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Review Apex > UNIT 11 Across the Lifespan > Flashcards

UNIT 11 Across the Lifespan Flashcards

1
Q

how does pregnancy affect minute ventilation?

A

progesterone is a respiratory stimulant. It increases MV up to 50%

  • Vt increases by 40%
  • rr increases by 10%
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2
Q

how does pregnancy affect the mother’s ABG?

A

progesterone is a respiratory stimulant, increasing MV up to 50%. In consequence, mom’s PaCO2 falls and she develops a respiratory alkalosis. Renal compensation eliminates bicarb to normalize blood pH.

increased PaO2 d/t reduction in physiologic shunt that increases driving pressure of oxygen across the fetoplacental interface + improves fetal gas exchange

pH = no change
PaO2 = 104-109
PaCO2 = 28-32
HCO3- = 20
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3
Q

how does pregnancy affect the oxyHgb dissociation curve?

A

R shift, facilitates O2 unloading to the fetus

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4
Q

how does pregnancy affect the lung volumes and capacities?

A

FRC is reduced as a function of a decrease in ERV and RV (ERV decreases more than RV)

increased O2 consumption paired w/ decreased FRC hastens the onset of hypoxemia.

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5
Q

how does CO change during pregnancy and delivery?

A

CO increases 40% (uterus receives 10% of CO, uterine contraction causes autotransfusion = increased preload)

  • HR increases 15%
  • SV increases 30%

CO returns to pre-labor values in 24-48hrs
CO returns to pre-pregnancy values in approx 2 weeks

twins cause CO to increase 20% above a single fetus pregnancy

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6
Q

how do BP and SVR change during pregnancy?

A

increased blood volume + decreased SVR = net even effect on MAP
- decreased DBP 15%

progesterone causes increased NO (vasodilation) and decreased response to angiotensin and NE

  • SVR decreases 15%
  • PVR decreases 30%
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7
Q

who is at risk for aortocaval compression and how do you treat it?

A

in the supine position, the gravid uterus compresses the vena cava and the aorta –> decreased venous return + decreased arterial flow
- compromised fetal perfusion and can also cause the mother to lose consciousness

LUD 15degrees = tx
- should be used for anyone in 2nd or 3rd trimester

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8
Q

how does the intravascular fluid volume change during pregnancy?

A

increases 35% (prepares mom for hemorrhage w/ labor)

plasma volume increase 45%
erythrocyte volume increase 20%
- creates dilutional anemia

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9
Q

what hematologic changes accompany pregnancy?

A

clotting factors increase (I, VII, VIII, IX, X, XII) = hypercoaguable state

anticoagulants decrease (protein C, S) = 6x risk of DVT

increased fibrin breakdown = counteracts state of hypercoaguability

decreased antifibrinolytic system = reduction in fibrin polymerization

**makes more clot, but breaks it down faster; tendency to develop consumption coagulopathy

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10
Q

how does MAC change during pregnancy?

A

decreased by 30-40% d/t increased progesterone

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11
Q

how does pregnancy affect gastric pH and volume?

A

increases volume
decreases pH
- d/t increased gastrin

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12
Q

how does pregnancy affect gastric emptying?

A

before onset of labor = no change

after onset of labor = delayed

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13
Q

how does pregnancy affect uterine blood flow?

A

at term, UBF increases to 500-700mL/min (10% of CO)

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14
Q

what conditions can reduce uterine blood flow?

A

uterine blood flow does NOT autoregulate –> therefore, it is dependent on MAP, CO, and uterine vascular resistance

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

causes of decreased UBF:

  • decreased perfusion: maternal hypotension
  • increased resistance: uterine contraction, hypertensive conditions that increase UVR
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15
Q

discuss the use of phenylephrine and ephedrine in the laboring patient.

A

classic teaching = phenylephrine increases uterine vascular resistance and reduces placental perfusion

new evidence = phenylephrine is as efficacious as ephedrine in maintaining placental perfusion and fetal pH.

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16
Q

which law determines which drugs will pass through the placenta?

A

Fick
rate of diffusion = (diffusion coefficientsurface areaconcentration gradient)/ membrane thickness

drugs that favor placental transfer:

  • low molecular weight
  • high lipid solubility
  • unionized
  • nonpolar
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17
Q

define the 3 stages of labor

A 
1 = beginning of regular contractions to full cervical dilation (10cm)
2 = full dilation to delivery of fetus (pain in the perineum begins during stage 2)
3 = delivery of the placenta
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18
Q

how does uncontrolled labor pain affect the fetus? Why?

A

uncontrolled pain may result in:

  • increased maternal catechols –> HTN –> reduced UBF
  • maternal hyperventilation –> L shift of oxyHgb curve –> reduced delivery of O2 to fetus
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19
Q

compare and contrast the pain that results from the first and second stages of labor.

A

first

  • pain begins in the lower uterine segment and the cervix
  • origin: T10-L1 posterior nerve roots

second

  • adds in pain impulses from the vagina, perineum, and pelvic floor
  • origin: S2-S4 posterior nerve roots
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20
Q

compare and contrast regional anesthetic techniques that can be used for first and second stage labor pain

A

1st stage (T10-L1), 2nd stage (S2-4)

uterus and cervix (diffuse, dull, cramping pain)

  • neuraxial
  • paracervical nerve block
  • paravertebral lumbar sympathetic block

perineum (well localized, sharp pain)

  • neuraxial
  • pudendal nerve block
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21
Q

describe the “needle through needle” technique for CSE

A
  • epidural space is ID-ed w/ the epidural needle
  • spinal needle is placed through the epidural needle, LA injected into intrathecal space
  • spinal needle is removed
  • epidural catheter is threaded through epidural needle
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22
Q

compare and contrast bupivacaine and ropivacaine for labor.

A

bupi: amide, long DOA
- racemic mixture
- minimal tachyphylaxis
- low placental transfer (high PB, ionization)
- sensory >motor block
- cardiac toxicity (before sz)
- 0.75% contraindicated via epidural d/t risk of toxicity w/ IV injection

ropi: amide, long DOA
- S isomer of bupi w/ propyl group substituation
- decreased risk of CV toxicity
- decreased potency c/w bupi
- decreased motor block

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23
Q

discuss the use of 2-chloroprocaine for labor

A
  • useful for emergency c/s when epidural already in place (d/t fast onset)
  • metabolized by plasma pseudocholinesterase (minimal placental transfer)
  • antagonizes opioid receptors (reduces efficacy of epidural morphine)
  • risk of arachnoiditis w/ intrathecal injection d/t preservatives
  • those w/out methylparaben, metabisulfite don’t cause neurotoxicity
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24
Q

discuss the consequences of an epidural that is placed in the subdural space.

A

w/in 10-25mins after dosing, pt will experience symptoms of excessive cephalad spread
- subdural space is a potential space; holds very low volume –> block will go high quicker

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25
Q

what is the treatment for a total spinal?

A 
vasopressors
IVF
LUD
elevation of the legs
intubation if LOC
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26
Q

discuss the fetal heart rate.

