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Principles II- Josh > Ms. Harmons focused review > Flashcards

Ms. Harmons focused review Flashcards

this is what harmon told us to focus on

1
Q

Pulmonary changes in reference to inhalation agents

A

-MV is increased by 50% TV by 40% and RR by 10% the increased MV and decreased FRC => causes rapid increased alveolar concentrations of inhaled anesthestics basically gas uptake is faster!!!

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2
Q

uterine blood flow is up to how much mL/min

A

500-700 mL/min

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3
Q

Is the uterus autoregulated

A

no, it depends on the mothers BP

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4
Q

what causes decreases in uterine blood flow?

A

mothers hypotension

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5
Q

do epidurals or spinal anesthesia alter uterine blood flow?

A

not if maternal hypotension is avoided

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6
Q

what do contractions do to uterine blood flow?

A

Decreases it

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7
Q

An Anesthetic consideration is that which pressor is NOT associated with significant decreases in uterine blood flow?

A

Ephedrine

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8
Q

Placental exchange occurs primarily by what?

A

diffusion

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9
Q

1st stage Pain what type of pain? what causes the pain? what type of nerve fibers? where to the fibers origionate? pain characteristics?

A

-VISCERAL -caused by uterine contractions an ddilation of cervix -Autonomic C fibers -enter the dorsal horn of the spinal cord T10-L1 -dull- aching pain (how to remember For Jake) know the C visCeral pain caused by Contractions and dilation Cervix autonomic C fibers

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10
Q

2nd stage Pain what type of pain? what causes the pain? what type of nerve fibers? name of the nerves? where to the fibers origionate?

A

-SOMATIC -caused by the stretching of the vagina and perineum by desecent of the fetus -A-Delta -pudendal nerves -enter spinal cord at posterior roots S2-4 (how to remember Somatic Seecond stage remember the S)

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11
Q

what is the treatment for aspiration prophylaxis for all pregnant women? give doses and route!

A

Reglan 10mg IV Zantac 50mg IV Bicitra 30 mL PO

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12
Q

what is Beat to beat variability? Is it normal? what does it indicate?

A

FHR that varies 5-20 BPM yes (completly normal) nothing no worries

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13
Q

what is early decelerations? is it normal? what does it indicate?

A

-the slowing of the FHF that begins with the onset of uterine contraction -yep (no worries no problems) -nothing NOT indicative of fetal distress

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14
Q

what is a late deceleration is it normal? what does it indicate? what test is recomended?

A

-slowing of FHF that begins 10-30 seconds after the onset of uteine contractions. -nope never - fetal distress - fetal scalp pH

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15
Q

what are variable decelerations? they are generally characterized by what? thought to be caused by what? are the bad? how can you fix it?

A
  • variable in magnitude, duration and time of onset - generally characterized by a steep descent of FHR -umbilical cord compression -unless prolonged, they are usually benign - changing maternal position (all caused by compression of the cord)
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16
Q

what is it and what are the 6 defining characteristics?

A

early decelerations have the following characteristics:

  • Occur with each uterine contraction
  • Start and end with the contraction
  • Gradually decrease in rate and then end in a return to baseline
  • Are uniform in appearance
  • Are associated with a mild decrease in FHR (20 bpm or less)
  • Are accompanied by a loss in beat-to-beat variability during the deceleration (Plaus 1112)
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17
Q

what is this and what are the 4 defining characteristics

A

variable decelerations have the following characteristics:

  • Vary in appearance, duration, depth, and shape
  • Demonstrate abrupt onset and recovery
  • Maintain beat-to-beat variability with the deceleration
  • Are classified as severe if the FHR decreases by 60 bpm, if the FHR decreases to less than 60 bpm, or if the decelerations last 60 seconds or longer (Plaus 1112)
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18
Q

what is this and what are it’s 7 defining characteristics

A

late decelerations have the following characteristics:

  • Occur with each uterine contraction
  • Start between 10 and 30 seconds after the uterine contraction
  • Gradually decrease in rate and end in a return to baseline
  • Are uniform in appearance
  • Vary in depth according to the strength of the uterine contraction
  • May or may not be accompanied by beat-to-beat variability
  • Are classified as severe if the FHR decreases by more than 45 bpm

Late decelerations are probably caused by a problem in the uteroplacental interface that results in fetal hypoxia and acidosis. Any late deceleration is a reason for concern. Even small (Plaus 1112)

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19
Q

WHat is this

A

normal beat-to-beat and long-term variability with fetal heart rate (FHR) of 150 to 160 beats per minute (bpm). The distance between the heavy vertical lines represents 60 seconds. The lighter vertical lines are 10 seconds apart (Plaus 1110)

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20
Q

What is this?

