Respiratory Flashcards

1
Q

3 factors (pathophys) leading to RDS

A

decrease lung volume
decrease FRC
decrease compliance

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2
Q

A chest x-ray may show hyperinflation, prominent perihilar vascular markings, edema of interlobar septae, or fluid in the fissures. What is diagnosis?

A

TTN

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3
Q

Adenosine leads to increased or decreased apnea?

A

leads to increased apnea
caffeine competitive antagonist for adenosine, and less apnea when caffeine is used

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4
Q

airway resistance is comprised of what 3 components?

A

Chest wall resistance (25%), airway resistance (55%), lung tissue resistance (20%)

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5
Q

At what embryological stage would CDH occur?

A

Before 10th week
due to failure of pleuro-peritoneal closure

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6
Q

At what embryonic stag is lung considered viable?

A

Cannicular

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7
Q

Does airway resistance increase or decrease with postnatal age?

A

Increases

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8
Q

does high or low PcO2 lead to increase IVH risk?

A

both do

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9
Q

name 5 ways caffeine helps

A

decreases hypoxic depression of breathing
decreases periodic breathing
improves CO2 sensitivity
increased diaphragmatic activity
increases minute ventilation

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10
Q

How is oxygen content determined?

A

can be calculated by adding amount of O2 bound to hgB ot the amount of dissolved O2 in blood

(1.34 ml O2/ghb x hgb (g/dl) x 02 sat ) + (.002 x paO2)

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11
Q

How is surfactant synthesized?

A

Predominantly Choline incorporation pathway, induced by steroids, cAMP or beta agonists

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12
Q

Meconium aspiration releases which chemical vasoconstrictors?

A

endothelin-1, thromboxane A2 and prostaglandin E2

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13
Q

Name 3 physical factors of lung development

A

Lung Fluid: Promotes growth through chronic stretch (due to pressure)
Fetal breathing (increased pressure when coupled from upper airway contractions)
Peristaltic airway contractions (pressure on distal buds)

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14
Q

name 5 things that can cause pulmonary hypoplasia

A

Renal agenesis
urinary outlet obstruction
loss of amniotic fluid (PPROM)
CDH
Large pleural effusions

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15
Q

name some factors associated with delayed lung maturation

A

Diabetes, Rh isoimmunoization with hydrops, 2nd born twin, c-section

mediated by insulin, androgens, and transforming growth factors

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16
Q

New BPD vs old BPD

A

new BPD interferes with luing development

old BPD is caused by direct injury to lungs

new BPD have decrease in alveolar septation, and microvascular development
(arrest of pulmonary alveolarization, with increased alveolar deimateres and fewer alveoli)

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17
Q

pressure controlled ventilation what happens when compliance increases?

A

Tidal volume increases, PIP, stays same

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18
Q

Volume targeted ventilation what happens when compliance increases

A

pressure drops (PIP), and TV stays same

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19
Q

What abnormalities might you see in Pseudoglandular phase of lung development, if something is amiss?

A

BRANCHING ABNORMALITIES OF LUNG

bronchogenic cysts
CDH
Congenital lobar emphysema
Cystic adenomatoid malformations

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20
Q

what are 5 variables that impact distribution of surfactant

A
  1. gravity (position of lung)
  2. volume of instillation
  3. Speed of instillation
  4. Surfactant type and properties
  5. Fluid volume in lung
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21
Q

what are benefits of permissive hypercapnia?

A

need for less MV
less lung injury
direct protective effect of lung
neuroprotection
ensures maximal respiratory drive
less danger of hypocapnia

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22
Q

What are the hydrophilic surfactant proteins

A

Sp-A Tubular Myelin
sp-D Surfactant lipid homeostasis (host defense)

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23
Q

What are the hydrophobic Surfactant proteins?

A

SP-B Type II surface tension reduction
SP-C tension reduction film stability

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24
Q

What information does the alveolar-arterial (A-a) gradient provide?

A

provides information about whether the lungs are transferring oxygen from atmosphere to pulmonary circulation.
the larger the A-a gradient, the poorer O2 transfer

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25
Q

What is a pulmonary artery sling?

A

anomalous origin of the left pulmonary artery from right pulmonary artery

LPA supplies left lung goes posterior to trachea, and anterior to esophagus
LPA aberration compresses distal trachea, and right mainstem bronchus

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26
Q

What is ABCA 3 Transporter?

A

ATP Binding cassette protein that helps with transport of lipids
Autosomal recessive,
30-40% of all refractory acute respiratory failure
abnormal accumulation of lamellar bodies in type 2 cells, and inablity to transport to surface

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27
Q

what is hyperoxia test?

A

determining if low O2 sats are due to Cardiac or Respiratory reasons
if paO2 >100, it’s respiratory

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28
Q

What is physiological deadspace, and how can it be calculated?

