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Inhalation is the inward movement of respiratory gas into the lungs. During ordinary spontaneous breathing, contraction of the respiratory diaphragm and contribution from external intercostal muscles expand the thoracic space; the resulting pressure relationships permit inward flow.^[ref] Positive-pressure ventilation can instead assist inward flow by raising pressure at the airway opening.

The flow-driving difference is between airway-opening pressure and alveolar pressure. In a simple resistive model,where $R$ is airway resistance. For constructed gauge pressures $p_{\mathrm{opening}}=0$ and $p_{\mathrm{alv}}=-2$ cm H${}_2$O, with $R=4$ cm H${}_2$O·s/L, inward flow is 0.5 L/s. These are illustrative pressures, not a measurement or a prescribed breathing pattern.

Transpulmonary pressure answers a separate question:with $p_{\mathrm{pl}}$ the pleural pressure. If the same example has $p_{\mathrm{pl}}=-7$ cm H${}_2$O, the distending difference is 5 cm H${}_2$O. At a later no-flow instant, $p_{\mathrm{alv}}$ can equal atmospheric pressure while $p_{\mathrm{pl}}$ remains negative. The expanded lung can then have positive transpulmonary pressure without continued inward airflow.

It is consequently misleading to use any single negative intrathoracic pressure as a synonym for inspiration. Pleural pressure, alveolar pressure, the applied airway pressure and volumetric flow rate refer to different parts of the mechanical system. Inhalation names the flow phase; the relevant pressure differences explain how it is produced.

Mechanical ventilation assists or replaces the movement of gas into and out of the lungs using a machine. A ventilator can deliver that assistance through a mask or a breathing tube.^[ref] This supports pulmonary ventilation; it does not replace every function of the lungs, circulation or gas exchange.

In positive-pressure ventilation, pressure applied at the airway opening helps drive inhalation. The resulting tidal volume depends on both that pressure history and respiratory mechanics. For a passive single-compartment model, a useful equation isHere $V$ is volume above the selected end-expiratory reference, $C$ is respiratory-system compliance, $R$ is airway resistance, and $p_0$ represents the baseline positive end-expiratory pressure. The model neglects active respiratory muscle pressure and changes in these coefficients.

For constructed $C=0.05$ L/cm H${}_2$O, $R=5$ cm H${}_2$O·s/L, $V=0.5$ L, $\dot{V}=0.5$ L/s and $p_0=5$ cm H${}_2$O, the predicted airway pressure is $5+10+2.5=17.5$ cm H${}_2$O. At zero flow with the same volume, the resistive term vanishes and the model gives 15 cm H${}_2$O. Thus an airway-pressure peak contains different information from a no-flow pressure measurement. These numbers illustrate the equation, not patient settings.

The importance of testing ventilation strategies was demonstrated by a 2000 randomized trial in acute respiratory distress syndrome and acute lung injury. It compared lower and traditional tidal volume strategies indexed to predicted body weight, with different plateau-pressure limits. In 861 participants, reported mortality was 31.0% versus 39.8%.^[ref] The experiment compared complete specified protocols in a defined population; it does not establish one universal setting from tidal volume alone. Physical models explain how pressure and flow interact, while controlled clinical evidence tests consequences that those models cannot supply by themselves.