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Neo Board Review MAP > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Fetal Lung Fluid

A

Lung spaces filled with fluid due to net chloride influx into lungs
Periodic laryngeal movements allow exit of fluid into amniotic sac
Pressure gradient 3-5 cmH2O across larynx

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2
Q

Channels involved in secretion of FLF (into alveoli)

A 
Na/K/2Cl transporter
Chloride channels (ClC2, ClCN2)
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3
Q

Channels involved in absorption of FLF

A

Epithelial Na channel (ENaC)

Na/K-ATPase

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4
Q

Composition of fetal lung fluid

A 
High Cl (150)
Low pH (6.27)
Low protein (0.03)
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5
Q

Clearance of FLF postnatally

A



35% cleared
- lung distention (incr transpulmonary pressure)
- increased lymphatic oncotic pressure a/w low fetal alveolar protein


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6
Q

Sodium channels (FLF)

A

ENaC on apical surface - Bring sodium into the cell from alveoli
Na/K-ATPase - allow sodium to leave cell and enter interstitium
Water follows sodium out of alveoli and into interstitial space


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7
Q

Fetal breathing

A

Discrete episodes that resemble REM sleep and periods of low-voltage cortical activity
During later half of gestation 40-50% FBM alternating with apnea
No FBM = reduction and lung volume

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8
Q

Bradycardia after delivery

A

Due to lack of pulmonary stretch
Asphyxia -> hypoxia -> carotid chemoreceptor activation -> bradycardia
Periglottic stimulation activates laryngeal reflex

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9
Q

Lung inflation in the DR

A

Immediate increase in HR and BP

Gradually: establishes FRC, improves pulmonary and blood flow, improves gas exchange

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10
Q

Hering Breuer reflex

A

Lung overinflation leads to cessation of inspiration (apnea)

Pulm stretch receptors -> vagus

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11
Q

Paradoxical reflex of Head

A

Inhibition of Hering Breuer reflex results in extended inspiration
Periodic deep sighs = initial newborn breaths

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12
Q

J receptor reflex

A

Juxtacapillary receptors -> rapid, shallow breathing (TTN)

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13
Q

Laryngeal chemoreflex

A

Age related response to stimulators of larynx
Response: hypertension, bradycardia, swallowing, apnea
Stimulus: water, milk, suction catheter
Enhanced by sedation and hypoxemia

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14
Q

Carotid body reflex

A

Stimulus: hypoxemia (not hypoxia)
Response: initial increase in ventilation, followed by depression
Leads to peripheral vasoconstriction, stimulation of breathing, vagal (bradycardia)



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15
Q

Distal esophageal reflex

A

Afferent: vagal nerve
Stimulus: irritation of distal esophagus
Response: laryngospasm and stridor

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16
Q

Lung expansion and pulmonary vasodilation

A

Lung aeration -> increased oxygen and pH -> Vasodilation
NO, PGs further increase pulmonary blood flow
Stimulates FLF clearance and surfactant release

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17
Q

Diving reflex

A

Response to asphyxia
Redistribution of cardiac output to heart, brain, adrenals
High PVR with R to L shunting
Increase in BP followed by hypotension

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18
Q

Nitric oxide

A

Activation of guanylyl cyclase-> increased CGMP -> K channels -> pulmonary vasodilation

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19
Q

Sildenafil

A

Inhibits PDE5 to prevent degradation of cGMP

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20
Q

At end of which stage of lung development is the lung considered viable?

A

Canalicular

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21
Q

Late stages of lung development

A

Alveolar and microvascular

  • secondary crests
  • capillary bilayer
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22
Q

Timing of lung development stages

A 
Embryonic: 0-6 weeks
Pseudoglandular: 6-16 weeks
Canalicular: 16-26 weeks
Saccular: 26-36 weeks
Alveolar and vascular: 36 weeks to 3-5 years
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23
Q

Embryonic phase

A

Ventral lung buds off of esophagus at 4 weeks
Progressive elongation & dichotomous branching to form proximal airway
Pulmonary vascular development from 6th aortic arch
Coincides with development of kidneys

