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APEX Study Guide > 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 – Increases minute ventilation up to 50%

-Vt increases by 40%
-RR increases by 10%

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2
Q

How does pregnancy affect the mother’s arterial blood gas?

A

Arterial pH = no change
PaO2 = Increased (104-108 mmHg)
PaCO2 = Decreased (28-32 mmHg)
HCO3 = Decreased (20 mmol/L)

-progesterone = respiratory stimulant –> minute ventilation increases 50% –> Mom’s PaCO2 falls and develops respiratory alkalosis
-renal compensation eliminates bicarb to normalize blood pH
-small reduction in physiologic shunt explains mild increase in PaO2 –> increases driving pressure of O2 across the fetoplacental interface and improves fetal gas exchange

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3
Q

How does pregnancy affect the oxyhemoglobin dissociation curve?

A

Right Shift (increases P50) –> 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 (decreased expiratory reserve volume and residual volume) – ERV decreases more than RV

*increased oxygen consumption paired with decreased FRC hastens the onset of hypoxemia

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5
Q

How does cardiac output change during pregnancy and delivery?

A

Cardiac Output - increases 40%
-heart rate increases 15%
-stroke volume increases 30%

-uterus receives 10% of the CO
-uterine contraction causes autotransfusion (increased preload)

Compared to pre-labor values, CO during labor:
-increases 20% in 1st stage
-increases 50% in 2nd stage
-increases 80% in 3rd stage

-CO returns to pre-labor values in 24-48hr
-CO returns to pre-pregnancy values in ~2 weeks

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

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6
Q

How do blood pressure and systemic vascular resistance change during pregnancy?

A

MAP = no change
SBP= no change
DBP = decreases 15%
*increased blood volume + decreased SVR = net even effect on MAP

SVR = decreases 15%
PVR = decreases 30%
*progesterone causes increased nitric oxide (vasodilation) and decreased response to angiotensin and norepi

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7
Q

Who is at risk for aortocaval compression, how do you treat it?

A

In supine position – gravid uterus compresses both the vena cava and the aorta – decreases venous return to the heart as well as arterial flow to the uterus and lower extremities

-decreased CO compromises fetal perfusion and can also cause the mother to lose consciousness

Treatment: displacing uterus away from the vena cava and aorta can reduce the compressive effects – elevate mother’s right torso 15 degrees
*should be used for anyone in their 2nd and 3rd trimester

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8
Q

How does the intravascular fluid volume change during pregnancy?

A

Intravascular Fluid - increases 35%

Plasma volume - increases 45%

Erythrocyte volume - increases 20%

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9
Q

What hematologic coagulation changes accompany pregnancy?

A

-Clotting factors: 1, 7, 8, 9, 10, 12 increase
-Anticoagulants: Protein S decreases and no change in Protein C
-Fibrin breakdown increases
-Anto-fibrinolytic system: 11 & 13 decrease

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10
Q

How does MAC change during pregnancy?

A

Decreased by 30-40%

-probably due to increased progesterone

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11
Q

How does pregnancy affect gastric pH and volume?

A

Increases gastric volume

Decreases gastric pH

*due to 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 = slowed

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13
Q

How does pregnancy affect uterine blood flow?
What is the non-pregnant flow rate vs pregnancy at term flow rate?

A

Non-Pregnant State = 100 mL/min

Pregnancy at Term = up to 700 mL/min or 10% of CO

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14
Q

What is uterine blood flow dependent on? What conditions can reduce uterine blood flow?

A

Uterine blood flow does NOT autoregulate – dependent on MAP, CO, and uterine vascular resistance

-decreased perfusion: maternal hypotension (sympathectomy, hemorrhage, aortocaval compression)
-increased resistance: uterine contraction, hypertensive conditions that increase UVR

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15
Q

Which law determines which drugs will pass through the placenta?

A

Fick’s Principle

Rate of Diffusion = [Diffusion Coefficient x Surface Area x Concentration Gradient (between mom/fetus)] / [Membrane Thickness]

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16
Q

What drug characteristics favor placental transfer?

A

-Low molecular weight <500 Daltons (most anesthetic drugs are smaller than 500 Daltons)
-High lipid solubility
-Nonionized
-Nonpolar

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17
Q

What are the 3 stages of labor?

A

Stage 1: beginning of regular contractions to full cervical dilation (10cm)

Stage 2: full cervical dilation to delivery of the fetus (pain in the perineum begins during stage 2)

Stage 3: delivery of the placenta

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18
Q

How does uncontrolled labor pain affect the mother and the fetus?

A

Increased maternal catecholamines –> HTN –> Reduced uterine blood flow to fetus

Maternal hyperventilation –> Leftward shift of oxyhgb curve –> Reduced O2 delivery to fetus

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19
Q

What spinal levels does the pain that results from the first and second stages of labor originate? What is the quality of pain during each stage?

A

Stage 1:

  • T10-L1 posterior nerve roots
  • pain begins in the lower uterine segment and the cervix
  • dull, diffuse, cramping

Stage 2:

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

What anesthetic techniques can be used for 1st and 2nd stage labor pain? What spinal levels are targets for each stage?

A

Stage 1 – target T10-L1

  • neuraxial (spinal, epidural, CSE)
  • paravertebral lumbar sympathetic block
  • paracervical block (high risk of fetal bradycardia

*afferent pathway = visceral C fibers hypogastric plexus

Stage 2 – target S2-S4

  • neuraxial (spinal, epidural, CSE)
  • pudendal nerve block

*afferent pathway = pudendal nerve

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21
Q

Explain the “needle through the needle” technique for CSE

A

-Epidural space is identified with epidural needle
-Spinal needle is placed through the epidural needle
-Local anesthetic and/or opioid is injected into the intrathecal space
-Spinal needle is removed
-Epidural catheter is threaded through the epidural needle

*CSE provides dual benefit of a rapid onset of spinal anesthesia and the ability to prolong the duration of anesthesia with an indwelling epidural catheter

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22
Q

Compare and contrast bupivacaine and ropivacaine in labor

A

Bupivacaine = amide, long duration

  • racemic mixture
  • minimal tachyphylaxis
  • low placental transfer d/t increased protein binding and increased ionization
  • greater sensory block relative to other LAs
  • cardiac toxicity more common with R-enantiomer
  • cardiac toxicity occurs before seizures
  • 0.75% contraindicated via epidural due to risk of toxicity w/ IV injection

Ropivacaine = amide, long duration

  • S-enantiomer of bupivacaine + substitution of propyl group
  • when compared to bupivacaine – less risk of CV toxicity, decreased potency, and decreased motor block
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23
Q

Discuss the use of 2-Chloroprocaine for labor

A

-Useful for emergency c-section when epidural is already in place (very fast onset)
-Metabolized by pseudocholinesterase in the plasma –> minimal placental transfer
-Antagonizes opioid receptors (mu & kappa) and reduces efficacy of epidural morphine
-Risk of arachnoiditis when used for spinal anesthesia due to preservatives
-Solutions without methylparaben and metabisulfite do not cause neurotoxicity

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24
Q

What are the consequences if an epidural is placed in the subdural space?

A

Within 10-25 minutes after epidural is dosed – patient will experience symptoms of excessive cephalad spread of LA

-subdural space is a potential space (hold very low volume) –> block height for a given amount of LA will be much higher than if the same volume was administered in the epidural space

*neither test dose or aspiration will rule out subdural placement

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25
Q

What might a total spinal result from? What is the treatment?

