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OB Flashcards

1
Q

What causes swelling of the maternal airway?

A

Increased progesterone, estrogen, and relaxin combined with an increase in ECF.
These tissues also become very friable

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2
Q

Risk of difficult and failed intubation

A

8x higher than normal

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3
Q

What things make airway edema even worse in parturients?

A

Pre-eclampsia, tocolytics, and prolonged trendelenburg position

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4
Q

This hormone is a respiratory stimulant

A

Progesterone
Causes MV to increase by 50%
(40% increase in TV + 10% increase in RR)

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5
Q

Lung volume changes in pregnancy

A

Increased:

  • TV and MV
  • RR

Decreased:
- FRC (d/t decreases in ERV and RV)

No changes in other lung volumes! It’s actually pretty easy to think this through.

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6
Q

CV changes in pregnancy

A
  • O2 consumption increased 20%
  • CO increased 40% (up to 80% in 3rd stage of labor)
  • HR increased 15%
  • SV increased 30% (similar to respiratory, with volume increasing more than rate)
  • SBP and MAP unchanged (increase in blood volume and decrease in SVR even out)
  • DBP decreased 15%
  • SVR and PVR both increased d/t NO
  • No change in filling pressures (CVP or PAOP)
  • Left axis deviation (d/t pushing of diaphragm)
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7
Q

3 Major effects of progesterone

A

1) Increases RAAS activity
- Increased blood volume and CO

2) Vascular muscle relaxation
- Decreased SVR and increased flow

3) Increased MV
- Rightward shift of dissociation curve

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8
Q

With LUD, the right torso should be elevated ___ degrees

A

15 degrees

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9
Q

Heme changes in pregnancy

A

Overall, increasing circulating blood volume and preparing for hemorrhage in labor

  • Increase circulating volume and erythrocyte volume (dilution anemia)
  • Increased clotting factors
  • Decreased natural anticoagulants (C&S)
  • Decreased fibrin polymerization and increased fibrin breakdown

Mom makes more clot, but breaks it down faster too

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10
Q

What happens to serum albumin?

A

Decreases

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11
Q

What happens to pseudocholinesterase?

A

Decreases (not enough to be clinically relevant though)

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12
Q

Drug characteristics that favor placental transfer

A
  • Low MW
  • Non-ionized and non polar
  • Lipid soluble
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13
Q

Stages of labor

A

Stage 1

  • Beginning of regular contraction to full dilation
  • Divided into latent, and then active phases
  • Most cervical dilation occurs during active phase
  • Thoracic pain (T10-L1)

Stage 2

  • Full dilation to delivery
  • Perineal pain begins here (Sacral S2-4)

Stage 3
- Delivery of placenta

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14
Q

2 Major effects of uncontrolled pain in labor

A

1) Catecholamine release
- Maternal HTN and reduced UBF

2) Hyperventilation (leftward shift and decreased O2 transfer to fetus)

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15
Q

Only LA that decreases efficacy of morphine

A

2-Chlorprocaine

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16
Q

How is chlorprocaine metabolized?

A

Pseudocholinesterase (minimal placental transfer)

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17
Q

Presentation of high spinal

A

Rapid sensory and motor block
Dyspnea
Difficulty phonating
Hypotension (hypotension leads to apnea)

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18
Q

Management of high spinal

A

Get her BP back up so she will start breathing on her own! (Overall pressers and increase venous return)

  • Pressors
  • IVF
  • LUD
  • Leg elevation

If unable to manage her own airway, then INTUBATE

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19
Q

Normal fetal heart rate (FHR)

A

110-160

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20
Q

Fetal and maternal causes of low FHR (

A

Fetal:

  • Asphyxia
  • Acidosis

Maternal:

  • Hypoxia
  • Drugs that decrease placental perfusion
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21
Q

Fetal and maternal causes of high FHR (>160)

A

Fetal:

  • Hypoxia
  • Arrhythmias

Maternal:

  • Fever
  • Placental infection (chorioamnionitis)
  • Meds given to mother (atropine, ephedrine, or terbutaline)
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22
Q

These things decrease FHR variability

A
  • CNS depressants (opioids, sedatives, propofol, barbs, and magnesium)
  • Hypoxia
  • Fetal sleep
  • Acidosis
  • Anencephaly
  • Cardiac anomalies
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23
Q

Type of decels and what they mean

A

1) Early
- Occur with uterine contraction
- Compression of fetal head increased vagal tone
- Loss of variability with each deceleration
- NO RISK OF FETAL HYPOXIA (benign)

2) Late
- Deceleration occurs AFTER contraction
- Due to decreased placental perfusion leading to fetal compromise**
- GRADUAL decal that happens with each contraction
- Caused by maternal hypotension, hypovolemia, acidosis, and preeclampsia

3) Variable
- No pattern between contraction and FHR
- RAPID drop in FHR
- Variability is maintained during decel
- Often due to compression of cord (causing baroreceptor mediated reduction in FHR)

