Respiratory Flashcards
Lung development
1) respiratory tract is derived from ___
2) what first branches from esophagus to form the lungs?
3) does this arise from forgot, Midgut, or hindgut
1) Endoderm
2) Ventral Bud
3) Foregut
Vascular Supply
1) which aortic arch does the pulmonary vasculature form from?
2) where do the bronchial arteries come from? What did they supply?
3) how do pre-Acenar arteries develop? When are they complete?
4) how do intra-Acenar arteries develop? When are they complete?
1) sixth aortic arch
2) aorta to the conducting airways, visceral, pleura, connective tissue
3) angiogenesis (16 weeks)
4) vasculogenesis (alveolar development to 8-10 years)
Alveolarization
1) what phase does this occur? (Timeline)
2) how many alveoli at term? Adult?
3) what enhances alveolarization?
4) what delays alveolarization?
1) alveolar phase (36 weeks to 8 years)
2) 50 – 150million -> 200–600 million
3) vitamin a and thyroxine
4) postnasal steroids, oxygen, malnutrition, ventilation, insulin, inflammation
Lung development
List the stages of lung development and gestational age
Embryonic (0–5)
pseudoglanular (5–15)
canalicular (15–25)
Sacular (25–35)
Alveolar (36+)
Embryonic
1.) structures?
2.) developmental abnormalities?
-Ventral bud, bronchi, five branches/lobes (“5 branches by 5 weeks”)
-Pulmonary vasculature from 6th aortic arch
-laryngeal cleft, tracheostenosis, tracheoesophageal fistula, bronchogenic cyst
Pseudoglandular
1) structures?
2) developmental abnormalities
Branching up to terminal bronchi
Bronchopulmonary epithelium -> amniotic fluid
Pneumocyte precursors
Vasculature (artery/veins)
Separation of thorax/peritoneal (7wk)
Branching abnormalities, CDH, CLE, CPAM, pulmonary lymphangiectasia
Cannulicular
1) structures?
2) developmental abnormalities?
-Terminal bronchioles/respiratory bronchioles
-Type two-> type one pneumocytes
-Viable lung at 25 weeks
Pulmonary hypoplasia, surfactant deficiency, alveolar capillary dysplasia
SACCULAR
1) structures?
2) developmental abnormalities?
-alveolar ducts
-Complete bronchial division
-Gas exchange = alveolar/capillary membrane
2) pulmonary hyperplasia, surfactant deficiency
ALVEOLAR
1) structures?
2) developmental abnormalities?
1) alveoli
-Microvasculature
2) surfactant deficiency, CLE, PHTN
PNEUMOCYTES
1) percent surface area of alveoli?
2) which secrete surfactant?
3) which is progenitor cell?
1) I = 90% II = 10%
2) type 2
3) type 2
FETAL LUNG FLUID
1) how much volume? Equal to what on PFT?
2) production rate near term?
3) how is Cl- transported and pulmonary epithelia?
4) what inhibits fetal lung fluid production?
1) 20–30 ML/KG; FRC
2) 4–5, ML/KG/HR
3) actively on basal side
4) Epi (delivery stress), B-adrenergic agonists
ABSORPTION OF FLF
1) prior to birth, function of respiratory epithelium changes from _____ secreting to _____ absorbing.
2) FLS decreases by ___, prenatally, ___ during active labor and ___ postnatal.
3) why is it helpful to have fluid in lungs at birth?
1) chloride, sodium
2) 1/3
3) P~T/r ⬆️ radius of airways allows for a lower pressure to overcome surface tension
SURFACTANT
1) what is the largest composition?
2) what percentage is surfactant proteins
1) 50% disaturated Phosphatidylcholine
2) 8%
SURFACTANT
1) chromosome for SP-A
2) chromosome for SP-B
3) chromosome for SP-C
4) chromosome for SP-D
1) 10
2) 2
3) 8
4) 10
SURFACTANT
1) which is the most abundant?
2) hydrophobic?
3) express last (early third trimester)
4) assist w/ tubular myelin formation?
5) promotes surface absorption of phospholipid?
6) aids in host defense?
1) SP-A
2) SP-B, C
3) SP-D
4) SP-A, B
5) SP-B, C
6) SP-A, D
SURFACTANT
1) which SP has no known mutations?
2) which homozygotes deficiency is autosomal recessive? Timeline of symptoms?
3) which is autosomal dominant? Timeline?
1) SP-A, D
2) SP-B @birth
3) SP-C months ➡️ interstitial lung disease
SURFACTANT
1) what is the most common known genetic cause of surfactant deficiency? Inheritance?
2) mechanism of action of this protein?
3) timeline?
1) ATP-binding Cassatt member A3 deficiency (ABCA3 deficiency); autosomal recessive
2) assist with transport of lipids; deficiency lacks DPPG, and PG. Decreased lamellar bodies.
3) soon after birth to childhood
SURFACTANT
1) ___ % of secreted surfactant is recycled
2) what is the turnover time?
1) 95%
2) 10 hours
SURFACTANT
what is Survanta made from and what does it contain?
Minced bovine long
SP-B and C (small amounts.)
No SP -A
SURFACTANT
What is infasurf and what does it contain?
Bovine lung lavage
SP-B, C
No SP -A
SURFACTANT
What is Curosurf made from and what does it contain?