A

-Epidural dose injected into subarachnoid space
-Epidural dose injected into subdural space
-Single shot spinal after failed epidural block

Initial Treatment: vasopressors, IVF, left uterine displacement, elevation of legs, and intubation if LOC

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26
Q

What might cause fetal bradycardia and tachycardia?

A

Fetal Bradycardia = <110

  • fetal causes: asphyxia, acidosis
  • maternal causes: hypoxemia, drugs that decrease uteroplacental perfusion

Fetal Tachycardia = >160

  • fetal causes: hypoxemia, arrhythmias
  • maternal causes: fever, chorioamnionitis, atropine, ephedrine, terbutaline

*fetal oxygenation is a function of uterine and placental blood flow – fetus responds to stress w/ peripheral vasoconstriction, HTN, and baroreceptor-mediated reduction in HR

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27
Q

What are the causes of each fetal deceleration? Which are unremarkable and which are cause for concern?

A

-Variable Decels = Cord Compression
-Early Decels = Head Compression
-Accelerations = Ok of Give Oxygen
-Late Decels = Placental Insufficiency

*Early decelerations do not present a risk of fetal hypoxemia
*Late and Variable decelerations require urgent assessment of fetal status

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28
Q

What is defined as premature delivery? What are potential complications from preterm delivery?

A

Premature Delivery = delivery before 37 weeks gestation or less than 259 days from last menstrual cycle

Complications:
-respiratory distress syndrome
-intraventricular hemorrhage
-NEC
-hypoglycemia
-hypocalcemia
-hyperbilirubinemia

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29
Q

How are steroids and tocolytic agents used in the prevention of premature delivery?

A

Corticosteroids (betamethasone) - hasten fetal lung maturity (begin to take effect within 18 hours and peak benefit at 48hrs)

Tocolytic Agents - stop labor ~24-48 hours (provide a bridge that allows the corticosteroids time to work)

*seldom given after 33 weeks gestation

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30
Q

What are the side effects of beta-2 agonists when used for tocolysis?

A

-Hypokalemia results from intracellular K+ shift
-Cross placenta and may increase FHR
-Hyperglycemia results from glycogenolysis in the liver

*newborn of hyperglycemic mother is at risk of post-delivery hypoglycemia (glucose supply is gone, but neonatal insulin remains)

*Terbutaline and Ritodrine = examples

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31
Q

What are the side effects of hypermagnesemia?

A

-Apnea
-Hypotension
-Skeletal muscle weakness (synergism w/ NDMRs)
-CNS depression
-Reduced responsiveness to ephedrine and phenylephrine

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32
Q

What is the treatment for hypermagnesemia?

A

Supportive measures

Diuretics (to facilitate excretion)

IV Calcium (to antagonize Mg)

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33
Q

How can oxytocin be administered? What are the potential side effects?

A

Can be given IV (diluted in IVF) or can be injected directly into the uterus

Side Effects:
-water retention
-hyponatremia
-hypotension
-reflex tachycardia
-coronary vasoconstriction

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34
Q

How can methergine be administered? What is the dose?

A

Methergine = Ergot Alkaloid

Can be given 0.2 mg IM (not IV)

*IV admin can cause significant vasoconstriction, HTN, and cerebral hemorrhage

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35
Q

What are the pros and cons of general anesthesia for c-section?

A

Benefits:

  • speed of onset
  • secured airway
  • greater hemodynamic stability

Drawbacks:

  • risk of difficult mask ventilation
  • risk of difficult laryngoscopy
  • risk of difficult intubation
  • risk of aspiration
  • potential MH
  • absence of maternal awareness
  • neonatal respiratory & CNS depression

*mortality is 17x higher w/ general anesthesia – failure to manage airway is most common cause of maternal death

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36
Q

What is the triple prophylaxis against aspiration for a c-section?

A
  1. Sodium Citrate 15-30 mL within 15-30 min of induction (neutralize gastric acid)
  2. H2 Receptor Antagonists (Ranitidine) 1 hour before induction (reduce gastric acid secretion)
  3. Gastrokinetic Agent (Metoclopramide) 1 hour before induction (hasten gastric emptying and increase LES tone)
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37
Q

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

A

18-20 weeks gestation – considered “full stomach”

-require RSI w/ aspiration prophylaxis

*also apply to the immediate postpartum period

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38
Q

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

A

NSAIDs may close the ductus arteriosus

*AVOID after 1st trimester

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39
Q

What is the diagnostic criteria for gestational hypertension, preeclampsia, and eclampsia?

A

Gestational HTN:
-onset = after 20 weeks gestation
-severity = mild
-proteinuria = no
-seizures = no

Preeclampsia:
-onset = after 20 weeks gestation
-severity = mild to severe
-proteinuria = usually present
-seizures = no

Eclampsia:
-onset = after 20 weeks gestation
-severity = severe
-proteinuria = usually present
-seizures = yes

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40
Q

What happens to the balance of prostacyclin and thromboxane in the patient with preeclampsia?

A

Healthy placenta produces thromboxane and prostacyclin in equal amounts – Patient with preeclampsia produces up to 7x more thromboxane than prostacyclin

*increased thromboxane favors vasoconstriction, platelet aggregation, and reduced placental blood flow

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41
Q

What is the difference between mild and severe preeclampsia?

A
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42
Q

Why is magnesium used in preeclampsia?

A

Seizure Prophylaxis w/ magnesium sulfate

-Load: 4g over 10 min
-Infusion: 1-2 g/hr

*treatment for Mg toxicity = 10mL of 10% calcium gluconate IV

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43
Q

What is the anesthetic management for the patient with preeclampsia?

A

-Fluid management is balanced between a volume contracted patient and a “leaky” vasculature from endothelial dysfunction
-Neuraxial anesthesia assists w/ blood pressure control and also provides better uteroplacental perfusion
-Be sure to rule out thrombocytopenia (<100,000) before performing a neuraxial block
-Due to airway swelling, these pts have higher incidence of difficult intubation
-Have an exaggerated response to sympathomimetics and methergine
-If receiving Mg therapy – exhibit increased sensitivity to neuromuscular blockers
-Mg relaxes the uterus and increases the risk of postpartum hemorrhage

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44
Q

What is HELLP syndrome? What is the definitive treatment?

A

HELLP = Hemolysis, Elevated Liver enzymes, and Low Platelet count

-develops in 5-10% of those with preeclampsia
-experience epigastric pain and upper abdominal tenderness

Definitive Treatment = delivery of the fetus

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45
Q

What are the anesthetic considerations for maternal cocaine abuse?

A

Cocaine = ester-type local anesthetic that inhibits NE reuptake in presynaptic SNS neuron.. flooding the synaptic cleft with NE increases SNS tone

-CV risks: tachycardia, dysrhythmias, and myocardial inschemia
-Acute intoxication increases MAC
-Chronic use decreases MAC
-OB risks: spontaneous abortion, premature labor, placental abruption, and low APGAR scores
-HTN is best treated with vasodilators
-Beta-blockers can cause heart failure if the SVR is significantly elevated
-Hypotension may not respond to ephedrine in chronic cocaine abusers (d/t catecholamine depletion)
-Chronic cocaine abuse is associated with thrombocytopenia – check platelet count before neuraxial anesthesia

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46
Q

What is the difference between placenta accreta, increta, and percreta? What is the major risk that these complications present?

