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NICU Board Review Cards > Pulmonology > Flashcards

Pulmonology Flashcards

1
Q

CDC criteria for ventilator associate pneumonia

A

​Mech Vent for at least 2 days and

  1. Worsening gas exchange
  2. Radiographic evidence (infiltrate, consolidation, cavitation, pneumatocele)
  3. Three of the following
  • temp instability
  • WBC <4K or >15 K, bands >10
  • cough
  • sputum/ inc secretions
  • apnea/ inc WOB
  • wheezing, rales, rhonchi
  • HR <100, >170
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2
Q

Most common organism with vent assoc pneu

A

Pseudomonoas

Enterobacter

Klebsiella

Staph aureus

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3
Q

Indicence of VAP

A

2.7-37.2 episodes/1000 ventilator days

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4
Q

Risk factors for VAP

A

BPD

Sedation

reintubation

Bld transfusion (inc pul edema)

acid suppressive med

ETT (reservoir bactaria, impedes physiologic clearnace)

Surfactant deficiency

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5
Q

Preventive measure for VAP

A

hand hygiene

closed ventilator circuit (avoid unnecessary equipment change/ disconnection)

dec standing water within the circuit

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6
Q

Management for suspected VAP

A

Linzolid/Vanco plus Pip-Taz/gent

severe cases: antipsuedomonal: cefepime/ceftaz, carbapenem

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7
Q

What is main mechanism of gas exchange in HFOV

A

Diffusion (there is constant entry of fresh gas)

Other mechanisms:

taylor dispersion, regional variation of turbulent and laminar flow, pendelluft movement

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8
Q

What is main mechanism of gas exchange on conventional vent and normal human ventilation

A

Bulk convective gas movement (actual entry and exit of gas through the patient= tidal volume)

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9
Q

Forces need to overcome for ventilation to happen

A
  1. Resistance
  2. Imepdence (mechanical barries to flow)
    * R= 8nl/r4 - Can affect flow (length of ETT, diameter of ETT) in terms of HFOV decrease MAP in distal airway
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10
Q

What is primary risk factor for BPD

A

invasive mechanical ventilation

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11
Q

Stage of lung development for extremely premature infant

A

Canalicular stage

  • set up for shear force injury (inc volutrauma with dec GA)
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12
Q

Strategies for invasive ventilation for extremely premature infant

A
  • Limit tidal volume (avoid volutrauma)
  • Optimal MAP and PEEP for alveolar stability (avoid atelectrauma)
  • Minimizing oxygen toxicity
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13
Q

Effects antenatal steroids

A
  • Accelerate maturation of type II alveolar cells for surfactant production
  • Increased thinning of alveolar septa
  • Accelerated invasion of capillaries into the airspaces
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14
Q

Benefits of antenatal steroids
For infants between 22 and 25 weeks GA

A

reduces: mortality (39 to 18%), severe IVH, neurodevelopmental impairment

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15
Q

Benefits of SIMV vs nonsynchronized

A
  • improves gas exchange
  • inc pt comfort with dec need for sedation and muscle relaxation
  • dec WOB, risk for barotrauma, volutrauma and IVH
  • faster weaning
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16
Q

Settings for pressure limited vent

A

PIP: provide chest wall excursion

  • needs PIP to manual adjusted with change in pulmonary dynamics
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17
Q

Settings for volume controlled

A

Desired tidal volume is set

  • PIP automatically changed with change in pulm dynamics
  • challenge if with air leak
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18
Q

TV for Preterm RDS <700 g

A

5.5–6 mL/kg 24 cm H2O

Rationale: Dead space of the flow sensor/decreased compliance, risk of air leak

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19
Q

Advantage of Volume targeted ventilation over pressure limited ventilation

A

Reduction of:

  • in death or BPD at 36 weeks’ gestation
  • duration of mechanical ventilation,
  • air leaks
  • hypocarbia
  • grade 3 to 4 IVH as well as PVL and/or severe IVH
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20
Q

Initial setting for VTV based on wt/GA

A
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21
Q

What is the mechanism of gas exchange in HFJV

A

Taylor dispersion

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22
Q

Rationale for pressure support during weaning from conventional vent in extremely preterm infant

A

Unable to generate adeq TV, effective alveolar vent during spon breaths

  • Poor lung compliance
  • Increased airway resistance from the ET
  • Inc chest wall compliance
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23
Q

Risk factors for TTN

A

Maternal:

  • before completion of 39 weeks gestation
  • CS without labor
  • GDM
  • maternal asthma

Fetal:

  • male gender
  • perinatal asphyxia
  • prematurity
  • SGA/LGA
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24
Q

