physiology Flashcards
forces keeping alveoli open
transmural gradient
pulmonary surfactant - reduces alveolar surface tension
alveolar interdependence - If alveolus starts to collapse the surrounding alveoli are stretched then recoil exerting expanding forces in collapsing alveolus to open it
elastic forces promoting alveolar collapse
elastic recoil of lungs + chest wall
alveolar surface tension (surfactant REDUCES surface tension - premature babies need to overcome high surface tension to inflate lungs)
how does a pneumothorax effect transmural pressure gradient?
abolishes it - by raising intrathoracic pressure -> leading to lung collapse
which pressure must decrease to allow air to flow into lungs during inspiration
interalveolar pressure must become less than atmospheric pressure for air to flow into lungs during inspiration
- before inspiration they are equal, expansion of lungs makes intralveolar pressure fall (boyles law)
boyles law
at any constant temp the pressure exerted by a gas varies inversely with the volume of the gas
(increase in size of lungs makes intraalveolar pressure fall)
muscles of respiration (major, acessory of inspiration, muscles of active respiration)
major = diaphragm + external intercostal muscles
accessory of inspiration (contracts only on forceful inspiration) = sternocleidomastoid, scalenus, pectoral
muscles of active expiration (contracts only during active expiration) = abdominal muscles, internal intercostal muscles
what can be measured by spirometry
tidal volume
inspiratory reserve volume
expiratory reserve volume
inspiratory capacity
vital capacity
whatlung measurements can NOT be measured by spirometry
residual volume
functional residual capacity
total lung volumes
inspiratory / expiratory reserve volumes
IRV = extra volume of air that can be maximally inspired over + above the typical resting tidal volume
ERV = extra volume of air that can be actively expired by maximal contraction beyond the normal volume of air after a resting tidal volume
residual volume
minimum volume of air remaining in the lungs even after a maximal expiration
(tidal volume = volume of air entering or leaving lungs during a single breath)
inspiratory capacity? how can it be calculated?
max volume of air that can be inspired at the end of a normal quiet expiration
IC = IRV + TV
*functional residual capacity? how can it be calculated?
volume of air in lungs at end of normal passive expiration
(FRC = ERV + RV)
vital capacity
max volume of air that can be moved out during a single breath following a maximal inspiration
VC = IRV + TV + ERV
how does emphysema affect residual volume?
residual volume increases as elastic recoil of lungs is lost
affect of airway obstruction on FVC, FEV1 + FEV1/FVC%
FVC - normal
FEV1 = low
FEV1/FVC% = low!
affect of lung restriction on FVC, FEV1 + FEV1/FVC%
FVC = low
FEV1 = low
FEV1/FVC% = normal!
affect of combination of airway obstruction + restriction on FVC, FEV1 + FEV1/FVC%
all LOW
FVC, FEV1 in asthma vs COPD
COPD - smaller FVC + FEV1,
–> FEV1/FVC post bronchodilator - <70%
asthma –> FEV1/FVC = <75%
does parasympathetic or sympathetic activation cause bronchodilation
sympathetic -> bronchodilation
para -> bronchoconstriction
effect of decreased pulonary compliance
greater change in pressure needed to produce a given change in volume (lungs are stiffer), causes SOB (esp on exertion)
restrictive pattern on spirometry
causes of decreased lung compliance
pulmonary fibrosis
pulmonary oedema - **heart failure
lung collapse
pneumonia
absence of surfactant
causes of increased pulmonary compliance
if elastic recoil lost -> emphysema, hyperinflation of lungs (have to work harder to get air out)
compliance increases with age
when is work of breathing increased
decreased pulmonary compliance
airway resitance increased
elastic recoil decreased
a need for increased ventilation
pulmonary ventilation vs alveolar ventilation
Pulmonary ventilation = volume of air breathed in + out per minute
- increase -> increase tidal volume + resp rate
–> more advantageous to increase depth of breathing due to dead space
Alveolar ventilation = volue of air exchanged between atmosphere + alveoli per min
–> Alveolar ventilation is less than pulmonary ventilation due to presence of anatomical dead space
ventilation vs perfusion
Ventilation = rate gas passes through lungs
Perfusion = rate blood passes through lungs
alveolar dead space
mismatch between air in alveoli + blood in pulmonary capillaries
- Ventilated alveoli not adequately perfused with blood = alveolar dead space
o V small, of little significance in healthy
o Could increase significantly in disease
- Accumulation of CO2 in alveoli as a result of increased perfusion decreases airway resistance leading to increased airflow
- Increased alveolar O2 conc as a result of increased ventilation causes pulmonary vasodilation which increases blood flow to match larger airflow
affect of pulmonary arterioles on decreased O2
vasoconstriction
- vasodalite on increased O2
(systemic arterioles do opposite)
HbF compared to Hb
interact less with 2,3 biphophoglycerate in RBCs
has a higher affinity for O2 - compared to adult Hb
HbF curve shifted to left compared to Hb
ALLOWs O2 transfer from mother to foetus even if pO2 is low