A

Types of abnormal placental implantation:

Accreta = attachment to the surface of myometrium
Increta = invades myometrium
Percreta = extends beyond the uterus

*uterine contractility is impaired and potential for tremendous blood loss

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47
Q

What is placenta previa? How does it present?

A

Occurs when placenta attaches to the lower uterine segment

-partially or completely covers the cervical os
-associated with PAINLESS vaginal bleeding
-potential for hemorrhage

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48
Q

What conditions increase the risk of placenta previa?

A

Previous c-sections

History of multiple births

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49
Q

What are the risk factors for placental abruption? How does it present?

A

Placental Abruption = partial or complete separation of placenta from uterine wall prior to delivery – results in hemorrhage and fetal hypoxia

Risk Factors:
-PIH
-preeclampsia
-chronic HTN
-cocaine use
-smoking
-excessive alcohol use

Presents: PAINFUL vaginal bleeding (pain may be so severe as to cause breakthrough when epidural is in place

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50
Q

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

A

Uterine Atony

Risk Factors:
-multiparity
-multiple gestations
-polyhydramnios
-prolonged oxytocin infusion prior to surgery

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51
Q

What IV medication can you give to help with the extraction of retained placental fragments?

A

IV nitroglycerine

*provides uterine relaxation

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52
Q

What are the treatment options for uterine atony?

A

-Uterine massage
-Oxytocin
-Ergot alkaloids
-Intrauterine balloon

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53
Q

What is the Apgar score? What does each value represent?

A

-Used to assess newborn and guide resuscitative efforts
-Five parameters are evaluated at 1 and 5 minutes after delivery
-Score at 1 min correlates with fetal acid-base status
-Score at 5 min may be predictive of neurologic outcome

Normal = 8-10
Moderate Distress = 4-7
Impending Demise = 0-3

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54
Q

How do you calculate the Apgar score?

A
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55
Q

What is the best indicator of ventilation during neonatal resuscitation?

A

Resolution of bradycardia

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56
Q

How do you dose epinephrine and fluids during neonatal resuscitation?

A

Epi: 10-30 mcg/kg (IV) or 0.05-0.1 mg/kg (intratracheal) of 1:10,000 concentration

Fluids: 10 mL/kg over 5-10 min of PRBCs, NS, or LR

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57
Q

What are normal vital signs for a newborn, 1yr, 3yr, and 12yr old?

A

Newborn: BP 70/40, HR 140, RR 40-60

1 yr: BP 95/60, HR 120, RR 40

3 yr: BP 100/65, HR 100, RR 30

12 yr: BP 110/70, HR 80, RR 20

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58
Q

Why is the neonate’s minute ventilation higher than the adult?

A

Oxygen consumption and CO2 production are 2x those of the adult – neonate must increase alveolar ventilation accordingly

-metabolically more efficient to increase respiratory rate than it is to increase tidal volume

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59
Q

What is the primary determinant of blood pressure in the neonate?

A

Heart Rate = primary determinant of CO and SBP

-neonatal myocardium lacks the contractile elements to significantly adjust contractility or SV (ventricle is noncompliant)
-frank-starling relationship is underdeveloped
-heart rate must be maintained to ensure adequate tissue perfusion and oxygen delivery

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60
Q

Explain the autonomic influence on the newborns heart

A

Autonomic regulation of the heart is immature at birth – SNS being less mature than the PNS

-stressful situations (i.e. laryngoscopy or suctioning) may cause bradycardia
-atropine may be administered prior to induction to mitigate this response

*baroreceptor reflex is poorly developed – fails to increase HR in the setting of hypovolemia

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61
Q

What is the difference between the breathing patten in adults and infants?

A

Adult = Mouth or Nose

Infant = Preferential Nose breather up to 5 months of age
-most infants convert to oral breathing if the nasal passages are obstructed
-bilateral choanal atresia may require emergence airway management if the infant is unable to mouth breathe

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62
Q

What is the difference between the relative size of the tongue in adults and infants?

A

Adult = Small relative to oral volume

Infants = large relative to oral volume
-tongue is closer to soft palate (makes it easier to obstruct upper airway)
-more difficult to displace during laryngoscopy

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63
Q

What is the difference between the epiglottis shape in adults and infants?

A

Adult = Leaf (C shape), floppier, shorter

Infant = U (omega shape), stiffer, longer
-makes it more difficult to displace during laryngoscopy

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64
Q

What is the vocal cord position in adults and infants?

A

Adult = perpendicular to trachea

Infant = anterior slant
-visualization and passage of ETT may be more difficult
-ETT may get stuck in anterior commissure

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65
Q

What is the laryngeal position in adults and infants?

A

Adult = C5 - C6

Infant = C3 - C4
-larynx more superior/cephalad/rostral but NOT anterior
-same position as the adult at age 5-6 years old

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66
Q

Where is the narrowest point of the airway in the adult and infant?

A

Adult = Glottis (vocal cords)

Infant = Cricoid or Glottis
-resistance to ETT insertion beyond vocal cords 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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67
Q

What is the difference between the orientation of the right mainstem bronchus in adults and infants?

A

Adult = more vertical

  • right bronchus takes off at 25 degrees and left at 45 degrees

Infant = less vertical

  • up to age 3 both bronchi take off at 55 degrees
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68
Q

What is the optimal intubation position for adults and infants?

A

Adult = Sniffing position

Infant = head on bed with shoulder roll
-large occiput
-sniffing position will place glottic opening in a more anterior position

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69
Q

How does oxygen consumption, alveolar ventilation, respiratory rate, and tidal volume in neonates compare to adults? What are the values for each?

A

Oxygen Consumption:
-neonate = 6 mL/kg/min
-adult = 3.5 mL/kg/min

Alveolar Ventilation:
-neonate = 130 mL/kg/min
-adult = 60 mL/kg/min

Respiratory Rate:
-neonate = 35 bpm
-adult = 15 bpm

Tidal Volume:
-neonate = 6 mL/kg
-adult = 6 mL/kg

*neonatal alveolar surface area is only 1/3 of the adult and O2 consumption is 2x that of the adult – neonate must increase alveolar ventilation in order to sustain normal arterial gas tensions

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70
Q

Why do neonates desaturate faster than adults?

A

Neonates Have:
-Increased O2 consumption to support metabolic demand
-Increased alveolar ventilation to increase O2 supply
-Slightly decreased FRC reflects a reduced O2 reserve

*Net Result = increased ratio of alveolar ventilation relative to size of its FRC –> faster gas turnover means O2 supply in FRC is quickly exhausted during apnea

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71
Q

Why is inhalation induction faster with a neonate than with an adult?

A

Due to the increased alveolar ventilation relative to size of the FRC

*faster turnover of the FRC allows speedier development of anesthetic partial pressure inside the alveoli and consequently a more rapid change in anesthetic partial pressure inside the brain and spinal cord

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72
Q

What is the difference between fast and slow twitch muscle fibers? How does this relate to neonatal pulmonary mechanics?

A

Diaphragm and intercostal muscles are composed of:

  • type 1 = slow twitch muscle fibers (built for endurance) – resistant to fatigue
  • type 2 = fast-twitch fibers (built for short bursts of heavy work) – tire easily

Smaller number of type 1 fibers within the diaphragm increases neonate’s risk for respiratory fatigue and developing respiratory failure

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73
Q

Compare and contrast the FRC, VC, TLC, RV, CC, and Vt of neonates to adults

A
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74
Q

How does the newborn’s ABG change from delivery to the first 24 hours of life?