A

Anatomical dead space (gas in conducting areas of respiratory system) does not come into contact with alveoli +
Alveolar dead space (air contacting alveoli without blood flow in adjacent pulmonary capillaries)

can be calculated by Bohr equation

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29
Q

What is the Haldane effect

A

Decrease in hgb Saturation
enhances removal of CO2 from oxygen

increased Hgb Saturation decreases its ability to carry CO2
promotes dissociation of CO2 from hgb in oxygen rich capillaries of lungs

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30
Q

What is the most sensitive test for evaluating phrenic nerve injury?

A

ultrasound

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31
Q

What respiratory measurements are increased in neonates compared to adults

A

Respiratory Rate
Residual Volume
Minute Ventilation
Alveolar Ventilation [(TV - dead space) x RR]

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32
Q

Where do majority of CDH take place?

A

They occur posteriorly and are a result of the failure of pleuroperitoneal membrane closure in utero.

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33
Q

Why is MCT formula recommended for patients with chyolothorax?

A

if lymphatic vasculature has been injured, the lymphatic vessels are not necessary for absorption of MCT

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34
Q

How does iNO work

A

increases soluble guanlyate cyclase, which increases cyclic GMP

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35
Q

What do you see in all patients with Congenital Lobar emphysema?

A

hyperinflation of affected lung segment

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36
Q

Best way to position infant with PIE

A

on affected side lateral decubtius, allows unaffected lung to oxygenate

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37
Q

Reciprocal of time constant is equal to what in flow volume curve on vent?

A

slope of exhalation

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38
Q

What is reciprocal of compliance?

A

elastance?

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39
Q

What is reciprocal of conductance?

A

resistance

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40
Q

How is resistance represented on flow volume curve?

A

Resistance is represented by the distance from the slope of the curve to the outer portion of the loop

When resistance to flow is increased, the distance will increase and the loop will become wider

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41
Q

Which aortic arch derivates stick, of the 6?

A

3, 4, 6
pulmonary structures arise from 6th arch

42
Q

Do antenatal steroids improve alevorization?

A

No, but they do increase surface area
and they do increase surfactant production

43
Q

Time constant measures what?

A

resistance x compliance
time required for inflation for deflation by 63%

44
Q

Embryologically where do lungs derive from

A

from ventral bud of esophagus

45
Q

Type I pneumocytes differ from Type 2 pneumocytes how

A

Type 1 cover alveolar surface, help in gas exchange,
Type 2 mainily in alveolar lining (only 10% of surface), and play role in surfactant metabolism

46
Q

Boyle’s Law

A

P1V1 = P2V2
as pressure of a gas decreases, the volume in that space increases

47
Q

Chemoreceptors on medulla respond to what kind of changes?

A

Changes in CO2, increase in H
There are no O2 sensors in medulla

48
Q

Peripheral chemoreceptors are located where?

A

carotid and aortic bodies
they responde to decrease in PaO2, and increase in PaC02

49
Q

Alveolar Ventilation equation

A

Va= (Tidal volume- dead space) x RR

50
Q

Va/Q >1
(the ____________ effect)

A

excessive ventilation and blood from that area in lung will have high PaO2 and low PaCO2
dead space effect

51
Q

Va/Q <1
(the __________ effect)

A

some gas exchange, but lower than normal PaO2 and higher PaCo2
(shunt effect)

52
Q

What kind of blood is intrapulmonary shunt

A

any blood that goes through systemic circulation without going through ventilated lung region.

53
Q

What is anatomic dead space?

A

areas of lung, not involved in gas exchange

54
Q

What is physiologic dead space?

A

WASTED VENTILATION
anatomic deadspace + alveolar dead space

55
Q

What does the Bohr equation measure?

A

Physiologic dead space

56
Q

Bohr equation

A

[Arterial CO2- Expired CO2/(Arterial CO2) ] x tV

57
Q

Poiseuille’s law

A

length x viscosity /radius to 4th power

58
Q

bronchoconstriction increases or decreases dead space?

A

decreases

59
Q

What is equation for elastance?

A

inverse of compliance
change in pressure/ Change in volume

60
Q

hypoxemia vs hypoxia

A

hypoxemia is low O2 in blood (not necessarily reflective of O2 sat)
hypoxia is low O2 in tissues

61
Q

What does A-a gradient measure?

A

how well lugs are transferring O2 from atmosphere to pulmonary circulation?

62
Q

Calculation of A-a gradient

A
63
Q

Equation for O2 Delivery

A

Cardiac Output x O2 content

64
Q

Fick Principle

A

O2 consumption in blood is difference between O2 delivered to tissues (arterial blood) and blood returning form tissues (venous blood)

65
Q

O2 consumption equation

A

VO= 1.34 x (hgb) (arterial O2 sat - venous O2 sat)

66
Q

If O2 delivery is decreased to tissue, how will body compensate?

