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Board Exam COPY > Neonates > Flashcards

Neonates Flashcards

1
Q

Why is phenylephrine not a good choice for neonates?

A

Their hearts are immature and unable to increase contractility to overcome increases in after load.

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2
Q

Why do infant have such a high respiratory rate?

A
  • To compensate for their high metabolic rate (twice the rate of O2 consumption and CO2 production as adults)
  • Thus the neonate must increase their minute ventilation accordingly.
  • Also, neonates only have about 1/3 the alveolar surface area of adult.
  • Metabolically, it’s more efficient to increase RR than TV
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3
Q

In the setting of hypovolemia and bradycardia, which is better for the neonate, EPI or atropine?

A

EPI

Will increase HR and will increase contractility (even though only by a little bit)

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4
Q

How does contractility improve over time in neonates?

A

Neonates are initially born with very low SVR, but this begins to rise over time.
The LV has to push against a higher after load, so contractile elements multiple and mature, thus improving contractility. Over time, this means that kids become less dependent on HR for CO.

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5
Q

Baroreceptor response in neonates

A

Immature.

Because of this, the reflex will not increase HR in the setting of hypovolemia and can vastly worsen BP.

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6
Q

The number of alveoli continue to rise until this age

A

8-10 years of age

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7
Q

Why do neonates have very fast inhalation inductions?

A

High minute ventilation and low FRC

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8
Q

Type I and Type II muscle fibers

A 
II = Fast twitch (strong, but tire easily)
I = Slow twitch (endurance)
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9
Q

Muscles of inspiration

A

DIAPHRAGM IS MAIN ONE

Intercostals are immature (ribs thus more horizontal and unable to significantly increase thoracic volume)

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10
Q

Newborn lungs are compliant or noncompliant?

A

None-compliant

The CHEST WALL is very compliant d/t cartilaginous ribs

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11
Q

Why does chest wall collapse on inspiration occur in neonates?

A

Low lung compliance + high chest wall compliance

Diaphragm has to work hard to expand the lung. High negative intrathoracic pressures lead to chest wall collapse

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12
Q

FRC and CC in newborns

A

CC overlaps with FRC, causing small airway collapse with tidal breathing

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13
Q

Clamping of the cord causes this in the newborn

A

Rhythmic breathing

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14
Q

Acute rise in ____ promotes continuous breathing in the newborn

A

Acute rise in O2 promotes continuous breathing

Hypoxia causes apnea.

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15
Q

Respiratory control doesn’t mature until this age

A

42-44 weeks

BEFORE this time, hypoxia will cause apnea.

AFTER this time, hypoxia stimulates breathing.

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16
Q

Lifespan of RBCs with HgbF

A

70-90 days

Compared to 120 days with HgbA

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17
Q

P50 of HgbF and HgbA

A

HgbF = 19mmHg

HgbA = 26.5mmHg

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18
Q

HbF’s ability to bind 2,3-DPG

A

HgbF is unable to bind 2,3-DPG, which is why it has a higher affinity for O2 and lower partial pressure in the tissues

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19
Q

When is HgbF replaced by HgbA?

A

First 2 months of life

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20
Q

RBC transfusion guidelines

A

Depends on if patient is older or younger than 4 months old

Younger than 4 months:

  • Kids still have HgbF, so transfusion trigger is higher (their Hgb isn’t as efficient in delivering O2!)
  • Trigger of 10 for kid having major surgery or if they have moderate CP disease
  • Trigger of 13 (earlier transfusion) for kids with SEVERE CP disease

Older than 4 months:
- Same guidelines for adults (6-10g/dL stuff)

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21
Q

FFP transfusion guidelines

A

For coagulopathies only (not volume expansion). Give if:

  • Need to quickly reverse warfarin
  • PT > 1.5 or increased PTT
  • To correct coagulopathic bleeding if > 1 blood volume has been replaced and you can’t get coats drawn easily
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22
Q

This pH abnormality is associated with massive transfusion

A

Either may happen

1) Acidosis from poor oxygenation and increased lactate
2) Alkalosis from metabolism of citrate to bicarbonate in the liver

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23
Q

Massive transfusion may have this effect on GB

A

Hyperglycemia 2/2 dextrose in the blood

24
Q

Why are PRBCs radiated?

A

To destroy leukocytes, which can cause graft-vs-host disease

25
Q

Newborns and ABO antigens

A

ABO antigens are poorly expressed in newborns. Some say they can be given uncross matched blood. q

26
Q

Renal function in the neonate and it’s implications

A

Compared to the adult, the neonatal kidney has:

1) Decreased perfusion pressure
2) Decreased GFR
3) Decreased ability to concentrate ruin

As a result, the neonate is bad at handling fluids:

  • Bad at concentrating urine, so it loses lots of water 2/2 lack of sodium reabsorption (bad at handling fluid restriction)
  • However, low GFR, so unable to excrete large volumes, and are bad at handling fluid overload as well
  • Fluid management is essential!

