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95 Cards in this Set

  • Front
  • Back
Structures that make up the conducting zone of respiratory tree

What do its walls contain?

where is there cartilage?
nose, pharynx, trachea, bronchi, bronchioles, terminal bronchioles

walls contain smooth muscle

cartilage in trachea, and bronchi
respiratory zone of the respiratory tree
respiratory bronchioles, alveolar ducts, alveoli
what makes up the anatomic dead space
conducting zone of the respiratory tree
what is the job of the conducting zone of the respiratory tree?

respiratory zone?
condicting zone: brings air in and out; warms, humidifies, and filters air

respiratory zone: gas exchange
Pneumocytes

What type of cells?
2 types?
where?
pseudostratified ciliated columnar cells extend to respiratory bronchioles

Type I (alveolar surfaces) for gas diffusion; Type II (only 3%) secrete surfactant
What clears debris in lung alveoli?

How are mucus secretions cleared?
macrophages clear debris in alveoli

swept out of lung to mouth by ciliated cells
Type I pneumocytes

a. where do you find them
b. type of cells
c. job
a. cover 97% of alveolar surfaces
b. squamous cells
c. thin for gas diffusion
Type II pneumocytes
a. type of cells
b. where
c. jobs
a. cuboidal, clustered
b. cover 3% of alveolar surfaces
c. produce surfactant, serve as precurosrs to type I and other type II cells, proliferate in lung damage
Clara cells
a. structure
b. 3 jobs
a. columnar w/secretory granules, nonciliated, lamellar bodies

b. secrete component of surfactant, degrade toxins, act as reserve cells
bronchopulmonary segments

What makes up each bronchopulmonary segment
tertiary (segmental) bronchus + 2 arteries (bronchial and pulmonary) in the center

veins and lymphatics drain along the borders
How are pulmonary arterial pressures kept constant throughout the cardiac cycle
elastic walls
how many lobes

right lung?

left lung?
right = 3

left = 2 lobes + lingula
What is the relationship between the pulmonary artery to the bronchus at the right and left lung hilus
RALS

right anterior, left superior
If you aspirate a peanut, where will it go if you are upright?

if you are supine?
right bronchus (wider and more vertical) --> lower portion of right inferior lobe

superior portion of right inferior lobe
what rib line demarcates the border of the superior and middle lobe in the right lung?
4th rib (horizontal fissure)
In what dermatomal level would you find the oblique fissure from the posterior view of the lung
T2
3 structures that perforate the diapharagm
T8: IVC
T10: esophagus, vagus
T12: aorta (red), thoracic duct (white), azygous vein (blue)

I (IVC) ate (8)
10 eggs (esophagus)
at (aorta) 12
Innervation of the diaphragm

pain in diaphragm refers to where
C3-C5

referred pain to shoulder
What muscles do you use?
a. quiet inspiration
b. quiet expiration
c. exercise inspiration
d. exercise expiration (4)
a. diaphragm
b. passive
c. external intercostals, Scalene, Sternomastoids
d. rectus abdominis, internal and external obliques, transversus abdominis, internal intercostals
You detect a lecithin-to-sphingomyelin ratio of >2.0 in the amniotic fluid.

what does this tell you
fetal lung maturity
Surfactant
-3 jobs
-produced by what type of cells
-decreases alveolar surface tension
-increases compliance
-decreases the work of inspiration

produced by type II pneumocytes
surfactant is made up of what chemical?

In what condition do you see a deficiency
dipalmitoyl phosphatidylcholine (lecithin)

neonatal RDS
5 important lung products
1. surfactant
2. prostaglandins
3. histamine (bronchoconstricts)
4. ACE (AII; inactivates bradykinin)
5. kallikrein (activates bradykinin)
how do ACE inhibitors work in the lung
prevent production of ACE, so increases bradykinin --> cough and angioedema
how do you calculate collapsing pressure on the alvolus?

what happens to collapsing pressure as radius of the alveolus decreases?
collapsing pressure = (2 * surface tension) / radius

tendency to collapse on expiration as the radius decreases (law of Laplace)
Lung volumes

what is the residual volume (RV)? can it be measured with spirometry?
Air in lung after maximal expiration

cannot be measured on spirometry
Lung volumes

Expiratory reserve volume (ERV)
air that can be still breathed out after normal expiration
Lung volumes