A

surrogate measure of overall fetal wellbeing (fetal hypoxia and acidosis)

normal 110-160

  • intact CNS, ANS + normal pH
  • normal uteroplacental perfusion

bradycardia <110

  • asphyxia, acidosis
  • hypoxemia, drugs that decrease uteroplacental perfusion

tachycardia >160

  • hypoxemia, arrhythmias
  • fever, chorioamnionitis, atropine, ephedrine, terbutaline
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27
Q

what type of fetal decelerations are unremarkable? which cause concern?

A

early decels (head compression) don’t present a risk of fetal hypoxemia, while late and variable decels require urgent assessment of fetal status.

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28
Q

what are the common causes of fetal deceleration patterns?

A

VEAL CHOP

Variable: Cord compression
Early: Head compression
Accels: OK (or give O2)
Late: Placental insufficiency

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29
Q

define premature delivery, and list the potential complications from its occurrence.

A

delivery <37 weeks gestation

  • leading cause of perinatal M&M
  • risk is even higher w/ newborns <1500g
  • incidence increases w/ multiple gestations and PROM

complications:
- respiratory distress
- intraventricular hemorrhage
- NEC
- hypoglycemia
- hypocalcemia
- hyperbilirubinemia

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30
Q

discuss the use of steroids and tocolytic agents in the prevention of premature delivery

A

corticosteroids (betamethasone) hasten fetal lung maturity

  • begin to take effect w/in 18hrs
  • peak benefit 48hrs

tocolytic agents stop labor approx 24-48hrs

  • provide a bridge that allows the corticosteroids time to work
  • abx prophylaxis for chorio is also given at this time

neither of these are often given after 33 weeks gestation

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31
Q

what are the side effects of B2 agonists when used for tocolysis?

A

(terbutaline, ritodrine)

  • hypokalemia d/t intracellular K+ shift
  • cross placenta, may increase FHR
  • hyperglycemia d/t glycogenolysis in the liver
  • newborn of hyperglycemia mother is at risk for post-delivery hypoglycemia
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32
Q

how does the serum magnesium level correspond w/ its clinical effects?

A

two different ways to measure Mg++ in the plasma:

1.8-3mg/dL = normal

4-8mg/dL = tocolysis

7-9.5mg/dL or 2-3.5mEq/L = anticonvulsant

10-12mg/dL or 4-6.5mEq/L = loss of patellar reflex, N/V, diplopia, somnolence

12-18mg/dL = resp depression

> 18mg/dL or 6.5-7.5mEq/L = skeletal m weakness, apnea

> 25mg/dL or >10mEq/L = cardiac arrest

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33
Q

what are the side effects of magnesium?

A 
pulmonary edema
hypotension
skeletal m weakness 
CNS depression
reduced responsiveness to ephedrine/phenylephrine
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34
Q

what is the treatment for hypermagnesemia?

A

supportive measures
diuretics
IV calcium

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35
Q

how can oxytocin be administered? what are the potential side effects?

A

synthesized by suproptic and paraventricular nuclei of the hypothalamus, released from posterior pituitary

give it IV (diluted), or it can be injected directly into the uterus

side effects:

  • water retention
  • hyponatremia
  • hypotension
  • reflex tachycardia
  • coronary vasoconstriction
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36
Q

how can methergine be administered?

A

ergot alkaloid
0.2mg IM (NOT IV)

IV administration = significant vasoconstriction, hypertension, and cerebral hemorrhage

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37
Q

what are the pros and cons of GA for c/s?

A

mortality is 17x higher w/ GA
- failure of successful a/w securement is the most common cause

benefits

  • speed of onset
  • secured airway
  • greater hemodynamic stability

drawbacks

  • difficult BMV, DL, intubation
  • risk of aspiration
  • potential MH
  • absence of maternal awareness
  • neonatal respiratory, CNS depression
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38
Q

describe aspiration prophylaxis for the patient scheduled for a c/s

A

triple prophylaxis against aspiration:

  • sodium citrate
  • H2 receptor antagonist
  • gastrokinetic agent
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39
Q

when is the pregnant patient who presents for non-obstetric surgery at risk for aspiration?

A

if mom is >14 weeks gestation

  • administer antacid w/in 30mins of induction
  • H2 blocker 1hr pre-induction
  • reglan +/-

if mom is >14 weeks gestation, use RSI + 6.0-7.0 ETT

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40
Q

what is the risk of NSAIDs when used in the pregnant patient?

A

avoid in first trimester, as they may close the ductus arteriosus

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41
Q

compare and contrast the diagnostic criteria for gestational HTN, preeclampsia, and eclampsia.

A

gest HTN
- HTN after 20 weeks

preeclampsia

  • HTN after 20 weeks
  • proteinuria
  • edema

eclampsia

  • HTN after 20 weeks
  • proteinuria
  • edema
  • seizures

(edema is no longer a requirement for diagnosis)

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42
Q

discuss the balance of prostacyclin and thromboxane in the patient w/ preeclampsia

A

the healthy placenta produces thomboxane and prostacyclin in equal amounts, however, the pt w/ preeclampsia produces up to 7x more thromboxane than prostacyclin
–> favors vasoconstriction, platelet aggregation, and reduced placental blood flow

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43
Q

compare and contrast mild and severe preeclampsia.

A

mild

  • <160/<110
  • <5g proteinuria/24hrs
  • 24 UOP >500mL
  • generalized edema w/out pulmonary edema, cyanosis, HA, visual impairments, epigastric pain

severe

  • > 160/>110
  • > 5g proteinuria/24hrs
  • generalized edema + pulmonary edema
  • cyanosis
  • HA + visual impairment
  • epigastric pain
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44
Q

discuss the use of magnesium for preeclampsia

A

the presence of seizures differentiates b/n preeclampsia and eclampsia.

sz prophylaxis w/ mg sulfate

  • load: 4g over 10min
  • gtt: 1-2g/hr
  • tx for mag toxicity: 10mL of 10% calcium gluconate IVP
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45
Q

detail the anesthetic management for the patient w/ preeclampsia.

A
  • balanced fluid management
  • RA = good, but r/o thrombocytopenia
  • higher incidence of difficult intubation d/t a/w swelling
  • exaggerated response to sympathomimetics + methergine
  • if on mag, increased NMB sensitivity
  • mag also relaxes uterus = increased risk of postpartum hemorrhage
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46
Q

what is HELLP syndrome? what is the definitive treatment?

A

HELLP: hemolysis, elevated liver enzymes, low platelet count

  • develops in 5-10% of those w/ preeclampsia
  • s/s: epigastric pain and upper abdominal tenderness

definitive tx = delivery

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47
Q

discuss the anesthetic considerations for maternal cocaine abuse.

A
  • CV risks: tachycardia, dysrhtyhmias, MI
  • acute intoxication increases MAC, chronic decreases
  • OB risks: spontaneous abortion, premature labor, placental abruption, low APGAR scores
  • HTN treated w/ vasodilators
  • BB can cause HF is SVR is elevated
  • hypotension may not respond to ephedrine (d/t catechol depletion); use phenylephrine
  • chronic cocaine abuse is associated w/ thrombocytopenia
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48
Q

what is the difference b/n placenta accreta, increta, and percreta? What is the major risk that these complications present?

A

accreta: placenta attaches to the surface of the myometrium
increta: invades the myometrium
percreta: extends beyond the uterus

uterine contraction is impaired and there is potential for tremendous blood loss, GA is preferred (though RA is safe)

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49
Q

what conditions increase the risk of abnormal placental implantation

A

placenta previa

previous c/s

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50
Q

what is placenta previa? How does it present?

