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ANPR550 Pediatric Anesthesia > Pediatric Anesthesia Week 2 Flash Cards > Flashcards

Pediatric Anesthesia Week 2 Flash Cards

1
Q

What is the normal hemoglobin and hematocrit (H&H) for a neonate?

A

Hemoglobin: 18- 19 grams/dL
Hematocrit: 60 %

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2
Q

At birth, what is the percentage of hemoglobin is fetal hemoglobin?

A

50- 70%

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3
Q

How does fetal hemoglobin (HgbF) different from adult hemoglobin (HgBA)? How does it affect its Oxyhemoglobin Dissociation Curve?

A

Fetal hemoglobin (HgBF) has a higher affinity for oxygen, picking up more oxygen, but does not deliver it to the tissues. HgBF holds on to O2 not delivering it to the tissues, thus SHIFTING curve TO THE LEFT

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4
Q

At what age does H&H change in infants? How?

A

Around 2- 3 months. H&H DECLINE steadily. Hemoglobin declines to 9- 11 grams/dL and HgBF is largely replaced with HgBA

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5
Q

When does HgBA start to increase? At what level? At what age does HgBA normalize?

A
  • After 3 months
  • HgBA: 12- 13 grams/dL
  • Usually at or around puberty
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6
Q

How does a preterm neonate’s H&H transition from HgBF to HgBA? Or does it?

A

It occurs EARLIER and has a more PRONOUNCED DECREASE in hemoglobin

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7
Q

How much does a preterm neonates hemoglobin decrease when transitioning from HgBF to HgBA?

A

Decreases to about 7- 8 grams/dL

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8
Q

How does a preterm neonate’s drop in hemoglobin affect its Oxyhemoglobin Dissociation Curve?

A

Despite the reduction of HgB, the O2 delivery to the tissue may not be compromised due to the curve SHIFT TO THE RIGHT (more HgBA)

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9
Q

At what age does hemoglobin “normalize” (comparable to full-term neonates) in preterm neonates?

A

At or about 1 YEAR of AGE

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10
Q

Is the Oxyhemoglobin Dissociation Curve of a newborn shifted to the LEFT or RIGHT? Why?

A
  • LEFT (more HgBF vs HgBA)

- HgBF does not bind with 2, 3 DPG, shifting the curve to the LEFT

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11
Q

How is HgBF beneficial to a fetus?

A

Allows the loading of more O2 at lower fetal O2 partial pressures (fetal arterial PO2 of 20- 30 mmHg)

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12
Q

What happens to the Oxyhemoglobin Dissociation Curve during the first few months of life? Why?

A
  • It TRANSITIONS to a SHIFT TO THE RIGHT
  • As HgBF is replaced by adult HgBA (2-3 or 3-4 months) decreasing levels of 2, 3 DPG increasing the infants P50 enhancing O2 delivery, shifting curve TO THE RIGHT
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13
Q

What are the Dubowitz & Ballard scoring system?

A
  • A means of estimating GESTATIONAL AGE
  • Dubowitz: external score using physical characteristics with neurologic score
  • Ballard: uses simplified scoring criteria
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14
Q

When are the systems MOST ACCURATE? When are they not?

A
  • 30- 42 hours AFTER delivery

- In very small, preterm neonates

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15
Q

What is the most accurate means of assessing gestational age?

A

By measuring the CROWN-RUMP LENGTH OF THE FETUS during the FIRST TRIMESTER during ultrasound

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16
Q

What is the hemoglobin concentration at 2 weeks? 2- 3 months of age? 2 years of age?

A
  • 2 weeks: 13- 19 grams/dL (100 ml of blood)
  • 2- 3 months: LESS than 10- 11 grams/dL
  • 2 years: LESS than 12.5 grams/dL
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17
Q

What is the NORMAL range for hemoglobin level in a FULL-TERM newborn?

A

14 to 19 grams/dL

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18
Q

What happens to the Hgb of a FULL-TERM newborn after birth? What happens to the hematocrit?

A
  • It transitions from HgBF to HgBA and at 2-3 months (9th to 12th week) it “bottoms out” to a minimum of 10 to 11 grams/dL
  • Hematocrit drops from 60% to around 33%
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19
Q

When does hemoglobin levels START to stabilize in a FULL-TERM newborn?