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24
Q

Pseudoglandular phase

A

Branching continues
Trachea & segmental bronchi by 7 weeks
Closure of pleuroperitoneal folds at 7 weeks (CDH)
By 16 weeks all bronchial divisions are done (24 total)

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25
Q

Canalicular phase

A

Completion of conducting airways through terminal bronchioles
Rudimentary gas exchange units

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26
Q

Saccular phase

A

Gas exchange enabled by alveolar capillary membrane by 24 weeks
Expanding surface areas
Double capillary network

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27
Q

Alveolar phase

A

True alveoli appear at 36 weeks
Expansion of surface area via formation of septae or secondary crests
Postnatal alveolar growth for 3-5 years

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28
Q

Vascular phase of lung development

A

Birth to 3 years
Micro vascular maturation with single capillary bed
Late alveolarization 2-20 years

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29
Q

Early mediators of lung development

A

FGF 10, 9, 2 (fibroblast growth factor)
Sonic hedgehog (SHH)
Bone morphogenetic protein (BMP)

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30
Q

Fibroblast growth factor (FGF)

A

Polypeptide ligand
Works with tyrosine kinase receptor (FGF-R)
FGF 10 initiates primary branching


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31
Q

Mediators of lung development (C & S)

A

FGF1, FGF7, keratinocyte growth factor
TGFB super family: Regulates cell proliferation, differentiation, migration, and extracellular matrix formation
Linked to glucocorticoid signaling -> maturational effect of betamethasone on type 2 cells

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32
Q

Morphogens

A

Concentration gradients to give different developmental signals to growing tissue

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33
Q

Transcription factors in lung development

A

T-Box
FOX
HOX
TITF1

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34
Q

What leads to left-right asymmetry during cardiac development?

A

Lefty 1
Lefty 2
Nodal
Defects in these can lead to transposition, situs inversus

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35
Q

Vascular development of lungs

A

Vascular endothelial growth factor (VEGF)

FLT1, FLK1 (high affinity receptors)

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36
Q

Mesenchyme

A

Development of lungs regulated by mesenchyme

Removal arrests branching

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37
Q

Physical mediators of lung development

A

Lung fluid: promotes growth through chronic stretch
FBM: increased pressure when coupled with upper airway contractions
Peristaltic airway contractions: pressure on distal buds

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38
Q

Vitamin A and lung development

A

No vitamin A -> tracheal stenosis & pulmonary agenesis

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39
Q

Inhibition of alveolarization

A 
Mechanical ventilation of preterm lungs
Glucocorticoids, insulin, PKC
Inflammatory cytokines (TGF-a, TNF-a, IL11, IL6
Hyperoxia or hypoxia
Poor nutrition
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40
Q

Abnormal development in embryonic phase

A 
Atresias (laryngeal, esophageal, tracheal)
Bronchogenic cysts
TEF
Pulmonary agenesis/aplasia
Pulmonary sequestration
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41
Q

Abnormal development in pseudoglandular phase

A 
Renal agenesis -> pulmonary hypoplasia
CPAM
Pulmonary lymphangiectasia
CDH
Tracheo/bronchomalacia
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42
Q

Abnormal development in cannalicular phase

A

Renal dysplasia and pulmonary hypoplasia
Alveolar capillary dysplasia
Surfactant deficiency

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43
Q

Abnormal development in saccular phase

A

Oligohydramnios and pulmonary hypoplasia
Alveolar capillary dysplasia
Surfactant deficiency

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44
Q

Abnormal development in alveolar phase

A

Lobar emphysema
Pulmonary hypertension
Surfactant deficiency

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45
Q

Tracheoesophageal fistula

A

M&raquo_space; F
1:2500 births
Due to incomplete fusion of TE folds in embryonic phase
Five types

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46
Q

Bronchopulmonary sequestration

A 
Mass of abnormal pulmonary tissue
Not connected to tracheobronchial tree
Blood supply from aorta
No gas exchange
COMPLETELY ABNORMAL
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47
Q

