RESPIRATION PHYSIOLOGY: VENTILATION
Ventilation Pathophysiology

PATHOPHYSIOLOGY OF RESPIRATORY VENTILATION

A. Physiological Classification

CAUSE EXAMPLE PATHOPHYSIOLOGY
Muscle Excitation Inadequate muscle
excitation
Polio Destruction of motor nerves
CNS depression
Elastic Force Increased stiffness (or Compliance decrease)
chest wall Skeletal deformity (e.g. kyphoscoliosis)
lung tissue Fibrosis (e.g. silicosis, asbestosis, black lung)
surface tension Hyaline membrane disease (e.g. respiratory distress syndrome of the newborn)
space occupying lesion Thoracic cancer
Airway Resistance Increased airway resistance
upper airway Aspirate solid object
Laryngospasm
Croup
lower airway: acute Asthma
lower airway: chronic COLD or COPD (Chronic Obstructive Lung Disease or Chronic Obstructive Pulmonary Disease) chronic bronchitis
emphysema

(Note:  SIDS -- Sudden Infant Death Syndrome)

B. Clinical Classification

1. Restrictive

a. associated with reduced total lung capacity
b. due to increased stiffness
c. diagnosed from TLC or C

2. Obstructive

a. associated with reduced air velocity
b. due to increased airway resistance
c. diagnosed from Raw or FEV1/VC (< 80%) or Peak Exp. Flow Rate (PEF)
d. "pink puffer" = emphysema & "blue bloater" = chronic bronchitis
e. acute (e.g. asthma) and chronic pulmonary disease can be distinguished as acute disease is relieved by broncodialator but chronic disease is not releaved

3. CNS Disease

a.    reduced muscle stimulation by the nervous system
b.    reduced muscle strength
c.    reduced muscle strength can be diagnosed from maximum inspiratory and expiratory pressure measurement

SUMMARY (==>)

C. Pathophysiology of Emphysema

1. characteristics (==>)

a. degeneration of lung tissue (irreversible) -- pathological diagnosis
b. high RV and FRC and TLC (large, barrel chest)
c. low VC (frequently)
d. high Raw on expiration, while inspiration may be normal (check-valve effect)

2. physiological basis

a. loss of lung tissue causes RV & FRC & Ppl in the relaxed position
b. forced expiration leads to further Ppl, which increases airway compression on expiration
c. hence, on expiration, increased airway resistance and gas trapping