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NICU Board Review > Respiratory Flash Cards > Flashcards

Respiratory Flash Cards

1
Q

How does CPAP affect Laplace’s law?

A

P=2(surface tension)/radius

CPAP increases the radius and decreases the pressure needed to keep alveoli open

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2
Q

What are the 3 effects of CPAP in respiratory system?

A
  1. Increases transpulmonary pressure
  2. Reduced apnea by activating stretch receptors and preventing airway collapse
  3. Reduces collapsing alveoli by increasing FRC, larger TV, reduced VQ mismatch and improved compliance
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3
Q

What are the air dispersion mechanisms for HFOV?

A
  1. Convection: Bulk flow for proximal airways (convection)
  2. Convection and diffusion: Turbulent flow and Taylor dispersion (asymmetric flow velocities->mixing of inspiratory and expiratory flows)
  3. Diffusion: Penduluft & collateral ventilation (gas flows from alveoli with short time constant to alveoli with longer time constants)
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4
Q

Differences between HFOV and HFJV

  • is exhalation passive or active?
  • is I:E fixed?
  • is Vt dependent on frequency?
A 
HFOV 
CPAP system with piston displacement of gas 
Exhalation active 
Rate is Hz
I:E fixed
TV dependent of frequency (Hz)
HFJV
Jet pushes bursts of gas on top of conventional ventilator
Exhalation passive
Rate is breaths/min
IT is variable
TV independent of frequency/rate
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5
Q

What type of air flow does sigh breaths deliver on HFJV?

A

Bulk flow

conventional breath used to increase lung recruitment via augmenting bulk flow

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6
Q

How can mean airway pressure be adjusted on ventilator?

A

By adjusting PIP PEEP and insp times

Paw=(Ti x PIP) + (Te x PEEP)/ Ttot

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7
Q

Minute ventilation calculation

A

Minute ventilation=TVxRR

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8
Q

What are some of the issues when you set flow rate on the ventilator too low or high?

A

Usually 6-10 L/min

Low flow rates

  • might not allow to reach targeted pressures or volume
  • increases dead space ventilation
  • can cause air hunger

High flow rates

  • too rapid achievement of targeted P or V
  • increased turbulence->inc resistance and inadvertent PEEP
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9
Q

Time constant equation

How many time constants are needed to empty lungs?

A

Time constant=Resistance x compliance

3 time constants=95% empty

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10
Q

How does time constant differ between RDS and BPD?

A

Time constant is shorter in RDS because the compliance is much lower

Time constant is longer in BPD because of increased resistance

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11
Q

What are the reported advantages of volume targeted ventilation?

A
  1. Decrease in BPD
  2. Decreased rate of pneumothorax
  3. Less hypocarbia
  4. Decreased risk of IVH
  5. Decreased risk of PVL
  6. Shorter duration of MV
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12
Q

What is difference between volume control vs volume targeted?

A

Volume control constant preset Vt with pressure rising passively and cycles off after reaching peak volume. Doesn’t measure Vt reaching patient lungs.

Volume targeted is modification of PC ventilation delivering target Vt by adjusting pressure over time. Exhaled Vt more closely resembles flow reaching pt lungs

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13
Q

How does pulse oximetry detect arterial saturation sP02?

A

Looks at the differences in frequencies of light absorbed through light source and photo sensor during pulsation. Oxygenated Hgb absorbs infrared light and deoxygenated Hgb absorbs red light. Photosensor detects red light and therefore % is extrapolated to give SpO2.

Can have false readings w poor perfusion position difficulties and presence of other hemoglobin species

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14
Q

How does NIRS work?

A

Assesses regional tissue oxygenation through light of varying frequencies passing from source through tissue and to near-infrared detector sensors

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15
Q

For every 1mmHg change in PaCO2 we expect inverse change in pH of?

A

0.006

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16
Q

Anion gap calculation

A

Na -(Cl+Hco3)

Normal AG: 6-12
Elevated AG: lactate or ketones
Normal AG: renal losses GI, losses

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17
Q

Winters formula

A

Expected PaCO2= [1.5x(serum HCO3)] +(8+/-2)

Used in the case of primary metabolic disturbance to assess degree of resp compensation

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18
Q

What does Poiseuille’s law refer to?

