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
How does PPV affect the right heart vs left heart?
``` 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
26
What are the 4 mechanisms for pulmonary edema according to starlings equation?
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)
27
What is the mechanism of Nitric oxide?
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.
28
There is no data to support iNO use in which 3 populations?
Premature infants Congenital heart disease CDH
29
OI index
OI=MAPxFiO2/paO2
30
When should iNO be initiated?
To optimize lung recruitment | OI>25 or paO2 <100 despite 100% FiO2
31
Why is rebound effect noted in rapid weaning of iNO?
Inhibition of endogenous nitric oxide synthase (eNOS)
32
Risks associated with use of iNO
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
33
Contraindications of iNO use
Structural heart defects depending on right to left shunting - Critical AS - interrupted aortic arch - coarctation - HLHS Obstructive TAPVR
34
Factors that decrease RDS risk?
Antenatal corticosteroids | Chronic intrauterine stress
35
How does RDS appear histologically?
Appear as an eosinophilic membrane that lines airspaces
36
Antenatal corticosteroids have been found to decrease the incidence of which diseases?
RDS IVH NEC Neonatal death Too many doses can be associated w fetal growth restriction
37
Porcine or bovine surfactant contain which surfactant proteins?
Surfactant proteins B and C | Phospholipids
38
What is the pathophysiology of TTN?
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
39
Risk factors for TTN
``` Male <38 weeks gestation LBW Macrosomia Maternal diabetes or asthma ```
40
How to prevent TTN?
Avoid elective c/s prior to 39 weeks
41
What is the difference between congenital, early onset or late onset Pneumonia?
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)
42
What are the 2 signaling pathways that lead to vasodilation and decrease in PVR at birth in neonate?
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.
43
PPHN is characterized by 3 types
Maladaptation (MAS, pneumonia) Maldevelopment (ACD) Underdevelopment (hypoplastic) Hypoplastic vasculature CDH has hypoplastic and excessive muscularization
44
What is a normal A-a gradient in RA? | How about in 100% FiO2?
RA is 10-15 | 100% FiO2 is 80-100
45
An A-a gradient > what number is strongly suggestive of patient needing ECMO?
>600
46
Sildenafil acts in which pathway?
It’s acts in the nitric oxide pathway | It inhibits PDE5 and therefore blocks the conversion of cGMP to its inactive form GMP
47
What is the pathophysiology of PIE?
Air dissects and gets trapped in the perivascular connective issue. In preterm infants this connective tissue is more abundant and less dissectible trapping air.
48
Does collateral ventilation occur in the alveolus in newborns?
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
49
How does nitrogen washout theoretically help in pneumothoraces?
100% O2 decreases partial pressure of nitrogen in alveolus compared to the pleural space leading to diffusion of nitrogen out of pleural space.
50
Name the proven preventative management strategies for BPD?
Vitamin A Caffeine Less invasive surfactant administration (1 retrospective review)
51
What value is considered abnormal for a sweat chloride test to diagnose cystic fibrosis?
>60meq/L of chloride
52
Name the early marker for pancreatic exocrine insufficiency in CF?
Low fecal elastase 1
53
Describe the complete spectrum for a patient with CF?
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
54
Which is the most common vascular ring type?
Double aortic arch (40%) | Right aortic arch w ligamentum arteriosum/PDA (30%)
55
Name the 3 types of incomplete vascular rings
Aberrant R subclavian artery (20%) Anomalous origin of the innominate artery (10%) Aberrant left pulmonary artery (rare)
56
CDH Most common side for defect? %associated anomalies Name associated anomalies
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
57
Describe pathophysiology of CDH | -most common site?
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
Right sided CDH is most commonly associate with which type of infection?
GBS
59
Describe lung head circumference ration that may help predict CDH outcomes?
LHR<1 poor prognosis LHR>1.4 good prognosis Liver + LHR<0.8 high mortality
60
Which lobe is most commonly affected in congenital lobar emphysema? Describe pathophysiology Treatment?