Minced porcine lungs
SP-B, C
No SP-A
SURFACTANT
What is Alveofact made from and what does it contain?
Bovine lung lavage
SP-B, C
No SP-A
SURFACTANT
Laplace’s Law
P=2T/r
“LaPressure’s Law”
Pressure is directly proportional to ST and indirectly to radius.
CONTROL OF BREATHING
Boyles Law
P1V1=P2V2
APNEA
1) define apnea
2) define periodic breathing
1) no airflow for >20 seconds
2) 3 respiratory pauses with more than 3 sec between for up to 20 seconds
Ventilation
Ideal ventilation:perfusion
Va/Q should = 1
Anything else = VQ mismatch = hypoxemia
VENTILATION
ventilation equation
Va= (tidal volume - dead space) x RR
MECHANICS
1) resistance equation
2) most respiratory resistance
R = change in pressure (cmH2O / change in flow(L/s)
Chest wall (25%), airway (55%), lung tissue (20%)
What part of the respiratory system has the most resistance?
About 50% of airway resistance is due to nasal resistance
Poiseuille’s Law
Flow = [change in pressure x constant x (radius)4] / [8 (length X viscosity)]
Radius to the 4th power
What happens to the resistance if the diameter of an ETT increases from 2 to 4 mm
If the diameter goes from 2 to 4 than the radius will increase from 1 to 2. And the resistance will be 16 times less because resistance is indirectly proportional to r ^ 4.
Compliance equation
Elastance equation
C=changing vol / changing pressure
-Compliance is the slope of the volume pressure curve
E= changing pressure / changing vol
-elastance is inverse of compliance
How does compliance differ from neonates to adults?
Greater chest wall compliance because bones are more Cartlidge and soft and compliant compared to hard adult ribs.
1) How does compliance differ from premature to term infants?
2) How does RDS change compliance?
1) premature infants, have more compliant lungs
2) sentence with RDS have stiffer lungs. Flat volume pressure curve. Less compliant lungs
MECHANICS
What happens to compliance at both high and low lung volumes?
Compliance decreases because very small volume changes require large pressure changes.
What are disease states that lead to low FRC, and high FRC
1) low: RDS-> atelectasis and collapse
2) high: MAS, chronic lung disease, using excessive vent pressures
MECHANICS
Define “time constant”
Time constant equation
How quickly the lungs can empty.
Also, how long it takes for alveolar and proximal airway pressure to equilibrate.
TC= resistance x compliance 
MECHANICS
One time constant = ____% volume
Two time constant
Three time constants
3-5 time constants
63%
86%
95%
3-5: necessary to allow adequate time for inspiration and expiration
MECHANICS
1) Healthy, newborn time constant?
2) RDS
3) CLD
1) 0.09-0.15
2) lower 0.05 (decreased lung compliance, and mildly increased airway resistance)
3) higher >0.15 (decreased lung compliance, and markedly, increased airway resistance
MECHANICS
What is increase in neonates compared to adults?
Respiratory rate
Residual volume
Minute ventilation (TV x RR)
Alveolar ventilation
Chest wall compliance (soft compliant ribs)
Lung tissue resistance (more dense)
Oxygen consumption
MECHANICS
What is decreases in neonates compared to adults?
Tidal volume
Total lung capacity
Inspiratory capacity
Vital capacity
Time Konstant
Lung compliance (stiffer lungs)
Muscle strength
MECHANICS
What is the same in neonates and adults?
 Dead space
Functional residual capacity
PATH
Sequestration vs CPAM
Sequestration: “sequestered in time out” not functioned, not connected to bronchial tree, systemic circulation, most likely to cause respiratory distress
CPAM: fed by Pulm circulation,
Both unilateral, both regress in utero.
OXYGEN
1) Define paO2
2)Each hemoglobin contains ___ sites that combine to oxygen
3) define O2 sat
1) Partial pressure of oxygen dissolved in the plasma of arterial blood. (Not bound to Hgb)
2) 4 Fe++ Heme
3) % hgb O2 binding sites that are saturated with O2.
OXYGEN
1) O2 content equation
1) O2 con= bound to hgb + dissolved
= (1.34 x Hb x O2sat) + (0.003 x paO2)
CO2
1) how is majority transferred in blood
1) bicarb ions (70%) vs 10% dissolved
BPD
classification
mild: 02 at 28d + room air at 36 wks
Moderate: 02 at 28D + < 30% at 36WKS
Severe: 02 at 28D + >= 30% at 36WKS or CPAP
Factors associated with accelerated long maturation and surfactant production
1) chorioamnionitis
2) chronic maternal hypertension
3) hemoglobinopathy
4) incompetent cervix
5) IUGR
6) maternal cardiovascular disease
7) placenta, infarction
8) pregnancy, induced, hypertension
9) prolong rupture of membranes 
Pulsus paradoxus occurs when the <increase/decrease> in <systolic/diastolic> blood pressure during <inspiration/expiration> is exaggerated and > ___mm Hg.
decrease in systolic blood pressure during inspiration is exaggerated and > 10 mm Hg.
Which surfactant protein is not associated with human disease.
A, B, C are associated with human disease. D Does not
Most critical: b chromosome 2 (b is the second letter), c on chromosome 8 causes disease later.
A tubular myelin formation.
8% of surfactaht.
La places law
P = 2T/r
