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My board review cards > Respiratory Day > Flashcards

Respiratory Day Flashcards

from Pediatrix review

1
Q

ENaC is inhibited by what

A

Amiloride

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2
Q

Fetal lung fluid and aminoic fluid

A

lung fluid go to aminoic fluid but amnioci fluid don’t go to lung (small)

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3
Q

amount of FLF secreted daily

A

250-300ml/day in human (4-5ml/kg/hr in near term infants)

20-30ml/kg, similar to FRC.

pressure gradient 3-5 cm H2O across laryn. –> CPAP volume.

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4
Q

secretion FLF:
inhibit by what
Driven by what molecule

A

inhibit by: Bumetanide, beta adrenergics, vaspressin, epinephrine

Na-K-2Cl Tri-transporter and Chloride
channels (ClC2, CLCN2)

Cl

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5
Q

absorption of FLF by what channel
Driven by what molecule

inhibited by what medications?

A

Epithelial Na Channel (ENaC) (face alveolar lumen)
Na-K-ATPase (face blood)

Na

Inhibited by Amiloride.
Na-K-ATPase inhibited by Ouabain

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6
Q

FLF composition

A

rich in Na
rich in Cl
protein content is ZERO –> allow the fluid to be absorbed after birth
low bicarb
very acidic

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7
Q

FLF Clearance

Before Birth

During Labor

After Birth

A

35% cleared during days prior to birth (decrease secretion of FLF through decrease Cl secretion, increase Na transport from alveolar space, increase lymhatic oncotic pressure)

30% cleared during labor:
- ENac Channel, active Na absorption
From catecholamine surge, higher cortisol and thyroid hormone
- mechanical force compresse fetal chest
- epinephrine suppress FLF secretion (cl channels)

35% cleared postnatally: lung distention (↑transpulmonary pressure), ↑ Lymphatic oncotic pressure associated with low fetal alveolar protein, crying.

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8
Q

Fetal Breathing Movement
( not a good card)

A

occurs in discrete episode (resemble REM sleep in periods of low voltage crotical activity)
principle musles: diaphgragm and glottis.
later half of gestation 40-50% FBM alternates with complete apnea.
without breathing movement, lung cannot grow.

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9
Q

REM sleep in baby
(not a good card)

A

irregular breathing
loss of upper airway and intercostal muscle activity, leading to a greater risk of airway obstruction

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10
Q

what causes bradycardia after birth

(Maybe not a good card)

A

lack of pulmonary stretch
Asphyxia -> hypoxia -> carotid chemo-rectorps -> bradycardia.

In addition:
Periglottic stimulation -> laryngeal reflex (tickle vocal cord with suctioning, vocal cord close)

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11
Q

Lung inflation and vagal tone

A

lung inflation, -> decrease vagal tone -> increase heart rate

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12
Q

What are these respiratory reflexes:

Hering-Breur inflation Reflex

Parodoxical reflex of head

Hering-Breuer Deflation Relex

J receptor reflex ?

A

Hering Breur Reflex: Lung over-inflation leads to cessation of inspiration. Protective. increase with GA, strongest in first few months. NB>Adults (via pulmonary stretch receptor (on airway smooth muscle > medulla > vagal nerve )

Parodoxical reflex of Head
* Inhibition of Hering Breur reflex results in extended inspiration. initial NB breaths in term infant (parodoxical increase in diaphgramatic contraction during inflation)
* probably important in causing periodic deep sighs breath.

Hering-Breuer Deflation Relex:
increase in ventilatory rate with abrupt deflation of the lungs (i.e. pneumothorax)
associated with deep sign breath.
Help maintain FRC in infant’s

J Receptor Reflex: Juxta capillary receptors; Rapid shallow breathing (can be dissociated from chemoreceptor)

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13
Q

iNO
where does it come from and how does it work?

A

Arginine becomes NO (nitric oxide, using NO synthase)
iNO convert GTP -> cGMP (guanyl cyclase)

cGMP -> K+ channels -> vasodilation

Sildenafil block PDE5, whcih break down cGMP.
PDE5 = phosphodiesterase 5

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14
Q

what’s most rapidly depleted in neuronal injury and cell death.