A

Increase O2 extraction (less venous O2)
Recruiting more capillaries

67
Q

What is Haldane effect

A

Changes im CO2 binding to Hb based on amount of O2

68
Q

Haldane effect on tissues

A

O2 is removed from Hb, thus greater amount of CO2 can bind to Hb

69
Q

Haldane effect on lungs

A

binding of O2 to hb in alveolar capillaries increases CO2 unloading from capillary to alveoli.

70
Q

Co2 elimination is dependent on

A

Alveolar minute ventilation (Resistance, compliance, time constant)
Diffusion across alveolar capillary membrane ( distane between alveoli and capillaries)

71
Q

What decreases if you increase PEEP

A

TV will decrease, but if you increase PIP by same TV remains same

TV decreases because you reduce pressure gradient

72
Q

which manipulation of vent parameter will increase O2 and decrease PcO2

A

increasing flow

73
Q

Benefits of VV ECMO?

A

spares carotid artery
lower risk of arterial emboli

74
Q

Benefits of VA Ecmo

A

provides respiratory and cardiac support
can use femoral vessels

75
Q

HFJV requires ________ time for gas to get OUT of lungs?

A

MORE

76
Q

HFOV requires __________ time for gas to get IN to lungs

A

MORE

77
Q

Why are majority of infants asymptomatic with pneumomediastinum?

A

because air is seldom under tension

78
Q

What causes a pulmonary hemorrhage

A

acute increase in capillary hydrostatic pressure
(From L to R shunting of PDA, or vasoconstriction from illness)

79
Q

How to manage pulmonary hemorrhage

A

increase PEEP, to impede pulmonary blood flow

80
Q

What is more worrisome, inspiratory stridor, biphasic stridor or Expiratory Stridor?

A

Expiratory stridor
(region narrows during expiration)
Tracheomalacia, tracheal stenosis
Vascular rings, mediastinal mass

81
Q

How do you diagnose vascular ring?

A

barium swallow (might show indentation in esophagus)

82
Q

LHR < 1.0 good or bad prognosis in CDH

A

bad

83
Q

How do you distinguish between Pneumothoraces and Congenital Lobar emphysema on xray?

A

both have hyperinflated lobe and mediastinal shift, but in CLE, lung markings will extend to the periphery

84
Q

Most affected lob in Congenital Lobar Emphysema

A

left upper lobe > right middle lone> right upper lobe

85
Q

How do CPAMs differ from bronchopulmonary sequestrations?

A

blood supply from pulmonary circulation
CPAMS also have communication with tracheo-broncial tree

86
Q

What types of CPAM have most favorable prognosis

A

Types 1 and 4
(2 and 3 usually associated with other morbidities, syndromes TEF etc)

87
Q

What leads to lymphagneictasia?

A

failure of lymphatic vessel regression at 20 weeks gestation, or lymphatic obstruction

88
Q

Is Extralobar or intralobar sequestration more common in neonates?

A

extralobar, but overall intralbor more common in general population

89
Q

where are majority of extralobar sequestrations located?

A

mainly left side between lower lobe and diaphragm

90
Q

Prognosis of Alveolar-capillary dysplasia

A

poor, respiratory failure in first 48 hours

91
Q

Pulmonary veins are misaligned, and inadequate vascularization of alveoli with decreased number of capillaries adjacent to alveoli

A

Alveolar-capillary dysplasia

92
Q

What does Guanyl Cyclase do?

A

with NO increases cyclic GMP

93
Q

In what CHD legion might you see WPW

A

Ebstein’s anomaly

94
Q

What happens when there is an increase in resistance (either CLD&raquo_space;» or RDS) without a concomitant decrease in compliance, what happens to time constant?

A

time constant increases and takes longer for lung to empty

95
Q

If a ventilator does not allow for sufficient time for expiration what happens

A

lungs will have long time constant, and gas trapping occurs

96
Q

Where are most intrapulmonary sequestrations located?

A

posterior basal segment, mainly in left lung
blood supply by anomalous usually from aorta

97
Q

What is immediate goal in treatment of of hyperammonemia?

A

to remove ammonia
hemodialysis
allso

IV sodium benzoate and sodium phenylacetate will remove glycine and glutamate from body

98
Q

In Methemglobinemia what happens to Hgb?

A

Iron changes from ferrous (reduced) state to ferric (oxidized) state, decreasing ability of hemoglobin to bind O2.

99
Q

What happens during an intrathoracic obstruction?
(kind of sound)

A

Region narrows during expiration, expiratory stridor
tracheomalacia, tracheal stenosis, external compression (vascular ring)

100
Q

What happens during laryngeal obstruction?
(kind of sound)

A

region is fixed in size, larynx is narrowest part of airway, so this is the most common type of stridor
layrngomalacia, vocal cord paralysis

101
Q

With surfactant surface tension is greater in expiration or inspiration?

A

Lowest at expiration, highest at inspiration

102
Q

What are side effects of therapeutic hypothermia?

A

platelet dysfunction, decreased surfactant, pulmonary hypertension, vasoconstriction