Tidal volume
air that moves into the lung with each quiet inspiration typically 500mL
Lung volumes

Inspiratory reserve volume (IRV)
air in excess of the tidal volume that moves into the lung on maximum inspiration
Lung volumes

Vital capacity
TV + IRV + ERV

everything except the residual volume
Lung volumes

Functional residual capacity
RV + ERV = volume in lungs after normal expiration
Lung volumes

Inspiratory capacity
IRV + TV
Lung volumes

Total lung capacity
lc = IRV + TV + ERV + RV
Lung volumes

what is a capacity?
capacity is a sum of 2 or more volumes
What is physiologic dead space?
What are 2 components?
Where do you find the largest component?

how do you calculate it?
volume of inspired air that does not take place in gas exchange

conducting airways (anatomic) + alveoli (functional)

largest contributer is apex of lung

VD = tidal vol. * [(PaCO2 - PeCO2)/PaCO2)]
What is the system pressure at functional residual capacity and how does this affect the balance of lung and chest wall forces?
system pressure is atmospheric

tendency for inward pull of lungs is balanced by the outward pull of the chest wall
FRC
a. what is the airway/alveolar pressure
b. what is the intrapleural pressure
a. 0
b. negative (prevents pneumothorax)
what is compliance?

what are 3 causes of decreased compliance?
change in lung volume for a given change in pressure


pulmonary fibrosis, insufficient surfactant, pulmonary edema
Hb

how many subunits
4 polypeptide subunits (2 alpha, 2 beta)
2 forms of Hb and what are their affinities for O2
T = taut, low affinity

R = relaxed, high affinity (300x)
(When you're relaxed, you do your job better - carry O2)

-positive cooperativity, negative allostery (unlike myoglobin)
5 things that shift Hb from R to T form?

what does this do to the dissociation curve of oxygen?
Cl, H, CO2, 2,3BPG, temperature

shifts dissociation curve right --> decreases O2 affinity --> increases O2 unloading
How does fetal Hb compare to adult Hb
a. in structure
b. affinities
a. fetal has 2alpha and 2gamma subunits

b. lower affinity for 2,3 BPG than HbA --> higher affinity for O2
Methemoglobin
a. what is it?
b. what does it bind?
c. how do you treat?
a. oxidized Hb (ferric Fe3+)
b CN, binds O2 less well
c. use nitrites to oxidize to methemoglobin (binds CN to allow cytochrome oxidase to function)

Then use thiosulfate to bind to CN --> renal excretion

treat Methemglobinemia w/ Methylene blue
Carboxyhemoglobin
a. what does it bind
b. effect
a. binds CO with 200x greater affinity than O2
b. decrease oxygen binding capacity with a left shift in the oxygen-Hb dissociation curve, decreases unloading in tissues
Why does the oxygen-Hb dissociation curve have a sigmoidal shape?

what does it mean if the curev shifts to the right?

what does it mean if the curve shifts to the left?
Hb has positive cooperativity for Hb - affinity increases for each subsequent oxygen molecule bound

right = decreased affinity for oxygen (more unloading)

left = increased affitiny for oxygen, (harder to unload)
5 factors that cause a right shift in the Hb-oxygen dissociation curve
Increase in:
CO2
Acid/Altitude
DPG (2,3 DPG)
Exercise
Temperature

CADET
5 factors that cause a right shift in the Hb-oxygen dissociation curve
Decrease in CADET
CO2
Acid/Alcohol
DPG
Exercise
Temperature

+fetal Hb (higher affinity for oxygen than adult Hb)
Pulmonary circulation

a. resistance?
b. compliance?
a. low resistance
b. high compliance
What is the effect of a decrease in PAO2 (alveolar oxygen) on lung perfusion
causes hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung
3 gases that have perfusion limited ventialtion in the lung

what does this mean
O2, CO2, N2O

gas equilibrates early along the length of the capillary, such that diffusion can increase only if blood flow increases
2 gases that have diffusion limited ventilation in the lung

what does this mean
O2 (emhysema, fibrosis)
CO

Gas does not equilibriate by the time blood reaches the end of the capillary
Patient has pulmonary HTN

if this progresses, what can it lead to
cor pulmonale (RVH/dilation) --> RV failure (JVD, edema, hepatomegaly)
What is the equation for diffusion ventilation of a gas