A
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75
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

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76
Q

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

A

19 mmHg

-fetal hemoglobin shifts curve to the left (left = love)
-benefits the fetus by creating an oxygen partial pressure gradient across the uteroplacental membrane that facilitates the passage of O2 from the mother to fetus

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77
Q

Why does fetal Hgb have a higher affinity for oxygen?

A

Fetal Hgb has 2 alpha and 2 gamma chains – (adults have 2 alpha and 2 beta chains)

-2,3-DPG shifts the curve to the right – the beta chains are the binding sites for 2,3-DPG –> fetal hgb doesn’t have beta chains, so it doesn’t bind 2,3-DPG – shifting curve to the left

78
Q

What are the indications for FFP transfusion in the neonate?

A

-Emergence reversal of warfarin
-Correction of coagulopathic bleeding with increase PT > 1.5 or increased PTT
-Correction of coagulopathic bleeding if >1 blood volume has been replaced and coagulation studies are not easily obtained

**FFP is NOT indicated for expansion of intravascular volume

79
Q

What is the dose for FFP transfusion in the neonate?

A

10 - 20 mL/kg

80
Q

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

A

Recommended for invasive procedures to maintain a platelet count above 50,000

Dose if obtained from apheresis = 5 mL/kg
Dose if pooled platelet concentrate = 1 pack/10 kg

81
Q

What physiologic changes occur as a result of massive transfusion?

A

-Alkalosis –> due to citrate metabolism to bicarb in the liver
-Hypothermia –> due to transfusion of cold blood
-Hyperglycemia –> due to dextrose additive to stored blood
-Hypocalcemia –> due to binding of calcium by citrate
-Hyperkalemia –> due to admin of older blood

*admin of PRBCs to neonates can lead to hyperkalemia and cardiac arrest – risk reduced by admin of washed or fresh cells that are <7 days old

82
Q

What physiologic changes occur as a result of massive transfusion?

A

-Alkalosis –> due to citrate metabolism to bicarb in the liver
-Hypothermia –> due to transfusion of cold blood
-Hyperglycemia –> due to dextrose additive to stored blood
-Hypocalcemia –> due to binding of calcium by citrate
-Hyperkalemia –> due to administration of older blood

83
Q

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

A

Newborn = 14-20 and 45-65%

3 Months = 10-14 and 31-41%

6-12 Months = 11-15 and 33-42%

*adult female = 12-16 and 37-47%
*adult male = 14-18 and 42-50%

84
Q

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

A

Premature Neonate = 90-100 mL/kg

Term Neonate = 80-90 mL/kg

Infant = 75-80 mL/kg

> 1 year = 70-75 mL/kg

85
Q

A 3-kg term neonate requires emergency exploratory laparotomy for necrotizing enterocolitis. Her perop hematocrit is 50%. What is the max allowable blood loss to maintain a hematocrit of 40%?

A

Max Allowable Blood Loss = EBV x [(Hct starting - Hct target) / Hct starting]

  1. EBV = 3 kg x 80 to 100 mL/kg = 240 to 300 mL
  2. Hct starting - Hct target = 50 - 40 = 10
  3. MABL = 240 to 300 mL x [(50-40) / 50] = 48-60 mL
86
Q

When do GFR and renal tubular function achieve full maturation?

A

Normal GFR is reached at 8-24 months of age

  • before maturation, neonates do a poor job conserving water (intolerant of fluid restriction) and unable to excrete large volumes of water (don’t do well with volume overload either)

Normal tubular function is reached at 2 years of age

  • in first few days of life neonate is an obligate sodium loser – after they are better able to retain sodium than to excrete it
  • also have tendency to lose glucose to the urine
87
Q

What is the distribution of body water in the premature neonate, neonate, child, and adult?

A

Premature Neonate:
-TBW = 85% – ECF = 60% – ICF = 25%

Neonate:
-TBW = 75% – ECF 40% – ICF = 35%

Child:
-TBW = 60% – ECF = 20% – ICF = 40%

Adult:
-TBW = 60% – ECF = 20% – ICF = 40%

88
Q

What signs suggest dehydration in the neonate?

A

-Sunken anterior fontanel
-Weight loss (a 10% reduction in the first week is normal)
-Irritability or lethargy
-Dry mucus membranes
-Absence of tears
-Decreased skin turgor
-Increased hematocrit in absence of transfusion

89
Q

What is the 4:2:1 rule of fluid management?

A

4 mL/kg/hr for 0-10kg

Add 2 mL/kg/hr for 10-20 kg

Add 1 mL/kg/hr for >20kg

*for pts >20kg –> take patient’s weight in kg + 40

90
Q

How should the NPO fluid deficit be replaced?

A

Multiply the pt’s hourly fluid maintenance rate by the number of hours NPO time

-replace deficit over 3 hours: 50% 1st hour – 25% 2nd hour – 25% 3rd hour

91
Q

How should third space losses be replaced in the neonate?

A

Replace fluid lost to 3rd spacing and evaporation

-Minimal surgical trauma = 3-4 mL/kg/hr
-Moderate surgical trauma = 5-6 mL/kg/hr
-Major surgical trauma = 7-10 mL/kg/hr

*general rule – 3rd space loss is not included in the first hour of anesthesia

92
Q

What ratio should be used to replace blood loss with crystalloid, colloid, and blood?

A

Crystalloid = 3:1 ratio

Colloid = 1:1 ratio

Blood = 1:1 ratio

93
Q

Which pediatric populations should receive an IVF that contains glucose?

A

Infants and children at risk of developing hypoglycemia including:
-prematurity
-less than 48hrs old
-small for gestational age
-newborns of diabetic moms
-children w/ DM who received insulin on day of surgery
-children who receive glucose-based parental nurtition

94
Q

What is the cardiac output in the newborn? How does this affect pharmacokinetics?

A

CO = 200 mL/kg/min

-drugs are delivered to and removed from the rest of the body at a faster rate than the adult

95
Q

How is plasma protein binding different in the neonate?

A

Before 6 months of age – lower concentrations of albumin and alpha-1 acid glycoprotein

So, highly-protein bound drugs will display higher free drug levels (increase risk of toxicity)

96
Q

How does MAC differ in children? Does this rule apply to all the volatile anesthetics?

A

Neonate (0-30 days): MAC is lower than the infant
Premature: MAC is lower than the neonate
Infant 1-6 months: MAC is higher than the adult
Infant 2-3 months: MAC peaks at its highest level

MAC requirement pattern for Sevo is different
-0 days to 6 months: MAC is higher (3.2%)
-6 months to 12 years: MAC is lower but still higher than the adult (2.5%)

97
Q

How do you dose SUX in the neonate?

A

SUX = 2 mg/kg

-largely due to a relatively higher ECF (Vd is larger)

98
Q

How do you dose nondepolarizing neuromuscular blockers in the neonate? Why?

A

Dose = same as the adult on mg/kg basis

-although the ECF is larger the NMJ is highly sensitive to the effects of NDMRs
-this cancels each other out – explaining the same dosing as adults

99
Q

What is the dose for IM SUX? Which IM site has the fastest onset of action?