A

Poor beat-to-beat and long-term variability. The fetal heart rate was measured with a scalp electrode. (Plaus)
Plaus, Nagelhout and. Nurse Anesthesia, 4th Edition. W.B. Saunders Company, 022009. .

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21
Q

are VAA’s teratogens? and why or why not?

A

yes (potentially)
b/c unethical to test in prego

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22
Q

LA, VAAs, induction agents, opioids, and MR are all safe for the fetus when?

A

in clicical circumstances

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23
Q

Name14 teratogenic drugs?

A

ACEi’s
ETOH
COCAINE
COUMADIN
androgens
antithyroid
chemo
Diethystibesterol
Lead
Lithium
Mercury
Phenytoin
Streptomycin
Thalidomide
Trimethadione
Valproic acid

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24
Q

Pregnancy cat A

A

no risk identified in well controlled studies

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25
Q

Pregnancy Cat B

A

no adequate and well controlled studies in PREGNANT WOMEN, however animal studies have revealed no fetus harm

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26
Q

Pregnancy Cat C

A

no adequate and well controlled studies in PREGNANT WOMEN, however an adverse effect has been shown in animals
or
Adequate and well controlled studies in PREGNANT WOMENhave failed to show a risk to the fetus; but an adverse effect has been shown in an animal

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27
Q

Pregnancy Cat D

A

a risk to the fetus has been demonstrated in adequate, well controlled or observational studies in pregnant women; however the benefits of therapy may outweigh the potential risk

28
Q

Pregnancy cat X

A

positive evidence of fetal abnormalities has been demonstrated in adequate well controlled studies or observational studies in pregnant woman or animals, the drug is contraindicated in women who are or may became pregnant

29
Q

what teratogenic effect do benzo’s cause

A

cleft anomalies

30
Q

what teratogenic effects does cocain how

A

vasoconstriction

hypoxia

abruption

31
Q

what teratogenis effects do halogenated inhalation drugs have

A

in animal studies after 8-12 hours of exposure during organogenesis( effects were seen)

32
Q

what teratogenic effects do NSAIDs have

A

constrict or close ductus arteriosis (usually avoided)

33
Q

complications of tocylitics

A

pulm edema
arrythmias
hypokalemia

34
Q

what is present when the placenta implants in advance of the fetal presenting part?

A

Placenta previa

35
Q

3 types of placenta previa? and what are they?

A

total

partial

marginal

36
Q

what is marginal placenta previa?

A

placenta just reaches the internal OS but does not cover it AKA (low-lying)

37
Q

what is partial placenta previa?

A

placenta partially covers the internal OS

38
Q

what is complete placenta previa?

A

placenta completely covers internal OS

39
Q

what can cause placenta previa?

A

multiparity

advanced maternal age

previous C-section (or uterine sx)

Previous placental previa

40
Q

*****************************

what is the classic presentation of placentia previa

A

PAINLESS vaginal bleeding during the second or third trimester

41
Q

what is defined as separation of placenta from the decidua basilis (endometrium) before delivery of fetus?

A

Placental abruption

42
Q

look at all 3 and see differences

A
43
Q

what are associated factors with placental abruption

A

HTN

advanced age and parity

tobacco use

COCAINE

trauma

PROM

Hx of placental abruption

44
Q

what is a uterine wall defect resulting in fetal distress and/ or maternal hemmorrhage sufficient enough to require a C-section or post partum laparotomy?

A

uterine rupture

45
Q

where does uterine rupture usually occur?