A

Resistive pressure is relative to air viscosity and length of tube and inversely related to radius to power 4

R=8nL/pi r^4

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19
Q

What are the limitations (3) of ventilator graphics to asses pulmonary function?

A
  1. Not validated in ELBW infants
  2. Does not capture poor compliance in very distal airways
  3. Cannot accurately represent heterogenous lung disease
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20
Q

During inspiration what happens to cardiac output?

-How does systemic venous return and pulmonary venous capacitance affect this?

A

Cardiac output decreases
There is an increases venous return
Blood in R heart Increases displacing IV septum leading to increase RV stroke volume and decrease LV stroke volume
Pulmonary venous capacitance increases w negative intrathoracic pressure reducing return PV return to LA

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21
Q

What is the overall influence of respiration on cardiac output?

A

During inspiration there’s a transient BP decrease 2/2 decrease in CO that is physiologic and will equilibrate w increase in CO during expiration

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22
Q

What is pulsus paradoxus?

A

Exaggerated decrease in systolic pressure during inspiration

cardiac tamponade - there is R heart compression and decrease venous return during inspiration

Severe airway obstruction - more negative intrathoracic pressure—-> increase pulmonary capacitance and decrease left atrial return

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23
Q

How does alveolar vessel resistance and extraalveolar vessel resistance change with inflation and deflation?

A

Alveolar vessel resistance increases with inflation (decrease in radius and increase in length of vessels when alveolus is extended) while extraalveolar resistance decreases (intrapleural P decreases, transmural P increases->vessel dilated and R decreases

With deflation the opposite occurs

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24
Q

How does positive pressure ventilation affect pulmonary venous return and LV after load?

A

PPV increases alveolar pressure-> inc intrathoracic and intrapleural pressure
which in turn
-Decreases pulmonary venous capacitance lead to increased PV return
-Decreased aortic transmural pressure leads to decreased LV afterload

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25
Q

How does PPV affect the right heart vs left heart?

A 
Increases intrathoracic P
Decreases systemic venous return
Decreases RV preload 
Decreases RV stroke volume 
Increases RV afterload

Left heart
Increases pulmonary venous return
Increases LV stroke volume
Decreases LV afterload

right heart effects predominates therefore PPV decreases overall cardiac output

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26
Q

What are the 4 mechanisms for pulmonary edema according to starlings equation?

A
  1. Increased vascular hydrostatic P (ie LV dysfunction, pulmonary venous hypertension, volume overload)
  2. Decreased interstitial hydrostatic P (ie post-obstructive pulmonary edema)
  3. Decreased transmural oncotic P (decreased proteins ie poor nutrition)
  4. Increased permeability (sepsis, aspiration)
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27
Q

What is the mechanism of Nitric oxide?

A

In endothelial cell l-arginine is converted to NO via eNOS.

NO goes into smooth muscle cell and stimulates guanylate cyclase enzyme.

Guanylate cyclase converts GTP to cGMP which causes vasodilation of smooth muscle.

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28
Q

There is no data to support iNO use in which 3 populations?

A

Premature infants
Congenital heart disease
CDH

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29
Q

OI index

A

OI=MAPxFiO2/paO2

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30
Q

When should iNO be initiated?

A

To optimize lung recruitment

OI>25 or paO2 <100 despite 100% FiO2

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31
Q

Why is rebound effect noted in rapid weaning of iNO?

A

Inhibition of endogenous nitric oxide synthase (eNOS)

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32
Q

Risks associated with use of iNO

A

Formation of peroxinitrite which can lead to vasoconstriction and lipid peroxidation affecting surfactant function

Can be oxidized into nitrogen dioxide->causes methHgb, hypoxemia, pulmonary edema

Inhibits platelet aggregation

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33
Q

Contraindications of iNO use

A

Structural heart defects depending on right to left shunting

  • Critical AS
  • interrupted aortic arch
  • coarctation
  • HLHS

Obstructive TAPVR

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34
Q

Factors that decrease RDS risk?

