1
Q
what are the effects of caffeine on apnea
A
decreased: periodic breathing, depressed effect on breathing
increased: CO2 sensitivity, diaphragm activity and minute ventilation
2
Q
Phys reasons for apnea of prematurity :
A
- carotid bodies are silenced in response to oxygen due to hyperoxia after birth
- decreased central sensitivity to CO2
- laryngeal mucosa stimulation causes apnea due to exaggerated inhibitory reflex
- unregulated inhibitory neurotransmitters: GABA + adenosine
- hypoxic stimulation of carotid body may cause bradycardia
3
Q
A-a gradient equation
A
A-a= FiO2 x (barometric pressure- pressure of H2O) - (paCO2/0.8)- paO2
= FiO2 x 713 - paCO2- paO2
* if at sea level
* water 47mm Hg
* atmosphere 760 mmm Hg
4
Q
characteristics of dead space:
1. equation
2. ratio
3. physiologic =
4. bronchoconstriction -
A
- can be calculated using the Bohr equation
- high V/P ratio
- physiologic = anatomic + alveolar
- bronchoconstriction decreases dead space
5
Q
Bohr equation for dead space
A
VD/VT = (PaCO2- PeCO2)/ PaCO2
Volume of dead space over tidal volume = arterial Co2 minus expired co2 over the arterial co2
6
Q
what increases surfactant distribution
A
- surface activity
- gravity
- volume of surfactant
- rapid rate of administration
- higher PIP and PEEP
- more fluid in the lungs or edema
7
Q
iNO contraindications
A
critical aortic stenosis, interrupted aortic arch, HLHS , TAPVR
8
Q
what are the differences in new BPD vs Old
A
NEW BPD has less fibrosis, less inflammation, less PHTN
overall characteristics of bpd are : less microvascular development, decreased alveolar septation
9
Q
most abundant item in surfactant
A
phosphatidylcholine desaturated = 50%
(lecithin)
aka DPPC
10
Q
LaPlace’s law
A
P= 2T/r
pressure to maintain an open alveoli
11
Q
surfactant proteins needed for survival
A
B>C
12
Q
organisms for early vs late pneumonia
A
early: GBS, listeria, Ecoli, klebsiella
late: pseudomonas, staph, fungal, chlamydia
13
Q
ventilator management of pneumothorax
A
decrease: PEEP, PIP, iTime
increase: rate
14
Q
spinnaker sail sign
A
pneumomediastinum
the outline of the thymus - it gets pushed up and out laterally
15
Q
meconium aspiration –> lung injury leading to –>
A
- mechanical obstruction
- chemical inflammation
- surfactant inactivation
16
Q
pulmonary dysfunction due to meconium aspiration
A
- air trapping and air leaks
- V/P mismatch leading to hypoxia
- increased pulmonary vascular resistance ( due to pulmonary vasoconstriction and maladaptive leading to PPHN)
17
Q
Chylothorax
A
> 80% lymphocytes
110 Tigs
low cholesterol content, presence of chylomicrons
*jury is out on WBC count/ exudative vs transudative
change to MCT formula
more common on R due to thoracic duct location
18
Q
traditional exudative effusions
A
> 1000 wbc
200 LDH
19
Q
risk factors for TTN
A
maternal sedation
maternal diabetes
c-section
quick birth
perinatal depression
20
Q
risk factors for RDS
A
prematurity
maternal diabets
perinatal depression
males
- thinks that inactivate surfactant
21
Q
compared to adults, neonates have — respiratory measurements
A
higher:
respiratory rate
residual volume
minute ventilation
alveolar ventilation
similar: dead space and FRC
22
Q
ATP- binding cassette member A3 deficiency
A
ABCA3 deficiency
autosomal recessive
most common known inherited surfactant deficiency
lack DPPC and PG, decreased lamellar bodies bc ABCA3 transports these lipids to the lamellar bodies
presents similar to protein B deficiency / classifies as interstitial lung disease
23
Q
increased lung maturation by -
A
chorio , HTN, hemoglobinopathes, IUGR, prolonged rupture
inhibited by : diabetes, males, c-section, twins, prematurity
