Mechanisms of Gas exchange Flashcards
the most important muscle in inspiration is? What happens when it contracts
diaphragm
- contraction:
- pushes abdominal contents downward
- increase intrathoracic volume
- decrease in intrathoracic pressure
function of sternocleidomastoid and scalenes in inspiration
- sternocleidomastoid: elevates sternum
- scalenes: elevates upper ribs

air is driven out of the lungs by what between the lungs and atmosphere
reverse pressure gradient
what are the expiratory muscles. Which is most important
- abdominal muscles: most important
- internal intercostals: pull ribs inward and downward
What nerves are responsible for the diaphragm descending and the external intercostal muscles enlarging the thoracic cavity during inspiration
- phrenic nerve
- intercostal nerves
is expiration a passive or active process? Why?
- passive
- accomplished by elastic property of lungs (stretched lungs recoil) and relaxation of the inspiratory muscles
What are the pressures involved in ventilation
- atmospheric
- intra-alveolar
- intra-pleural
**when intra-alveolar < atmospheric; flow of air into lungs
relationship between intra-alveolar pressure and intrapleural pressure throughout the cycle? This creates what type of pressure gradient?
- intra-alveolar pressure > intrapleural pressure
-
transmural pressure gradient
- lung is always stretched
transmural pressure
= alveolar pressure - intrapleural pressure
- lung is always stretched to some degree, even during expiration
lung elastic recoil is due to
- collagen and elastic fibers
- **favors collapse
why are changes in thoracic dimensions accompanied by changes in lung dimensions?
- antagonist action of lung elastic recoil and chest wall elastic forces generates negative intrapleural pressure
- intrapleural pressure and fluid cohesiveness counteract the elastic forces
lung compliance
change in lung volume for a given pressure change
C= change in V/change in P
relationship between lung compliance and lung elasticity
lung compliance is inversely correlated with the lungs elastic properties
- more elastic tissue = decreased compliance
- **if lungs have high compliance, inflation is easier but elastic tissue is less
relate volume of lung with negative pressure outside the lung
- lung is inflated with negative pressure outside
- lung is deflated by decreasing negative pressure outside
Slope of lung volume vs negative pressure outside of lung gives
lung compliance
relate compliance between inspiration and expiration
compliance is different for inspiration and expiration
- for a given pressure, expiratory volume > inspiratory volume
What is pneumothorax? what is the consequence?
- object punctures intrapleural space
- air is introduced
- intrapleural P = atmospheric P
- consequence
- lungs collapse bc no negative intrapleural pressure to keep lungs open
- chest wall springs out bc no negative IPP to prevent chest wall from springing out
what happens to lung compliance in emphysema (obstructive disease)? consequence?
- emphysema: less of elastic fibers in lungs
- compliance increases
- compliance increases with lower lung volumes
- therefore, at a given volume the elastic recoil (collapsing) force on the lungs decreases
- chest becomes barrel shaped

what happens to lung compliance in fibrosis (restrictive disease)?
- stiffning of lung tissues
- compliance decreases
- **lung compliance decreases with high lung volumes

Law of Laplace
- pressure generated by each sphere (alveolus)
-
P = 2T/r
- P= collapsing pressure on alveolus
- T: surface tension
- r: radius
role of surfactant in alveolus
surfactant reduces the collapsing pressure
- disrupts intermolecular forces in the fluid lining the alveoli
collapsed alveoli are called
atelectasis
synthesis of surfactant begins at week what in a fetus?
- week 24
- always present by week 35
equation relating flow of air to resistance
-
Q = change of pressure/R
- Q= airflow rate
what is the primary determinant of resistance
airway radius
R= 8nl/π(r^4)
what is the major site of airway resistance
medium sized bronchi
what ANS system is responsible for relaxation of bronchial smooth muscle
- SNS adrenergic
- via activation of B2 receptors
- i.e. epinephrine/albuterol
what ANS system is responsible for constriction of bronchial smooth muscle
- PNS cholinergic
- activation of muscarinic agonists
presentation
- airway resistance increased
- thickening of walls from inflammation and histamine induced edema
- plugging of airway by secretion of mucus
- airway hyperresponsiveness, constricting spasms
asthma
treatment of asthma
- B adrenergic agonist -> relax SM
- corticosteroids -> decrease inflammation
lungs are protected by a1-antitrypsin. What happens in emphysema?
- collapse of airways and destruction of alveolar walls
-
macrophages release trypsin
- overrides the protective ability of a1-antitrypsin
-
macrophages release trypsin
type A emphysema
-
pink puffers
- mild hypoxemia
- normal PCO2
type B emphysema
- Blue bloaters
- hypoxemia
- hypercapnia: Increased PCO2
elastic forces of the chest wall favor
expansion
Fick’s law
volume of gas transferred/unit time (Vx) = (D x A x change in P) / change in X
- D: diffusion coeff
- A: surface area
- P: partial pressure difference of gas
- X: membrane thickness
the driving force for the diffusion of a gas comes from
partial pressure difference of gas
diffusion coefficient of a gas (D) depends on
- molecular weight
- solubility
diffusion for CO2 is what compared to diffusion of O2
D for CO2 is 20x higher than for O2
how does lung diffusing capacity vary in emphysema? In fibrosis? In anemia? In exercise?
-
emphysema: DL decreases
- destruction of alveoli -> decreased surface area
-
Fibrosis: DL decreases
- diffusion distance increases
-
Anemia: DL decreases
- decreased Hb in RBC
-
Exercise: DL increases
- additional capillaries perfused-> increased surface area
Henry’s law of dissolved gas
Cx = Px x solubility
in solutions (blood), gas is carried in what three forms? give ex
-
dissolved
- nitrogen: only in dissolved form
-
bound
- O2, CO2 bind to proteins in blood
-
chemically modified
- conversion of CO2 to HCO3-