A

when the placenta attaches to the lower uterine segment

  • partially or completely covers the cervical os
  • associated w/ painless vaginal bleeding
  • potential for hemorrhage
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51
Q

what are the risk factors for placental abruption? how does it present?

A

partial or complete separation of the placenta from the uterine wall prior to delivery. results in hemorrhage and fetal hypoxia

risks:
- PIH
- preeclampsia
- chronic HTN
- cocaine use
- smoking
- excessive EtOH

presents w/ painful vaginal bleeding; pain may be so severe as to cause breakthrough even w/ epidural placement

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52
Q

what is the most common cause of postpartum hemorrhage? What are the risk factors?

A

uterine atony is the most common cause. Increased by:

  • multiparity
  • multiple gestations
  • polyhydramnios
  • prolonged oxytocin infusion prior to surgery
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53
Q

a patient suffers from retained placental fragments. What IV medication can you give to help w/ the extraction?

A

IV NTG for uterine relaxation

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54
Q

what are the treatment options for uterine atony?

A

uterine massage
oxytocin
ergot alkaloids
intrauterine balloon

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55
Q

what does the APGAR score mean?

A

used to assess the newborn and guide resuscitative efforts. Five parameters are evaluated at 1 and 5 minutes after delivery.
1 min score correlates w/ fetal acid-base status
5min score may be predictive of neurologic outcome

normal 8-10
moderate distress 4-7
impending demise 0-3

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56
Q

know how to calculate the apgar score

A

HR: absent, <100, >100

resp effort: absent, slow, normal

muscle tone: limp, some flexion, active motion

reflex irritability: absent, grimace, cough/sneeze/cry

color: pale/blue, body pink/extremities blue, completely pink

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57
Q

what is the best indicator of ventilation during neonatal resuscitation?

A

resolution of bradycardia

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58
Q

how do you dose epi and fluids during neonatal resuscitation?

A

epi 1:10,000

  • 10-30mcg/kg IV
  • 0.05-0.1mg/kg intratracheal

PRBCs, NS, LR
- 10mL/kg over 5-10mins

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59
Q

what are the normal VS for a newborn? How do they trend as the child ages?

A

newborn

  • 70/40
  • HR 140
  • rr 40-60

1yr

  • 95/60
  • HR 120
  • rr 40

3yr

  • 100/65
  • HR 100
  • rr 30

12yr

  • 110/70
  • HR 80
  • rr 20
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60
Q

why is the neonates minute ventilation higher than the adult?

A

O2 consumption and CO2 production are twice those of an adult (ventilation increases accordingly)

it is metabolically more efficient to increase the rr than it is to increase the Tv (explains why rr increases, but Tv/weight is the same)

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61
Q

what is the primary determinant of BP in the neonate?

A

HR
BP = HRSVSVR

neonatal myocardium lacks the contractile elements to significantly adjust contractility or SV; the ventricle is noncompliant. Furthermore, the frank-starling relationship is underdeveloped (but not entirely absent) in the newborn

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62
Q

describe the autonomic influence on the newborns heart.

A

immature at birth, with the SNS being less mature than the PSN.
stressful situations (DL, sxning, etc.) may cause bradycardia
- consider atropine pre-induction

additionally the baroreceptor reflex is poorly developed so the reflex fails to increase HR in the setting of hypovolemia

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63
Q

contrast the breathing pattern in adults and infants.

A

adult: mouth or nose

infant: preferential nose breather up to 5 months of age
- most convert to oral breathing if the nasal passages are obstructed
- bilat choanal atresia may require emergency airway management if the infant is unable to mouth breathe.

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64
Q

contrast the relative size of the tongue in adults and infants.

A

adult: small relative to oral volume

infant: large relative to oral volume
- tongue is closer to the soft palate, which makes it more likely to obstruct the upper airway
- more difficult to displace during DL

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65
Q

contrast the relative neck length in adults and infants.

A

adult = longer
infant = shorter
- more acute angle required to visualize the glottis

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66
Q

contrast the epiglottis shape in adults and infants

A

adults: leaf (C-shaped), floppier, shorter

infant: U (omega shape), stiffer, longer
- makes it more difficult to displace during DL

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67
Q

contrast the vocal cord position in adults and infants

A

adult = peripendicular to trachea

infant = anterior slant

  • visualization and passage of ETT may be more difficult
  • ETT may get stuck in the anterior commissure
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68
Q

contrast the laryngeal position in adults and infants.

A

adults C5-6
infants C3-4
- larynx more superior/cephalad/rostral but NOT anterior. The only time the infants airway is more “anterior” is during neck flaxion
- same position as the adult at age 5-6yrs

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69
Q

contrast the narrowest point of the airway in adults and infants

A

adult = glottis (VC)
infant = cricoid or glottis
- resistance to ETT insertion beyond the VC is likely at the cricoid ring
- cricoid tissue is prone to inflammation and edema formation –> stridor or obstruction
- Poiseuille’s law: small changes in radius can significantly increase resistance to airflow

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70
Q

Why is the “narrowest region of the infant airway” controversial?

A

classic teaching = infant’s airway is narrowest at cricoid ring and funnel shaped ariway

current evidence to support that the classic teaching may not be entirely accurate. New insight suggests that pediatric airway is likely more cylindrical than previously believed, and in the paralyzed child the VC is the narrowest point

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71
Q

contrast the orientation of the R mainstem bronchus in adults and infants.

A

adult = more vertical
infant = less vertical
- up to age 3, both bronchi take off at 55 degrees
- in the adult, the R bronchus takes off at 25 and the L at 45

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72
Q

contrast the optimal intubation position for adults and infants.

A

adult = sniffing position
infant = head on bed w/ shoulder roll
- infant has large occiput
- sniffing position will place the glottic opening in more anterior position

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73
Q

contrast the oxygen consumption, alveolar ventilation, respiratory rate, and tidal volume in neonates and adults?

A

bc neonatal alveolar surface area is only 1/3 of the adult and oxygen consumption is twice that of an adult, the neonate must increase alveolar ventilation in order to sustain normal arterial gas tensions.
It is metabolically more efficient to increase respiratory rate than it is to increase Tv.

oxygen consumption:
6mL/kg/min neonate
3.5mL/kg/min adult

alveolar ventilation:
130mL/kg/min neonate
60mL/kg/min adult

respiratory rate
35bpm neonate
15bpm adult

Tv 6mL/kg for both

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74
Q

why do neonates desaturate faster than adults?

A

they have:

  • increased O2 consumption to support metabolic demand
  • increased alveolar ventilation to increase O2 supply
  • slightly decreased FRC reflecting a decreased O2 reserve

the net result = increased ratio of alveolar ventilation relative to FRC size. A faster gas turnover means that the O2 supply in the FRC is quickly exhausted during apnea.

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75
Q

why is inhalation induction faster w/ a neonate than w/ an adult?

A

increased ratio of alveolar ventilation to FRC

faster FRC turnover (fewer alveoli are needed to achieve steady state) allows for a speedier development of anesthetic partial pressure inside the alveoli and consequently a more rapid change in the anesthetic partial pressure inside the brain and SC

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76
Q

what is the difference b/n fast and slow twitch muscle fibers? how does this relate to neonatal pulmonary mechanics?