A

Antenatal corticosteroids

Chronic intrauterine stress

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35
Q

How does RDS appear histologically?

A

Appear as an eosinophilic membrane that lines airspaces

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36
Q

Antenatal corticosteroids have been found to decrease the incidence of which diseases?

A

RDS
IVH
NEC
Neonatal death

Too many doses can be associated w fetal growth restriction

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37
Q

Porcine or bovine surfactant contain which surfactant proteins?

A

Surfactant proteins B and C

Phospholipids

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38
Q

What is the pathophysiology of TTN?

A

Delayed activation of fetal lung fluid clearance through

  • abnormal functioning Na/K atpase and eNac
  • lack of proceeding labor results in lack of trigger switch from secretory to resorptive processes in type II epithelial cells
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39
Q

Risk factors for TTN

A 
Male 
<38 weeks gestation
LBW
Macrosomia
Maternal diabetes or asthma
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40
Q

How to prevent TTN?

A

Avoid elective c/s prior to 39 weeks

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41
Q

What is the difference between congenital, early onset or late onset Pneumonia?

A

Congenital -intrauterine aspiration of infected amniotic fluid or trans placental transmission

Early onset-aspiration during or after birth of vaginal organisms or infected amniotic fluid (1st week)

Late onset-environmental, inhalation or nosocomial (>1 week)

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42
Q

What are the 2 signaling pathways that lead to vasodilation and decrease in PVR at birth in neonate?

A

Nitric oxide generation from l-arginine via eNOS which converts to GTP to cGMP via guanylate cyclase.

Prostacyclin signaling from arachidonic acid via COX 1 prostacyclin synthase which coverts ATP to cAMp via adenylate cyclase.

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43
Q

PPHN is characterized by 3 types

A

Maladaptation (MAS, pneumonia)
Maldevelopment (ACD)
Underdevelopment (hypoplastic)
Hypoplastic vasculature

CDH has hypoplastic and excessive muscularization

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44
Q

What is a normal A-a gradient in RA?

How about in 100% FiO2?

A

RA is 10-15

100% FiO2 is 80-100

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45
Q

An A-a gradient > what number is strongly suggestive of patient needing ECMO?

A

> 600

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46
Q

Sildenafil acts in which pathway?

A

It’s acts in the nitric oxide pathway

It inhibits PDE5 and therefore blocks the conversion of cGMP to its inactive form GMP

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47
Q

What is the pathophysiology of PIE?

A

Air dissects and gets trapped in the perivascular connective issue. In preterm infants this connective tissue is more abundant and less dissectible trapping air.

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48
Q

Does collateral ventilation occur in the alveolus in newborns?

A

No. Develops ~3-4 years and likely reason why more likely to get pneumothoraces with proximal obstruction or atelectasis

  1. Intraalveolar through the pores of kohn. (Not developed in newborns)
  2. Bronchioalveolar through the channels of Lambert
  3. Interbronchial through the channels of Martin
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49
Q

How does nitrogen washout theoretically help in pneumothoraces?

A

100% O2 decreases partial pressure of nitrogen in alveolus compared to the pleural space leading to diffusion of nitrogen out of pleural space.

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50
Q

Name the proven preventative management strategies for BPD?

A

Vitamin A
Caffeine
Less invasive surfactant administration (1 retrospective review)

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51
Q

What value is considered abnormal for a sweat chloride test to diagnose cystic fibrosis?

A

> 60meq/L of chloride

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52
Q

Name the early marker for pancreatic exocrine insufficiency in CF?

A

Low fecal elastase 1

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53
Q

Describe the complete spectrum for a patient with CF?