- insulin, androgens, TGF-b
24
Q
inspiratory stridor
A
supraglottic obstruction that narrows with inspiration
pierre robin/treacher collins
macrogossia - beckwith weidemann syn, hypothyroid, glycogen storage, t21
choanal atresia
25
biphasic stridor
laryngeal obstruction- vocal cords, subglottis, extra thoracic trachea
laryngomalacia
vocal cord paralysis
sublotteic stenosis
26
expiratory stridor
intrathoracic trachea and bronchi
tracheomalacia
tracheal stenosis
27
complete vascular rings
double aortic arch
right aortic arch with PDA
persistant 4th branchial arch
encircles trachea and esophagus
28
incomplete rings
aberrant right subclavian
anomalous innominate artery
aberrant left pulmonary artery
* barium swallow/echo for diagnosis
29
mcc site for CDH
foramen of bochdalek
30
right side CDH
most have liver in chest
associated with Strep pneumoniae infection
31
diaphragm paralisis
Right more common
belly dancer sign- belly button moves up and toward the affected side during inspiration
32
high pH
low - WBC, protein, lDH and spec gravity
transudative effusion
<1000 abc
<3 G protein
< 200 LDH
due to disruption of hydrostatic and oncotic forces
CHF, nephrotic syndrome, hydrops
33
low pH
high - wbc, protein, LDH and spec grav
exudative
inflammation/infection
due to increased permeability of pleura or capillaries
34
congenital LOBAR emphysema
one lobe
LEFT = MCC
over dissension leads to displaced PMI, compression of remaining lung with respiratory distress
looks like a pneumo with lung markings
usually resolves
35
CPAM
branching abnormality
COMMUNICATES with bronchial tree
PULMONARY circulatioon
CPam (C= communicates, Pulmon circulation )
36
CPAM types
Type 0 = rarest
Type 1 = MCC, usually one large cyst
Type 2 multiple cysts + lots of anomalies
Type 3 =Large mass
Type 4= most likely to be malignant
Types 0&2 do worse bc associated with other anomalies
37
bronchopulmonary sequestration
NOT connected to trachealbrocheal tree , NOT suppled by pulmonary vessels
neonatal : usually extra lobar (own visceral and outside normal lung)
childhood : intralobar
usually regress
should get genetic studies and echo
can connect to GI track
38
alveolar capillary dysplasia
blood vessels are not properly formed near alveoli, causes severe RDS and PPHN soon after birth
lung biopsy
100% mortality
associated with other anomalies
39
acetazolamide / diamox
carbonic anhydrase inhibitor , blocks reabsorption of NaHCo3 in the proximal tubules
causes hypokalemia, mild hyperchloremic metabolic acidosis
40
furosimide and bumetanide
loop off henle
loose k, na, cl, ca, mg
ototoxicity
nephrocalinosis
41
chlorothiazide
inhabits nacl reabsorption in the distal tubule
lose na. k, mg, cll, HCO3, phos
less loss of calcium
inhibits release of insulin
displaces bilirubin from albumin
hyperuricemia
42
methyxanthines
maybe increase cyclic AMP
concentration increased by erythromycin, ketoconazole
lowered by phenobarbital
relaxes respiratory smooth muscle
decreases central apena
increased contraction of diaphragm
shifts CO2 curve left
increases minute ventilation
increases sensitivity of medulla to Co2
decreased incidence of BPD
43
Nitric oxide path
L-arginine + nitric oxide synthase = nitric oxide
nitric oxide + guanylate cyclase = cGMP
cGMP = increase in calcium out of cell = smooth muscle relaxation
the last step is inhibited by phosphodiesterase
therefore a phosphodiesterase inhibitor would prolong calcium leaving and therefore smooth muscle relaxation = sildenafil
44
PPHN classification
> 5-10% sat differential
sat lability
OI >15
or a PaO2 differential >20
