52
Q

3 Medications used as uterotonics

A
  1. oxytocin
  2. methergine (ergot alkaloid)
  3. prostaglandin F2 (hemabate or carboprost)
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53
Q

Where is oxytocin synthesized and store/released

A 
synthesis = the paraventricular nuclei of hypothalamus
store/released = posterior pituitary gland
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54
Q

Stimulation of what 3 areas can release endogenous oxytocin

A
  1. Cervix
  2. vagina
  3. breasts
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55
Q

What hormone is pitocin equivalent to

A

It is a synthetic equivalent of oxytocin

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56
Q

What are 3 indications for oxytocin

A
  1. induction or augmentation of labor
  2. stimulating uterine contraction
  3. combating uterine hypotonia and hemorrhage
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57
Q

Why is oxytocin used during C/S

A

uterine contraction following placental delivery

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58
Q

What are 5 side effects of oxytocin

A
  1. Water retention
  2. hyponatremia
  3. HoTN
  4. reflex tachycardia
  5. coronary vasoconstriction
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59
Q

What is a consequence of rapid oxytocin IV administration

A

CV collapse

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60
Q

How is oxytocin metabolized

A

hepatic metabolism

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61
Q

What is the half-life of oxytocin

A

4-17 minutes

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62
Q

What type of medication is methergine

A

Ergot alkaloid

63
Q

What are the second-line and third-line uterotonics

A 
2nd = methergine
3rd = hemabate
64
Q

What is the dose of methergine

A

0.2 mg IM

65
Q

What are the consequences of methergine IV administration

A
  1. significant vasoconstriction
  2. HTN
  3. Cerebral hemorrhage
66
Q

How is methergine metabolized and the half-life

A 
metabolism = hepatic
half-life = 2 hrs
67
Q

What type of medication is hemabate

A

prostaglandin F2

68
Q

What is the dosing for hemabate

A

250 mcg IM

69
Q

What are 5 side effects of hemabate/carboprost

A
  1. N/V
  2. Diarrhea
  3. HoTN
  4. HTN
  5. bronchospasm
70
Q

At what point during a c-section should oxytocin be used

A

after delivery of the placenta

71
Q

What are 5 situations that general anesthesia should be used for CS

A
  1. Maternal hemorrhage
  2. Fetal distress
  3. Coagulopathy
  4. Pt refusal of RA
  5. Contraindications to RA
72
Q

How does general anesthesia affect maternal mortality

A

It is 17-times higher in this population

73
Q

What is the most common cause of maternal death associated with GA

A

failure to successfully manage the airway

74
Q

What are 3 prophylactic medications used in the maternal population undergoing GA for CS

A
  1. sodium citrate
  2. H2 receptor antagonist (ranitidine)
  3. Gastrokinetic agent (reglan)
75
Q

Why is neonatal depression not a concern with GA induction drugs

A

Depression is short-lived b/c of redistribution

76
Q

What are 11 steps for a GA C/S

A
  1. Plan for difficult intubation.
  2. Triple aspiration prophylaxis
  3. LUD
  4. Place monitors
  5. Surgical prep and drape
  6. Preoxy while prepping
  7. Induction
  8. Once ETT passes through cords yell “CUT”
  9. Use MAC<0.5 + nitrous to prevent uterine atony
  10. Give oxytocin once placenta delivered (BZDs for amnesia)
  11. Extubate when fully awake
77
Q

How much amniotic fluid may be present in the EBL suction

A

~700 mL

78
Q

What are 3 benefits of GA for C/S

A
  1. Speed of onset
  2. Secure airway
  3. Greater hemodynamic stability
79
Q

What type of non-obstetric surgeries have the greatest risk of preterm labor

A

abdominal and pelvic procedures

80
Q

What are fetal risks associated with non-obstetric procedures

A
  1. growth restriction
  2. low birth weight
  3. fetal demise
  4. increased incidence of preterm labor
81
Q

What are 2 maternal risks associated with non-obstetric surgeries

A
  1. Difficult intubation

2. Risk of aspiration

82
Q

When is the best option for timing of surgical procedures in the parturient and why

A

2nd trimester

It avoids high risk of teratogenicity during 1st trimester and increased risk of preterm delivery during 3rd trimester

83
Q

Why should N2O be avoided in the first 2 trimesters

A

It may be linked with congenital disabilities due to DNA synthesis inhibition

84
Q

At what point during the pregnancy are pts considered full stomach

How does this affect the anesthetic

A

18-20 weeks

RSI with aspiration prophylaxis

85
Q

How much sodium citrate should be given to a parturient and when should it be given before a procedure

A 
Dose = 15-30 mL
timing = 15-30 min before induction
86
Q

What 4 physiologic abnormalities should be avoided in the parturient during non-obstetric procedures