A

Pancreatic insufficiency (80-90%) > fat malabsorption and FTT
Chronic obstructive airway disease (90%)> bacterial overgrowth
Bilateral genesis of vas deferens (90%)>male sterility (not female)
Other: meconium ileus in newborn (in 15% of newborns w CF),
polyposis, mucocele, sinusitis, gastrointestinal cancer,
CF related diabetes if pancreatic fibrosis, osteoporosis
CFTR-related disorder = CFTR gene mutation
e.g., recurrent pancreatitis isolated bilatera

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54
Q

Which is the most common vascular ring type?

A

Double aortic arch (40%)

Right aortic arch w ligamentum arteriosum/PDA (30%)

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55
Q

Name the 3 types of incomplete vascular rings

A

Aberrant R subclavian artery (20%)
Anomalous origin of the innominate artery (10%)
Aberrant left pulmonary artery (rare)

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56
Q

CDH
Most common side for defect?
%associated anomalies
Name associated anomalies

A

Left 85%
40% associated anomalies
CHD, undescended tested, meckels diverticulum, unilateral kidney

Assoc’d with
Fryns Syndrome (AR, CDH, limb abnormalities, abnormal facies)
Aneuploidies - Turners (XO), T13, T18

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57
Q

Describe pathophysiology of CDH

-most common site?

A

Herniation of intestines through diaphragm secondary to failure of closure of pleuroperitoneal canal at 8 weeks gestation

Foramen of Bochdalek (70-90%)-posterior lateral region
Less common at anterior midline-morgagni hernia

58
Q

Right sided CDH is most commonly associate with which type of infection?

A

GBS

59
Q

Describe lung head circumference ration that may help predict CDH outcomes?

A

LHR<1 poor prognosis
LHR>1.4 good prognosis
Liver + LHR<0.8 high mortality

60
Q

Which lobe is most commonly affected in congenital lobar emphysema?
Describe pathophysiology
Treatment?

A

Left upper lobe (45%)

Occurs secondary to disruption of bronchi pulmonary development, possibly due to cartilaginous deficiency within large airways

25..% associated with obstruction of airway—> over distention

If doesn’t resolve spontaneously may need lobectomy

61
Q

What is the blood supply of CPAM?

Does it communicate w tracheobronchial tree?

A

Pulmonary circulation

It communicates with tracheobronchial tree via small tortuous passage

Typically only involves one lobe of lung

62
Q

Which is most common type of CPAM

A

Type 1
Occurs at 7-10 weeks gestation
Has large cysts 2-10cm
Usually single cyst but can be multi loculated
Lined with ciliated pseudostratified epithelium
Often p/w compression of remaining lung

63
Q

Which CPAM type is associated with other congenital anomalies?

A

Type 2
60% w other congenital anomalies
P/w multiple cysts and solid areas
Lining of ciliated cuboidal or columnar epithelium

64
Q

Does Bronchopulmonary sequestration have a connection to travheobronchial tree?
What is the blood supply?
Which type is neonatal presentation?

A

No connection to tracheobronchial tree. It’s non functioning lung tissue

Supplied by anomalous systemic artery (ie aorta)

Extralobar type, less common but presents in neonatal period

65
Q

What is management of CPAM if large in utero vs postnatal?

A

In utero watch for hydrops->if develops then needs fetal surgery for thoracoamniotic shunt (can decrease CPAM volume by 70%) to decrease risk for pulm hypoplasia

Postnatal
May need vent or even ecmo
Consider elective intubation of contra lateral bronchus
Complete resection in 2-6 months for all types bc complications (risk of developing hamartomas or infection)

66
Q

What are outcomes of CPAM by type?

A

Types 1 and 4-surgery curative
Type 0 and 2: poor as result of associated anomalies
Type 3: poor bc of large size causes pulmonary hypoplasia/pphn

All have increased risk of focal dysplasia (hamartomas) and infection

67
Q

Describe pathophysiology of congenital pulmonary lymphangectesia and associated syndromes

A

Dilated lymphatic vessels of lung 2/2 abnormal development (failure of regression at 20wks) or lymphatic obstruction

Increased risk of pleural effusion
Needs biopsy for dx which increases risk for effusion

If primary etiology it’s associated w T21, turner and noonan.