A

Phosphocreatine most rapidly depleted

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15
Q

apoptotic cell death
vs.
necrotic cell death

A

caspases (in apototic cell death)
Cytochrome c released from mitochondria
activates caspase-8 & caspase-9

Initial hypoxia and glucose deprivation disrupts cellular
homeostasis and ATP depletion
* Loss of Na-K-ATPase, membrane depolarization, influx
of Na, Ca, and H2O
* Excess extracellular glutamate increases Ca entry
* Phospholipases, Xanthine oxidase, nNOS
* Cell swelling and death

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16
Q

what are some of scavengers (or lack of scanvengers) in oxidative stress

(might not be important?)

A

Lack of scavengers:
glutathione, SOD, catalase,
cholesterol

Radicals with unpaired electrons react with proteins, lipids and DNA producing oxidative damage

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17
Q

inflammatory damage from chorioamnionitis is due to what chemicals

A

release of cytokines like IL-6, IL-8, interferon gamma as well

(cause iNO production, vasodilation, capillary leak)
Temporal relationship to CP

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18
Q

Prolonged intrauterine hypoxia shows up as what in the cord gas

A

profound metabolic acidosis
BE high.

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19
Q

what stage in lung development is consider viable

A

canalicular

primitive alveoli = respiraotry bronchioles

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20
Q

lung buds is from what germ layer

A

endoderm

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21
Q

pulmonary arteries originated from what?
Pulmonary vein originated from what

A

6th pair of aortic arches
(also where PDA comes from, the 6th left arch, same as L pulmonary artery)

left atrium

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22
Q

Airway development under control of what signaling

A

Airway development under control by retinoic acid signaling

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23
Q

In pseudoglandular phase, what gene/signaling pathway control development

A

*Early branching is regulated by the insulin-like growth factor

*Cellular differentiation (ciliated, goblet, basal) under the control of FGF-10 and FGF-7
*Disruption of FGF-10 results in lung agenesis
*Excess FGF-7 leads to poor differentiation, resembles CPAM
*Mutations on FGFR2 –Pfeiffer, Apert, Crouzons – variety of defects (laryngomalacia, tracheomalacia, lobar atresia, pulmonary aplasia)
*Note: *FGFR3 = achondroplasia

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24
Q

what disease happened during Embryogenic stage of lung development

A

TEF
tracheal stenosis
laryngeal cleft
Bronchiogenic cyst

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25
Q

what disease happened during Pseudoglandular stage of lung development

A

CDH (7 weeks)
Congenital lobar emphysema (air trapping, mimic pneumothorax)
Bronchiogenic Cyst ?
Bronchopulmonary sequestration.
Pulmoanry Lymphangiectasia

CPAM (MOST COMMON CONGENITAL LUNG LESION, may. be reduced with steroid. may regress after 25 weeks, Cystic or adenomatous tissue lined with ciliated pseudostratified epithelium)

Scimitar syndrome (R pulmonary vein drains to IVC)

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26
Q

What disease happened during Canalicular stage of lung development

A

pulmonary hypoplasia
surfactant deficiency
alveolar capillary dysplasia
(FOXF 1 gene)

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27
Q

When does primary septa happen?

A

Saccular stage:
- terminal sacs / primitive alveoli form.
- sacs are separated from each other by primary septa (start of alveolarization)

Type I and Type II pneumocytes lines the wall.

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28
Q

what stage in lung development does double-capillary network first start to develop

A

Saccular stage:
walls between the sacs contain double capillary network

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29
Q

Congenital Pulmonary lymphangiectasis

A

*Extremely rare, males 2:1
*Dilated pulmonary lymphatics, chylothorax
*Associated with Noonan, Ulrich-Turner and Downs
*Primary – fatal , associated with syndromes
- Present with RDS and pleural effusions
- Hemihypertrophy and lymphedema may be present
*Secondary – associated with CHD
- HLHS, Cor Triatum
- Thoracic Duct Agenesis
- Infections (TORCH)

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30
Q

when does secondary septae form

A

alveolar stage

terminal sacs are separated by secondary septae (adult alveoli).
new double-capillary layers form –> remodeling to form mature single layer (blood-air barrier)

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31
Q

Surfactant’s predominant lipid
(also most abundant proportion of component)

A

DPPC:
disaturated phosphatidylcholine

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32
Q

what are the principle proteins in surfactant?
what about the rest of them?

A

SP-B and SP-C are the principle proteins
Hydrophobic.