What is responsible for fetal lung fluid

A

Chloride channels

  • Volume of fetal lung is maintained by the larynx, which acts as a one-way valve, allowing only outflow of fluid
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25
Q

How is fetal lung fluid is reabsorbed

A
  • through ENaC
    • activated with onset of labor: maternal epinephrine and glucocorticoids
    • ENac is found in apical membranes of type II pneumocytes.
  • starling forces and thoracic squeeze(minor role)
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26
Q

Effect of neck position in ET position for infant <1kg

A
  • neck flexion: decrease lip-to-carina distance by up to 1.5 cm,
  • neck extension: increases the distance by up to 1.3 cm.
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27
Q

What is arterial oxygen content (CaO2)

A

CaO2 = (1.36 mL/g × Hb g/dL × SaO2) + (PaO2 mm Hg x 0.003 mL/[dL × mm Hg])

For every gram of Hgb, it carries 1.36 ml of O2
SaO2 in decimal

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28
Q

In lung development, what is responsible for branching of the mesoderm

A

Mesenchyme

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29
Q

Where is the respiratory tract derived from?

A

Endoderm

Forms from the ventral bud of the esophagus

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30
Q

Lung development is dependent on:

A
  1. fetal lung fluid
  2. Fetal breathing efforts
  3. Peristalsis of the airway
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31
Q

Origin of the pulmonary vasculature

A

6th aortic arch
* Pulmonary arteries : intrapulmnary structures for gas exchange
* Bronchial arteries: fr aorta supplies conducting airways, visceral pleura, connective tissue, pulm arteries

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32
Q

How does does pre-acinar arteries develop

A

Angiogenesis

new vessels from preexisting

supplies airways incl non resp bronchioles

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33
Q

How does does Intra-acinar arteries develop

A

Vasculogenesis

de novo from mesoderm

  • supplies respiratory brochioles and alveolar ducts
  • growth with alveolar devt
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34
Q

True or false:
fetus has greater vascular wall thickness vs adult

A

True

In terms of total vessel diameter

  • Fetal pulm arteries has smooth muscles until preacinar
  • Fetal to near term: Intra-acinar arteries lack muscle (all vessels around alveoli)
  • In adults: all have smooth muscles but thin
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35
Q

How many aveoli present at birth

A

50-150M

Adults: 200-600M

Inc in alveolar phase until 3-8 yrs
Enhanced by Vit A and thyroxine
Delayed by steroids, O2, NTN def, MV, insulin, inflam

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36
Q

When are adult airways completed?

A

24 wks gestation

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37
Q

Pulmonary embryology
Embryonic stage:
a. Structural dev’t
b. abnormality

0-5 wks

A

a. Upper airway, tubes (until 5 lobes)
b. TEF, bronchogenic cyst

38
Q

Pseudoglandular
a. Structural dev’t
b. abnormality

6-15 wks

A

a. Up to terminal bronchiole, separation of thorax and peritoneal cavity
b. CPAM, Cong emphysema, diaphragmatic hernia

39
Q

Canalicular
a. Structural dev’t
b. abnormality

16-25 wks

A

a. Bronchioles, pneumocytes II to I
b. Pulm hypoplasia, surf def, alveolar cap dysplasia

Lung is viable

40
Q

Saccular
a. Structural dev’t
b. abnormality

26-35 wks

A

a. multiple sacs fr terminal bronchiole; gas exchange via alveolar-capillary membrane
b. pulmonary hypoplasia, surf def

41
Q

Alveolar stage
a. Structural dev’t
b. abnormality

36wks- 8y/o

A

a. alveoli inc, microvascular growth and vessel maturation
b. pulmonary hypoplasia, surf def, pulm HTN

42
Q

Difference of Type I and II pneumatocytes

A
43
Q

what is volume of fetal lung fluid

A

20-30 ml/kg
same as FRC

production near term 4-5 ml/kg/hr

44
Q

How is fetal lung fluid produced

A

Cl actively out in the future air space

via net negative intracellular potential

Inhibited by epinephrine, beta adrenegic agonist
cough it out

45
Q

How is fetal lung fluid abosrbed/ cleared prenatally

A
  • dec FTF
  • eNac
  • Inc lymphatic oncotic p

Absorb sodium
suck in

46
Q

How is fetal lung fluid absorbed/ cleared during labor

A
  • mechincal forces
  • catecholamine surge- eNac
  • higher cortisol and thyroid- eNac
47
Q