A

Neonate & Infant Dose = 5 mg/kg
Older Children = 4 mg/kg

-Intralingual administration via the submental approach likely has the fastest onset

100
Q

What is the primary hemodynamic concern when a small child receives a second dose of SUX?

A

Children less than 5 years old –> SUX may cause bradycardia or asystole

*can occur following the first dose but is more likely after repeat administration – IV atropine pretreatment (0.02 mg/kg) will mitigate this response

101
Q

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

A

Rocuronium
-only NDMR that can be given IM

<1 yr: 1mg/kg
>1 yr: 1.8 mg/kg

102
Q

What is tracheoesophageal atresia? What are the five types?

A

Esophageal atresia = most common congenital defect of the esophagus and most of these children also have a tracheoesophageal fistula

103
Q

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

A

Esophageal atresia prevents fetus from swallowing amniotic fluid –> maternal polyhydramnios is a key diagnostic indicator

Diagnosis is confirmed by the inability to pass a gastric tube into the stomach
-other symptoms include: choking, coughing, and cyanosis during oral feeding

104
Q

What is the VACTERL association w/ tracheoesophageal atresia?

A

Approximately 25-50% of patient with tracheoesophageal atresia suffer from other congenital anomalies (VACTERL association)

V - vertebral defects
A - imperforated anus
C - cardiac anomalies
T - tracheoesophageal fistula
E - esophageal atresia
R - rectal dysplasia
L - limb anomalies

105
Q

Where should the tip of the ETT be positioned in a patient with a type C tracheoesophageal atresia?

A

Below the fistula but above the carina

-if too high – respiratory gas is delivered to the stomach
-if too low – endobronchial intubation is likely

106
Q

How should you induce anesthesia in a patient undergoing a type C tracheoesophageal atresia repair?

A

-Head up position and frequent suctioning minimize risk of gastric aspiration
-Awake intubation or inhalation induction w/ spont ventilation
-Positive pressure ventilation –> Gastric distension –> decrease thoracic compliance –> increased PIP required to ventilate –> downward spiral
-Placement of g-tube allows for gastric decompression (open g-tube to atmosphere before induction)
-Place ETT below fistula but above carina
-Precordial stethoscope placed on the left chest will immediately detect right mainstem intubation
-Right lung compression during surgical repair is common (right mainstem intubation will cause rapid desaturation

107
Q

What is the pathophysiology of respiratory distress syndrome?

A

Neonates who don’t produce enough surfactant are at risk for respiratory distress syndrome (RDS):

  • in the absence of adequate surfactant, alveoli remain stiff and non-compliant
  • small alveoli tend to collapse
  • larger alveoli become over distended (accept gas from collapsed alveoli)
  • this promotes atelectasis, reduces surface area where gas exchange can take place, creating V/Q mismatch
  • hypoxemia leads to acidosis and possibly the return to fetal circulation
108
Q

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

A

Amniocentesis

-ratio of lecithin (surfactant) to sphingomyelin (surfactant precursor) gives advanced warning about state of fetal lung

L/S ratio > 2 suggests adequate lung development
L/S ratio <2 is associated with increased risk of respiratory distress syndrome

109
Q

Why is a pre- and post-ductal SpO2 monitored in the newborn?

A

Pre-ductal pulse ox placed on right upper extremity
Post-ductal pulse ox placed on lower extremity

Difference between values suggest:
-pulmonary hypertension
-right to left cardiac shunt
-return to fetal circulation via the PDA

110
Q

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

A

Congenital diaphragmatic hernia – diaphragmatic defect that allows the abdominal contents to enter the thoracic cavity

-foramen Bochdalek = most common site of herniation (usually left side)
-other sites of herniation include foramen of Morgagni and around the esophagus

111
Q

What signs/symptoms suggest a congenital diaphragmatic hernia?

A

-Scaphoid abdomen (sunken in) and likely experience respiratory distress
-Barrel chest
-Cardiac displacement
-Fluid filled gastrointestinal segments in the thorax

112
Q

Describe the ventilatory management of a patient with a congenital diaphragmatic hernia

A

Mass effect of abdominal contents within the chest impairs lung development – leads to pulmonary hypoplasia (one or both lungs can be affected) – increased PVR & decreased compliance

-Keep PIP <25-30 cmH20 (minimize barotrauma and risk of pneumo of “good” lung)
-Avoid other conditions that increase PVR (hypoxia, acidosis, hypothermia)
-Abdominal closure may increase PIP (surgeon can create a temporary ventral hernia to increase abdominal volume)
-Pulse ox place on lower extremity can warn of increased intra-abdominal pressure

113
Q

What is the difference between Omphalocele and Gastroschisis?

A
114
Q

What are the anesthetic concerns for a patient with omphalocele or gastroschisis?

A

-If gastroschisis – abdominal contents are placed in a bag after delivery (minimizes water and heat loss)
-Monitor peak airway pressure (if PIP > 25-30 cmH2O then surgical closure of abdomen may require staging)
-Closure may increase intra-abdominal pressure: Increased intra-abdominal pressure = decreased venous return = decreased CO = decreased systemic perfusion
-Measure SpO2 on lower extremity to monitor for impaired venous return
-N2O distends bowel and may impair surgical closure
-Expect major fluid and electrolyte shifts

115
Q

How and when does pyloric stenosis present?

A

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

-infant presents with non-bilious projectile vomiting
-occurs in first 2-12 weeks of life
-more common in males

116
Q

What is the pathophysiology of pyloric stenosis?

A

Vomiting depletes water and causes hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis

  • Lungs compensate with respiratory acidosis
  • Kidneys try to correct metabolic alkalosis by excreting bicarb

As dehydration continues – aldosterone increases (Na+ & water retention) – to maintain electroneutrality the kidneys lose hydrogen to urine –> causes paradoxical acidification of urine

If dehydration is not corrected – impaired tissue perfusion increases lactate production and produces metabolic acidosis (LATE complication)

117
Q

What is the anesthetic management of a patient with pyloric stenosis?

A

-Surgical correction should be postponed until the fluid, electrolyte, and acid-base status are optimized (Pyloric stenosis = medical emergency NOT surgical emergency)
-Anticipate a full stomach (empty stomach before induction) – awake intubation or RSI and extubate awake
-Place an OG or NG after induction (use it to assess the pylorus for an air leak following surgical repair (air leak suggests mucosal perforation)
-Liberal hydration to correct dehydration (may require glucose supplementation)
-Postop apnea is common

118
Q

What is necrotizing enterocolitis? Who is at risk?

A

NEC = necrosis of the bowel, usually terminal ileum and proximal colon

-likely the result of early feeding – impaired absorption by the gut leads to stasis, bacterial overgrowth, and infection

Babies at Risk:
-prematurity (<32 weeks)
-low birth weight (<1500g)

119
Q

What is the management of patients with NEC?

A

Medically managed

-bowel perforation necessitates bowel resection and usually colostomy
-pts often have a metabolic acidosis and require substantial fluid replacement

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

120
Q

What is retinopathy of prematurity?

A

Vasculogenesis occurs 16 and 44 weeks post conception – process begins at the macula then continues outwards towards the edges of the developing retina over time

ROP is define by two phases:
-Phase 1: inhibited growth of retinal vessels
-Phase 2: overgrowth of abnormal vessels with fibrous bands that extend to the vitreous gel which can precipitate retinal detachment

121
Q

What are the risk factors for retinopathy of prematurity (ROP)?