SP-A and SP-D: these are hydrophilic. NO known human mutations.
A: tubular myelin formation and host defense
D: surface lipid homeostatis, host denfense, anti-oxidation

ABCA3 protein (ATP-Binding Cassette membra A3):
assist w/ transport of phospholipid into lamella bodies and involved in lamellar body formation
infant with ABCA3 deficiency does not have DPPC and PG, decreased lamella bodies.
AR, most COMMON known genetic cause of surfactant deficiency.

90% surfactant recycled

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33
Q

L/S Ratio

A

if L/S ratio > 2, lecthin/sphingomyelin ratio
marker of lung maturity
usually around 35 weeks

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34
Q

SP-B deficiency

A

Autosomal recessive.
Chromosome 2
present with: term RDS, unsustained response to surfactant.

no lamellar bodies, no tubular myelin or surfactant function.

fatal

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35
Q

SP-C deficiency

A

Autosomal dominant (50% de novo)
gene on chromosome 8.
C: Chronic lung disease of infancy (CPI)
RDS, ARDS, non-specific interstitial lung disease
ILD > RDS

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36
Q

ABCA3 Deficiency

A

Autosomal Recessive
Chromosome 16

critical for the formation of lamella body.
(can be seen under electromiscoscopy)
RDS > ILD

E/M: Small abnormal vesicles with electron dense inclusions. LB & TM in surfactant layer are absent. Excess LB in type II cells.

lamella body is where surfactant is stored.

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37
Q

Cystic Fibrosis

A

Autosomal Recessive (1:2500)
immunoreactive trypsinogen
increased Na absorption (dehydration of luminal content in gut)

Can have hypoChloremic metabolic alkalosis

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38
Q

what’s the next stage in management in vocal cord paralysis

A

MRI to exclude Chiari malformation.

Treatment: conservative

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39
Q

Boyles Law

A

P1V1 = P2V2
air flow from high pressure to low pressure
P: pressure
V: volume

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40
Q

What determines the type of gas flow (laminar vs. turbulent flow)

A

Reynolds Number

Laminar flow: molecules travel in straight line
Turbulent: branching airways and large airways. occurs at high rate of gas flow.

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41
Q

total respiratory resistance is the sum of what

A

Rrs (total respiratory system resistance) = lung tissue resistance (high in neonate, generate during inflation and deflation) + airway resistance (nasal) + chest wall resistance (decreased in premature infants)

Airway is the majority (55%, mostly nasal)

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42
Q

Time constance calculation
(IMPORTANT)

A

Time constant = resistance x compliance

R = delta P/delta Q
C = delta V/delta P

Time constance = delta V/ delta Q

take 3-5 TC for relatively complete inspiratory or expiratory phase. （or 3x TC to reach 95% equilibrium)

long TC = slow filling/emptying
(i.e. BPD, LGA w. normal lung)

Healthy infant TC = ~ 0.12s.
for RDS = ~ 0.05s.

larger animals has more compliance and higher time constance => larger baby, need longer iTime.

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43
Q

What is anatomic dead space, alveolar dead space, and physiological dead space

A

Physiological dead space = anatomic + alveolar

Vd/Vt = (PaCO2 - PeCO2) / PaCO2

Bohr equation

Vt = Va + Vd

Vd is dead space volume
Vt is tidal volume
PaCO2 is CO2 in arterial blood
PeCO2 is the partial pressure of CO2 in the expired air

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44
Q

where’s the respiraotry center in brainstem

A

Medulla and pons

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45
Q

PaCo2 affect what receptors in control of breathing

A

Central chemoreceptor in medulla oblongata

PcCO2 and H+

and peripheral chemo receptors (carotid and aortic bodies)

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46
Q

PaO2 affect what receptors in control of breathing

A

peripheral chemoreceptor in carotid and aortic arch

preterm has decreased response to hypoxia.

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47
Q

larger animal and time constant

A

larger animals has more compliance and higher time constance

TC = R x compliance

3x TC to reach 95% equilibrium.
larger baby, need longer iTime.