A

the diaphragm and intercostal muscles are composed to two types of muscle fibers:

Type I = slow twitch (endurance, fatigue-resistance)
Type II = fast twitch (fast, tire easy)

neonatal diaphragm has 25% type I (adults have 55%) and this explains why neonates fatigue more easily (increased risk for respiratory fatigue, distress, and failure)

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77
Q

compare and contrast neonates to adults in terms of: FRC, VC, TLC, RV, CC, and Vt.

A

FRC:
34mL/kg adult
30mL/kg neonate

VC:
70mL/kg adult
35mL/kg neonate

TLC
86mL/kg adult
63mL/kg neonate

RV
16mL/kg adult
23mL/kg neonate

CC
23mL/kg adult
35mL/kg neonate

Tv 6mL/kg both

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78
Q

how does the newborn’s ABG change from delivery to the first 24hrs of life?

A

mother at term:
7.40 pH, PaO2 90, PaCO2 30

umbilical vein (placenta to fetus)
7.35/30/40
umbilical artery (fetus to placenta)
7.30/20/50

newborn at time after delivery:

10min: 7.20/50/50
1hr: 7.35/60/30
24hr: 7.35/70/30

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79
Q

how does hypoxemia affect ventilation in the newborn?

A

respiratory control doesn’t mature until 42-44 weeks

  • before maturation: hypoxemia depresses ventilation
  • after maturation: hypoxemia stimulates ventilation.
80
Q

what is the P50 of fetal hemoglobin? Why is this important?

A

P50 = 19mmHg

Hgb shifts the curve to the L (L=love)
it benefits the fetus by creating an O2 partial pressure gradient across the uteeroplacental membrane that facilitates the passage of O2 from the mother to the fetus

81
Q

Why does HgbF have a higher affinity for O2?

A

adult hgb (hgbA) consists of 2 alpha and 2 beta chains, while hgbF contains 2 alpha and 2 gamma chains.

2,3 DPG causes a R shift on the oxyHgb dissociation curve
2,3 DPG only has a binding site on the beta chain
therefore, HgbF doesn’t bind 2,3 DPG, shifting the curve to the L and creating a higher affinity for O2 in the HgbF

82
Q

discuss the physiologic anemia of the infant.

A

in the first 2 months of life, erythrocytes containing HgbF are replaced by those that produce HgbA. After about 6 months, HgbF has been completely replaced by HgbA (P50 is now the same as the adult)

birth: Hgb = 17g/dL
2months: RBC production begins to shift to HgbA
2-3months: Hgb = 10g/dL
4months: erythropoiesis increases and Hgb rises
4-6months: HgbA has completely replaced HgbF and P50 is adult level

83
Q

what is the dose for PRBC transfusion in the neonate? How much will this increase Hgb?

A

10-15mL/kg

10mL/kg will raise Hgb by 1-2g/dL

84
Q

what are the indications for FFP transfusion in the neonate?

A

emergency reversal of warfarin

correction of coagulopathic bleeding w/ increase PT >1.5 or increased PTT

correction of coagulopathic bleeding if >1 blood volume has been replaced and coagulation studies aren’t easily obtained.

FFP is NOT indicated for expansion of intravascular volume

85
Q

what is the dose for FFP transfusion in the neonate?

A

10-20mL/kg

86
Q

when is platelet transfusion indicated in the neonate? What is the dose?

A

invasive procedures to maintain platelet count >50K

dose if obtained from apheresis: 5mL/kg
dose if pooled from platelet concentrate: 1 pack/10kg

87
Q

describe the physiologic changes that occur as a result of massive transfusion.

A

massive transfusion is associated with:

  • acidosis (inadequate oxygenation and increased lactate)
  • alkalosis (citrate metabolism to bicarb in the liver)
  • hypothermia
  • hyperglycemia (dextrose additive)
  • hypocalcemia (citrate binding)
  • hyperkalemia (administration of older blood d/t dysfunctional cell membrane. Risk is decreased is <7 day old blood)
88
Q

what is the normal H&H at birth, 3 months, and 6-12months?

A

newborn: 14-20/45-65%
3months: 10-14/31-41%
6-12months: 11-15/33-42%

adult
female 12-16/37-47
male 14-18/42-50

89
Q

what is the estimated blood volume in the premature neonate, term neonate, infant, and child >1yr?

A

preterm 90-100mL/kg
term 80-90mL/kg
infant 75-80mL/kg
>1yr 70-75mL/kg

90
Q

a 3kg term neonate requires emergency ex lap for necrotizing enterocolitis. Her pre-op Hct is 50%. What is the maximum ABL to maintain Hct of 40%?

A

ABL = EBV*(Hct-Hct target)/Hct

EBV = 3kg*(80 to 100mL/kg)
= 240-300mL

ABL = 300(50-40)/50 = 60mL

91
Q

when do GFR and renal tubular function achieve full maturation?

A

normal GFR is reached at 8-24months of age
- before maturation, neonates do a poor job of conserving water, so they are intolerant of fluid restriction. On the flip side, they are unable to excrete large volumes of water, so they don’t do well w/ fluid overload either

normal tubular function is reached at 2yrs of age
- in the first few days of life, they are an obligate sodium loser. After that, they’re better able to retain Na+ than excrete it. They have a tendency to lose glucose in the urine.

92
Q

compare and contrast the distribution of body water in premature neonate, child, and adult.

A

premature:
TBW 85%: ECF 60%, ICF 25%

neonate
TBW 75%: ECF 40%, ICF 35%

child & adult
TBW 50%: ECF 20%, ICF 40%

93
Q

what signs suggest dehydration in the neonate?

A
  • sunken anterior fontanel
  • weight loss (10% decrease in first week is normal)
  • irritability or lethargy
  • dry mucus membranes
  • absence of tears
  • decreased skin turgor
  • increased Hct w/out transfusion
94
Q

describe the 4:2:1 rule of fluid management.

A

0-10kg: 4mL/kg/hr
10-20kg: add 2mL/kg/hr to previous total
>20kg: add 1mL/kg/hr to previous total

95
Q

how should the NPO fluid deficit be replaced?

A

multiply the patient’s hourly fluid maintenance rate by the number of hours NPO time, replace over three hours:
1st hr: 50%
2nd hr: 25%
3rd hr: 25%

96
Q

how should third space losses be replaced in the neonate?

A

minimal surgical trauma: 3-4mL/kg/hr
moderate surgical trauma: 5-6mL/kg/hr
major surgical trauma: 7-10mL/kg/hr

as a general rule, 3rd space loss is not included in the first hour of anesthesia.

97
Q

what ratio should be used to replace blood loss w/ crystalloid, colloid, and blood?

A

crystalloid 3:1 ratio
colloid 1:1 ratio
blood 1:1 ratio

98
Q

which pediatric patient populations should receive an IVF that contains glucose?

A

infants and children that are at risk of hypoglycemia:

  • prematurity
  • newborns of diabetic mothers
  • those w/ diabetes who received insulin on day of surgery
  • those who received glucose based parental nutrition
99
Q

what is the cardiac output in the newborn? how does this affect pharmacokinetics?