* if there is no PDA,= or if there is an intracardiac mixing lesion there may not be a sat differential. conversely a left obstructive lesion there may be a differential with out PPHN
45
reversed O2 sat differential seen with
D- transposition with either a coarct or PPHN
46
echo evidence of PPHN
RV pressure: tricuspid jet
shunt: flow at atrial or ductal level ( reversal of flow> bidirectional)
septal motion: paradoxical = septal bowing (bowing > flattening)
47
antenatal steroids cause :
decreased fetal movements and fetal breathing
decreased fetal HR variability
do no affect fetal blood flow
may cause a lower BPP but should return to baseline after 7 days
48
alveolar partial pressure of O2
PAO2
PAO2=
= [fio2 x (PB- pH2O] - PaCo2/0.8
49
embryonic stage malformations
TEF/ esophageal atresias
bronchogenic cysts
pulmonary sequestrations
50
To evaluate for intrinsic lung disease :
Thin sectioned CT
Genetic testing : SFTPB, SFTBC, ABCA3, thyroid transcription factor NKX2.1
51
Lung defenses include
Mucins, cilliary clearance , surfactant proteins , tubular mylein which stores surfactant and proteins, and alveolar macrophages
52
Laws :
Boyle
Charles
Dalton
Fick
Henry
Boyle : volume of gas is inversely related to pressure
Charles: higher temp will produce higher volume of gas
Dalton: mixed gas pressure is equal ro the sums of the parts
Fick : diffusion is directly proportional to surface area
Henry : a gas will dissolve in a liquid directly related to its partial pressure
53
pseudoglandular
pulmonary sequestrations
pulmonary lymphangiectasias
CPAMs
CDH
54
canalicular
alveolar capillary dysplasia
surfactant deficiency
( and for saccular and alveolar)
55
importance of Vit A
induces TBX4, HOX and FGF (10 and 7)
56
hormones involved in surfactant production
cortisol
thyroid hormones
57
hydrophobic surfactant proteins
B and C
reduce surface tension
58
surfactant protein that plays a role in making tubular myelin and is part of host defense
A
59
surfactant protein B deficiency
pulmonary alveolar proteinosis
no lamellar bodies no tubular myelin
non sustained response to giving surfactant, needs transplant
60
surf C deficiency
AD
chronic lung disease
61
compared to adults, infants have ___ resistance and --- compliance
higher resistance and lower compliance
62
resistance =
R = change in pressure/change in flow
63
Poiseuille's law
flow = (Pie x Px r^4)/( 8 x n x L)
flow = pie x pressure x radius^4 / 8 x viscosity x length
64
time constant
the amount of time it takes for filling or emptying
takes 3-5 time constants to complete full filing or full emptying
Time constant = Resistance x Compliance
so if compliance is low, low time constant = infants compared to adults
long time constant = BPD
65
ventilation and perfusion zones of lung
I : PA>Pa>Pv
* high alveolar pressure but low pulmonary artery pressure = highest V/Q ratio
II : Pa>PA>Pv
* normal V/Q ratio
III: Pa>Pv>PA
* ventilation is reduced, perfused but not ventilated so small V/Q ratio
* most of neonatal lung
66
O2 saturation
amount of hemoglobin that is saturated with oxygen
is not related to amount of hemoglobin , you saturation may be normal even if anemic, carbon monoxide poisoning
67
O2 content in blood =
(1.34 x Hgb X O2 sat) + ( 0.003 x PaO2)
bound O2 + dissolved O2
is dependent on Hgb
68
O2 delivery =
O2 content x cardiac output
69
Oxygen consumption =
Venous O2 or VO2= Cardiac output x (Arteria O2 Content- Venous O2 Content )
70
Bohr effect
high CO2 or acid (H+) will decreases hemoglobins affinity for oxygen making it want to dump oxygen at tissues , and vice versa
71
Haldane effect
High O2 decreases hemoglobin affinity for CO2 making it easy for unloading CO2 at the lung tissue to be expelled.