A

Usually after the 3rd month (12th week) until about 2 years of age

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20
Q

When does hemoglobin normalize to adult levels? What are normal adult hemoglobin levels?

A
  • Begin to rise after 2 year of age and normalize at puberty

- Adult HgB: 14.0- 15.5 grams/dL

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21
Q

How does a hemoglobin levels differ in the PRETERM vs the FULL-TERM neonate?

A
  • In PRETERM, HgB transitions EARLIER and DECREASE MORE (around 7 to 8 grams/dL by 4 to 8 weeks)
  • PRETERM neonate’s transition catch up to their FULL-TERM counterparts at or around 1 year of age
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22
Q

What is the minimum hemoglobin concentration necessary before O2 carrying capacity is jeopardized in a neonate? An infant older than 3 months?

A
  • Neonate: LESS THAN 13 grams/dL

- Infant > 3 months: LESS THAN 10 grams/dL

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23
Q

A 3 month old infant, scheduled for surgery, has a HgB of 10.5 grams/dL. What action should be taken?

A

Continue with the surgery as it is > 10 grams/dL and the infant is 3 months of age (normal: 10- 11 grams/dL)

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24
Q

During pre-op of a 6 month old infant, you note physiologic anemia. What is the likely cause?

A

Most likely a FORMER PREMATURE INFANT (ex-premie). They tend to remain anemic because of poor nutrition and delayed hematopoiesis, induced by earlier transfusions
*Tend to catch up with full-terms at 1 year of age

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25
Q

In fetal circulation, PVR is ________ and SVR is _________.

A
  • Increased

- Decreased

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26
Q

In fetal circulation, the Foramen Ovale connects the ________ with the _________. Shunting blood from ________ to _________.

A
  • Right Atrium
  • Left Atrium
  • Right
  • Left
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27
Q

How does the Foramen Ovale naturally close?

A

The transition of pressure with the SVR increase and PVR decrease changes the direction of shunt from fetal R to L shunt to a normal L to R shunt, thus closing the flap over the Foramen Ovale

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28
Q

What factors close the Ductus Arteriosis and Foramen Ovale?

A
  • PRESSURE CHANGES within the two circulations and REDUCED levels of PROSTAGLANDINS
  • DECREASE in PVR w/ CONSTRICTION of Ductus Arteriosis s/t Oxygenation
  • Increase in pulmonary blood flow
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29
Q

What factors may cause a neonate/infant to return to fetal circulation?

A
  • Preterm neonates/infants

- Metabolic derangement (asphyxia, sepsis, meconium aspiration, congenital diaphragmatic hernia)

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30
Q

What 4 factors precipitate persistant fetal circulation in neonates?

A
  • Hypoxemia
  • Acidosis
  • Pneumonia
  • Hypothermia
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31
Q

What is the pathologic mechanism common in persistent fetal circulation?

A

Increased pulmonary vascular resistance (PVR) leading to R to L shunting

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32
Q

What does ASD stand for? What is it?

A
  • Atrial Septal Defect

- “Hole” within the atrial septum (between RA and LA)

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33
Q

What does VSD stand for? What is it?

A
  • Ventricular Septal Defect

- “Hole” within the ventricular septum (between RV and LV)

34
Q

With this defect, the high pressures in the left side of the heart allows oxygenated blood to flow back to the right side increasing blood flow to the lungs potentiating pulmonary congestion/ hypertension. What type of shunt is this?

A
  • ASD/VSD

- LEFT to RIGHT shunt

35
Q

What is a RIGHT to LEFT shunt? What results?

A
  • Blood bypasses the lungs because of obstruction to the lungs (like in pulmonary stenosis) causing deoxygenated blood to flow through the ASD/VSD or both to the SYSTEMIC side
  • Cyanosis
36
Q

What are the 4 classifications of Congenital Heart Defect?

A
  1. “Simple” LEFT to RIGHT Shunt- INCREASED pulmonary blood flow potentiating PULMONARY CONGESTION/ HYPERTENSION
  2. “Simple” RIGHT to LEFT Shunt- Decreased pulmonary blood flow potentiating CYANOSIS
  3. COMPLEX Shunt- Mixing of pulmonary & systemic blood flow with CYANOSIS
  4. OBSTRUCTIVE LESIONS
37
Q

What are examples of “Simple” LEFT to RIGHT Shunts?