A

200mL/kg/min, which means that drugs are delivered to and removed from the rest of the body at a faster rate than the adult.

100
Q

discuss plasma protein binding in the neonate.

A

plasma proteins should be thought of as a storage site or a “sink” for drugs in the plasma. A drug bound to a plasma protein cannot exert a physiologic effect.

  • <6months, there are lower concentrations of albumin and alpha1 acid glycoprotein
  • highly PB drugs = higher free drug levels, increased toxicity risk
101
Q

discuss MAC in children. Does this rule apply to all volatile anesthetics?

A 
MAC varies w/ age: 
1-6months: MAC > adult MAC
2-3months: MAC peaks
neonate: MAC < infant
premature MAC
102
Q

how do you dose succinylcholine in the neonate?

A

2mg/kg

- largely d/t a relatively higher ECF (Vd is higher)

103
Q

how do you dose NDMR in the neonate? Why?

A

same as adult on a mg/kg basis.

- although ECF is larger, the NMJ is highly sensitive to the effects of NDMR. These things cancel each other out.

104
Q

what is the dose for IM succinylcholine? Which IM site has the fastest onset of action?

A

5mg/kg for infants and neonates (4mg/kg for child)

intralingual administration via the submental approach has the fastest onset.

105
Q

what is the primary hemodynamic concern when a small child receives a second dose of succinylcholine?

A

bradycardia or asystole (in child <5hrs)

this can occur following the first dose, but is more likely w/ repeated administration. IV atropine pretreatment (0.02mg/kg) will mitigate this response.

106
Q

An infant that is susceptible to MH develops a laryngospasm during induction of anesthesia. There is no IV in place. What’s the best drug to give at this time?

A

roc is the only NDMR that can be given IM

if <1yr= 1mg/kg
if >1yr = 1.8mg/kg

107
Q

describe the 5 types of tracheoesophageal atresia. Which is the most common?

A
  • most common congenital defect of the esophagus
  • most of these children also have a tracheoesophageal fistula

A: “missing” piece of esophagus (two blind pouches), no tracheal involvement
B: upper esophagus communicates w/ trachea, lower esophagus not connected
C: upper esophagus blind pouch, lower esophagus communicates w/ trachea
D: both upper and lower esophagus communicate w/ trachea, not each other
E: communicating esophagus w/ tracheoesophageal fistula

Type C accounts for approx 90% of all TEFs

108
Q

what prenatal finding suggests esophageal atresia? How is the diagnosis confirmed after birth?

A

prevents the fetus from swallowing amniotic fluid (it can’t reach the stomach), thus maternal polyhydramnios is a key diagnostic indicator for TEF.

diagnosis is confirmed by inability to pass a gastric tube into the stomach. Other symptoms: choking, coughing, and cyanosis during oral feeding.

109
Q

what is the VACTERL association?

A

approx 25-50% of patients w/ TEF suffer from other congenital anomalies. Collectively, these are known as the VACTERL association.

Vertebral defects
Anus imperforated
Cardiac anomalies
Tracheoesophageal fistula
Esophageal atresia
Renal dysplasia
Limb anomalies
110
Q

a patient has a type C TEF> Where should the tip of the ETT be placed?

A

below the fistula but above the carina

  • if too high: stomach is insufflated
  • it too low: endobronchial intubation is likely.
111
Q

how should you induce anesthesia in the patient undergoing a type C TEF repair?

A
  • head up and frequent suctioning to minimize gastric aspiration
  • awake intubation or inhalation w/ maintenance of spontaneous ventilation (PPV = gastric distention and decreased thoracic compliance)
  • gastric decompression w/ G tube prior to induction
  • ETT below fistula, above carina
  • precordial stethoscope on L chest to detect R mainstem intubation
  • R lung compression during repair is common; if R mainstem intubation, rapid desat will occur.
112
Q

discuss the patho of respiratory distress syndrome.

A

neonates who don’t produce enough surfactant are at risk.

  • alveoli remain stiff and noncompliant
  • small alveoli collapse
  • large alveoli become overdistended
  • this promotes atelectasis, reduces surface area for gas exchange = VQ mismatch
  • hypoxemia –> acidosis and possible return to fetal circulation
113
Q

what test can be done to assess fetal lung maturity in utero? What value suggests adequate lung development?

A

amniocentesis.

ratio of lecithin to sphingomyelin (L/S ratio) gives advanced warning about the state of the fetal lung
- L/S ratio >2 suggests adequate lung development

114
Q

discuss the use of pre- and postductal SpO2 monitoring the newborn.

A

preductal on RUE
postductal on LE (either side)

difference b/n pre and postductal suggests:

  • pHTN
  • R to L shunt
  • return to fetal circulation via PDA
115
Q

a patient has a herna at the foramen of Bochdalek. Which congenital condition does this patient have?

A

congenital diaphragmatic hernia allows the abdominal contents to enter the thoracic cavity.

  • foramen of Bochdalek is the most common site (usually on L)
  • other sites: foramen of Morgagni and around the esophagus
116
Q

what s/s suggest a congenital diaphragmatic hernia?

A

scaphoid abdomen (sunken in) and likely experience respiratory distress.

other findings:

  • barrel chest
  • cardiac displacement
  • fluid filled gastrointestinal segments in thorax
117
Q

describe the ventilatory management of the patient w/ congenital diaphragmatic hernia.

A

mass effect of the abdominal contents w/in the chest impairs lung development –> pulmonary hypoplasia (one or both lungs w/ increased PVR and decreased compliance)

  • keep PIP <25-30 (may require permissive hypercapnia
  • avoid other conditions that increase PVR (hypoxia, acidosis, hypothermia)
  • abdominal closure may increase PIP (surgeon can create temporary ventral hernia to make room)
  • LE pulse ox can warn of increased intraabdominal pressure
118
Q

compare and contrast omphalocele and gastroschisis.

A

omphalocele:
- midline defect involving the umbilicus
- involves bowel and sometimes liver
- covering is present
- incidence 1:3000-10000
- coexists w/ Trisomy 21, cardiac defects, Beckwith-Wiedemann syndrome
- surgery is less urgent + requires cardiac workup first

gastroschisis

  • off midline defect (R usually)
  • bowel involvement
  • no covering present
  • incidence 1:30,000
  • coexists w/ prematurity
  • surgery is more urgent + higher risk of fluid/heat loss (IVF 150-300mL/kg/day)

both primary closures are w/ prosthetic silo and may be staged procedures.

119
Q

describe the anesthetic concerns for a patient w/ omphalocele or gastroschisis.

A
  • gastroschisis: abdominal contents in bag after delivery to minimize water/heat loss
  • monitor PIP, keep <25-30
  • closure may increase intraabdominal pressure and decrease systemic perfusino
  • SpO2 LE
  • avoid N2O
  • expect major fluid/e-lyte shifts
120
Q

how and why does pyloric stenosis present?

A

occurs when hypertrophy of the pyloric muscle creates a mechanical obstruction at the gastric outlet. An olive shaped mass can be palpated just below the xiphoid process.