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48
Q

Fick’s Equation of diffusion

A

dQ/dt = k * A * dC/dl

49
Q

how to calculate alveolar minute ventilation

A

alveolar minute ventilation = alverolar tidal volume * RR
VTalv = Vt - Vds

MValv = VTalv * RR = VtRR - VdsRR
MV = Vt * Rate

50
Q

Alveolar-arterial gradient (A-a gradient)

A

PAO2 - PaO2 = FiO2 x (PB - PH2O) - PaCO2 / R - PaO2

PAO2 = FiO2 x (PB - PH2O) - PaCO2 / R

R = 0.8 (respiratory quotient)
PB = 760 mmHg (atmosphere), barometric pressure
PH2O = 47 mmHg

higher A-a gradient, poorer gas exchange
A-a gradient > 600 for 4-12 hours indicates need for ECMO

51
Q

Oxygen Content Calculation

A

Oxygen Content = Hgb x % sat x 1.34 + 0.003 x PaO2

venous 75% of arterial oxygen content.

52
Q

antenatal steroid work mechanism

A

Activation of ENaC channels
Induce production of surfactant proteins and lipid synthesis
Alter preterm respones to oxidative stress

53
Q

compliance calculation

A

compliance = delta V / delta P

54
Q

LaPlace’s Law

A

P = 2T/R

P is the pressure
T is surface tension
R: radius

55
Q

Jensen BPD criteria (2019)

A

No longer based on O2 requirement.
Low flow (< / = 2L), grade 1
High flow to nimv (> 2L) : grade 2
Intubate: grade 3

56
Q

does antenatal BMZ reduce BPD

A

No.

antenatal steroid helps mature the fetal lung primarily by decreasing the amount of mesenchymal tissue and increase potential airspace volumes.
These anatomic changes result in an arrest in alveolar (saccular) septation.

Also postnatal steroid arrest alveolar septation and microvascular development.

57
Q

physiological pulmonary HTN in fetus is mediated by what chemicals??

A

Mediated by Arachidonic acid, LOX, CYP450, Isoprostanes, Endothelin, Serotonin

58
Q

Medication for PPHN and their mechanisms

(need to work on it)

A

Three pathways to drop PVR:

  • Prostacyclin (PGI2)
    COX pathway
    cAMP (milrinone block PDE 3A, which break down CAMP, cleared by kidney)
  • Nitric Oxide (NO)
    cGMP (sildenafil block PDE 5, which breaks down cGMP, induces CYP, cleared by liver)
  • Endothelin (vasoconstrictor)
    Blocked by bosentan
59
Q

PaO2 > ? number can avoid hypoxic vasoconstriction

A

PaO2 >/= 50mm Hg will avoid hypoxic vasoconstriction

60
Q

PVR and its relationship to lung volume

A

PVR is lowest at FRC.
PVR increases at both high and low lung volumes

High lung volume:
- large vessel distend (resistance low)
- capillaries compress (resistance high)
- net effect: higher PVR (capillary compression wins out)

Low lung volume:
- positive intrapleural pressure
- capilaries dilated (resistance low)
- large vessels compressed
- net effect: higher PVR (large vessel compression wins out)

61
Q

renal agenesis happened in what stage of lung development

A

pseudoglandular

62
Q

balance between outward pull of chest wall and tendency of lungs to collapse determines what?

A

FRC

63
Q

Does surfactant helps in CDH

A

No

64
Q

what cardiac condition is contradicting for iNO

A

TAPVR

65
Q

Oxygenation Index Calculation

A

MAPx FiO2 / PaO2 (postductal) x 100

> 25 is considered severe lung disease.

66
Q

which side of diaphragm is more likely to be impacted in diaphragm paralysis

A

R side

in paralysis, diaphragm rise during inspiration and fall during expiration. The impacted side has less movement and chest appears more collapsed.

67
Q

oxygen content calculation

A

O2 content = 1.34 (ml O2/gHb) x Hb (g/dL) x O2 Sat + 0.003 x PaO2

68
Q

mechanisms of of HFOV (5 total)

A
  1. Bulk convection (bulk axial gas flow)
  2. Pendelluft effect (differential movement of gas as a result of different time constants)
  3. Taylor Dispersion (parabolic movement of the inspired gas that allows for increased area of diffusion)
  4. Molecular diffusion across alveolar gradients all factor in gas exchange
  5. Asymmetric velocity of gas during inspiration and expiration
69
Q

main difference between CPAM and bronchopulmonary sequestration (what are two typs of sequestration)

A

CPAM (most common type 1 and type 2): supply by pulmonary circulation

Bronchopulmonary sequestration:
receive blood from systemic circulation (aorta) and not connect to tracheobronchial tree.
might be associated with other anomalies.

