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Exhalation is the outward movement of gas from the lungs through the airways. During ordinary quiet breathing, relaxation after inhalation allows elastic recoil to reduce lung volume. Forceful expiration can additionally involve active muscles.^[ref] The term identifies a flow phase, rather than one universal muscle-activation pattern.

For an ideal passive compartment, let $V$ be the excess volume above equilibrium with the outlet pressure. With airway resistance $R$ and respiratory-system compliance $C$,An original example uses $R=10$ cm H${}_2$O·s/L, $C=0.06$ L/cm H${}_2$O and $V_0=0.60$ L. The time constant is 0.60 s, leaving about 0.221 L excess volume after one time constant. After three time constants, only about 0.030 L remains. These are model calculations, not recommended expiration times.

The flow-driving pressure difference is between alveolar pressure and the pressure at the open airway. Pleural pressure affects the distension and geometry of the lung and airway but is not interchangeable with either of those endpoint pressures. Active expiration can also narrow intrathoracic airways, so greater effort need not produce proportionally greater flow.^[ref]

The linear decay model is therefore useful for isolating resistance, compliance and available time, while measured flow can reflect changing airway geometry, active effort or multiple compartments. Completing one expiratory interval is a mechanical event; removing a given amount of carbon dioxide additionally depends on the composition and origin of the expired gas.

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.

Inspiratory capacity, IC, is the maximum volume that can be inhaled from the end of a quiet expiration to maximal inspiration. Its lower reference is functional residual capacity, and its upper reference is total lung capacity:The last expression combines tidal volume with inspiratory reserve volume.^[ref]

For stipulated total lung capacity 6.0 L and functional residual capacity 2.5 L, IC is 3.5 L. If tidal volume is 0.5 L, the corresponding inspiratory reserve volume is 3.0 L. The two descriptions use the same maximum inspiratory endpoint but different starting points.

The starting point is essential when interpreting a change. In an original comparison, keep total lung capacity at 6.0 L while moving the quiet end-expiratory level from 2.5 to 3.2 L. IC falls from 3.5 to 2.8 L, although the maximum inspiratory volume has not changed. Thus a lower inspiratory capacity need not imply a lower total lung capacity; an independently specified baseline is required to distinguish the possibilities.

Inhalation through a volume-measuring apparatus can determine an inspiratory increment without directly measuring the gas already present in the lungs. A stable starting level and complete endpoint connect that increment to the defined capacity. The technical standard therefore links capacity maneuvers with an identified FRC-level measurement.^[ref] The values in the example illustrate endpoint bookkeeping rather than reference limits for a particular person.

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.

Negative-pressure ventilation assists inhalation by reducing the pressure outside the chest relative to that at the airway opening. A chamber encloses the torso while the mouth and nose communicate with gas outside the chamber. Lower external pressure allows chest expansion and makes alveolar pressure transiently lower than the airway opening, drawing gas into the lungs.

The original 1929 apparatus report by Philip Drinker and Louis A. Shaw describes a sheet-metal tank, a sealing neck collar and the head supported outside the tank. Alternating tank pressure moved the chest while the head remained exposed to atmospheric pressure.^[ref] This is a concrete distinction between applying a pressure change to the body surface and applying it through an airway interface.

An original static example uses transpulmonary pressure $P_L=P_{\mathrm{alv}}-P_{\mathrm{pl}}$. With an open airway and no flow, suppose alveolar pressure is zero on an atmospheric gauge. Changing pleural pressure from $-6$ to $-10$ cm H${}_2$O raises $P_L$ from 6 to 10 cm H${}_2$O. For stipulated lung compliance $0.05$ L/cm H${}_2$O, the linear model predictsDuring the actual filling transient, pressure differences also overcome airway resistance. The static calculation does not predict the instantaneous flow waveform.

Tank pressure is a boundary condition, not a direct measurement of pleural pressure. Chest-wall mechanics and body geometry affect pressure transmission. Consequently, an equal numerical pressure at a positive-pressure airway interface and a negative-pressure body chamber need not produce identical volume changes or circulatory effects. The useful unifying quantity for lung distension is the pressure difference across the lung, together with its mechanical response.

Positive-pressure ventilation assists inhalation by raising pressure at the airway opening, driving gas into the lungs when that pressure exceeds alveolar pressure. It differs mechanically from spontaneous expansion of the thorax or negative-pressure ventilation, which lowers pressure around the lungs to produce the relevant distending difference. A ventilator's mask or tube supplies the applied airway connection.^[ref]

The direction of flow still depends on a pressure difference, not on whether either pressure is above atmospheric. For a simple resistive path,with positive $Q$ directed inward and $R$ the airway resistance. In an original example, pressures 10 and 8 cm H${}_2$O and $R=4$ cm H${}_2$O·s/L give inward flow 0.5 L/s. Pressures 8 and 10 cm H${}_2$O give outward flow 0.5 L/s. Both pairs are positive relative to atmosphere.

This explains why positive end-expiratory pressure can coexist with exhalation. The applied pressure can remain above atmospheric while elastic recoil produces a still higher alveolar pressure and drives gas outward. At equal opening and alveolar pressures, the same ideal resistive model gives zero flow.

The resulting tidal volume also depends on respiratory-system compliance, airway resistance, duration and any active respiratory muscle effort. The no-flow interval used to interpret plateau airway pressure removes one resistive contribution only under the required measurement conditions.^[ref] Positive pressure is therefore a mode of applying mechanical assistance, not a guarantee of a particular inward flow, volume or gas-exchange result.