  • infant presents w/ nonbilious projectile vomiting
  • occurs in first 2-12 weeks
  • more common in males
121
Q

describe the patho of pyloric stenosis

A

vomiting depletes water
–> hypoNa+, hypoK+, hypoCl-, met alkalosis

lungs compensate w/ resp acidosis
kidneys excrete bicarb

as dehydration continues, aldosterone increases (Na+ and H2O retention) + kidneys lose H+ to urine
–> paradoxical acidification o the urine

if dehydration isn’t corrected, impaired tissue perfusion increases lactate production and produces met acidosis (LATE complication)

122
Q

describe the anesthetic management of the pt w/ pyloric stenosis.

A
  • not surgical emergency (optimize fluids/pH/e-lytes first)
  • anticipate full stomach (OGT pre-induction) + RSI
  • liberal hydration +/- glucose supplementation
  • post-op apnea is common possibly d/t residual alkalotic CSF
123
Q

what is necrotizing enterocolitis and who is at risk?

A

NEC is necrosis of the bowel, usually the terminal ileum and proximal colon.
patho isn’t completely understood, but likely the result of early feeding.
- impaired absorption by the gut –> stasis, bacterial overgrowth, and infection, increasing risk of bowel perforation

those at risk:

  • premie <32 weeks
  • low birth weight <1.5kg
124
Q

discuss the management of patients w/ NEC.

A

medically managed unless bowel perforation (requires bowel resection and usually colostomy)

  • often have met acidosis
  • often req substantial fluid replacement

bowel resection early in life can lead to short gut syndrome (nutrient malabsorption) as the patient ages.

125
Q

what is retinopathy of prematurity?

A

causes abnormal vascular development in the retina. The immature retinal blood vessels are at risk of vasoconstriction and hemorrhage. Dysfunctional healing causes scars, and as the scars retract, they pull on the retina –> retinal detachment and blindness.

126
Q

what are the risk factors for ROP?

A

prematurity
low birth weight
hyperoxia

127
Q

discuss the relationship b/n FiO2 and ROP.

A

until retinal maturation is complete (up to 44 weeks post-conception), FiO2 should be titrated to SpO2 85-93%

128
Q

what is apoptosis?

A

programmed cell death.
while this is a healthy response during normal development, there are concerns that commonly used anesthetic agents can kill neurons, potentially causing neurocognitive delays later in life.

129
Q

which anesthetic agents have been implicated in apoptosis?

A 
those that tend to antagonize the NMDA receptor, stimulate the GABA receptor, or both: 
- halogenated anesthetics
- N2O
- propofol, ketamine, etomidate
- barbs
benzos

those not associated w/ apoptosis:

  • opioids
  • precedex
  • xenon
130
Q

give the name, location, and function of the 3 fetal shunts.

A

ductus venosus

  • allows umbilical blood to bypass the liver
  • umbilical vein –> IVC

foramen ovale

  • shunts blood from RA to LA to bypass lungs to perfuse upper body (heart, brain)
  • RA –> LA

ductus arteriosus

  • shunts blood from pulmonary trunk to aorta to perfuse lower body
  • PA –> proximal descending aorta
131
Q

when does each fetal shunt close? what is the adult remnant of each?

A

ductus venosus closes w/ clamping of umbilical cord
- remnant: ligementum venosus

foramen ovale closes in 3 days
- remnant: fossa ovalis

ductus arteriosus closes several weeks after birth
- remnant: ligamentum arteriosum

132
Q

list the 5 ways the fetal circulation is different from the adult circulation.

A

placenta is the organ of respiration (adult = lungs)

circulation is arranged in parallel (adult = series)

R-L shunting occurs across the foramen ovale and ductus arteriosus

PVR is high: lungs are collapsed and filled w/ fluid, so there is little pulmonary blood flow

SVR is low: placenta provides, large, low resistance vascular bed

133
Q

describe the circulatory changes that occur during the transition to extrauterine life.

A

first breath –> lung expansion –> increased PaO2, decrased PaCO2 –> decreased PVR

placenta separates from uterine wall (or cord clamp) –> increased SVR

decreased PVR and increased SVR –> LAP > RAP –> flap valve of foramen ovale closes

decreased PVR –> reversal of blood flow through the ductus arteriosus exposes the ductus to O2, prompting closure

decreased circulating PGE1 (released from placenta) –> DA closure

134
Q

what is the risk of a patent foramen ovale?

A 
paradoxical embolism (embolism goes to the brain instead of the lungs) 
- 30% of the adult population has a probe PFO
135
Q

what drugs can be used to close the ductus arteriosus? Which can be used to open it?

A

close: indomethacin
open: PGE 1

136
Q

what is an intracardiac shunt?

A

describes an abnormal blood flow pattern that occurs from an abnormal communication b/n the pulmonary and systemic circulations

137
Q

what conditions affect PVR? how?

A

PVR = 80*(mPAP-PAOP)/CO
- normal 150-200

PVR increased by:

  • hypercarbia, acidosis
  • hypoxemia
  • collapsed alveoli
  • T-burg
  • hypothermia
  • increased SNS, vasoconstrictors, light anesthesia, pain

PVR decreased by:

  • hypocarbia, alkalosis
  • adequate O2
  • hemodilution
  • vasodiltors
  • NO
138
Q

what conditions affect SVR? How?

A

SVR = 80*(MAP-CVP)/CO
- normal 800-1500

increased by:

  • vasoconstrictors
  • fluids
  • increased SNS, pain, anxiety

decreased by:

  • IA, propofl
  • decreased SNS tone
  • histamine, anaphylaxis
  • hemodultion
  • sepsis
139
Q

what is a cyanotic shunt? List 5 examples.

A

R-L shunt
venous blood bypasses the lungs. Since the blood isn’t exposed to O2 in the lungs, LV ejected blood is lower in O2 (diluted)

examples (5 T’s)

  • Tet
  • transposition of great arteries
  • tricuspid valve abnormality (Ebstein’s anomaly)
  • Truncus arteriosus
  • total anomalous pulmonary venous connection
140
Q

what are the hemodynamic goals for the patient w/ a R-L shunt?

A

patho: decreased pulmonary blood flow results in:
- hypoxemia
- LV volume overload
- LV dysfunction

hemodynamic goals:

  • maintain SVR
  • decrease PVR: hyperoxia, hyperventilation, avoid lung hyperinflation
141
Q

what is an acyanotic shunt? list 4 examples.

A

L-R shunt. blood from L heart recirculates through the lungs instead of perfusing through the body

ex:
- VSD (most common)
- ASD
- PDA
- coarctation

142
Q

what are the hemodynamic goals for a patient w/ a L-R shunt?

A

patho: decreased systemic blood flow (low CO, hypotension) and increased pulmonary blood flow (pHTN, RVH)

goals:
- avoid increased SVR
- avoid decreased PVR (decrease FiO2, hypoventilation)

143
Q

how do intracardiac shunts affect an inhalation or IV induction?

A

inhalation induction:
R-L = slower induction
L-R = minimal effect

IV induction:
R-L = faster induction
L-R = slower induction most likely

144
Q

what is Eisenmenger syndrome?

A

occurs when a patient w/ a L-R shunt develops pHTN

This reverses the flow through the shunt, which causes a R-L shunt, hypoxemia, and cyanosis

145
Q

what are the 4 defects associated w/ tetralogy of Fallot?