Intralobular BPS

A

Within visceral pleural lining of lobe, most often LLL

Present with recurrent pulmonary infections

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48
Q

Extralobular BPS

A

Outside pleural lining, has own pleural sac
Associated with CDH
Most asymptomatic, some become infected

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49
Q

Bronchogenic cyst

A

Abnormal budding & branching of tracheobronchial tree
Most in mediastinal area
Neonates there can be a one-way valve between the cyst and the bronchial tree
Can get rapid expansion & CV compromise/death
Can fill with serous fluid and enlarge over time
On chest x-ray there is no lung parenchyma appears clear dark/black

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50
Q

Congenital lobar emphysema

A

Usually upper/middle lobe
Becomes overinflated and causes compression of other lobes/mediastinum
Most cases caused by partial bronchial obstruction
- extrinsic: pulmonary vessels, excessive pulmonary flow
- intrinsic: defects in bronchial cartilage leading to collapse and distal air trapping

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51
Q

Pulmonary aplasia

A

In embryonic phase - lung bud fails to partition

Only rudimentary bronchi are present which end in a blind pouch

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52
Q

Lung volume in lung hypoplasia

A

<2/3 of normal lung volume

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53
Q

Causes of pulmonary hypoplasia

A 
Renal agenesis/dysplasia
Urinary outlet obstruction
Anhydramnios/PROM
CDH
Large pleural effusions
Neuromuscular abnormalities
Aneuploidy
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54
Q

Bronchiolar and alveolar cysts

A 
Communicate with proximal branches of bronchiolar tree and alveolar ducts
Restricted to single lobe, well defined
Fluid +/- Air filled
R>L lung
Lower lobes>upper lobes
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55
Q

CPAM

A

Lung immaturity and malformation of airways/lung parenchyma
25% of all congenital lung lesions
5 types - type 1 most common (>1 cyst 3-10 cm)
Frequently diagnosed on prenatal ultrasound
Small CPAMs may present with recurrent infections

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56
Q

Alveolar capillary dysplasia (ACD)

A

Inadequate vascularization of alveolar parenchyma -> reduced number of capillaries in alveolar wall
Pulmonary lobules can be malformed
Pulmonary veins are frequently misaligned
Presents as PPHN early, 10-15% can present at 2-6 weeks of life
Due to failure of fusion of double capillary network
Diffuse disease in 85% of patients

57
Q

Congenital pulmonary lymphangiectasis

A

Extremely rare, males 2:1

Dilated pulmonary lymphatics, chylothorax

58
Q

CDH

A

1:2200-4000 births
85% on left side, 1% bilateral
Posterolateral (Bochdalek, more common) or central (Morgagni) defects in diaphragm
20-60% have multiple anomalies
Frequently have pulmonary hypoplasia and PPHN
Severity related to size of defect, early onset in gestation, presence of liver

59
Q

CDH severity assessment

A 
Observed/expected LHR (lung area/head circumference)
- Extreme < 15%
- Severe 15-25%
- Moderate 26-35%
- Mild 36-45%
Lung/chest transverse diameter ratio
Fetal liver in chest
Fetal lung volume by MRI/US
Size of pulmonary artery
60
Q

Surfactant

A

Made up of highly organized lipids and surfactant proteins

Reduces surface tension, regulates surfactant structure/metabolism, enhances host defense

Decrease surface tension: saturated phosphatidylcholine, surfactant proteins B & C

61
Q

Advantages of surfactant

A

Low surface tension increases compliance and reduces work of breathing

Stabilizes alveoli

Keeps alveoli dry by reducing transudation of fluid

62
Q

Surfactant composition

A 
Disaturated phosphatidylcholine (DPPC) = 40%
Monounsaturated PC = 25%
Protein = 10%
Phosphatidylglycerol = 8%
Other = 8%
Neutral fat = 5%
Cholesterol = 4% 
63
Q

Surfactant life cycle

A

Starts in endoplasmic reticulum (ER) of type 2 cell
Goes to Golgi body
Forms a lamellar body and adds proteins/lipids/ABCA3 transporter
Forms tubular myelin
Stretches across surface of alveolus
Then destroyed by alveolar macrophage or recycled