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24
Q

Three-tier system for evaluation of FHR

A

Category I

  • FHR is normal
  • Fetus is good

Category II

  • There’s some weird shit going on with the FHR
  • Could be ok, but maybe not

Category III

  • There’s some serious shit going on
  • Oh fuck
  • Oh God, why?
25
What is sinusoidal pattern?
Regular up and down waves of FHR
26
Corticosteroids for fetal lung maturity begin to work at ___ hours and peak at ___ hours
Begins at 18 hours | Peaks at 48 hours
27
Tocolytic agents stop labor for how long?
24-48 hours
28
Examples of tocolytic agents
1) Beta- 2 Agonists - Work by increasing intracellular cAMP - Ex- Terbutaline and Ritodrine - SE include hyperglycemia (places fetus at risk for hypoglycemia), hypokalemia, and may cross placenta to increase FHR 2) Mag Sulfate - Ca++ antagonist 3) CCBs - Block influx of Ca+2 into uterine muscle - Ex- oral Nifedipine - Given with mag sulfate can exacerbate weakness 4) NO Donors - Rarely given d/t hypotension
29
How does mag sulfate work?
Calcium Antagonist | Turn off myosin light chain kinase and hyper polarizes excitable membranes
30
Order of magnesium's effects with increasing serum concentrations
``` Normal Level Tocolysis Anticonvulsant Patellar Reflex Abolished Skeletal muscle weakness Resp Depression Apnea Cardiac Arrest ```
31
SE of mag sulfate
Hypotension and decreased response to ephedrine and phenylephrine Pulmonary edema Muscle weakness CNS depression (b/c it depresses excitable tissue)
32
Treatment for hpermagnesemia
- IV Calcium! (Mag antagonist) - Diuretics (to excrete Mag) - Supportive measures
33
Details of Oxytocin (Pitocin)
- Endogenous oxytocin is release after stimulation of cervix, vagina, and/or breasts - Can be given IV or injected into uterus - Metabolism: hepatic - 1/2 life = 4-7 minutes (very short acting!) - SE = water retention and hyponatremia, hypotension, reflex tachycardia, and coronary vasoconstriction
34
Details of Methergine
- Ergot alkaloid - Second line uterotonic (after pitocin) - Dose = 0.2mg IM - Giving IV can cause massive HTN (may result in cerebral hemorrhage) - 1/2 life is 2 hours
35
Details of Hemabate/Carboprost
- Prostaglandin F2 - Third line uterotonic - Dose = 250mcg IM or injected into uterus - SE = bronchoconstrition, N/V/D, and hypoTN or HTN
36
In the case of coagulopathy, which is preferred for C/S? Regional or GA?
GA
37
In the case of fetal distress, which is preferred for C/S? Regional or GA?
GA (d/t greater hemodynamic stability --> no sympathectomy)
38
Triple prophylaxis against respiration
1) Bicitra 2) H2 antagonist (Ranitidine) 3) Gastrokinetic agent (Reglan)
39
VA usage in GA for emergent C/S
0.8 MAC with 50% Nitrous VAs relax the uterus and can contribute to bleeding post-delivery
40
When is oxtocin given during C/S
After delivery of the placenta
41
When can opioids and benzos be used during C/S?
After delivery of newborn
42
Why is C/S tried to be performed as quickly as possible?
Risk of neonatal acidosis increases if time from incision to delivery exceeds 3 minutes This is also why patient is prepped and draped prior to induction
43
Why are NSAIDs avoid for women after their first trimester?
They can close the ductus arteriosus When it comes to GA in parturients, KISS! Keep it simple, stupid! Stick to things with a proven track record. Nothing risky.
44
Aspiration prophylaxis if mother is > ___ weeks
14 weeks | Triple prophylaxis and RSI
45
Patho of pre-eclampsia
Abnormal placental implantation results in elevated uterine VR and reduction in BF. Placenta and fetus thus don't get enough O2 and nutrients to develop normally. The shitty placenta ends up making 7x more thromboxane than prostacyclin (normally 1:1). - Results in vasoconstriction, plt aggregation, and further decreased placental BF. - Diseased placenta also releases cytokines that damage vascular endothelium
46
Why do we treat BP in preeclampsia?
Only need it once severe (>160/110) to prevent MI, cerebral hemorrhage, and placental abruption.
47
Dose of mag sulfate for sz prophylaxis
4g loading dose > 10 minutes | Then infusion of 1-2g/hr
48
Dose of calcium for mag toxicity
1g | 10mL of 10% calcium GLUCONATE
49
Major risk of placenta accreta
Uterine contractility is impaired --> potential for massive blood loss!
50
This med can provide uterine relaxation for placental extraction
NTG
51
These situations in pregnancy may lead to DIC
Intrauterine demise Amniotic fluid embolism Placental abruption
52
Meaning of APGAR score at 1 and 5 minutes
1 minute = acid-base balance 5 minutes = neurologic outcome ``` 8-10 = Normal 4-7 = Moderate distress 0-3 = Impending demise ```
53
SpO2 immediately after delivery
60% Should rise to 90% by 10 minutes
54
This is the best indicatory of adequate ventilation in the newborn
Resolution of bradycardia
55
3 routes that emergency drugs can be given to newborn
1) Umbilical vein 2) ETT 3) Intraosseous
56
Dose of epic for newborn
10-30mcg/kg IV OR 0.05 - 0.1mg/kg via ETT
57
Volume expander dose for newborn
10mL/kg over 5-10 minutes for PRBCs NS LR
58
Chest compressions are initiated in newborn if HR
60

Board Exam (21 decks)

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