A
  • RV outflow tract obstruction
  • RVH d/t high pressure
  • VSD d/t septal malalignment
  • overriding aorta that receives blood from both ventricles

PVR/SVR ratio determines how much blood travels to the lungs and the systemic circulation

146
Q

how does a “tet spell” present? What situations increase the risk of “tet spells”?

A

hypoxemia and cyanosis

classically, the pt presents w/ hx of squatting during activity, kinking the arteries in the groin area and in turn increasing SVR –> decreased R-L shunt, improving oxygenation.

stress increases myocardial contractility and may cause spasm of the infra-valvular region of the RVOT, so tet spells also occur during stressful circumstances (exercise, crying, defecation, IV placement, induction)

147
Q

what is the treatment for a “tet spell” that occurs during the peri-op period?

A
  • 100% FiO2
  • IVF
  • increase SVR w/ phenylephrine to augment PVR/SVR ratio
  • decrease SNS stim (deepen aneshesia, BB)
  • avoid inotropes
  • avoid excessive airway pressure
  • knee-chest position to mimic squatting
148
Q

what are the hemodynamic goals for tetralogy of Fallot?

A

increase SVR (phenylephrine, avoid vasodilation)

decrease PVR (reverse hypercarbia, hypoxia, acidosis, etc.; give NO)

maintain contractility and HR (esmolol, avoid SNS stim or inotropes)

increase preload (crystalloid, 5% albumin)

149
Q

what is the best IV induction agent for the pt w/ tetralogy of Fallot?

A

ketamine 1-2mg/kg IV or 3-4mg/kg IM (increases SVR and reduces shunting)

even though it can increase contractility, this effect is minor compared to benefit of increasing SVR

150
Q

what is the most common congenital cardiac anomaly in infants and children? How about adults?

A

VSD in infants and children
- most close by 2yrs

adults: bicuspid aortic valve

151
Q

what is coarctation of the aorta? which syndrome is highly associated w/ this anomaly?

A

narrowing of the thoracic aorta in the vicinity of the ductus arteriosus.

  • typically just after or before the ductus arteriosus
  • in rare cases can be proximal to SC artery

Turner syndrome is highly associated w/ coarctation of the aorta

152
Q

how is blood pressure affected in the patient w/ coarctation of the aorta?

A

SBP in UE = elevated

SBP in LE = reduced

153
Q

Discuss Ebstein’s anomaly.

A

most common congenital defect of the tricuspid valve. There is usually an ASD or PFO

characterized by a downward displacement of the tricuspid valve and atrialization of the RV (d/t the ASD or PFO)

  • TR can be severe
  • R-L shunting occurs at atrial level
  • SVT is common
  • RV failure is common in post-op period
154
Q

discuss the anesthetic management of the patient who has previously undergone Fontan completion.

A

single ventricle that pumps blood into the systemic circulation

There is no ventricle to pump blood into the pulmonary circulation, so..

  • blood flow into the lungs is completely dependent on negative intrathoracic pressure during spontaneous breathing
  • PPV should be avoided
  • preload dependent (AVOID dehydration)
155
Q

what is truncus arteriosus?

A

characterized by a single artery that gives rise to the pulmonary, systemic, and coronary circulations.

w/ only one artery, no specific pathway for blood to enter the pulmonary circulation before being pumped systemically

  • usually a VSD is present as well
  • decreasing PVR or increasing pulmonary blood flow steals from systemic and coronary circulations
156
Q

discuss the typical ages affected and speed of onset for epiglottitis and croup.

A

epiglottitis

  • bacterial (H.influenza, group A strep, pneumococci, staph)
  • 2-6yrs
  • rapid onset (<24hrs)

croup (laryngotracheobronchitis)

  • viral (influenza viruses), bacterial is rare (mycoplasma)
  • <2yrs
  • gradual onset (24-72hrs)
157
Q

contrast the regions affected by epiglottitis and group. How do these present on lateral neck xray?

A

epiglottitis affects the supraglottic structurs
- xray: swollen epiglottis (thumb sign)

croup affects the laryngeal structures
- xray: subglottic narrowing (Steeple sign)

158
Q

discuss the clinical presentation and treatment of epiglottitis.

A

presentation:
- high fever
- tripod positioning (helps breathing)
- 4 D’s: drooling, dysphonia, dyspnea, dysphagia

tx:
- O2
- urgent a/w management (ETT, trach)
- abx (if bacterial)
- induction w/ SV w/ ENT surgeon present
- post-op ICU care

159
Q

discuss the clinical presentation and treatment of croup.

A

presentation:
- mild fever
- inspiratory stridor
- barking cough

tx:
- O2
- racemic epi
- corticosteroids
- humidification
- fluids
- intubation rarely required

160
Q

discuss the patho and presentation of postintubation laryngeal edema

A

aka post-intubation croup

tracheal mucosa perfusion pressure is 25cmH2O; thus using an ETT too large or injecting an excessive amount of air into the cuff reduces tracheal perfusion –> edema –> decreased subglottic airway diameter –> increased WOB

presents w/ hoarseness, barking cough, and/or stridor
- typically w/in 30-60mins of extubation

161
Q

what are the risk factors for postintubation laryngeal edema?

A

all are from a small airway or airway trauma

  • age <4yrs
  • ETT too large or cuff volume too high
  • traumatic or multiple intubation attempts
  • prolonged intubation
  • coughing (cuff rubs)
  • head/neck surgery
  • head repositioning intra-op
  • hx of infectious or post-intubation croup
  • Trisomy 21
  • URI?
162
Q

what is the best way to minimize the risk of postintubation laryngeal edema?

A

prevention is the best treatment!

maintain an airleak <25cmH2O (use a manometer intermittently to measure cuff pressure)

163
Q

what is the treatment for postintubation laryngeal edema?

A

aims to reduce swelling and improve airflow.

  • cool, humidified O2
  • racemic epi 0.5mL of 2.25% sln in 2.5mL of NS
  • dexamethasone 0.25-0.5mg/kg IV (max effect in 4-6hrs)
  • heliox (helium + O2, improves laminar flow by reducing Reynold’s number)

observe patient for a minimum of 4hrs after the racemic epi tx is completed.

164
Q

a patient w/ a respiratory infection presents for a tonsillectomy. Which s/s favor postponing the procedure?

A

proceed w/ caution:

  • only runny nose
  • clear nasal discharge
  • no fever
  • active, appears happy
  • clear lungs
  • older child

cancel

  • purulent nasal discharge
  • fever
  • lethargic, poor appetite
  • persistent cough
  • wheezing/rales that don’t clear w/ cough
  • child <1yr or previous preemie
165
Q

how can you reduce the risk of airway complications while anesthetizing a child w/ a URI?

A
  • avoid a/w irritation (FM > LMA&raquo_space;» ETT)
  • ETT increases bronchospasm risk 10x
  • if ETT required, use smaller tube
  • decadron 0.25-0.5mg/kg
  • ensure deep before DL
  • propofol: decrease a/w reactivity + bronchospasm
  • sevo best (nonpungent)
  • pretx w/ inhaled bronchodiltor or glyco doesn’t provide a clear benefit
166
Q

describe the presentation of the child who presents w/ foreign body aspiration.