A
  • ASD (Atrial Septal Defect)
  • VSD (Ventricular Septal Defect)
  • AVSD (Atrioventricular Septal Defect)
  • AP Window (Aortapulmonary Window)
38
Q

What are examples of “Simple” RIGHT to LEFT Shunts?

A
  • TOF (Tetrology of Fallot)
  • Pulmonary Atresia (lung obstruction)
  • Tricuspid Atresia (valve obstruction)
  • Ebstein Anomaly (congenital malformation of tricuspid valve)
    - Occlusion
    - Stenosis
39
Q

What are examples of COMPLEX Shunts?

A
  • TGA (Transposition of Great Arteries)
  • Truncus Arteriosus
  • DORV (Double-Outlet Right Ventricle)
  • HLHS (Hypoplastic Left Heart Syndrome)
  • TAPVD (Total Anomalous Pulmonary Venous Drainage)

*Focus on these

40
Q

What will HLHS patients eventually need?

A

A heart transplant

41
Q

What are examples of OBSTRUCTIVE LESIONS?

A
  • Pulmonary Stenosis
  • Aortic Stenosis
  • Mitral Stenosis
  • Coarctation of Aorta
42
Q

List 3 congenital defects where there is a RIGHT to LEFT Shunt? What is the common characteristic with these defects?

A
  • TOF (Tetrology of Fallot)
  • Pulmonary Atresia w/ VSD
  • Patent (persistant) Foramen Ovale
  • The flow (direction) of the shunt is PRESSURE DEPENDENT
43
Q

How common is Atrial Septal Defect (ASD) in children?

A

10% of CHD is ASD

44
Q

What are the 2 types of ASD?

A

Primum vs Secundum

45
Q

What is the difference between the 2 types of ASD?

A

Location of the defect on the septum
Primum- superior portion of the septum
Secundum- inferior portion of the septum

46
Q

What hemodynamic alteration may worsen a LEFT to RIGHT intracardiac shunt? What drugs should you avoid?

A
  • An increase in SVR may increase shunt such as in an Atrial Septal Defect (ASD)
  • Drugs that may increase SVR in the patient with ASD
47
Q

Which is usually larger, a ASD or VSD?

A

VSD

48
Q

What is a COMPLETE Atrioventricular Septal Defect (ASVD)?

A

Complete LEFT to RIGHT Shunt through both Atrial and Ventricular Septums ALSO a SINGLE COMMON ATRIOVENTRICULAR VALVE

49
Q

What is the MOST common congenital defect in children?

A

VSD (20% of CHD is VSD)

50
Q

How does size of a VSD effect flow? What issues can be seen post-operatively?

A
  • Small VSD: Restrictive Flow
  • Large VSD: Unrestricted Flow
  • Pulmonary Hypertension frequently requiring Inotropes
51
Q

Is the shunt of a Patent Ductus Arteriosus (PDA) a R to L shunt? or L to R shunt?

A

PDA= LEFT to RIGHT Shunt

52
Q

What cardiovascular changes occur with a Patent Ductus Arteriosus (PDA)?

A
  • Oxygenated blood to flow from the AORTA to PULM ARTERY
  • Additional blood through the lungs causes INCREASED WORKLOAD on the LEFT SIDE
  • LEFT VENTRICULAR HYPERTROPHY
  • INCREASE PULM. VASCULAR CONGESTION/RESISTANCE
  • Most patients are SYMPTOMATIC
53
Q

What would you auscultate when PDA is suspected on a pediatric patient?

A
  • A systolic and diastolic murmur
54
Q

What surgical approach is used for a PDA Ligation?

A

Via thoracotomy

55
Q

Where is PDA Ligation performed with neonates w/ extremely low birth weight (1000 g)?

A

In the NICU

56
Q

What are the pre-operative requirements for a PDA Ligation?

A
  • Type & Cross
  • Antibiotics (risk for Endocarditis)
  • Vitamin K (for immature liver)
57
Q

What are some of the risks for PDA Ligation?

A
  • Difficult ventilation
  • Desaturation d/t lung retraction
  • Tearing of PDA w/ massive hemorrhage
  • Inadvertent ligation of aorta or pulmonary artery
  • Endocarditis
  • *Paradoxical Air Embolism (PAE)
58
Q

What is the relationship between eTCO2 and Pulmonary Vascular Resistance (PVR)?