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
What is the blood supply of CPAM? | Does it communicate w tracheobronchial tree?
Pulmonary circulation It communicates with tracheobronchial tree via small tortuous passage Typically only involves one lobe of lung
62
Which is most common type of CPAM
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
Which CPAM type is associated with other congenital anomalies?
Type 2 60% w other congenital anomalies P/w multiple cysts and solid areas Lining of ciliated cuboidal or columnar epithelium
64
Does Bronchopulmonary sequestration have a connection to travheobronchial tree? What is the blood supply? Which type is neonatal presentation?
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
What is management of CPAM if large in utero vs postnatal?
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
What are outcomes of CPAM by type?
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
Describe pathophysiology of congenital pulmonary lymphangectesia and associated syndromes
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
What additional workup do u need for bronchopulmonary sequestration?
Chromosomal analysis/microarray and echo bc of it’s associated w congenital heart disease
69
Which BPS is associated w anomalies and describe them
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
What presents as inadequate vascularization of alveoli with decrease number of capillaries adjacent to alveoli and malaligned pulmonary veins
Alveolar capillary dysplasia
71
What zone does lung work normally vs MAS vs PDA?
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
Lung develops from?
Foregut
73
When does branching morphogenesis occur
Embryonic
74
Mediators of Lung Development
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
Branching morphogenesis is driven by
Mesenchyme
76
Which growth factor is secreted by the mesenchyme for branching morphogenesis?
FGF-10
77
Which protein is most important for secondary septation?
Elastin
78
Characteristics of Fetal Lung Fluid
* 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
Fetal Lung Fluid Characteristics
• 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
Biphasic stridor, what is etiology?
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
MCC Inspiratory stridor in newborn
Laryngomalacia
82
MC pleural effusion in neonates
Chylothorax Assc’d with Noonans + T21
83
Which is the most common type of CPAM?
Type 1-macrocystic (large cysts 1-10cm) Best prognosis too with Type 4
84
Which pulmonary disease connects to to systemic circulation?
BPS
85
Which pulmonary disease connects to tracheobronchial tree
CPAM
86
CXR finding with cyst in upper lobe. Which pulmonary disease?
CLE (mostly Left upper lobe) Remember CPAM and BPS is preferentially lower lobes
87
Which is most common type of BPS?
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
Which is the most common type of choanal atresia and associated abnl?
Mixed bony membranous | 50% associated anomalies. ChArge
89
Surfactant lowers surface tension and it’s ____ at end of expiration
Lowest It’s directly related to radius
90
O2 receptors
Peripheral chemoreceptors in carotid body
91
Genetic Mutations seen in respiratory conditions
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
Patient w PPHN ends up on ecmo then dies. Which isn’t associated with this presentation? SPB, ABC3, TTF1 FOXF1 SPD
SPD is not associated w RDS SPB, ABC3 TTF1 can cause severe RDS Foxf1 is ACD
93
Compared to older children neonates have
FRC reduced bc increased chest wall compliance Chest wall compliance increased Type 1 fibers reduced in neonates Neonates have increased closing capacity
94
What is closing capacity ?
Volume in the lungs at which alveoli collapse It is increased in neonates
95
A 10% increase in FiO2 increased O2 content by which percent?
10-15%
96
Post natal systemic corticosteroids in BPD, what outcomes?
Decreased BPD and mortality but possible increase in CP
97
Antenatal corticosteroids have what effect in BPD?
No change in overall rate but decreases RDS and mortality
98
Glucocorticoids help alveolarization (t/F)
False Adversely affects but we still give antenatal glucocorticosteroids to reduce RDS and mortality
99
The secondary septa are critical during alveolarization. What is present at the tips of these structures?