Two types:

Intralobar
*Within visceral pleural lining of lobe
*Present with recurrent pulmonary infections
*Drains to pulmonary veins

Extralobar
*Outside pleural lining, has pleural sac
*May be above or below diaphragm (associated with CDH)
*May communicate with gut
*Mostly asymptomatic and noted at surgery, some become infected
*Drains to bronchial veins

70
Q

physiological change in pneumothorax:
PaO2, HR, CVP, pulse pressure, arterial blood pressure, cerebral oxygen delivery

A

decrease PaO2,
Increase HR, CVP (central venous pressure),
Decrease in pulse pressure, arterial blood pressure,
Decrease in cerebral oxygen delivery

71
Q

Flow Volume loops:
Describe the loop and associated disease in these conditions.
What’s x-axis and y-axis

A

x-axis volume, y-axis flow
Top expiration, Bottom inspiration

Restrictive Lung disease (sufactant deficiency, meconium aspiration) -> lung cannot expand to maximal volume

Obstructive Lung disease (Chronic lung disease) -> longer time to empty lung,expiratory line more scooped

Extrathoracic upper airway obstruction (vocal cord paralysis, laryngomalacia) –> flatten inspiratory phase

Intrathoracic upper airway obstruction (tracheomalacia, vascular ring) -> obstruction during expiratory phase while inspiratory loop is normal

Fixed upper airway obstruction (tracheal stenosis) -> flattening of both inspiratory and expiratory curves.

72
Q

Name the lesion locations of the following:

Congenital lobar emphysema
Pulmonary sequestration
CDH
bronchogenic cyst
CPAM unilobar
Scimitar syndrome

A

Congenital lobar emphysema (LUL > RML > RUL&raquo_space; LL)
Pulmonary sequestration (LLL > RLL)
CDH (L > R)
bronchogenic cyst (mediastinal)
CPAM unilobar (R > L, lower > Upper)
Scimitar syndrome (RLL)

73
Q

which type of CPAM is associated with other anomalies (renal, cardiac diaphragm).
Which one is most common

cystic or adenomatous tissue is lined with what cells?

A

Type 2 (and type 0, which is really rare)

Type 1, 4 have good prognosis.
Type 1 (most common)

peak size 25 week

Cystic or adenomatous tissue lined with ciliated pseudostratified epithelium

74
Q

poor CDH prognosis
(indicators)

Two type of defects

A

Lung-Head-Ratio (LHR) <0.85
*Liver in chest
*Low fetal lung volumes by MRI
*Low lung/chest transverse diameter ratio

Posterolateral (back… Bochblek? type) or Central
(failure of closure of pleuro-peritoneal fold)

75
Q

What formed during canalicular phase of lung development.

A

gas exchange units: respiratory bronchioles (from terminal bronchiole: end of conducting bronchial unit), alveolar duct, a few terminal sacs.
blood-air barrier forms: angiogenesis, prominent capillary meshwork within mesenchyme -> promote ability to exchange gas
surfactant synthesis began.

76
Q

Genetic regulation/signaling pathway in canalicular phase that promote surfactant expression

how is glucocorticoid help?

A
  • Thyroid transcription factor-1 (TTF-1) ^ expression of surfactant proteins

Thyroid hormones are required for development of the surfactant system.
–> thyroid is also from Endoderm

  • TTF-1, FOXa1, FOXa2, GATA 6 signal/control primitive cuboidal cells differentiate into type I and type II epithelial cells.
  • TGF beta Superfamily: linked to glucocorticoid signaling. => antinatal steroid help type II cell mature. (regulate cell proliferation, differentiation, migration, and extracellular matrix formation)

cortisol induce fetal lung fibroblasts > fibroblast pneumocyte factor > stimulate surfactant production.

77
Q

Alveolar capillary dysplasia:
what gene is implicated

A

FOXF1 gene

rare, fatal
reduced number of capillaries in alveolar wall
(inadequate vascularization of alveolar parenchyma),
misaligned pulmnary veins
PPHN early. 10-15% may present at 2-6 weeks after birth

77
Q

what molecule in surfactant is responsible for even spread of sufactant

A

PG
phosphatidylglycerol

77
Q

What factor regulate vascular development in lung development
what is angiogenesis and what is vasculogenesis?