A

-Prematurity
-Low birth weight
-Hyperoxia
-Mechanical ventilation
-Blood transfusion
-Intraventricular hemorrhage
-Sepsis
-Vitamin E deficiency

122
Q

What is the relationship between FiO2 and retinopathy of prematurity (ROP)?

A

Until retinal maturation is complete (up to 44 weeks post-conception), FiO2 should be titrated to SpO2 89-94%

123
Q

Which anesthetic agents have been implicated in apoptosis?

A

-Halogenated anesthetics
-N2O
-Propofol
-Ketamine
-Etomidate
-Barbiturates
-Benzos

*unknown effect - dexmedetomidine, opioids, xenon

124
Q

What are the 3 fetal shunts? Where are they located? What is their function?

A

Ductus Venosus:
-function = allows umbilical blood to bypass the liver
-location = umbilical vein –> inferior vena cava

Foramen Ovale:
-function = shunts blood from the RA to LA to bypass the lungs to perfuse the upper body (heart/brain)
-location = right atrium –> left atrium

Ductus Arteriosus:
-function = shunts blood from pulmonary trunk to aorta to perfuse lower body
-location = pulmonary artery –> proximal descending aorta

125
Q

When does each fetal shunt close? What is the adult remnant of each?

A

Ductus Venosus –> closes w/ clamping of the umbilical cord

  • adult remnant = ligamentum venosus

Foramen Ovale –> closes 3 days after birth

  • adult remnant = fossa ovalis

Ductus Arteriosus –> closes several weeks after birth

  • adult remnant = ligamentum arteriosum
126
Q

List the 6 ways fetal circulation is different from adult circulation

A
  1. Placenta is the organ of respiration (adults = lungs)
  2. Circulation is arranged in parallel (adults = series)
  3. Right-to-left shunting occurs across the foramen ovale and ductus arteriosus
  4. PVR is high – lungs are collapsed and filled w/ fluid (very little pulmonary blood flow)
  5. SVR is low – placenta provides a large, low resistance vascular bed
  6. Minimal pulmonary blood flow and left atrial pressure is low
127
Q

What circulatory changes occur during the transition to extrauterine life?

A

-First breath –> Lung expansion –> Increase PaO2 & Decrease PaCO2 –>Decreased PVR
-Placenta separates from uterine wall (or cord clamp) –> Increased SVR
-Decreased PVR + Increased SVR = LA pressure > RA pressure –> flap valve of foramen ovale closes
-Decreased PVR –> Reversal of blood flow through the ductus arteriosus –> Exposes the DA to increased PO2 –> DA closure
-Decreased circulating PGE1 (released from placenta) –> DA closes

128
Q

What is the risk of a patent foramen ovale?

A

Increases risk of paradoxical embolism (embolus goes to brain instead of the lungs)

*30% of adult population has a probe patent foramen ovale

129
Q

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

A

Closed with indomethacin

Opened with prostaglandin E1

130
Q

What is an intracardiac shunt?

A

Abnormal blood flow pattern from an abnormal communication between the pulmonary and systemic circulations

*blood follows the path of least resistance (balance between PVR and SVR)
* R –> L (right heart to left heart) : L –> R (left heart to right heart)

131
Q

What conditions increase pulmonary vascular resistance?

A

-Hypercarbia
-Hypoxemia
-Acidosis
-Collapsed alveoli
-Trendelenburg position
-Hypothermia
-Vasoconstrictors
-Increased SNS tone
-Light anesthesia
-Pain

*normal PVR = 150-200 dynes/sec/cm
PVR = [(mPAP - PAOP) / CO] x 80

132
Q

What conditions decrease pulmonary vascular resistance?

A

-Hypocarbia
-Adequate oxygenation
-Alkalosis
-Hemodilution
-Vasodilators
-Nitric oxide

*normal PVR = 150-200 dynes/sec/cm
PVR = [(mPAP - PAOP) / CO] x 80

133
Q

What conditions increase SVR?

A

-Vasoconstrictors
-Fluid bolus
-Increased SNS tone
-Pain
-Anxiety

*normal SVR = 800-1500 dynes/sec/cm
SVR = [(MAP - CVP) / CO] x 80

134
Q

What conditions decrease SVR?

A

-Volatile anesthetics
-Propofol
-Decreased SNS tone
-Histamine
-Anaphylaxis
-Hemodilution
-Sepsis

*normal SVR = 800-1500 dynes/sec/cm
SVR = [(MAP - CVP) / CO] x 80

135
Q

What is a cyanotic shunt? List 5 examples

A

Cyanotic Shunt = Right to Left shunt

  • venous blood bypasses the lungs
  • blood is not exposed to O2 in the lungs – dilutes the final PO2 of the blood ejected by the left ventricle

Examples: (Remember the 5 T’s)

  1. Tetralogy of Fallot (most common)
  2. Transposition of the Great Arteries
  3. Tricuspid valve abnormality (Ebstein’s anomaly)
  4. Truncus Arteriosus
  5. Total anomalous pulmonary venous connection
136
Q

What is the pathophysiology of right-to-left shunt? What are the hemodynamic goals?

A

Pathophysiology:
-decreased pulmonary blood flow –> hypoxia, LV volume overload, LV dysfunction

Hemodynamic Goals:
-Maintain SVR
-Decrease PVR (hyperoxia, hyperventilation, avoid lung hyperinflation)

137
Q

What is an acyonotic shunt? List 4 examples

A

Acyanotic Shunt = Left to Right shunt
-blood in left side of the heart recirculates through the lungs instead of perfusing the body

Examples:
1. Ventricular Septal Defect (most common)
2. Atrial Sepal Defect
3. Patent Ductus Arteriosus
4. Coarctation of the aorta

138
Q

What is the pathophysiology of left-to-right shunt? What are the hemodynamic goals?

A

Pathophysiology:
-decreased systemic blood flow –> low CO and hypotension
-increased pulmonary blood flow –> pulmonary HTN and RVH

Hemodynamic Goals:
-Avoid increased SVR
-Avoid decreased PVR by avoiding alkalosis, hypocapnia, high FiO2, vasodilators

139
Q

How do intracardiac shunts affect an inhalation or IV induction?

A

Inhalation Induction:
R –> L shunt = Slower induction
L –> R shunt = Minimal effect

IV Induction:
R –> L shunt = Faster induction
L –> R shunt = Slower induction (most likely)

140
Q

What is Eisenmenger syndrome?

A

When a patient with a left-to-right shunt develops pulmonary hypertension

Reverses the flow through the shunt –> causes right-to-left shunt, hypoxemia, and cyanosis

141
Q

What are the 4 defects associated with tetralogy of Fallot?

A
  1. Right ventricular outflow tract obstruction (RVOT)
  2. Right ventricular hypertrophy (due to high-pressure load from the RV obstruction)
  3. Ventricular septal defect (due to septal malalignment)
  4. Overriding aorta that receives blood from both ventricles

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

142
Q

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

A

“Tet Spell” is precipitated by increased sympathetic activity –> increased myocardial contractility can cause spasm on infra-valvular region of the RVOT –> net effect is increased R–>L shunting = hypoxemia

Presentation: hyperventilation with onset of hypoxemia – child will assume a squatting position (increases intraabdominal pressure and compresses the abdominal arteries –> increases RV preload, SVR, and blood flow through RVOT)

Precipitated by: crying, agitation, pain, defecation, fright, or trauma

*Only children w/ unrepaired tetralogy of Fallot can experience tet spells

143
Q

What is the treatment for a “tet spell” that occurs during the perioperative period?