Elastin secreted by myofibroblasts
100
Amniotic fluid entry is restricted into the fetal lung (T/F)
True FLF contributes to AF not the other way around
101
What is critical for lung development? FLF, AF, both, fetal urine
Fetal lung fluid
102
Half-life of surfactant is _____ than adults
Longer Exogenous surfactant given get recycled and used for a longer duration of time
103
Which surfactant proteins are involved in immune function vS surfactant production?
A and D in immune function (hydrophilic) B And C surfactant production (lipophillic)
104
Increased lung volume shortens inspiratory time and prolongs expiratory time, this reflex is called:
Hering-Bruer Reflex
105
When in utero does the fetus breathe ?
REM Sleep
106
Which neurotransmitter is implicated in SIDS?
Serotonin | Lower levels seen in autopsy
107
CPAP of 5 Fo2 30% at 36 weeks. Which severity of BPD?
Severe (Positive pressure and 30% or more)
108
Difference between moderate and severe BPD
Severe Oxygen requirement > 30% and positive pressure (CPAP) at 36 weeks Moderate FiO2 > 30%
109
PATHOLOGIC hallmark of new BPD
Arrest of alveolarization Vascular mal development Variable fibrosis
110
Alveolar gas equation
PA02= (PB-PH20)xFiO2]-pCO2/R PB 760 PH20=47 Newborn R =1 Adults R=0.8
111
Per boyle’s law if volume increases pressure _____
Decreases P1V1=constant
112
A change in pressure is equal to __ST over ___
Laplace’s law=2ST/radius
113
Alveolar pressure _____ during inspiration
Increases
114
Dead space calculation (Bohr’s method)
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
Compliance equation
Compliance=change in volume/change pressure
116
Time constant for RDS
Short Poor compliance which rapidly improves w surfactant
117
What percentage of surfactant is recycled?
95%
118
Which is the largest component of surfactant?
DPPC or saturated phosphatidyl choline
119
Most abundant surfactant protein is?
SP-A as it plays role immune defense
120
Which surfactant proteins are imp in host defense?
SPA and SPD
121
Why is preterm lung deficient in surfactant?
Low quantity, low quality and function is interfered with
122
Which deficiency presents similar to SP-B deficiency with RDS?
ABCA-3
123
After surfactant in RDS, how does time constant change?
Increase in time constant Giving surfactant instantly improves oxygenation by providing adequate volume
124
How do antenatal CS work?
• Induction of surfactant synthesis • Increase surface area for gas exchange • Improved response to postnatal surfactant • Also decreases: IVH, PDA, NEC and postnatal hypotension
125
Administration of surfactant decreases the risk of?
Mortality Not PDA, BPD, NEC or RDS
126
Therapies for Pulmonary HTN
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
Which syndrome is associated with PPHN and CDH?
Fryns syndrome
128
CDH
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
Mechanoreceptors
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
Which surfactant proteins are involved in promoting adsorption and spreading of surfactant?
SP-B and SP-C
131
Which surfactant proteins are collectins
SP-A and SP-D
132
MC SP-B mutation in Northern Europeans
Frameshift mutation (on chromosome 2)
133
Primary anti-inflammatory effect of glucocorticoids to wean baby off ventilator is mediated by?
Annexin A1 synthesis
134
Mechanism of pulmonary hypertension in MAS?
Abnormally constricted vessels Triggers vasoconstrictors (endothelin, thromboxane)
135
Contraindications to iNO?
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
Where does NO work?
Acts on guanyl cyclase This will’ increase cGMP L- argunine is a precursor
137
MOA of sildenafil?? | and milrinone ??
Sildenafil- inhibits Phosphodiesterase 5 Milrinone - inbits Phosphodiesterase 3 Therefore increase cAMP
138
What is resistance?
Resistance = change in pressure/change in flow Resistance = 8nL/πr4 In neonates primary resistance is airway
139
Use of Caffeine in preemies leads to ______.
``` 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
What are the effects of posnatal corticosteroids aftet 1 week of age?
Decreased BPD, mortality Possibly increased CP No diff in major neurosensory disability Increased ROP, no change in blindness