Why

A
  1. Hypoxemia
  2. Hyperventilation
  3. HoTN
  4. Acidosis

These states can reduce placental BF

87
Q

Why are NSAIDs avoided during pregnancy

A

To prevent closure of the ductus arteriosus

88
Q

How does gestational HTN differ from pre-eclampsia and chronic HTN

A

It is HTN that presents after 20 weeks w/o proteinuria. BP returns to normal after delivery

89
Q

How does preeclampsia differ from gestational HTN

A

PreE presents with proteinuria

90
Q

What are BP parameters for Pre-E

A 
mild = >140/90
severe = >160/110

develops after 20 weeks

91
Q

What are 5 other conditions that can be considered part of pre-E

A
  1. persistent RUQ or epigastric pain
  2. Persistent CNS or visual symptoms (i.e. HA)
  3. Fetal growth restriction
  4. Thrombocytopenia
  5. Elevated liver enzymes
92
Q

What is eclampsia

A

When a mother with pre-E develops seizures

93
Q

What maternal age-ranges are at greater risk for pre-E

A

<20 yrs and >35 yrs

94
Q

What 2 pt population are at highest risk for pre-E

A
  1. Chronic renal disease

2. Homozygous for angiotensinogen T235 allele

95
Q

What 2 products of arachidonic acid are produced by the placenta

A
  1. Thromboxane

2. Prostacyclin

96
Q

How are thromboxane and prostacyclin affected by pre-E

A

They produce 7 times more thromboxane than prostacyclin

97
Q

What 3 actions does elevated thromboxane have in the pre-E pt

A
  1. Favors vasoconstriction
  2. Favors plt aggregation
  3. Reduces placental BF
98
Q

What additional mediators may be released from the diseased placenta in pre-E
The effects

A

Cytokines

Promote endothelial dysfunction

99
Q

What are 4 purposes of prostacyclin release from the placenta

A
  1. dec plt aggregation
  2. dec vasoconstriction
  3. dec uterine activity
  4. increased uteroplacental BF
100
Q

What are key complications of pre-E on maternal physiology

A
  1. HF
  2. Pulmonary edema
  3. Intracranial hemorrhage
  4. cerebral edema
  5. DIC
  6. proteinuria
101
Q

What are 3 vasoactive substances that are released from placental ischemia

A
  1. Cytokines
  2. Radicals
  3. Peroxides
102
Q

Why does proteinuria occur with pre-E

A

There is glomerular leak d/t endothelial damage from thromboxane and vasoactive substances

103
Q

Why is BP elevated during pre-E

A

d/t increased thromboxane causing vasoconstriction

104
Q

What causes generalized or pulmonary edema in the pre-E pt

A

Decreased oncotic pressures

Increased vascular permeability d/t endothelial damage

105
Q

What causes HA and visual impairment with severe pre-E

A

HA = cerebral edema

Visual changes = vasoconstriction of ocular arterioles

106
Q

What can cause epigastric pain in the severely pre-E pt

A

Liver subcapsular hemorrhage or hypoxic liver

107
Q

Why does plt count drop in the pt w/ severe pre-E

A

d/t consumption by endothelial damage

108
Q

What is the definitive treatment for pre-E and eclampsia

A

Delivery of the fetus and placenta

109
Q

When is delivery mandatory in the pre-E pt

A

when fetal distress occurs or maternal symptoms are severe

110
Q

What is the reason to medicate BP > 160/110

A

To prevent

  1. CVA
  2. MI
  3. Placental abruption
111
Q

Wat are 4 treatments for acute maternal HTN

A
  1. labetalol 20 mg, max 220 mg
  2. hydralazine 5 mg, max 20 mg
  3. Nifedipine 10 mg PO, max 50 mg
  4. Nicardipine infusion
112
Q

Once the neonate is delivered, when does pre-E resolve

A

It can be up to 4 weeks postpartum before pre-E resolves

It can still occur after delivery

113
Q

What are the benefits of neuraxial anesthesia with pre-E

What is ruled out prior to performing

A

It assists with BP control and provides better uteroplacental perfusion

r/o thrombocytopenia (plt <100,000)

114
Q

In pre-E pts, what medication can affect NMB during GA

A

Many pts are on Mg drips. This increases the sensitivity to neuromuscular blockers

115
Q

What differentiates pre-E from eclampsia

A

Seizures are present w/ eclampsia

116
Q

How are seizures prevented in the pre-E pt

A

Prophylaxis w/ mag sulfate

117
Q

What is the dosing for seizure prophylaxis with magnesium sulfate

A 
load = 4 g over 10 min
infusion = 1-2 g/hr
118
Q

What is the treatment for Mg++ toxicity

A

10 mL 10% Ca++ gluconate IV (Mg antagonist)