decreased O2 makes it easy for hemoglobin to pick up CO2
72
Shift right the oxygen dissociation curve
less O2 affinity
hemoglobin A
lower pH
increased DPG
increased temp
73
shift left oxygen dissociation curve
increased O2 affinity
hemoglobin F
higher pH
low DPG
low temp
74
nasal CPAP for RDS shortly after deliver ---
associated with improved survival
reduced need for mechanical ventilation
decreased BPD
75
supplemental surfactant has these surface proteins
B and C
76
surfactant production
1. type 2 pneumocytes make surfactant proteins and absorb lipids
2. those items are moved to mulivesicular bodies
3. processed then sent for storage in lamellar bodies
4. B and C and lipids are then secreted from the pneumocyte to then interact with A to form tubular myelin
5. endocytosis by type 2 cells then allows for recycling of used components , macrophages pickup debris
77
things we know reduce BPD
early CPAP
caffeine
vitamin A
avoidance of infection
78
BPD modifiers
PH is common but is a later finding ~6 wks and is a predictor of mortality
symptomatic PDA increases risk for BPD however no standard practice
kids with BDP are at risk for growth failure and have 20-25% increased caloric needs
79
for MAS , _____ reduces need for ECMO
surfactant administration, if given early
80
pneumonia classification
early is within 3 days, late is after
81
most common transplacental pneumonia
viral - CMV, rubella, varicella, herpes, HIV, enterovirus , flu
82
transplacental bacterial pneumonia
listeria, TB and syphilis
83
perinatal pnenumonia causes - at birth but not transplacental
GBS and gram negatives (ecoli, klebsiella, hflu, psueomonas, ) and chlamydia
84
suppurative pneumonia microbes
staph, klebsiella, psuedomonas, ecloga and fungal
lung necrosis, abscess formation and pneumatoceles
85
three types of pulmonary HTN
1. postnatal vasoconstriction but normal development of vasculature
* perinatal hypoxia, MAS, sepsis, RDS, hypothermia
2. fixed small arterioles
* chronic pulmonary venous hypertension like in TAPVR, chronic hypoxia in utero, premature closure of PDA
* poor prognosis
3. decreased cross-sectional area of pulmonary vascular bed
* pulmonary hpyoplasia like with CDH, oligo, thoracic dystrophies
4. functional obstruction of pulmonary blood flow
* polycythemia
86
vent strategies for PPHN
high oxygen with avoidance of hyperoxia
high mean airways pressure increase the pulmonary vascular resistance and can worsen PPHN
avoid hyperventilation as associated with reduced cerebral blood flow and hearing issues
87
phosphodiesterase inhibitors
inhibit degradation of cAMP/cGMP and reduce intracellular calcium allowing for vasodilation
88
sildenafil
PDE5 inhibitor
89
milrinone
PDE3 inhibitor
90
description of the hypoplastic lung in CDH
1. the hypo plastic lung lacks all three components: alveoli, normal bronchiolar branching pattern and pulmonary vascular structure
2. the remain pulmonary artery have muscular hypertrophy and postnatal pulmonary hypertension
91
measurements for CDH prognosis
1. lung to head ratio from an US
less than 0.6 is 100% mortality prognosis but greater than 1.6 is a good prognosis
2. observed to expected total fetal lung volume - done with MRI
less than 20% is poor but over 50% is favorable
92
eventuation of the diaphragm
diaphragm is replaced by fibroelastic tissue leading to thinning and abnormal movement
floor shows paradoxical movement , US is preferred first test showing lack of movement
93
CPAM prenatal and management
can to a cyst volume ratio ( cyst volume / head circumforence ) if larger than 1.6 higher risk of hydrops
maternal steroids or fetal resection
postnatal resection due to risk of malignancy
94
central chemoreceptors respond to ___ in the ____
they cause
CO2 and H+ in the medulla
they cause increased respiratory rate and depth
this is diminished in preterm infants relative to degree of prematurity
95
peripheral chemoreceptors are located ____ and respond to ____
carotid bifurcation and respond to PaO2 and pH
transient hyperventilation followed by apnea
96
4 causes of apnea of prematurity
1. laryngeal stimulation causes protective airway reflex but then causes apnea
2. negative pressure generated during attempt to breath while obstructive leads to apnea
3. peripheral hypoxic ventilation depression
4. central blunted response to hypercarbia
97
CO2 is mostly affected by ____
O2 is mostly affected by
CO2 = tidal volume, rate and expiratory time
O2= mean airway pressure and FiO2
98
vent strategy for RDS
avoid atelectasis = optimal PEEP
surfactant replacement
high rate and low tidal volume
* ling has a short time constant because of low compliance so empties quickly
non-invasive is preferred
99
vent strategy for BPD
low rate with higher tidal volume to allow for adequate expiration
lungs have high resistance and long time time constant so empties slowly
100
vent strategy for MAS
optimized PEEP and MAP
shorter iTime to allow for expiration
101
dexamethasone before 14 days and after - outcomes
before 14 days- increase risk of CP, perforation
after 14 days decreased mortality and risk of BPD
LSU Neonatology study set
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