How is fetal lung fluid absorbed/ cleared postnatal

A
  • lung distend: inc transpulm pressure
  • inc lymphatic p
48
Q

What is the most active component of surfactant

A

Dipalmitoyl Phophatidylcholine (DPPC) 50%

49
Q

Surfactant can be deacivated by

A

Alveolar edema fluid
Meconium

50
Q

In L/S ratio which substance reflects lung maturity

A

Lecithin

increases with gestational age

L/S ratio >2 lung maturity
Another test for lung maturity: Phosphatidylglycerol (not necessary of normal surfactant function)

51
Q

What is Laplace’s law

A

P=2T/r

Plays role in surfactant by decreasing surface tension resulting in better compliance

52
Q

What law is involved in air movement into the lungs

A

Boyle’s Law
* pressure of gas decreases as volume increases

P1V1=P2V2

53
Q

What happens to the muscles of respiration during:
a. Inspiration
b Expiration

A

Chest wall and diaphragm
a. Contract
b. Relax

54
Q

It is a reflex that prevents over inflation

A

Hering Breuer Inflation Reflex

There is an increase in this reflex as volumes increase above FRC, limits inspiratory duration
- reason decrease in RR with CPAP

55
Q

This reflex helps maintain FRC, prevents atelectasis and involved in “sigh” breaths

A

Hering Breuer deflation reflex

  • In pneumothorax d/t decrease TV, there is an inc in RR
  • activity inverse with GA
56
Q

This reflex is important during the first few breaths after delivery

A

Paradoxical reflex of head

inhibits hering breuer reflex, results in inspiration extended

57
Q

Control of respiration

A

CSF: includes metabolic acidosis
No O2 receptor in central
Blood: dec O2, carotid and aortic bodies

58
Q

Formula for alveolar ventilation

A

(TV-Dead space) x RR

Dead space usually 1/3 of TV

change in TV and RR is proportional to alveolar vent and pCO2

59
Q

What is dead space

A

Space with no gas exchange
1. Anatomic- Upper airway
2. Alveolar- alveoli not involved in gas exchange
3. Physiologic= Anatomic + Alveolar dead space (also known as wasted ventilation)

= TV x (arterialCO2-expired CO2)/arterial CO2

  1. Bronchoconstrict- dec dead space, bronchodilate- inc dead space
  2. d/t shunting, abN vasculature
60
Q

What lung zone does the neonatal lung behave

A

Zone 3
Pa>Pv>PA

zone 1- alveolar dead space- MAS, inc pressure
zone 4 no ventilation- PDA, pulmonary edema

61
Q

What is A-a gradient

A

[FiO2 (barometric-H2O p)]- CO2/R- paO2

Barometric= 760
H20= 47
R= 0.8
-If A-a>600 for 8-12 hrs ECMO

62
Q

Formula oxygen delivery

A

CO x [(1.34xHgbxO2 sat)+0.0003 paO2]

N 150-170 ml/kg/min

Factors that affect O2 del- CO, SV, Hgb, O2 sat, PaO2
SV- preload, afterload, contractility

63
Q

What principle explains oxygen consumption

A

Fick Principle
- O2 consumption is the difference bet O2 del to tissues and the O2 returning from the tissue

  • O2 consump= VO2= CO x1.34x Hg x (Arterial-venous O2 sat)
  • O2 delivery dec what happens?
    inc blood flow (dilation of capillaries)
64
Q

Factors to increase oxygenation in assisted ventilation

A
  • FiO2
  • MAP
    1. PEEP
    2. PIP
    3. I time
    4. Flow

Caution: PEEP >6- not efficient
Inc MAP risk for overdistension
Inc I time- pneumothorax

65
Q

How to inc tidal volume

A

Inc pressure gradient (Inc PIP or dec PEEP)

Tidal volume is independent of I or E time

66
Q

Acute respiratory deterioration in ventilated neonates

A
  1. Displacement- include malposition
  2. Obstruction- secretions
  3. Pneumothorax
  4. Equipment

Think DOPE

If none of the above- IVH, seizure, hypoglycemia, hypotension, sepsis

67
Q

Formula for Oxygen Index

A

(MAP x FiO2)/ paO2 x 100

>25 severe disease

68
Q

Based on Poiseulis law, what affects resistance

A
69
Q

Risk factors of TTN

A
  • Delivery before 39 wks
  • CS without labor
  • Prematurity
  • Male
  • LGA/SGA
  • Perinatal asphyxia
  • M asthma
  • GDM
70
Q

CXR of TTN

A
  • fluid in the interloabr fissure
  • bilateral alveolar and interstitial edema
  • prominent pulmonary vascular pattern with inc hilar markings
  • lung hyperinflation
  • Clears after 24 hrs

BG: mild hypoxemia and hypocapnia
* if hypercapnea- think of fatigue or air leak

71
Q

It might not be TTN

A
  • Differential cyanosis: PPHN, CHD
  • Persistent tachypnea >4 days
  • Rule of 2 hrs- not getting better, FiO2 >0.4
72
Q