A

-FiO2 100%
-Intravascular volume expansion
-Increase SVR w/ phenylephrine to augment the PVR to SVR ratio
-Reduce SNS stimulation to improve dynamic RVOT obstruction (deepen anesthesia, beta-blockade w/ short acting agent (esmolol))
-Inotropes worsen RVOT obstruction and are best avoided
-Avoid excessive airway pressure
-Infant may be placed in a knee-chest position to mimic squatting

144
Q

What are the hemodynamic goals for tetralogy of Fallot?

A

Increase SVR:

  • avoid vasodilation
  • treatment = phenylephrine

Decrease PVR:

  • avoid hypercarbia, hypoxia, acidosis, etc
  • treatment = reverse conditions listed above, and nitric oxide

Maintain Contractility & HR:

  • avoid SNS stimulation, ephedrine, dobutamine, epi
  • treatment = esmolol

Increase Preload:

  • avoid dehydration
  • treatment = crystalloid and albumin 5%
145
Q

What is the best IV induction agent for the patient with tetralogy of Fallot?

A

Ketamine (1-2 mg IV or 3-4 mg IM) –> increases SVR and reduces shunting

*even though it increases contractility – this effect is minor compared to benefit of increasing SVR

146
Q

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

A

Infants/Children = Ventricular Septal Defect (VSD) – many close by 2 years old

Adults = Bicuspid Aortic Valve

147
Q

What is coarctation of the aorta? Which syndrome is highly associated with this anaomaly?

A

Narrowing of the thoracic aorta in the vicinity of the ductus arteriosus

-typically occurs just before or after the ductus arteriosus, but in rare instances can occur proximal to left subclavian artery

Turner syndrome is highly associated with coarctation of the aorta

148
Q

How is blood pressure affected in the pt with coarctation of the aorta?

A

SBP = elevated in upper extremities

SBP = reduced in lower extremities

149
Q

What is Ebstein’s anomaly?

A

The most common congenital defect of the tricuspid valve
-usually an ASD or PFO

Characterized by a downward displacement of the tricuspid valve and atrialization of the right ventricle (d/t ASD or PFO)

  • tricuspid regurgitation can be severe
  • right to left shunting occurs at level of the atria
  • SVT is common
  • RV failure is common in postop period
150
Q

What are the anesthetic considerations for a patient who has previously undergone Fontan completion?

A

Pt has a single ventricle that pumps blood into the systemic circulation

No ventricle to pump blood into pulmonary circulation so:

  • blood flow into lungs is completely dependent on negative intrathoracic pressure during spontaneous breathing
  • positive pressure ventilation disrupts this arrangement and should be avoided/minimized
  • preload dependent – do not let them get dry
151
Q

What is truncus arteriosus?

A

Characterized by a single artery that gives rise to the pulmonary, systemic, and coronary circulations
-no specific pathway for blood to enter pulmonary circulation before being pumped into systemic circulation
-usually a VSD as well

Decreasing PVR or Increasing pulmonary blood flow steals blood from systemic and coronary circulations

152
Q

What organisms cause Epiglottitis? What are the typical ages affected and speed of onset?

A

Bacterial:
-H. Influenza (less common today)
-Group A Streptococci
-Pneumococci
-Staphylococci

Ages Affected = 2-6 years old

Onset = Rapid (<24 hours)

153
Q

What organisms cause Croup? What are the typical ages affected and speed of onset?

A

Viral:

  • H. parainfluenzae
  • Respiratory syncytial virus (RSV)
  • Influenza viruses type A & B

Bacterial:

  • Mycoplasma pneumoniae

Ages Affected: <2 years old

Onset = Gradual (24-72 hrs)

154
Q

What regions are affected by epiglottitis and croup? How do these present on a lateral neck x-ray?

A

Epiglottitis = Supraglottic structures –> Thumb sign (swollen epiglottis)

Croup = Laryngeal structures –> Steeple sign (subglottic narrowing)

155
Q

What is the clinical presentation and treatment for epiglottitis?

A

Clinical Presentation:
-high fever
-tripod position helps breathing
-4 D’s = Drooling, Dysphonia, Dyspnea, Dysphagia

Treatment:
-O2
-urgent airway management (tracheal intubation or tracheostomy)
-Antibiotics (if bacterial)
-induction w/ spont ventilation (CPAP 10-15 cmH2O minimizes airway collapse
-ENT surgeon must be present
-post-op ICU care

156
Q

What is the clinical presentation and treatment for croup?

A

Clinical Presentation:
-mild fever
-inspiratory stridor
-barking cough

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

157
Q

What is the pathophysiology and presentation of postintubation laryngeal edema?

A

Postintubation Laryngeal Edema = Postintubation Croup
-complication of endotracheal intubation or rigid bronchoscopy

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

Presents w/ hoarseness, barky cough, and/or stridor – typically occurs within 30-60 min following extubation

158
Q

What are the risk factors for postintubation laryngeal edema?

A

-Age <4
-ETT is too large
-ETT cuff volume is too high
-Traumatic or multiple intubation attempts (one reason not to use an uncuffed tube)
-Prolonged intubation
-Coughing
-Head/neck injury
-Head repositioning during surgery
-History of infectious or post-intubation croup
-Trisomy 21
-Upper respiratory tract infection

**all due to small airway or airway trauma

159
Q

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

A

Best treatment = Prevention

-maintain air leak <25 cmH2)
-if using cuffed ETT use a manometer to intermittently measure cuff pressure

160
Q

What is the treatment for postintubation laryngeal edema?

A

-Cool and humidified O2
-Nebulized racemic epinephrine 0.5 mL of 2.25% solution in 2.5 mL of 0.9% NS
-Dexamethasone 0.25-0.5 mg/kg IV (max effect requires 4-6 hrs)
-Heliox (helium + O2 mixture that improves laminar airflow)

*Aims to reduce swelling and improve airflow

**not infectious thus abx are not indicated

161
Q

Which signs and symptoms of respiratory infection should you “proceed w/ caution” and which symptoms should you cancel a case?

A

Proceed with Caution:

  • clear rhinorrhea (runny nose)
  • no fever
  • active
  • appears happy
  • clear lungs
  • older child

Cancel:

  • purulent nasal discharge
  • fever (>38*C)
  • lethargic
  • persistent cough
  • poor appetite
  • wheezing and rales that do not clear with cough
  • child <1 year or previous preemie
162
Q

How can you reduce the risk of airway complications while anesthetizing a child with an upper respiratory infection?

A

-Avoid mechanical irritation of the airway (Facemask > LMA&raquo_space;> ETT)
-Mechanical irritation (ETT use) increases risk of bronchospasm 10 fold
-If ETT must be used – use smaller size than normal (have higher risk of postintubation croup)
-Dexamethasone 0.25-0.5 mg/kg will reduce risk of postintubation croup
-Ensure a deep plane of anesthesia before instrumenting the airway
-Propofol attenuates airway reactivity and may reduce risk of bronchospasm
-Sevo is best volatile agent (non-pungent)
-Pretreatment w/ inhaled bronchodilator (albuterol or ipratropium) or glyco dose not provide a clear benefit

163
Q

What is the presentation of a child who presents with a foreign body aspiration?