64
Q

Surfactant deficient lungs (RDS)

A

Stiff lungs = Low compliance
Increased WOB
Atelectasis/low lung volumes
Alveoli filled with transudate 2/2 lack of stretch
Gas diffusion block -> hypoxia and hypercapnia
PPHN

65
Q

Variables that impact distribution of surfactant

A 
Gravity
Volume of instillation (larger better)
Speed of instillation (faster better)
Surfactant type
Fluid volume in lung (helps early on, surfactant spreads more quickly/evenly)
66
Q

Phosphatidylglycerol test for fetal lung maturity

A

Appears at 35 weeks
If it is in the amniotic fluid the lungs are mature
Requires thin layer chromatography

67
Q

Lamellar body count for fetal lung maturity

A

10,000-200,000/mL
>45,000 = mature lungs
Requires infrared spectroscopy

68
Q

Fetal lung maturity testing

A

High sensitivity for diagnosing maturity (90%)
Lower specificity (60-80%)
Mature -> high PPV
Immature results -> accurate prediction of RDS only 30-50% of time

69
Q

L/S ratio

A 
Sphingomyelin: General membrane lipid
Lecithin (phosphatidylcholine)
- <0.5 at 20 wks
- 1 at 32 wks
- 2 at 35 wks
Not good with contaminated specimens
Long turnaround time
70
Q

Surfactant protein A

A

Hydrophilic
Gene on chromosome 10
Involved in tubular myelin and host defense

71
Q

Surfactant protein D

A

Hydrophilic
Gene on chromosome 10
Involved in surfactant lipid homeostasis, host defense, antioxidant
No human diseases found

72
Q

Surfactant protein B

A

Hydrophobic
Gene on chromosome 2
Involved in surface tension reduction, tubular myelin, type 2 cell functions

73
Q

Surfactant protein C

A

Hydrophobic
Gene on chromosome 8
Involved in surface tension reduction, film stability

74
Q

ABCA3 mutations

A

Autosomal recessive
30-40% of all refractory acute respiratory failure in a newborn
Most severe forms need lung transplant
Less severe forms can respond to steroids

75
Q

SP-B Deficiency

A

Autosomal recessive
Presents as term RDS
Lethal
No lamellar bodies, no tubular myelin, no surfactant function
No sustained response to exogenous surfactant
Treatment requires lung transplant

76
Q

SP-C Deficiency

A 
Autosomal dominant
50% de novo mutations
Chronic lung disease of infancy
RDS, nonspecific interstitial lung disease
Treatment is lung transplant
77
Q

Alveolar proteinosis

A

GM – CSF signaling

78
Q

Dead space

A

Physiological = anatomic + alveolar

Calculated by Bohr equation

79
Q

Comparison of lung mechanics (adult vs neonate)

A

Neonate

  • Inc RR
  • Inc MV
  • Inc alveolar ventilation
  • Inc oxygen consumption

Adult

  • Inc TV
  • Inc total lung capacity
  • Inc inspiratory capacity
  • Inc Vital capacity
80
Q

Hypoxic pulmonary vasoconstriction

A

Tries to keep ventilation and perfusion matched
Blood vessels constrict so that blood isn’t going to alveoli that are not ventilated
Normal physiology

81
Q

Pulmonary Vascular resistance and lung volume

A

PVR is lowest near FRC
Increases at both high and low lung volumes
-> septal capillaries in alveolar walls are stretched -> diameters reduced

82
Q

PPHN due to Maladaptation

A

Pulmonary structure normal but PVR elevated

  • hypoxia
  • hypothermia
  • hyperviscosity
  • pneumonia
  • meconium aspiration
  • sepsis
83
Q

PPHN from Maldevelopment

A

Abnormal pulmonary structural development
Smooth muscle hypertrophy
- intrauterine hypoxia, fetal ductal closure
Decreased total pulmonary artery cross-sectional area
- pulmonary hypoplasia (CDH, congenital)
- Alveolar capillary dysplasia

