respiratory 2 Flashcards
to move gas into the lung, respiratory muscles overcome
- elastic resistance
- resistance to air flow (non elastic resistance)
non-elastic resistance
airflow - 80%
viscous - 20%
the ability to inflate and deflate the lung depends on two properties
compliance and elastance
compliance
a highly compliant lung is easy to inflate
distensibility - stretchability - ease at which the lung will expand
lung is 100x more distensible than a balloon
pulmonary and/pr thoracic
elastance
tendency to recoil to initial size after the distention
elastance is created by
elastance proteins
- resist distension and cause recoil
a lung that is highly complaint will tend to have
low elastance
to be complaint we have to overcome
elastance
surface tension
important at low lung volumes
- alveolar air-liquid interface
- inwardly directed force 0 tends to reduce alveolar diameter
- oppose alveolar expansion
- lung collapse (particularly in small alveoli)
surfactant
lowers surface tension - reduces attractive forces of hydrogen bonding between H2O molecules
surfactant is produced by
alveolar type 2 pneumocytes
alveoli radius
small alveoli generate more surface tension
as alveolar radius decreases, surfactants ability to lower surface tension increases
why might we want smaller alveoli
to increase surface area
what do we do to reduce surface tension
line the alveoli with surfactant secreted by type 2 pneumocites
what happens when there is no surfactant
lack of surfactant creates huge surface tension requiring high expansion pressures
infant respiratory distress syndrome
premature birth
surfactant not produces at high levels until 34 weeks gestation so some very preterm babies don’t have enough surfactant
low compliance lung
stiff lung
extra work required for normal inspiration
low compliance lung may be caused by
fibrosis - decrease in pulmonary compliance
high compliance lung
floppy lung
extra work is required for expiration
elastic tissue is damaged
non-elastic resistance
35%
airway resistance
depends on the diameter
as airways get smaller this increases
mucous resistance
depends how much mucous there is in the transmitting pathways
increased in response to histamine (histamine increases mucous secretions and viscosity)
histamine receptors
HIR - volume
H2R - viscosity
mucosal oedema
release of fluid from the blood into the lungs
caused by increase in permeability leading to transduction of fluid and macromolecules through wide intercellular gaps
chronic bronchitis
too much mucous produced by the lungs
cystic fibrosis
CFTR mutation
chloride channel
loss of ability too regulate chloride loss which changes osmotic gradient and affects mucous production
bronchodilation
B2-adrenergic receptor activation
mostly endocrine but some nervous
bronchoconstriction
muscarinic cholinergic re emptor activation
also histamine H1 receptor
bronchomotor tone
parasympathetic tone controls bronchomotor tone
increase in parasympathetic tone increases acetyl choline produced and vice versa
other local effects controlling acetylcholine reflex constriction
inhalation of smoke, dust, chemical irritants
arterial hypercapnia
cold
pulmonary emboli
bronchodilator endocrine
adrenaline causes bronchodilator using b2 adrenergic receptor
beta agonists cause bronchodilation
beta antagonists cause bronchoconstriction
measuring R
hard to measure resistance directly
measure its effects on function instead
PEF
peak expiratory flow
FEV1
forced expiratory volume in one second
FEV1/FVC
FEV/forced vital capacity
FVC
forced vital capacity
how much air can be taken out of fully inflated lung
3 main things causing respiratory disease
- respiratory muscles fail
- restrictive disease decreases compliance
- obstructive disease increases resistance
restrictive lung disease
decreases compliance
decreases lung volume
limits expansion
decrease in flow and ventilation causing increase in work required
obstructive lung disease
increase in resistance
flow rate is decreased
increase in work required to overcome resistance to flow
decreased ein airflow causes increase n respiratory times
restrictive lung disorder stats
decreased vital capacity, residual volume, functional residual capacity
obstructive lung disorders
decreased vital capacity, inspiratory and expiratory reserve volume
increased residual volume, functional residual capacity, RV/TLC,
obstructive complications
increased resistance to airflow due to abnormalities within the airway lumen
changes in the wall of the airway
decrease in elastic recoil
obstructive complications examples
asthma, chronic obstructive lung disease
bronchiectasis
cystic fibrosis
bronchiolitis
restrictive defects are caused by
- loss of lung volume
- abnormalities of structure surrounding the lung
- weakness of the inspiratory muscles of respiration
- abnormalities of the lung parenchyma
parenchymal
sarcoidosis - fibrosis idiopathic pulmonary fibrosis pneumonia, pulmonary oedema drug or radiation induced interstitial lung disease
extraparenchymal
myasthenia gravis - Guillain-barre syndrome, muscular dystrophies
diaphragmatic weakness/paralysis
chest wall, kyphoscoliosis
normal FEV1/FVC
80%
normal flow-volume loop
inspiratory is symmetric and convex
expiratory limb is linear
obstructive flow volume loop
peak expiratory flow is reduced
increased residual volume
FEV1/FVC reduced
restrictive flow volume loop
reduction in total lung capacity
FEV1/FVC reduced