Prognosis of TTN

A
  • Associated with asthma (inc if delivered via CS)
  • Malignant TTN- develop PPHN
  • Majority resolve 48 hrs

  • No meds currently recommended
  • All supportive
73
Q

Benefits/Effects of Caffiene

A
  1. Improve minute ventiltion
  2. Improve CO2 sensitivity
  3. Dec periodic breathing
  4. Dec hypoxic resp depression
  5. Improve diaphargm activity

Long Term:
Dec Mech vent, dec BPD, Dec death, Dec CP, Dec congnitive delay

74
Q

What is old BPD

A

Gross distortion of lung architecture due to oxygen toxicity and baro trauma

75
Q

What is new BPD

A

Acquired developmental chronic lung disease that is a consequnece of premature birth; will have respiratory insufficiency

prevelance has not decrease over time

Based on GA
before 28 weeks up to 40%
before 24 weeks up to 80%
Based on BW <1000g: 16% with sBPD

76
Q

Definition of BPD severity based on mode of support at 36 weeks PMA

A

Grade 1- <2LPM
Grade 2- Non-invasive vent (HFNC/CPAP)
Grade 3- Invasive ventilation

Does not anymore include FiO2

NIH- before 32 weeks, 28 days oxygen; severe BPD O2 >30% and/or pos vent at 36 wks

77
Q

Pathophysiology of BPD

A

disorder of:
1. lung parenchyma
2. pulmonary vasculature
3. small and/or large airway dysfunction

less common finding- IV- gross distortion of lung architecture- large cystic area, fibrosis atelectasis, hyperinflation

78
Q

It characterized by episode of acute and severe hypoxemia attributed to airway collapse or PPHN in a BPD patient

A

BPD spell

Goal: Open lung management through MAP and airway positioning- PEEP adjusted to mitigate airway collapse and hyperinflation to optimize compliance and dec resistance

79
Q

Strategies for MV in BPD

A
  1. TV 8-13 ml/kg (d/t inc dead space)
  2. Inc PIP 30-40 (d/t poor compliance and high resistance)
  3. Slower rate <20/min
  4. Long IT >0.5s
  5. Pressure support for fast compartment
  6. PEEP 6-8 (d/t obstructive component, risk atelectasis, maintain FRC)

Same minute ventilation (TVxRR)

80
Q

Goal of non invasive ventilation in BPD

A

Provide adeqaute support for growth and development and not avoid MV

Goal avoid: volutrauma, atelectrauma and O2 toxicity

red flags: poor growth, worsening PH, inability to tolerate developmentally appropriate physical activity, repeat hypoxic spells

81
Q

Strategies for non-invasive vent in BPD

A

More reserved pacing of weaning (ie weekly/ twice weekly)

Goal: no significant tachypnea, WOB and able to participate in PT/OT activity
Pitfall: Inaqdequate support: worsen regional atelectasis and intermittent hypoxemia

82
Q

This occurs when expiration is prolonged by high airway resistance and interrupted by subsequent inspiratory effort resulting in higher end expiratory volume (hyperinflation)

A

Auto-PEEP (PEEPi)

PE:
1. higher RR above the vent and mod-severe WOB (patient-vent asynchrony)
2. inspiration that do not trigger ventilator supported breath

83
Q

When to consider tracheostomy

A

Unable to wean from NIV/MV as bby approaches or surpasses term-equivalent PMA

Has been associated with decreased resp suport, improved growth and participation in developmental activities in the short term

84
Q

Outcome of sBPD and MV

A
  • 97% free fr MV by 5 yrs
  • Median age off MV 2 yrs
  • Median age decannulation 3 yrs

d/t on going alveolarization

85
Q

What are the approaches to prevent BPD

A
  1. Vitamin A
  2. Caffeine
86
Q

Morbidities with BPD

A
  • recurrent resp infection
  • asthma
  • neuro dev abN
  • PPHN
87
Q

Initial vent setting for CDH

A
  • PIP: less than 25
  • PEEP: 3–5
  • rate of 40–60
  • Paco2 50-70 mmHg.
88
Q

what are the different congenital lung malformations

A
89
Q

A neonate presents with expiratory stridor with feeding difficulty
Ba swallow showed at indentation on the esophagus
What is the most likely etiology?

A

Vascular ring most probably double aortic arch (40%)

due to right and left 4th brachial arches

90
Q

What are the morbidity/mortality of congenital diaphragmatic hernia

A
  1. pulmonary hypoplasia
  2. abnormal pulmonary vasoreactivity
  3. Pulmonary hypertension

NICU Board Review Cards (19 decks)

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