Restrictive ventilatory defects Flashcards
Functions of alveoli
Mechanical- expand on inspiration
shrink on expiration
exert outward traction on small airways
Gas exchange- thin walls- allow gases to move between air and blood
Lung compliance/ elastance
Lung compliance is volume increase per unit pressure increase - measured statically at the functional residual capacity
Not often measured clinically as pleural cavity pressure hard to obtain- oesophageal pressure measured using catheter
Lung elastic recoil (elastance) is reciprocal of compliance
Alveolar wall
Endothelium
Interstitium
Epithelium- these layers are only around .2 micrometers
Type 2 pneumocyte- surfactant contained in lamellated inclusion bodies
Moist to prevent cell death, surfactant contain basement membrane- surface tension
Type I pneumocytes
Type I pneumocytes are involved in the process of gas exchange between the alveoli and the capillaries They are squamous (flattened) in shape and extremely thin (~ 0.15µm) – minimising diffusion distance for respiratory gases -connected by occluding junctions, which prevents the leakage of tissue fluid into the alveolar air space Type I pneumocytes are amitotic and unable to replicate, however type II cells can differentiate into type I cells if required
Type II pneumocytes
- responsible for the secretion of pulmonary surfactant, which reduces surface tension in the alveoli
- They are cuboidal in shape and possess many granules (for storing surfactant components)
- Type II pneumocytes only comprise a fraction of the alveolar surface (~5%) but are relatively numerous (~60% of total cells)
Factors that affect lung compliance
- elastin fibres- this along with surface tension through attraction of h2o molecules causes tension in alveolar wall (elastic recoil of lungs)
- collagen fibres
- surface tension
- surfactant: -reduces surface tension
- increases compliance
- reduces work of breathing
- prevents collapse of small alveoli
- stabilises pulmonary capillaries
- prevents material egress into alveoli
- alveolar size
- lung volume/history
Decreased lung compliance
replacement of elastin fibres with collagen fibres in alveolar walls- stiffening, harder to inflate
pulmonary fibrosis
Respiratory disease of premature newborn- surfactant deficiency
Not matured enough to produce surfactant
Lower compliance due to excess surface tension in alveolar walls for their first breath
Increased lung compliance
emphysema, loss of elastin, destruction of alveolar walls
NOT a restrictive defect
Elastin fibres help resist stretch of alveolar walls and provide support to complex structures of millions of alveoli- no wall means more air in lungs, increased TLC, FRC
INCREASED AIRWAY RESISTANCE
Increase of compliance > Loss of alveolar tethering > Increase of airway resistance
Restrictive ventilatory defect
Reduction of lung volumes
-all volumes/capacities reduced
-minute volume preserved early in disease, but fails later
-total lung capacity preferred for diagnosis
A restrictive ventilatory defect may be caused by a pulmonary deficit, such as pulmonary fibrosis (abnormally stiff, non-compliant lungs), or by non-pulmonary deficits, including respiratory muscle weakness, paralysis, and deformity or rigidity of the chest wall.
Forced expiratory manoeuvre
- Fully inflate lungs
- Forcefully exhale as fast as possible
- Forcefully exhale as far as possible
Spirometry- FVC forced vital capacity
FEV1 forced expiratory volume in first second
both lower in restrictive conditions
Loss of lung compliance
–more negative intra-pleural pressure
–increased work of breathing
–restricted lung volumes
Disturbances of alveolar mechanics
Replacement of elastin fibres with collagen fibres- pulmonary fibrosis
- decreased lung compliance
- restrictive ventilatory defect
- reduced lung volumes, TLC, FEV1, FVC
Surfactant deficiency
- Respiratory distress syndrome- premature newborn, adults in intensive care
Destruction of elastin fibres- emphysema
- increased lung compliance
- obstructive ventilatory defect
- increased airway resistance