What is the effect on the equation of emphysema?
Pulmonary fibrosis?
Vgas = A/T * Dk (P1-P2)

A = area
T = thckness
Dk (P1-P2) = difference in partial pressures

emphysema = A decreases
pulmonary fibrosis = T increases
What is normal pulmonary artery pressure?

Pressure associated with pulmonary HTN?

pulmonary pressure associated with exercise?
normal = 10-14 mmHg

HTN >= 25

>35 mmHg
What is the cause of primary pulmonary HTN
inactivating mutation in BMPR2 gene (which normally functions to inhibit vascular smooth muscle prolferation); poor prognosis
COPD
Mitral stenosis
thromboemboli
autoimmune disease
L-R shunt
sleep apnea
living at high altitude

common causes of what
Pulmonary HTN
How does COPD --> pulmonary HTN
COPD destroys lung parenchyma = increases resistance
How does mitral stenosis --> pulmonary HTN
increases resistance, leading to increased pressure
How does recurrent thromboemboli --> pulmonary HTN
decreases cross sectional area
How do autoimmune diseases --> pulmonary HTN
inflammation --> intimal fibrosis --> intimal hypertrophy
How do L to R shunts --> pulmonary HTN
Increase shear stress --> endothelial injury
How does sleep apnea or living at a high altitude --> pulmonary HTN
hypoxic vasoconstriction
If pulmonary HTN is left untreated, what does it cause?
severe respiratory distress --> cyanosis and RVH --> death from decompensated cor pulmonale
What is the formula for pulmonary vascular resistance
PVR = [(pulm. artery pressure) - (P left atrium or wedge)] / CO
equation for vascular resistance?
R = [8(viscosity)(length)]/[(pi)(r^4)]
Oxygen content of blood

how do calculate

What is the normal level of O2 binding capcity?
O2 content = O2 binding capacity * % saturation + dissolved O2

O2 binding capcity = 20.1 mL O2/dL
1g Hb holds how much O2?

How much Hb is in blood?

Cyanosis occurs when deoxygenated Hb reaches what level?
1.34mL O2

normal Hb amount is 15 g/dL

>5g/dL
Oxygen content of blood

how is it affected if Hb falls
oxygen content of blood decreases overall, but not % sat or dissolved O2
Oxygen content of blood

what is the effect of chronic lung disease
arterial PO2 decreases because physiologic shunt decreases the O2 extraction ratio
How do you measure oxygen delivery to tissues
CO * oxygen content of blood
What is the alvoelar gas equation

How can it be approximated
PAO2 = PIO2 - (PACO2/R)
PAO2 = 150 - (PACO2/0.8)

R = respiratory quotient = CO2 produced / O2 consumed
What is the A-a gradient?

what are 3 causes of its increase?
A-a gradient = PAO2 - PaO2 = 10-15 mmHg

increases in hypoxemia (shunting, V/Q mismatch, fibrosis = diffusion block)
Oxygen deprivation

Hypoxemia (low PaO2)

5 causes
High altitude, hypoventilation (normal A-a gradient)

V/Q mismatch, diffusion limitation, R-L shunt (A-a increase)
Oxygen deprivation

Hypoxia (decreased O2 delivery to tissue)

5 causes
low CO
hypoxemia
anemia
CN poisoning
CO poisoning
Oxygen deprivation

Ischemia (loss of blood flow)
Impeded arterial flow
Reduced venous drainage
V/Q

How does the apex of the lung compare to the base of the lung
apex: V/Q = 3 (wasted ventilation)

base: V/Q = 0.6 (wasted perfusion)

both V and Q are greater at the base of the lung
How does exercise affect the V/Q ratio
Exercise --> increase in CO --> vasodilation of apical capillaries (V/Q approaches 1)
Where does TB flourish in the lungs and why
apex - thrives in high O2
What does it mean if V/Q = 0?