84
Q

PPHN

A

Usually in term or post-term infants
Single S2
Pre- and post-ductal saturation differential if PDA present due to R ->L shunting
Suspect if hypoxic and failing to respond as expected
- for every 1% increase in FiO2, PaO2 to should increase by 7

HFV plus iNO is better than HFV or iNO alone in severe PPHN

85
Q

Factors affecting diffusion

A

Diffusion distance

  • immature lung
  • interstitial edema or emphysema

Area for diffusion

  • atelectasis
  • pulmonary edema
  • immature lung
  • new BPD

Partial pressure gradient
- alveolar MV
- PaCO2


86
Q

Factors affecting anatomical dead space

A 
ETT size
ETT length
Flow sensor
Suction apparatus
Acquired tracheomegaly
End tidal CO2 detector
87
Q

Factors affecting alveolar dead space

A

Hyperinflation
Heterogenous inflation
Decreased pulmonary blood flow

88
Q

Causes of elevated PaCO2

A

Decreased tidal volume - decreased lung compliance, increased airway resistance, decreased patient effort

Increased physiologic dead space - added instrument, overinflation

Diffusion block - pulmonary edema

Loss of surface area - atelectasis, alveolar edema

Increased CO2 production - fever, sepsis, cold stress

89
Q

Beneficial effects of acidosis

A
  • increased respiratory drive
  • increased release of oxygen
  • increased ionized calcium
  • dilation of small airways
  • improved V/Q matching
  • increased sympathetic tone (inc HR, inc contractility)
90
Q

Hypoxemia

A

Decreased oxygen tension (PaO2)

91
Q

Hypoxia

A

Decreased oxygen delivery to the tissues

92
Q

Factors that affect mean airway pressure

A

PEEP (biggest)
PIP
IE ratio
Rise time/flow

93
Q

Right shift on oxyhemoglobin dissociation curve

A

Decreased oxygen affinity

Increased temperature
Acidosis (inc H, inc pCO2)
Increased 2,3-DPG

94
Q

Left shift on the oxyhemoglobin dissociation curve

A

Increased oxygen affinity

Decreased temperature
Alkalosis (decreased H and pCO2)
Decreased 2,3-DPG
Fetal hemoglobin

95
Q

Bohr effect

A

Increased PCO2 leads to more unloading of oxygen from hemoglobin

96
Q

Haldane affect

A

Deoxygenation of blood increases its ability to carry CO2

97
Q

Type I pneumocytes

A 
Shaped like a fried egg
Spread thinly across the alveolar surface (covers 90%)
Fewer number of cells in alveolar lining
Important role in gas exchange
Derived from type II cells
98
Q

Type II pneumocytes

A

Cuboidal shape
Covers 10% of alveolar surface
Greater number of cells in alveolar lining
Important role in surfactant metabolism and secretion
Progender to type I cells

99
Q

Total respiratory system resistance

A

Chest wall 25%
Airway 55%
Lung tissue 20%

50% of airway resistance is contributed by resistance in the nasal passages

100
Q

How much FLF is actively secreted every day?

A

250-300 ml/day

101
Q

Average fetal lung volume

A

20-30 mL

102
Q

What medication inhibits the secretion of fetal lung fluid?

A

Bumetanide

103
Q

What medications inhibit absorption of FLF?

A

Na/K-ATPase inhibited by Ouabain

ENaC inhibited by amiloride

104
Q

FLF clearance prior to labor

A

35% cleared during days prior to birth

  • decreased secretion via decreased Cl secretion
  • increased Na transport from alveolar space (ENaC)
  • increased lymphatic oncotic pressure
105
Q

FLF clearance during labor

A

30% cleared

  • ENaC - active Na reabsorption
  • hormones increase Na uptake (epinephrine, glucocorticoids, vasopressin, aldosterone)
106
Q

How much FRC is established in the first hour after birth?

