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PICU/NICU/Lines > ICU/Lines > Flashcards

ICU/Lines Flashcards

1
Q

Umbilical Catheters. Where should the tip be placed?

A

Vein: IVC/RA junction - at the level of the diaphragm (T8-10)

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2
Q

Contraindications to umbilical catheters?

A

.

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3
Q

Short and long term complications of umbilical catheters?

A

.

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4
Q

Central access complications. Ports - common problems and fixes?

A

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5
Q

Broviac/Hickman. Common problems and fixes?

A

.

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6
Q

ASA classes?

A

.

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7
Q

Describe revers ratio ventilation?

A

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8
Q

Indications for reverse ratio ventilation?

A

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9
Q

Physiology of reverse ratio ventilation?

A

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11
Q

Explain mechanisms of gas exchange with ventilation, highlight HFO?

A

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12
Q

What parameters can be modified with HFO?

A

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13
Q

Antibiotic prophylaxis for cardiac patients? Who? When? Why?

A

.

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13
Q

How do you adjust for high PaCO2 and low PaO2?

A

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14
Q

What causes HUS?

A

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15
Q

What are the complications of HUS?

A

.

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16
Q

Hemolytic disease of the newborn.

A

.

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17
Q

Indications for ECMO?

A

.

18
Q

Contraindications to ECMO?

A

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19
Q

Compare/Contrast VV and VA ECMO?

A

.

20
Q

Complications of ECMO. Patient factors and Circuit factors?

A

.

21
Q

Meconium aspiration - describe physiology of the VQ mismatch?

List non-ECMO treatments?

A

.

22
Q

Calculate oxygenation index (OI)?

A

OI=MAP x FiO2 x PaO2/100

23
Q

Define SGA?

A

Under 10 percentile for weight at given gestational age.

24
Q

What are the cutoffs for LBW/VLBW/ELBW?

A

2500 g
1000 - 1500 g
< 1000 g

25
Q

Mechanisms and challenges of Acid base balance in the neonate?

A

Carbonic acid-Bicarb buffer.

Respiratory compensation - immediate for repisratory/CO2 disturbances, Delayed for metabolic/HCO3 disturbances.
- impaired with prem lungs/CLD

Renal compensation - regulates H+/HCO3 excretion. Mostly occurs in proximal tubules.

  • impaired by low GFR in firs 24-72 hours of life,
  • Maturation of tubular function also takes time and the ability to reabsorb bicarbonate does not reach adult levels until one yr of age. Most sever in prems.
26
Q

IVH mechanism:

A

Rarely occurs beyond 32 weeks.
Gelatinous germinal matrix provides little support for capillaries. The subependymal germinal matrix easily bleeds extending into the ventricles.
Periventricular leukomalacia develops from necrosis of adjacent white matter.

Decreased ability to regulate cerebral blood flow places prems at risk.

27
Q

Mechanism of hydrocephalus with IVH?

A

Blood in the ventricles leads to arachnoiditis and impaired CSF flow at the Sylvain aqueduct.

28
Q

Risk factors for IVH?

A 
Lower gestational age
Lower birth weight 
Male/white
APGAR , 3 at 5 min
Chorioamnionitis
Cardiac resuscitation
RDS
CO2 disturbances
HFO
PDA
29
Q

Factors to decrease the risk of IVH?

A
  • Antenatal steroids (2 doses given within a week of delivery and 12 hours prior to delivery)
  • Avoid rapid volume expansion with resuc
  • correct coags
  • avoid hypoxia/hypercarbia
30
Q

Diagnosis of IVH?

A

Physical signs: bulging fontanelle, Seizure

Labs: low HCT, hypotension, hyperglycemia, metabolic acidosis

Ultrasound/MRI

31
Q

IVH Grading:

A

Grade 1 - confined to germinal matrix
Grade 2 - IVH without dilated ventricles
Grade 3 - IVH with dilation
Grade 4 - IVH with periventricular hemorrhagic infarction

32
Q

IVH management:

A

Supportive care - maintain blood pressure and appropriate HCT. Control Seizures.

Monitor with Weekly U/S to monitor hydrocephalus

33
Q

Mechanisms of heat creation in neonates?

A

Increase metabolic rate through non-shivering thermogenesis I.e. utilization of brown fat.

34
Q

Mechanisms/risks of heat loss in neonates?

A

1) Increased surface area to mass
2) Immature skin and low fat content increase evaporative loss
3) Limited stores of fat and glycogen to increase metabolism
4) Impaired shivering response
5) Inability to communicate

35
Q

Mechanisms of heat loss in the OR?

A
  • exposure of viscera to low ambient temperatures
  • IV solutions
  • Irrigation solutions
  • impaired CNS/muscular thermoregulation from medications
  • Ventilatory heat loss
36
Q

Bilirubin metabolism from Heme to conjugated Bili:

A

RBC break down->Heme (heme oxygenase) -> biliverdin (biliverdin reductase) ->unconjugated bilirubin bound to albumin - at high concentrations crosses BBB.

Bili bound to albumin is conjugated in the liver and excreted into bowel where it has two fates - excretion or conversion to unconjugated by b-glucuronidase and reuptake.

37
Q

Mechanism of physiologic jaundice?

A

Immature hepatic conjugation leads to accumulation over the first week of life usually peaking at 48-72 hours and then resolving over the next 5 days.

38
Q

Causes of pathological jaundice in the neonate?

A

1) increased Bili production
2) Decreased clearance
3) Breast feeding jaundice

39
Q

Causes of increased Bili production in the neonate:

A

1) increased Bili production:
- Hemolytic disease of the newborn -> autoimmune, inherited red cell membrane defects, enzyme deficiencies, and hemoglobinopathies.
- sepsis/DIC
- blood loss/hematoma from birth trauma
- polycythemia

40
Q

Causes of decreased Bili clearance in the neonate:

A
  • bowel dismotility
  • prematurity
  • metabolic derangement
  • bowel obstruction or Ileus
41
Q

Breast feeding Jaundice vs breast milk jaundice?

A

Breast feeding: decreased caloric and fluid intake, possible increased intestinal reabsorption - treat with increasing the frequency of breast feeding to 8-12/day. Adequacy is measured by 4-6 wet diapers/day and 3-4 stools/day with transition to seedy at day 4.

Breast milk jaundice: peaks at 2-3 weeks. Deconjugating enzymes in breast milk (unproven)

PICU/NICU/Lines (1 decks)

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