119
Q

What is HELLP

A

Hemolysis
Elevated Liver enzymes
Low Platelet count

120
Q

What is the incidence of HELLP in the pre-E pt

A

5-10%

121
Q

Treatment for HELLP

A

delivery of fetus and placenta

122
Q

What 2 complications are pts with HELLP at high risk for

A
  1. DIC

2. Intra-abdominal bleeding form liver

123
Q

What is the MOA of cocaine

A

inhibition of NE reuptake in presynaptic SNS

Increased NE = increased SNS tone

124
Q

What are 4 CV risks with cocaine abuse

A
  1. tachycardia
  2. dysrhythmias
  3. coronary vasoconstriction
  4. myocardial ischemia
125
Q

How does cocaine affect MAC

A 
Acute = increases MAC
Chronic = decreases MAC
126
Q

What are 4 CNS risks with cocaine abuse

A
  1. cerebral vasoconstriction
  2. Ischemia
  3. Seizures
  4. Stroke
127
Q

What are 4 OB risks with cocaine use

A
  1. spontaneous abortion
  2. premature labor
  3. placental abruption
  4. low APGAR scores
128
Q

What anti-HTN medication should be used in the cocaine intoxicated parturient and why

A

labetalol

It blocks alpha-mediated peripheral vasoconstrictoin

129
Q

What anti-HTN medication should be avoided in the cocaine intoxicated parturient and why

A

Beta-blockers

B1 causes myocardial depression that can lead to heart failure if SVR is elevated

B2 leads to impaired vasodilation of muscular beds causing heart failure and a further increase in elevated SVR

130
Q

Why is ephedrine not appropriate to use in chronic cocaine abusers

A

Catecholamines are depleted

Phenylephrine is the best option

131
Q

What hematologic disorder is chronic cocaine use associated with
Significance in parturient

A

Thrombocytopenia

Check plt level before neuraxial

132
Q

What are 4 roles of thromboxane in the pre-E pt

A
  1. inc plt aggregation
  2. inc vasoconstriction
  3. inc uterine activity
  4. dec uteroplacental BF
133
Q

What are the 3 types of abnormal placental implantations from least to most severe

A 
Accreta = attaches to surface of myometrium
Increta = invades myometrium
Percreta = extends beyond the uterus
134
Q

How is a normal placenta implanted in the uterus

A

It’s implanted into the decidua of the ENDOmetrium

135
Q

Define placenta previa

A

Placenta attaches to the lower uterine segment and either partially or completely covers the cervical os

136
Q

What type of bleeding is associated with placenta previa

A

painless vaginal bleeding with potential for hemorrhage

137
Q

What are 2 risk factors for placental previa

A
  1. previous c/s

2. history of multiple births

138
Q

Define placental abruption

A

Partial or complete separation of the placenta from the uterine wall before delivery

139
Q

What are 6 risk factors for placental abruption

A
  1. PIH
  2. Pre-E
  3. chronic HTN
  4. Cocaine use
  5. smoking
  6. excessive etoh use
140
Q

What are associated maternal symptoms of placental abruption

A

pain and vaginal hemorrhage

141
Q

What other maternal complication is associated with placental abruption

A

amniotic fluid embolism leading to DIC

142
Q

What is the most common cause of postpartum hemorrhage

A

Uterine atony

143
Q

What are 4 factors that increase the risk of uterine atony

A
  1. multiparity
  2. multiple gestations
  3. Polyhydramnios
  4. prolonged oxytocin before surgery
144
Q

What are 7 other causes of obstetric bleeding besides uterine atony

A
  1. retained placenta
  2. laceration of cervix
  3. uterine inversion
  4. coagulopathy
  5. placenta previa
  6. placental abruption
  7. abnormal placental implantation
145
Q

What medication can be given for retained placenta and why

A

IV nitroglycerin provides uterine relaxation for placental extraction

146
Q

What 3 conditions are maternal DIC associated with

A
  1. AFE
  2. Placental abruption
  3. Intrauterine fetal demise
147
Q

When are Apgar scores calculated

A

At 1 and 5 minutes after delivery

148
Q

What do the Apgar scoring times correlate with what fetal conditions

A

1 min = fetal acid-base status

5 min = predictive of neurologic outcomes

149
Q

What are the following Apgar scores:
Normal =
Moderate distress =
Impending demise =

A

Normal = 8-10
Moderate distress = 4-7
Impending demise = 0-3

150
Q

What are the 5 measures of Apgar scoring

A
  1. HR
  2. Respiratory effort
  3. Muscle tone
  4. Reflex irritability
  5. Color
151
Q

What a normal neonatal HR and RR

A 
HR = 120-160
RR = 30-60
152
Q

Why should supplemental O2 be avoided in the neonate

A

It increases risk of an inflammatory response

153
Q

What is the dose for

PRBCs, NS, and LR volume expanders in the newly delivered neonate

A

10 mL/kg

APEX-across the lifespan (7 decks)

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