A

80-90%

107
Q

Early stages of lung development

A

Embryologic and pseudoglandular

Branching morphogenesis occurs

108
Q

Middle stages of lung development

A

Canalicular and saccular

  • terminal unit capable of gas exchange
  • type 2 -> type 1 cell differentiation
  • capillary bed formation
109
Q

Mutations on FGFR2

A

Pfeiffer, Apert, Crouzon (laryngomalacia, tracheomalacia, lobar atresia, pulmonary aplasia)

110
Q

Angiogenesis during lung development

A

Proximal development, new blood vessels from previous ones

111
Q

Vasculogenesis during lung development

A

Distal vessels form from blood lakes in mesenchyme

Linked with angiogenesis during pseudoglandular phase

112
Q

Stimulation of alveolarization

A

Vitamin A

Thyroxine (T4)

113
Q

What is tracheoesophageal fistula associated with?

A

VACTERL

Esophageal atresia

114
Q

What is the most common type of TEF?

A

EA with distal TEF

115
Q

Pulmonary agenesis

A

Embryonic phase - lung bud fails to partition

Complete absence of one or both lungs including bronchi, bronchioles, and vasculature (if unilateral has hyperplasia of contralateral lung, no clinical consequences)

116
Q

Primary congenital pulmonary lymphangiectasis

A

Fatal, a/w Noonan, Ulrich-Turner, T21

  • Present with RDS and pleural effusions
  • failure of normal regression of lymphatic channels in fetal lung (20 wk)
  • Hemihypertrophy and lymphedema may be present
117
Q

Secondary congenital pulmonary lymphangiectasis

A

Associated with CDH

  • HLHS, Cor triatriatum
  • thoracic duct agenesis
  • TORCH infections
118
Q

Fetal lung testing specimens

A

Most tests are affected by quality of the amniotic fluid specimen
Ideal is from amniocentesis
Vaginal pool specimens after ROM can be unreliable

119
Q

ABCA3

A

ATP – binding cassette transporter A3 (ABCA3)
Type 2 cells
Critical for formation of lamellar bodies and surfactant function

120
Q

Anatomical dead space

A

Gas in the conducting areas of the respiratory system, air does not come into contact with the alveoli

121
Q

Alveolar dead space

A

Air contacting alveoli without blood flow in their adjacent pulmonary capillaries
Ventilation without perfusion

122
Q

Echo findings in PPHN

A 
Structurally normal heart
R->L shunting
Flattening or bowing of the IVS
Tricuspid regurg
Must see all 4 pulmonary veins to rule out TAPVR
123
Q

Negative effects of acidosis

A
  • increased PVR
  • cerebral vasodilation
  • increased intracranial pressure
  • decreased cardiac output
  • hyperkalemia
  • altered cellular energy and enzyme functions
124
Q

Exudative effusion

A

pH <7.4
WBC >1000
LDH >200

125
Q

Transudative effusion

A

pH >7.4
WBC <1000
LDH <200

Chylothorax fluid - classically appears milky with >80% lymphocytes, elevated triglycerides, xanthochromia

126
Q

Is CPAM connected to tracheobronchial tree?

A

Yes

127
Q

Blood supply for CPAM?

A

Pulmonary vessels

128
Q

Location preference for CPAM

A

Slight predilection for lower lobes

R = L

129
Q

Ouobain

A

Inhibits Na/K-ATPase, decreased FLF absorption

130
Q

Amiloride

A

Inhibits ENaC channels

131
Q

Which surfactant protein is most abundant?

A

SP- A

132
Q

What happens if you knock out FGF10 during lung development?

A

Complete agenesis of lungs with only trachea visible

133
Q

Alveoli present at birth

A

50-150 million

134
Q

Composition of fetal lung lymph and plasma

A

Lower Chloride 107
Higher pH 7.31
Higher protein 3.27
(Than fetal lung fluid)

135
Q

Effect of antenatal corticosteroids on fetal lung fluid

A

Increases absorption of FLF

Increased expression and activity of ENaC channels

136
Q

Lung:body weight ratio for lung hypoplasia

A
  • <0.015 <28 weeks

- <0.012 >28 weeks

137
Q

Lung DNA content for lung hypoplasia

A

<100 mg/kg body weight

138
Q

Lung weight (for lung hypoplasia)

A
  • <1kg = 15g/kg

- >1kg = 12g/kg

Neo Board Review MAP (18 decks)

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