A

Vascular endothelial growth factor (VEGF), 2 high affinity receptors (FLT 1 & FLK 1)

Angiogenesis: proximal development, new blood vessels from previous ones
Vasculogenesis: distal vessels from blood lakes in mesenchyme.

Linking of the two during Pseudoglandular phase

77
Q

what phase in lung development does renal agensis or dysplasia happen?

A

pseudoglandular (renal agensis)
canalicular (renal dysplasia)

78
Q

static lung compliance vs. dynamic lung compliance

A

static: change in lung volume / change in transpulmonary pressure with NO AIR FLOW. lowest at extremes of lung volumes. highest in the middle.

78
Q

chylo and exudate differences

A

Chyle: pH 7.4- 7.8. Triglyceride > 110 mg/dl.
Exudate: pH < 7.4. WBC > 1000, LDH > 200

78
Q

Comparing to adult lung, neonate respiration and lung volume have what? (increase vs. decrease)

A

Neonate have increased:
RR, minute ventilation, chest compliance, alveolar ventilator, oxygen consumption and residual volume (RV)

Adult have increase:
Tidal volume, lung compliance.
TLC, VC and IC (inspiratory capacity)

FRC and dead space are SIMILAR

79
Q

what is “new BPD”

A

Arrest in alveolarization or altered lung development
1) increase alveolar (saccular) diameters
2) fewer alveoli (saccules)
3) disruption of collagen network around the saccules
4) localization of elastin that is absent from site of future secondary septation

both increase and decrease platelet/endothelial cell adhesion molecule (PECAM) staining.

less PPHN, minimal fibrosis.
CXR showed cystic change, hazy, hyperinflation. (similar to cystic emphysema)

old BPD: due to barotrauma and oxidative stress/exposure.

80
Q

what heart condition is iNO contraindicated

A
  • Lesions dependent of R-L shunting (obstructive Left outflow tract): critical aortic stenosis, HLHS, interrupted coarctation.
  • TAPVR.
81
Q

caffeine mechanism of action

A

Adenosine A1 and A2A receptor blocker.
anti-inflammatory effect.
-> excitation of respiration neural output, increase sensitivity to CO2 .

Effect:
Neuro:
v central apean, v inflammation. ^ CO2 responsiveness, ^ cerebral cortical activity

Pulm:
^ MV, TV, diaphragmatic contractility, surfactant b protein transcription
v inflammation and fluid

CV:
^ cerebral blood flow, BP, RV output, SVC flow, LV stroke volume
v PDA requiring treatment

GI:
^ GER, time to regaining birthweight

82
Q

if venous sat (SpO2 in venous) starts to decrease, what does it mean

A

it means oxygen delivery is significantly compromised.

83
Q

diet in chylothorax

A

medium chain triglyceride

MCT is not required to be absorbed by lymphatic system.

84
Q

how to calculate FiO2 needed to keep PaO2 at different altitude

A

FiO2 x (PB - PH2O) = FiO2 x (PB2-PH2O)
PH2O = 47 mmHg
PB = 760 mmHg

85
Q

How does progesterone change breathing pattern

A

Progesterone increase breathing in pregnant women

86
Q

how to calculate respiratory resistance (R)

A

R = delta P / delta Q
(Ohm’s law)

R = (8 x viscosity x length) / (pi x r^4)

87
Q

what’s combined gas law

A

PV/T = P2V2/T2

T is TEMPERATURE.
V = volume
P = pressure

88
Q

Poiseulle’s law

A

Q = pi P r^4/8 x viscosity x length

89
Q

Oxygen delivery

A

O2 Delivery = O2 content x cardiac output

90
Q

are BPD patients bronchodilator responsive?

A

no

91
Q

BPD ventilator strategies

A

increase TV, increase iTime, provide good PEEP, decrease ventilator rate.

