Chapter 4 of 5 - Physiology Course
Breathing moves air; diffusion and blood transport move gases. This chapter links mechanics to hemoglobin and control of ventilation.
Clinical vignettes about hypoxemia or hypercapnia usually require you to separate ventilation (airflow and dead space), perfusion (blood flow to ventilated alveoli), diffusion (barrier thickness and surface area), and binding/transport (hemoglobin content and affinity). The first figure traces oxygen from atmosphere to tissues; the second outlines chemoreceptor integration.
Tidal volume is each breath size; minute ventilation is respiratory rate times tidal volume. Alveolar ventilation subtracts dead space - the portion of each breath that does not reach gas-exchanging alveoli.
Anatomical dead space includes conducting airways that do not participate in gas exchange; physiological dead space also includes alveoli that are ventilated but not perfused (V/Q approaches infinity in the extreme). Rapid shallow breathing can increase the dead-space fraction of minute ventilation and impair CO2 elimination even when total minute ventilation looks high on paper - a pattern relevant to obstructive disease and some restrictive processes.
Each step can become rate-limiting; exam questions often isolate one broken step (shunt, V/Q mismatch, diffusion impairment, anemia).
Ventilation
Fresh air reaches alveoli; alveolar PO2 set by VA and metabolism.
Alveolar-capillary diffusion
Thin barrier; surface area and thickness affect equilibration.
Pulmonary capillary blood
Hemoglobin loads O2; dissolved O2 is a small fraction.
Systemic circulation
CO and regional flow deliver oxygenated blood.
Tissue extraction
Right-shifted Hb curve favors O2 offloading during exercise and fever.

O2 and CO2 move down partial pressure gradients across the thin alveolar-capillary barrier.
Oxygen is transported dissolved (small fraction) and bound to hemoglobin (majority); diffusion from alveolus to capillary depends on partial pressure gradients and barrier integrity.
Formula
O2
Mol. Weight
31.998 g/mol
Sigmoid binding reflects cooperative oxygen binding. Clinical interpretation ties P50 (partial pressure at 50% saturation) to shifts from temperature, pH/CO2, and 2,3-BPG.
Carbon dioxide transport couples to the curve through the Bohr effect (H+ and CO2 favor O2 unloading) and the Haldane effect (deoxygenated hemoglobin carries more CO2 as carbamino species and supports bicarbonate buffering). These links explain why acid-base disturbances and lung disease interact with oxygen delivery beyond simple alveolar gas equations.
Quick Check
Which condition typically shifts the oxyhemoglobin curve to the right, favoring O2 unloading in tissues?
Fill in the Blank
The ratio of alveolar ventilation to perfusion in an ideal lung unit is close to________, matching air delivery to blood flow.
Central chemoreceptors (medulla) respond chiefly to CSF pH reflecting CO2 levels. Peripheral chemoreceptors (carotid bodies) sense hypoxemia, hypercapnia, and acidemia. Integration adjusts minute ventilation to maintain arterial blood gases.
During chronic CO2 retention, renal compensation raises bicarbonate and can shift the central set-point - a reason some patients depend on hypoxic drive; abrupt supplemental oxygen may reduce ventilatory stimulus in selected cases. Sleep, opioids, and brainstem lesions can depress the same integrative pathways, producing patterns of hypoventilation with hypercapnic respiratory failure.
Central sensors are exquisitely sensitive to CO2-related pH changes; peripheral carotid bodies add hypoxemic drive.
Arterial blood gas / CSF chemistry
PaCO2, PaO2, pH, and bicarbonate context.
Peripheral chemoreceptors (carotid bodies)
Strong hypoxia signal; also hypercapnia/acidemia.
Central chemoreceptors (medulla)
Respond to brain ECF pH influenced by CO2 diffusion.
Respiratory pattern generators
Adjust rate and depth of breathing.
Alveolar ventilation changes
Restores blood gases toward the regulated range.
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