A

over 60% of children present w/ classic triad of coughing, wheezing, and decreased breath sounds on affected side (usually R)

a/w obstruction significant enough to impair gas exchange –> hypoxemia, cyanosis, AMS, cardiac arrest, death

  • supraglottic obstruction = stridor
  • infraglottic obstruction = wheezing
167
Q

what are the complications of rigid bronchoscopy?

A

rigid bronch is the gold standard to retrieve foreign body

complications:
- laryngospasm
- bradycardia w/ insertion
- post-intubation croup
- PTX

168
Q

which syndromes are associated w/ difficult airway management?

A

large tongue “Big Tongue”

  • Beckwith syndrome
  • Trisomy 21

small/underdeveloped mandible “Please Get That Chin”

  • Pierre Robin
  • Goldenhar
  • Treacher Collins
  • Cri du Chat

cervical spine anomaly “Kids Try Gold”

  • Klippel Feil
  • Trisomy 21
  • Goldenhar
169
Q

describe the airway in the patient w/ Trisomy 21.

A 
small mouth
large tongue
narrow palate w/ high arch
midface hypoplasia
AO instability (subluxation)
subglottic stenosis (small ETT)
OSA
chronic pulm infection
170
Q

What is the CHARGE association?

A 
Coloboma (hole in one of the eye structures)
Heart defects
Choanal atresia 
Retardation of growth/develp
Genitourinary probs
Ear anomalies
171
Q

what is CATCH 22?

A

You might also see this called DiGeorge syndrome or 22q11.2 gene deletion syndrome

Cardiac defects
Abnormal face
Thymic hypoplasia
Cleft palate
Hypocalcemia (d/t hypoparathyroidism)
22q11.2 gene deletion
172
Q

What are the unique anesthetic considerations for the patient w/ DiGeorge Syndrome?

A

hypocalcemia is common (remember hyperventilation, albumin, and citrated blood products lower free Ca++ in the blood)

if the thymus is absent, the child is at risk for infection

  • tx = thymus transplant or mature T cell infusion
  • use leukocyte reduced irradiated blood if transfusion required.
173
Q

what activities correspond w/ 1, 4, and 10 metabolic equivalents?

A

1 MET = poor functional capacity

  • self care acivities
  • working at computer
  • walking 2 blocks slowly

4METs = good functional capacity

  • climbing flight of stairs (w/out stopping)
  • walking up a hill
  • light housework
  • raking leaves, gardening

10METs + = outstanding functional capacity
- strenuous sports

174
Q

how does minute ventilation change in the elderly?

A

increases d/t increased dead space (compensates to maintain a normal PaCO2)

175
Q

how does lung elasticity change in the elderly?

A

decreases
this collapses small airways and causes the lung to become overfilled w/ gas.

consequences:
- increased Vd
- decreased alveolar SA
- VQ mismatch
- increased A-a gradient
- decreased PaO2

176
Q

how does chest wall compliance change in the elderly?

A

decreases
the chest is stiffer and more difficult to expand

d/t:

  • flatter diaphragm
  • increased AP diameter
  • increased intercostal muscle mass
  • joint calcification
  • loss of intervertebral disc height
177
Q

why does residual volume increase in the elderly? What are the consequences of this?

A

aged lung has a reduced elastic recoil, which causes it to become overfilled w/ gas This process increases residual volume, which explains why the FRC increases as we age.

  • CC surpasses FRC at approx 45yrs in the supine position and approx 65yrs when standing
  • when CC > FRC, the small airways collapse during tidal breathing –> VQ mismatch, increased Vd, decreased PaO2
178
Q

how does arterial compliance change in the elderly?

A

decreases as a function of loss of elastin and increased collagen

  • increased SVR, BP
  • increased pulse pressure
  • increased myocardial wall tension to overcome SVR
  • increased myocardial hypertrophy
179
Q

how does myocardial compliance change in the elderly?

A

decreases

  • impaired relaxation may cause diastolic dysfunction
  • atrial kick becomes more important for ventricular priming and maintenance of cardiac output
180
Q

how does the cardiac conduction system change in the elderly?

A

fibrosis of the conduction system and loss of SA node tissue
–> increased incidence fof dysrhythmias

181
Q

how do the BP and pulse pressure change in the elderly?

A

BP increases as a function of reduced arterial compliance (increased SVR)

PP is also increased for this region

182
Q

how do systolic and diastolic function change in the elderly?

A

systolic function = no change

diastolic function decreases as a function of reduced compliance and increased wall stiffness that impairs myocardial relaxation.

183
Q

how do HR, SV, and CO change in the elderly?

A

decrease

184
Q

describe the autonomic changes that occur in the elderly.

A
  • decreased adrenergic receptor density
  • decreased response to catechols
  • increased circulating catechols as partial compensation
  • reduced ability to increase HR during hypotension (decreased baroreceptor function)
  • impaired thermoregulation = risk of hypothermia
185
Q

how does MAC change in the elderly?

A

decreases by 6% each decade of life after 40

186
Q

contrast the onset of post-op delirium and post-op cognitive dysfunction.

A

postop delirium = early postop period

POCD = weeks to months after surgery

187
Q

contrast the treatment of postoperative delirium and postoperative cognitive dysfunction

A

delirium

  • treat underlying cause
  • antipsychotics
  • minimize polypharmacy

POCD

  • no specific tx
  • most causes are mild and tend to resolve after 3 months

to minimize the risk of either/both conditions, its best to use rapidly metabolized drugs

188
Q

how does sensitivity to LA change in the elderly?

A

increases

  • decreased # of myelinated nerves
  • decreased diameter of myelinated nerves
  • decreased conduction velocity
189
Q

do the elderly require a dosage adjustment for intrathecal or epidural anesthesia? Why?

A

yes, both

  • intrathecal: CSF volume is reduced = greater spread of LA
  • epidural: volume of epidural space is reduced = greater spread of LA
190
Q

why is it more difficult to place a neuraxial block in the elderly?

A

anatomic changes

  • less space b/n posterior spinous processes
  • decreased intravertebral disc height
  • narrow intervertebral foramen
  • calcification of joints
191
Q

how does GFR change in the elderly?

A

decreases

  • 125mL/min in adult male
  • decreases 1mL/min/year after age 40

consequences:
- risk of fluid overload
- impaired drug elimination (consider dose adjustments if age >60)

192
Q

how do serum creatinine and creatinine clearance change in the elderly?

A

serum creatinine doesn’t change

  • GFR decreases w/ age, but muscle mass also declines w/ age (less production
  • they cancel each other out –> net no change in creatinine

creatinine clearance is decreased, though
- this is the most sensitive indicator of glomerular function in the kidney

193
Q

How does production of plasma proteins change the elderly?

A

alpha1 acid glycoprotein increases
- decreased free fraction of basic drugs

albumin decreases
- increased free fraction of acidic drugs

pseudocholinesterase decreases (sux duration increases in men > women)

194
Q

how does circulation time change in the elderly?

A

circulation time increases. decreased CO prolongs the time of drug delivery from the site of administration to the site of action

  • slower IV induction
  • faster inhalation induction
195
Q

how does lean body mass change in the elderly? Why is this important?

A

decreases as a function of reduced muscle mass. This results in:

  • decreased BMR
  • decreased TBW
  • decreased blood volume
  • decreased plasma volume
  • decreased Vd for hydrophilic drugs
  • decreased neuromuscular reserve
  • hypothermia sets in faster

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