= Mechanical ventilation
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\b[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.<What Is a Ventilator? by NHLBI>[Opening explanation, machine and interfaces]{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 is
$$
p_{\rm aw}(t)=p_0+\frac{V(t)}{C}+R\dot V(t).
$$
Here $V$ 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%.<Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome by the Acute Respiratory Distress Syndrome Network>[Abstract, Methods and Results]{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.
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