If secondary etiology, ass w HLHS, thoracic duct a genesis and intrauterine infection

68
Q

What additional workup do u need for bronchopulmonary sequestration?

A

Chromosomal analysis/microarray and echo bc of it’s associated w congenital heart disease

69
Q

Which BPS is associated w anomalies and describe them

A

Extralobar BPS 40-60% risk of other anomalies: CDH, vetebral anomalies, CHD, colonic duplication, CPAM
-has minimal risk of infection and malignant transformation

Majority in left side between lower lobe and diaphragms
Located outside normal lung w it’s own visceral pleura and no bronchial connection but may connect w GI tract

70
Q

What presents as inadequate vascularization of alveoli with decrease number of capillaries adjacent to alveoli and malaligned pulmonary veins

A

Alveolar capillary dysplasia

71
Q

What zone does lung work normally vs MAS vs PDA?

A

Normal zone III Pa>Pv (alveolar P is neutral)

In MAS it’s Zone I/II PA>Pa>Pv (alveolar pressure increases)

PDA zone IV Pa>Pv>PA (vascular overload)

72
Q

Lung develops from?

A

Foregut

73
Q

When does branching morphogenesis occur

A

Embryonic

74
Q

Mediators of Lung Development

A

Formation of Primary bronchi
Factors Involved
FGF10, FGFR2, RA, RAR

Branching Morphogenesis
FGF(1,7,9, 10), RA, Shh, Gli2, GATA6,
HOX

Alveolarization
PDGF, PDGFRA, RA, RAR, FGF2, FGFR

Angiogenesis
VEGF

75
Q

Branching morphogenesis is driven by

A

Mesenchyme

76
Q

Which growth factor is secreted by the mesenchyme for branching morphogenesis?

A

FGF-10

77
Q

Which protein is most important for secondary septation?

A

Elastin

78
Q

Characteristics of Fetal Lung Fluid

A
  • High in chloride
  • Low in bicarbonate and protein
  • 4-5 ml/kg/hr (up to 400 ml/day)
  • Crucial for lung distension during lung development
79
Q

Fetal Lung Fluid Characteristics

A

• Fluid clearance after birth results from active transport
via the epithelial sodium channels (ENaC)
At birth, only 35% of FLF has to be absorbed with
breathing
• Most of the FLF goes to the interstitium and then to the
pulmonary vasculature
•
<20% of the FLF is cleared by the pulmonary lymphatics

80
Q

Biphasic stridor, what is etiology?

A

Subglottic stenosis

Inspiratory (Extrathoracic or upper airway obstruction)
Large tongue, laryngomalacia, laryngeal cyst, congenital
tracheal stenosis (tracheal rings)

Biphasic-(Glottic or subglottic)
Subglottic stenosis, subglottic hemangioma

Expiratory (Intrathoracic airway obstruction)
Arch anomalies, vascular rings, tracheomalacia of intrathoracic
segment of trachea

81
Q

MCC Inspiratory stridor in newborn

A

Laryngomalacia

82
Q

MC pleural effusion in neonates

A

Chylothorax

Assc’d with Noonans + T21

83
Q

Which is the most common type of CPAM?

A

Type 1-macrocystic (large cysts 1-10cm)

Best prognosis too with Type 4

84
Q

Which pulmonary disease connects to to systemic circulation?

A

BPS

85
Q

Which pulmonary disease connects to tracheobronchial tree

A

CPAM

86
Q

CXR finding with cyst in upper lobe. Which pulmonary disease?

A

CLE (mostly Left upper lobe)

Remember CPAM and BPS is preferentially lower lobes

87
Q

Which is most common type of BPS?

A

Intralobar (75-85-%)
Most common in males
Develops proximal to main lung bud
Venous return are pulmonary veins

Extralobar 15-25%
Develops distal to lung bud
Venous return Azygous vein

88
Q

Which is the most common type of choanal atresia and associated abnl?