A

A direct relationship, if eTCO2 increases, so does PVR

59
Q

How many pulse oximeters would you need in a PDA Ligation? Where?

A
  • 2
  • Preductal = RIGHT HAND
  • Postductal= LOWER LIMB
60
Q

How would you know if the Aorta has been clamped inadvertently?

A

If the pulse is lost from the lower limb during a test clamping of the duct

61
Q

What kind of fluids would you use for maintenance fluids during PDA Ligation?

A

Glucose containing crystalloids

62
Q

What anesthesia related specific actions does the surgeon perform for a PDA Ligation?

A

They place the intercostal nerve block and/or high-dose opioid and muscle relaxants

63
Q

Where should the arterial line be measured in a patient undergoing repair of a PDA?

A

Femoral Artery

64
Q

How do pediatrics exhibit different pharmacokinetics from adults?

A
  • Altered protein binding
  • Larger volume of distribution (Vd)
    - Less fat/muscle and more fluid
  • Smaller proportion of fat and muscle stores
  • Immature renal and hepatic function
65
Q

How does the difference of pharmacokinetics in pediatrics effect metabolism?

A
  • Reduce a drug’s metabolism and/or
  • Increase a drug’s metabolism
  • Delay elimination
66
Q

Why would pediatric pharmacokinetics sometimes INCREASE metabolism?

A

Extensive FIRST PASS METABOLISM with drugs such as Propanolol, Morphine, and Midazolam

67
Q

When do liver enzymes become completely functional in a neonate?

A

The cytochrome P450 enzyme system is fully functional at ONE MONTH of age

*Gist: Liver metabolism is DECREASED in the neonate until one month of age

68
Q

What is the most common cause for liver transplantation in children?

A

Cholestatic Liver Disease secondary to Biliary Atresia (obstruction), particularly in infants (50%)

*A Kasai Procedure is performed to correct Biliary Atresia

69
Q

What is the physiology behind Jaundice in a newborn?

A

Due to the breakdown of RBC’s,which release bilirubin (byproduct) into the blood where the immaturity of the newborn’s liver cannot effectively metabolize the bilirubin (conjugated form) and prepare it for excretion into the urine

70
Q

When does normal physiology jaundice of a newborn typically appear?

A

Between the 2nd and 5th day of life and clears with time (and sunlight)

71
Q

This is a grave form of jaundice of a newborn characterized by very HIGH LEVELS of unconjugated bilirubin in the blood, YELLOW STAINING and DEGENERATIVE LESIONS in the cerebral gray matter

A

Kernicterus (Bilirubin Encephalopathy)

72
Q

How do you treat Kernicterus?

A

Phototherapy and exchange transfusions

73
Q

What can potentially predispose a neonate to Kernicterus?

A

Some medications may displace unconjugated bilirubin from its protein binding sites and possibly predispose an neonate to Kernicterus

74
Q

What are the signs and symptoms of Kernicterus?

A
  • Hypertonicity
  • Opisthotonus
  • Spasticity
75
Q

Can unconjugated bilirubin cross a normal blood-brain barrier?

A

No. They are normally bound to protein (albumin) that is too large

76
Q

How is unconjugated bilirubin able to cross the blood-brain barrier in Neonates?

A

Neonates have an immature blood-brain barrier

77
Q

What drugs may cause Kernicterus in a neonate?

A

Any drug that competes for albumin binding sites such as:

  • Furosemide
  • Sulfonamides
  • The preservative, Benzyl Alcohol, in Diazepam
78
Q

What is one of a number of conditions that is associated with APNEA and BRADYCARDIA in PRETERM INFANTS?

A

Gastroesophageal Reflux (GERD)

79
Q

Why are neonates/infants prone to GERD? What would you see?

A
  • The immaturity of the pharyngo-esophageal sphincter (even in healthy newborns)
  • Frequent regurgitation or “spitting” of gastric contents
80
Q

What is the placenta impermeable to?

A

Insulin and Glucagon

81
Q

Where is insulin secreted from and at what stage of life?

A

The islets of Langerhans in the Pancreas of the fetus, but only from the 11th week of fetal life

ANPR550 Pediatric Anesthesia (7 decks)

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