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mechanism responsible for pulmonary gas exchange disorders
impaired ventilation;perfusion ratio
impaired diffusion capacity
alveolar hypoventilation
what is normal level of V/Q
(ventilation ~4L/min; perfusion ~5L/min). this balance ensures efficient gas exchange
changes in ventilation-perfusion ratio
decreased V/Q (<0.8, shunt/like states)
perfusion is preserved but ventilation is reduced
seen in = chronic bronchitis, asthma, pneumonia
consequences = alveoli are perfused but poorly ventilated → hypoxemia and hypercapnia
increased V/Q (>0.8, dead space states)
ventilation is adequate but perfusion is reduced
seen in = pulmonary embolism, emphysema
consequences = wasted ventilation, poor oxygen uptake, hypoxemia
pulmonary gas exchange abnormalities (impaired diffusion capacity)
reduced transfer of gasses (especially O2) across the alveolo-capillary membrane, even with normal ventilation and perfusion
determinants of diffusion = surface area, membrane thickness, partial pressure gradient, capillary transit time and gas solubility
causes:
- pulmonary fibrosis = thickened interstitium → decreased gas transfer
- emphysema = destruction of alveolar walls → decrease surface area
- pulmonary edema = fluid in alveoli/interstitium → thickened barrier
consequences = hypoxemia (more prominent than hypercapnia), exercise intolerance, dyspnea
describe alveolar hypoventilation syndrome
inadequate alveolar ventilation → hypercapnia and hypoxemia. occurs even if lung tissue is structurally normal
Types:
homogenous hypoventilation:
- primary = depressed central drive or neuromuscular weakness (e.g CNS trauma, drug overdose, myasthenia gravis)
- secondary = mechanical limitation of breathing (e.g obesity hypoventilation syndrome, chest wall deformities)
hetergenous hypoventilation=
- ventilation unevenly distributed across lung regions
- common in advanced COPD with emphysema → areas of obstruction, air trapping and V/Q mismatch
consequences = chronic hypercapnia, respiratory acidosis, secondary hypoxemia
breathing control disorders
impaired regulation of respiration by the central nervous system or faulty transmission to respiratory muscles. dysfunction of the respiratory centres in the medulla/pons or impaired chemoreceptor signalling
examples:
- central hypoventilation = absent or reduced automatic breathing
- congenital (“Ondine’s curse”), acquired (brainstem stroke, trauma,
tumor), or drug-induced (opioids, sedatives)
central sleep apnea = intermittent failure of CNS to initiate breaths → periods of apnea during sleep. seen in heart failure, opioid use, stroke
neurodegenerative diseases = parkinson’s, ALS → impaired motor neuron function, chest wall rigidity, autonomic dysfunction → hypoventilation
Cheyn-stokes respiration = abnormal pattern of periodic breathing characterised by a cyclical waxing and waning of tidal volume, followed by episodes of apnea (no breathing).
consequences = hypoxemia, hypercapnia, secondary systemic hypoxia, risk of respiratory failure