will this improve w/100% O2?
airway obstruction (shunt)

NO
What does it mean if V/Q = infinity?

will this improve w/100% O2?
blood flow obstruction(physiologic dead space)

YES
What are 3 forms in which CO2 is transported in the lungs?
1. Bicarbonate (90%)

2. Bound to Hb at N-terminus of globin (not heme) as carbaminoHb
--> CO2 binding favors taut form (O2 unloaded)

3. dissolved CO2 (5%)
Describe the haldane effect
In lungs, oxygenation of Hb caues a release of H+ --> binds to HCO3 --> H2CO3 --> CO2 and water --> release of CO2
Describe the Borh effect
In peripheral tissues, increase in H (from tissue metabolism) --> shift in oxygen dissociation curve to the right --> unloading of O2
High altitude effect
a. ventilation acutely
b. ventilation chronically
c. EPO
d. 2,3 DPG
e. cellular changes
f. bicarb
g. vessels
a. acute increase
b. chronic increase
c. increase EPO --> high Hct and Hb (chronic hypoxia)
d. increase in 2,3 DPG binds to Hb so that Hb releases more O2
e. Increase in mitochondria
f. increase renal excretion of bicarb to compensate for respiratory alkalosis (augment by acetazolamide)
g. chronic hypoxic pulmonary vasoconstriction --> RVH
Response to exercise
a. CO2 production
b. O2 consumption
c. ventilation rate
d. V/Q ratio
e. pulmonary blood flow
f. pH
g. PaO2, PaCO2
h. venous CO2 content
a. increase in CO2 production
b. increase in O2 consumption
c. inc. ventilation rate to meet O2 demand
d. V/Q from apex to base becomes more uniform
e. Increase flow do to inc. CO
f. pH down due to lactic acidosis
g. no change
h. increase
Coal miner's pneumoconiosis

a. type of lung disease
b. where in lung does it affect
c. 2 possible results
a. restrictive, interstitial
b. upper lobes
c. cor pulmonale, caplan's (rheumatoid arthritis, intrapulmonary nodules on CXR)
Type of pneumoconiosis associated with foundries, sandblasting, and mines

shows "eggshell" calcification of hilar LNs

dx? path?
increases susceptibility to what?
silicosis (interstitial, restrictive)

silica in upper lobes disrupts phagolysosomes and macrophages, release fibrinogenic factors --> fibrosis

TB
Type of pneumoconioses

associated with shipbuilding, roofing, plumbing

See white, calcified pleural plaques on lower lobes

histo: golden brown rods resembling dumbells inside of macrophages

dx?
associated with what 2 conditions?
asbestos

bronchogenic carcinoma and mesothelioma
stain to see asbestos

what happens once it is enhaled
Prussian blue

ingested by macrophages
What happens in neonatal respiratory distress syndrome?

what is the lecithin/sphingomyelin ratio in the amniotic fluid with this disease?

what is the risk associated with persistently low O2 tension
surfactant deficiency --> increased surface tension --> alveolar collapse

L/S < 1.5

PDA
Surfactant
a. type of cells that make it
b. when in gestation do they start production
a. type II pneumocytes
b. 35th week
Treatment for Neonatal respiratory distress syndrome? (3)

Why not supplemental oxygen?
maternal steroids before birth, artificial surfactant for infant, thyroxine

oxygen can result in retinapathy of prematurity
Prematurity
maternal diabetes (elevated insulin)
cesarean delivery (decreased release of fetal glucocorticoids)

risk factors for what?
neonatal respiratory distress syndrome
Trauma
Sepsis
Shock
Gastric aspiration
Uremia
Acute pancreatitis
Amniotic fluid embolism

risk factors for what?
acute respiratory distress syndrome
Acute respiratory distress syndrome

what causes it?

pathologically, what happens?
damage to alveoli from neutrophilic substances toxic to alveolar wall --> coag cascade or free radicals --> increased alveolar capilllary permeability --> exudate

Hyaline membranes + alveolar fluid