92
Q

elevated pulmonary vascular resistance in fetus is mediated by what chemicals

A

arachidonic acid, LOX, CYP 450, Isoprostanes, Endothelin, serotonin

93
Q

bugs in neonatal pneumonia

A

Early: GBS, E. Coli, Klebsiella, Listeria (fetal diarrhea)
*Late: add S. aureus, Pseudomonas, fungal, chlamydia
*Prematurity: Ureaplasma(worse BPD) –> cause of chorio

also common in asphyxia (due to gasping)

94
Q

why is meconium aspiration associated with air trapping

A

because meconium stick to wall of bronchiole and hard for air to get out.

95
Q

oxygen consumption

A

Ox consumption = V (dot) O2 = cardiac output x Hgb x (arterial O2 sat – venous O2 sat)

96
Q

effect of PaO2 on PVR

A

PaO2 below 50 mmHg, increase hypoxic vasoconstriction and increase PVR

97
Q

effect of PVR with acidosis

A

PVR increases with worsening acidosis

98
Q

sail sign on CXR

A

pneumomediastinum

99
Q

pneumothorax is air between what

A

air between parietal and visceral pleura

100
Q

what’s pulmonary interstitial empysema

A

premie with RDS. air leaks to interrstitial space. use HFV, reduce iTime and MAP

101
Q

CDH and brochopulmonary sequestration

A

they are associated

102
Q

The relationship of pressure and zones in the lung. PA, Pa, PV

Neonate operate at what zone

A

Zone I: PA > Pa > Pv
Zone II: Pa > PA > Pv
Zone III: Pa > Pv > PA
Zone IV: Pa > Pv

zone III

Can be at zone II or zone I during air trapping.

103
Q

V/Q and alveolar ventilation

A

V/Q is matched to alveorlar ventilation (VA) –> VA/Q
VA = (TV - dead space) x RR
PaCO2 is proportional to VA.
if double VA, PaCO2 halves

VA = alveolar ventilation

104
Q

V/Q = 0
V/Q < 1
V/Q > 1

A

V/Q = 0:
Anatomic shunt. VA = 0, Q is normal.

V/Q <1:
Intrapulmonary shunt. VA low. Q normal.

V/Q > 1:
VA= normal. Q = low or none.

V/Q = infinity:
anatomic dead space
Q is zero

105
Q

CO2 elimination and relationship to tidal volume in HFV

A

CO2 elimination is proportional to TV^2 in HFOV

106
Q

Bohr Effect:

Haldane Effect

A

Bohr effect: CO2 and H+ affect the affinity of the hemoglobin for oxygen.
Co2 bind, facilitate o2 unload. Oxygen delivery to tissue

Haldane effect is a phenomenon where an increase in PaO2 reduces the affinity of the hemoglobin to CO2

Gibbs-Donnan: the behavior of charged particles near a semi-permeable membrane that sometimes fail to distribute evenly across the two sides of the membrane.

Chloride shift: the movement of Cl(-) from the plasma into erythrocytes as blood moves from the arterial to the venous end of systemic capillaries.

107
Q

compliance and lung volume

A

compliance of lung is reduced at either atelectic lung or over distended lung.

108
Q

in premature infant, what is chest wall compliance (high or low) vs. lung compliance (high or low)

A

chest wall compliance: low
lung compliance: high.

109
Q

how does Na-K-ATPase pump help with fluid re-absorption?

A

establish Na gradient from alveolar lumen to respiratory cell.

located in basolateral cell membrane. transport Na from respiratory into the interstitium in exchange for K.

110
Q

what is a side effect of sildenafil and how long will it take to be effective

A

transient hypotension
2 week of therapy.

111
Q

diffuse or local linear or patchy infiltrate
consolidation or atelectasis
hyperaeration with or without air leak

what x-ray finding is this?

A

meconium aspiration

112
Q

Boyles Law
Charle’s law
Dalton’s law
Henry’s law

A

Boyles Law: PV= P2V2

Charle’s law: gas expand when warm and shrink when cold.

Dalton’s law: P toatal = P1 + P2 + P3…

Henry’s law: at constant pressure, any gas physically dissolved in a liquid in proprotion to its partial pressure

113
Q

end expiratory grunting,
nasal flaring,
tachypnea,
retraction,

+/- oxygen requirement

what is the condition? (term infant, no risk factors)
what is the xray finding?

A

TTN (most resolve by 48 hr but can be 2-5 days).

Perihilar streaking and fluid in the HORIZONTAL fissure.
(can also show pleural effusion and atelectasis)

114
Q

most abundant surfactant protein

A

SP-A

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