Solutes:
- Tend to lose sodium and glucose

27
Q

Renal maturation

A

1) GFR reaches adult levels at 8 months - 2 years

2) Renal tubular function achieves full concentrating ability at 2 years

28
Q

Total body water distribution is the same as adults by this age

A

1 year

29
Q

Third space losses

A

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

30
Q

Neonatal CO

A

CO is 200mL/kg/min

This is faster than the adult and results in faster circulation time compared to adults

31
Q

Protein binding in neonates

A

Decreased d/t low levels of circulating proteins

32
Q

Effect of fat soluble drugs

A

Drugs that rely on fat for redistribution and termination of effect will have a prolonged DOA 2/2 decreased body fat content.

These bitches are 80% water.

33
Q

Neonates and bilirubin

A

Neonates cannot conjugate bilirubin 2/2 a lack of glucuronyl transferase. This is the same enzyme that metabolizes tylenol.

34
Q

BBB in neonates

A

Immature.

Allows more drugs to pass. May explain the increased sensitivity to sedative hypnotics.

35
Q

Muscle relaxant dosing in neonates

A

Sux = NEED MORE! 2mg/kg (higher Vd + equal sensitivity to sux at the NMJ)

NDMRs = same as adult dosing (this is because even though there is a higher Vd, the NMJ is immature and more sensitive to NDMRs)

36
Q

Sux dosing

A

IV = 2mg/kg

IM = 5mg/kg for neonates and infants
4mg/kg for older children

37
Q

Sux and bradycardia

A

Happens in children

38
Q

This is the only NDMR that can be given IM

A

Roc

IM dose is 1mg/kg for kids 1 year

39
Q

This is an indication in the mother that their child might have TEF

A

Polyhydramnios (kid isn’t swallowing amniotic fluid)

40
Q

TEF is associated with these other congenital anomalies (25-50% of those with TEF will have another anomaly)

A

VACTERL

Vertebral defects
Imperforate Anus
Cardiac Abnormalities
TEF
Esophageal atresia
Renal Dysplasia
Limb anomalies

20% will have a significant cardiac defect. Pre-op ECHO should be performed

41
Q

When is surfactant made during gestation?

A

Begins at 22-26 weeks

Peaks at 35-36 weeksq

42
Q

This medication can hasten fetal lung development. When does it work?

A

Betamethasone
Starts to work at 18 hours
Peaks at 48 hours

43
Q

Another same for surfactant is

A

Lecithin

44
Q

How can we get an idea of how mature a fetus’s lungs are?

A

Do an amniocentesis to look at the L/S ratio.
Looks at ratio of lecithin (surfactant) to sphingomyelin (surfactant precursor).
L/S ratio > 2 means adequate maturation

45
Q

Risk factors for developing respiratory distress syndrome (RDS)

A 
Prematurity
Low birth weight
O2 Toxicity
Intubation
Barotrauma from PPV
Maternal DM
46
Q

pH imbalances with pyloric stenosis

A

Causes initial metabolic ALKALOSIS.

Patient continues to lose fluid, and if hypovolemia is not corrected, impaired tissue perfusion results in lactate production and metabolic ACIDOSIS.

47
Q

Symptoms of pyloric stenosis first appear when?

A

At 2-12 weeks

More common in males.

48
Q

Vomiting depletes these things

A

Water, H+, Na+, Cl-, and K+

49
Q

Why is urine acidic in pyloric stenosis?

A

Losing lots of fluid. RAAS activated and aldosterone is released. Kidney reabsorbs Na+, but loses H+ to maintain electroneutrality

50
Q

Anesthetic management of pyloric stenosis

A
  • Postpone surgery until fluids and electrolytes are optimized.
  • Correct severe dehydration with 20mL/kg of NS
  • Maintenance fluids should be D5 1/2NS at 1.5x calculated rate (volume depleted and poor nutritional status)
  • Anticipate full stomach (RSI or awake intubation). Extubatne awake.
  • Post-op apnea is common (could be b/c the CSF remains alkalotic even though serum pH has normalized)
51
Q

Patho of retinopathy of prematurity

A

Immature BVs are at risk of vasoconstriction and hemorrhage. Dysfunctional healing then causes scars. As the scars retract, they pull on the retina, causing detachment and blindness.

52
Q

Risk factors for retinopathy of prematurity

A 
Prematurity
High FiO2
Mechanical ventilation
Intraventricular hemorrhage
Sepsis
Vitamin E deficiency
53
Q

For how long do kids need to be given a low FiO2?

A

Until retinal maturation is complete (44 weeks post-conception)

Until then, keep SpO2 between 85-93%

54
Q

What drugs may cause neural apoptosis?

A

Those that stimulate GABA and inhibit NMDA:

  • Ketamine*
  • Midazolam*
  • Propofol
  • Etomidate
  • VAs
  • N2O
  • Barbs
  • Other benzos
55
Q

What are the Dubowitz and Ballard scoring systems?

A

Ways of estimating gestational age AFTER the baby has been born!

How old is dis baby?

Most accurate 30-42 hours after birth

56
Q

What is the MOST ACCURATE way to measure gestational age in a fetus?

A

Crown-rump length via ultrasound

Board Exam COPY (21 decks)

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