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Gas exchange in the lung occurs by passive diffusion following Fick's Law: the rate is proportional to the partial pressure gradient and membrane area, and inversely proportional to thickness. CO diffuses ~20× faster than O (greater solubility) so in lung disease hypoxemia precedes hypercapnia.

The oxyhemoglobin dissociation curve (Hill, n 2.8) has a sigmoidal shape due to cooperativity: the 4 subunits of Hb change their affinity for O progressively. P 27 mmHg under standard conditions. The Bohr effect shifts the curve to the right (lower affinity, greater O discharge) in conditions of acidosis, hypercapnia and hyperthermia: precisely the conditions of the active tissues that most need O.

The alveolar gas equation states that PAO depends on FiO, barometric pressure and PaCO/R_resp: at higher altitudes (low P_B), PAO falls (altitude hypoxia). The A-a difference (PAO - PaO > 15 mmHg) indicates alteration of gas exchange: shunt, V/Q imbalance (the most common), or diffusion alteration.

The shunt and dead space are the two mechanisms of ventilatory inefficiency. Shunting (Q_s/Q_t > 5%: atelectasis, pneumonia, ARDS) produces hypoxemia that does not respond well to supplemental O because the shunted blood never passes through the alveolus. Alveolar dead space (TEP, emphysema) produces hypercapnia by diluting effective alveolar ventilation.

The Henderson-Hasselbalch equation is the basis of acid-base balance: pH = 6.1 + log([HCO]/0.03·PCO). The lungs rapidly control pH by varying PCO; the kidney slowly controls [HCO]. The four primary disorders (respiratory or metabolic acidosis/alkalosis) and their compensations are diagnosed with arterial blood gases, interpreted in this framework.

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ID:('ky', 39)

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ID:(0, 39)