A

Class Triad: Cough, Wheezing, and Decreased breath sounds on affected side (usually right)

  • airway obstruction significant enough to impair gas exchange can quickly progress to hypoxemia, cyanosis, altered mental status, cardiac arrest, and death

Supraglottic Obstruction –> Stridor
Subglottic Obstruction –> Wheezing

164
Q

What are the complications of rigid bronchoscopy?

A

Rigid bronchoscopy = “gold standard” procedure to retrieve foreign body

Complications:
-laryngospasm
-bradycardia during scope insertion
-postintubation croup
-pneumothorax

165
Q

Which syndromes are associated with difficult airway management due to:
-Large Tongue (2)
-Small/Underdeveloped Mandible (4)
-Cervical Spine Anomaly (3)

A

Large Tongue: Remember “Big Tongue”
-Beckwith Syndrome
-Trisomy 21

Small/Underdeveloped Mandible: Remember “Please Get That Chin”
-Pierre Robin
-Goldenhar
-Treacher Collins
-Cri du Chat

Cervical Spine Anomaly: Remember “Kids Try Gold”
-Klippel-Feil
-Trisomy 21
-Goldenhar

166
Q

Describe the airway in the patient with Trisomy 21

A

-Small mouth
-Large tongue
-Palate is narrow with a high arch
-Midface hypoplasia
-Atlantoaxial instability (C1 & C2 subluxation - avoid neck flexion)
-Subglottic stenosis (use smaller ETT)
-OSA
-Chronic pulmonary infection

*at risk for difficult ventilation and intubation

167
Q

What is the CHARGE Association?

A

C - Coloboma (a hole in one of the eye structures)
H - Heart defects
A - Choanal atresia (back of nasal passage is obstructed)
R - Retardation of growth and development
G - Genitourinary problems
E - Ear anomalies

168
Q

What is CATCH 22?

A

C - Cardiac defects
A - Abnormal face
T - Thymic hypoplasia
C - Cleft palate
H - Hypocalcemia (due to hypoparathyroidism)
22 - 22q11.2 gene deletion

**Also called DiGeorge Syndrome or 22q11.2 gene deletion syndrome

169
Q

What are the unique anesthetic considerations for the patient with DiGeorge syndrome?

A

Hypocalcemia is common – remember hyperventilation, albumin, and citrated blood products lower free Ca2+ in the blood

If the thymus is absent – child is at high risk of infection

170
Q

What activities correspond with 1, 4, and 10 METs?

A

1 MET (Poor functional capacity):
-self care activities
-working at computer
-walking 2 blocks slowly

4 METs (Good functional capacity):
-climbing a flight of stairs w/o stopping
-walking up a hill (>1-2 blocks)
-light housework
-raking leaves
-gardening

10 METs (Outstanding functional capacity):
-strenuous sports – running, swimming, basketball

171
Q

How does minute ventilation change in the elderly?

A

Increases

-increased Vd necessitates an increase Ve to maintain a normal PaCO2

172
Q

How does lung elasticity change in the elderly?

A

Decreased

-this collapses the small airways and causes the lung to become overfilled with gas

-increased Vd
-decreased alveolar surface area
-V/Q mismatch
-increased A-a gradient
-decreased PaO2

173
Q

How does chest wall compliance change in the elderly? Why?

A

Decreases – chest is stiffer and more difficult to expand

Caused by:
-calcification of joints
-diaphragmatic flattening
-increased A:P diameter
-decreased intervertebral disc height
-decreased respiratory muscle strength
-decreased lung elastic recoil

174
Q

Why does residual volume increase in the elderly? What are the consequences?

A

Aged lung has a reduced elastic recoil –> causes it to become overfilled w/ gas –> increases residual volume (explains why FRC increases as we age)

-Closing capacity surpasses FRC at ~45 years old in the supine position and ~65 years old when standing
-When CC > FRC –> small airways collapse during tidal breathing (contributes to V/Q mismatch, increased anatomic dead space, and a reduction in PaO2)

175
Q

How does arterial compliance change in the elderly?

A

Decreases as a function of loss of elastin and increased collagen

-increase SVR –> increase BP
-increase pulse pressure
-increase myocardial wall tension to overcome higher afterload
-increase myocardial hypertrophy

176
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

177
Q

How does the cardiac conduction system change in the elderly?

A

There is fibrosis of the conduction system and loss of SA node tissue –> increases incidence of dysrhythmias

178
Q

How do the blood pressure and pulse pressure change in the elderly?

A

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

Pulse pressure also increases for this reason

179
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

180
Q

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

A

All decrease

181
Q

What autonomic changes occur in the elderly?

A

-Decreased adrenergic receptor density
-Decreased response to catecholamines
-Increased circulating catecholamines as partial compensation
-Reduced ability to increase HR during hypotension (decreased baroreceptor function)
-Impaired thermoregulation increases the risk of hypothermia

182
Q

How does MAC change in the elderly?

A

Decreases by 6% each decade of life after age 40

183
Q

What is the onset of postop delirium and postop cognitive dysfunction?

A

Postop Delirium = Early postop period

POCD = Weeks to months after surgery

184
Q

What is the treatment for postop delirium and postop cognitive dysfunction?

A

Postop Delirium:
-treat underlying cause
-antipsychotics
-minimize polypharmacy

POCD:
-no specific treatment
-most cases are mild and tend to resolve after ~3 months

**to minimize risk – best to use rapidly metabolized drugs

185
Q

How does sensitivity to local anesthetics change in the elderly?

A

Sensitivity to LA increases

-decreased number of myelinated nerves
-decreased diameter of myelinated nerves
-decreased conduction velocity

186
Q

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

A

Both require a dosage adjustment

Intrathecal: CSF volume is reduced –> Greater spread of LA

Epidural: Volume of epidural space is reduced –> Greater spread of LA

187
Q

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

A

Anatomic changes:
-less space between the posterior spinous processes
-decreased intravertebral disc height
-narrow intervertebral foramen
-calcification of joints

188
Q

How does the glomerular filtration rate change in the elderly?

A

GFR Decreases:
-125 mL/min in adult male –> decreases by 1 mL/min/year after age 40

Consequences include:
-risk of fluid overload (less plasma delivered to the nephrons per unit time)
-impaired drug elimination (consider dosage adjustments if age >60)

189
Q

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

A

Serum Creatinine does not change
-GFR decreases w/ age (should increases Cr) –> muscle mass declines w/ age (less creatinine is produces) –> net effect is Cr = unchanged

Creatinine Clearance is decreased (most sensitive indicator of glomerular function in elderly)

190
Q

How does the production of plasma proteins change in the elderly?

A

Alpha 1-acid Glycoprotein = increased (larger reservoir for basic drugs = decreased free fraction)

Albumin = production decreases (smaller reservoir for acidic drugs = increased free fraction)

Pseudocholinesterase = production decreases (SUX duration increases in men > women)

191
Q

How does circulation time change in the elderly?

A

Increases –> reduced CO prolongs the time of drug delivery from the site of administration to the site of action

-slower IV induction
-faster inhalation induction

192
Q

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

A

Decreases as a function of reduced muscle mass

It Causes:
-decreased basal metabolic rate
-decreased total body water
-decreased blood volume
-decreased plasma volume
-decreased Vd for hydrophilic drugs (higher than expected Cp for a given dose)
-decreased neuromuscular reserve
-Hypothermia sets in faster

APEX Study Guide (13 decks)

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