A

Mixed bony membranous

50% associated anomalies. ChArge

89
Q

Surfactant lowers surface tension and it’s ____ at end of expiration

A

Lowest

It’s directly related to radius

90
Q

O2 receptors

A

Peripheral chemoreceptors in carotid body

91
Q

Genetic Mutations seen in respiratory conditions

A

SPB, ABCA3, TTF1 can cause severe RDS phenotype
FOXF1 is associated with Alveolar capillary dysplasia with misalignment
of pulmonary veins (ACD-MPV)
SP-D mutations not associated with RDS

92
Q

Patient w PPHN ends up on ecmo then dies. Which isn’t associated with this presentation?
SPB, ABC3, TTF1 FOXF1 SPD

A

SPD is not associated w RDS

SPB, ABC3 TTF1 can cause severe RDS
Foxf1 is ACD

93
Q

Compared to older children neonates have

A

FRC reduced bc increased chest wall compliance

Chest wall compliance increased

Type 1 fibers reduced in neonates

Neonates have increased closing capacity

94
Q

What is closing capacity ?

A

Volume in the lungs at which alveoli collapse

It is increased in neonates

95
Q

A 10% increase in FiO2 increased O2 content by which percent?

A

10-15%

96
Q

Post natal systemic corticosteroids in BPD, what outcomes?

A

Decreased BPD and mortality but possible increase in CP

97
Q

Antenatal corticosteroids have what effect in BPD?

A

No change in overall rate but decreases RDS and mortality

98
Q

Glucocorticoids help alveolarization (t/F)

A

False

Adversely affects but we still give antenatal glucocorticosteroids to reduce RDS and mortality

99
Q

The secondary septa are critical during alveolarization. What is present at the tips of these structures?

A

Elastin secreted by myofibroblasts

100
Q

Amniotic fluid entry is restricted into the fetal lung (T/F)

A

True

FLF contributes to AF not the other way around

101
Q

What is critical for lung development?

FLF, AF, both, fetal urine

A

Fetal lung fluid

102
Q

Half-life of surfactant is _____ than adults

A

Longer

Exogenous surfactant given get recycled and used for a longer duration of time

103
Q

Which surfactant proteins are involved in immune function vS surfactant production?

A

A and D in immune function (hydrophilic)

B And C surfactant production (lipophillic)

104
Q

Increased lung volume shortens inspiratory time and prolongs expiratory time, this reflex is called:

A

Hering-Bruer Reflex

105
Q

When in utero does the fetus breathe ?

A

REM Sleep

106
Q

Which neurotransmitter is implicated in SIDS?

A

Serotonin

Lower levels seen in autopsy

107
Q

CPAP of 5 Fo2 30% at 36 weeks. Which severity of BPD?

A

Severe (Positive pressure and 30% or more)

108
Q

Difference between moderate and severe BPD

A

Severe
Oxygen requirement > 30% and positive pressure (CPAP) at 36 weeks

Moderate
FiO2 > 30%

109
Q

PATHOLOGIC hallmark of new BPD

A

Arrest of alveolarization
Vascular mal development
Variable fibrosis

110
Q

Alveolar gas equation

A

PA02= (PB-PH20)xFiO2]-pCO2/R

PB 760
PH20=47
Newborn R =1

Adults R=0.8

111
Q

Per boyle’s law if volume increases pressure _____

A

Decreases

P1V1=constant

112
Q

A change in pressure is equal to __ST over ___

A

Laplace’s law=2ST/radius

113
Q

Alveolar pressure _____ during inspiration

A

Increases

114
Q

Dead space calculation (Bohr’s method)

A

VD/VT=PaCO2-PeCO2/PaCO2

VD= Dead space volume
VT = Tidal volume
PaCO2= the carbon dioxide in the arterial blood
PeCO2= is the partial pressure of carbon dioxide in the expired air.

Paco-Peco/Paco

115
Q

Compliance equation

A

Compliance=change in volume/change pressure

116
Q

Time constant for RDS

A

Short

Poor compliance which rapidly improves w surfactant

117
Q

What percentage of surfactant is recycled?

A

95%

118
Q

Which is the largest component of surfactant?