A

classic rupture of uterine scar

46
Q

what is the prefered definative approach to uterine rupture?

A

hysterectomy

47
Q

postpartum hemorrhage is defined as what?

A

> 300 ml after delivery

(or a 10% decrease in HCT from admission to portpartum period)

48
Q

what is primary postpartum hemorrhage

A

occurs during first 24 hrs after delivery

49
Q

what is 2ndary postpartum hemorrhage

A

occurs b/t 24 hrs and 6 wks postpartum

50
Q

what are 3 abnormal placental implantations

A

Accreta- adherance to myometrium no invasion or passage to muscle

Increata- invasion on myometrium

Percreta- invasion of uterine serosa or other pelvic structures

51
Q

5 categories of tocolytics and names and SE if known

A

Beta receptor agonist (terbutaline, ritodine) s/e of tachycardia

Magnesium sulfate (Ca++ antagonist)

CCB (procardia, Nifidipine)

Prostaglandin sysnthesis inhibitors (ASA, NSAIDs, Indomethacin) s/e ductus arterious closure

Oxytocin antagonist

52
Q

MAgnesium sulfate

  1. used for what 2 things?
  2. causes relaxation of ______, ________, and ________ smooth muscle
  3. Alters _______ transport and availability
  4. normal serum levels are ____ - _____ mg/dL
  5. therapeutic serum level is _____-____ mg/dL
A
  1. tocolysis and PIH
  2. vascular, bronchial, and uterine
  3. calcium
  4. 1.8-3
  5. 4-8
53
Q

Magnesium s/e

  1. DTR loss at _____ mEq/L
  2. Cardiac arrest at ______ mEq/L
  3. think of it as a partial _________ ___________
  4. rapidly removed from the body, can be antagonized with _______ ___________
  5. side effect s/s
A
  1. 10
  2. 25
  3. neiromuscular blockade
  4. calcium chloride (3x’s more Ca++ than glucanate)
  5. muscle weakness/ loss of DTR/ head ache/ dizziness/ nausea/ respi changes/ ECG changes/ flushing
54
Q

what is important to remamber about magnesiums s/e

A

it crosses the placenta so all s/e mom gets baby gets also

55
Q

s/s of PIH (preeclampsia)?

A

HTN

edema

proteinuria

h/a

visual disturbances

confusion

RUQ pain

Epigastric pain

Oligohydroaminious

impaired renal fxn

oliguria <500 ml/day

pulm edema

anemia

thrombocytopenia <100,000

fetal inpired liver fxn

56
Q

Diagnosis of PIH preeclamsia is based on what?

A

sustained BP > 140/90

2+ or 300 mg/24hr proteinuria

pretibial edema

57
Q

what is used to control PIH

A

magnesium

58
Q

preeclampsia anesthesia preference

A

regional (as long as plt is ok)

can decrease BP

59
Q

what are predisposing factors to PIH/preeclampsia

A

highest is primigravidas <20 y/o

and older the 35

60
Q

what about esmolol use in PIH/ preeclampsia

A

held great promise, but found to be a BAD idea

crosses the placenta and causes a clinically significant feta beta blockade

BABY WILL COME OUT WITH ASYSTOLE

61
Q

est blood loss for vaginal birth

A

approx 500ml

62
Q

est blood loss for c-section

A

700 for c-section (somewhere she said 1500 was ok)

63
Q

CV compensatory response to aortocaval compression

A

decreased venous return = decreased SV and CO

response is

tachycardia

casoconstriction of lower extremities

64
Q

G2P2002

A

G# of pregnancies

P # of kids

F P and L (full term, preterm, abortion, living)

2 pregnancies

2 full term

0 preterm

0 abortions

2 living

65
Q

G1P0000

A

1 pregnancy

0 fullterm

0 preterm

0 abortion

0 living

(this is her first pregnancy)

66
Q

severe preeclampsia is said to exist when what conditions are present?

A

Bp > 160/110

3+ or 4+ proteinuria

UOP < 20 ml/hr

CNS signs (blurred vision, changes in metation)

Pulm edema

epigastric pain

Principles II- Josh (17 decks)

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