A

DPPC or saturated phosphatidyl choline

119
Q

Most abundant surfactant protein is?

A

SP-A as it plays role immune defense

120
Q

Which surfactant proteins are imp in host defense?

A

SPA and SPD

121
Q

Why is preterm lung deficient in surfactant?

A

Low quantity, low quality and function is interfered with

122
Q

Which deficiency presents similar to SP-B deficiency with RDS?

A

ABCA-3

123
Q

After surfactant in RDS, how does time constant change?

A

Increase in time constant

Giving surfactant instantly improves oxygenation by providing adequate volume

124
Q

How do antenatal CS work?

A

• Induction of surfactant synthesis
• Increase surface area for gas exchange
• Improved response to postnatal surfactant
• Also decreases: IVH, PDA, NEC and postnatal
hypotension

125
Q

Administration of surfactant decreases the risk of?

A

Mortality

Not PDA, BPD, NEC or RDS

126
Q

Therapies for Pulmonary HTN

A

Increase cGMP
INO - stimulates soluble guanylyl cyclase
Sildenafil (blocks PDE5)

Increase cAMP:
Alprostidil
Milrinone (blocks PDE3)
Prostacyclin (inhaled - Flolan)

Increase eNOS
Bosentan (blocks ET-B and ET-A)

127
Q

Which syndrome is associated with PPHN and CDH?

A

Fryns syndrome

128
Q

CDH

A

0.8-5/10,000 births
M>F
40-60% cases are isolated, associations include cardiac,
renal, gastrointestinal, and CNS, also chromosomal
aneuploidy
*Syndromic associations including Fryns syndrome

Location
70-75% postero-lateral - Bochdalek hernia, L»R
23-28% anterior - Morgagni hernia

Low Lung to Head ratio <0.6 can indicate poor outcome

129
Q

Mechanoreceptors

A

Stretch receptors
Respond to Tidal volume changes

Ventrolateral surface medulla
Chemo receptor - co2 changes

Peripheral chemo receptors in carotid bodies and aortic bodies

Hypoxemia - breathes faster then decreased resp effort

Hypercarbia
Decrease respiratory rate due to
blunting of peripheral chemoreceptors

130
Q

Which surfactant proteins are involved in promoting adsorption and spreading of surfactant?

A

SP-B and SP-C

131
Q

Which surfactant proteins are collectins

A

SP-A and SP-D

132
Q

MC SP-B mutation in Northern Europeans

A

Frameshift mutation (on chromosome 2)

133
Q

Primary anti-inflammatory effect of glucocorticoids to wean baby off ventilator is mediated by?

A

Annexin A1 synthesis

134
Q

Mechanism of pulmonary hypertension in MAS?

A

Abnormally constricted vessels

Triggers vasoconstrictors (endothelin, thromboxane)

135
Q

Contraindications to iNO?

A

Critical Ao stenosis (left sided obstructive cardiac lesion)

TAPVR (obstructive) [pulm edema is aleady present - and iNO will make this worse]

TGA with intact ventricular septum (Vasodilating will compromise forward flow)

136
Q

Where does NO work?

A

Acts on guanyl cyclase
This will’ increase cGMP

L- argunine is a precursor

137
Q

MOA of sildenafil??

and milrinone ??

A

Sildenafil- inhibits Phosphodiesterase 5

Milrinone - inbits Phosphodiesterase 3
Therefore increase cAMP

138
Q

What is resistance?

A

Resistance = change in pressure/change in flow

Resistance = 8nL/πr4

In neonates primary resistance is airway

139
Q

Use of Caffeine in preemies leads to ______.

A 
Improved resp drive
Increased MV and CO2 sensitivity 
Decreased hypoxic ventilator depression 
Improved contractility of diaphragm 
Reduced risk of BPD
Improved lung compliance secondary to weak diuretic effect
140
Q

What are the effects of posnatal corticosteroids aftet 1 week of age?

A

Decreased BPD, mortality
Possibly increased CP
No diff in major neurosensory disability
Increased ROP, no change in blindness

NICU Board Review (19 decks)

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