Relation between airway pressure intrathoracic pressure and lung volume

The degree to which both ITP and lung volume increase during PPV is a function of airways resistance and lung compliance. With reduced compliance, fixed tidal volumes generate greater mean and plateau airway pressures than when compliance is normal. However, for the same tidal increase in lung volume, ITP and pericardial pressure increase similarly in both normal and acute lung injury states despite varying levels of compliance. If lung inflation is sustained and ventricular function normal, as may occur with positive end-expiratory pressure (PEEP), ITP increases more than pericardial pressure, presumably because cardiac volume decreases. Accordingly, ITP may overestimate pericardial pressure during PEEP when left ventricular function is normal. In congestive heart failure, pericardial pressure often exceeds ITP because the pericardium functions as a limiting membrane. However, with progressive increases in PEEP, ITP rises until it approximates pericardial pressure; both pressures will then increase in parallel as PEEP increases further. In heart failure states, hemodynamic effects of PEEP are only seen once ITP and pericardial pressure equalize.

The proportion of airway pressure transmitted to the pleural surface is highly variable. Even the percentage of the increase in airway pressure transmitted to the pericardial surface as PEEP is increased is not constant between individuals. The amount by which either ITP or pericardial pressure will increase cannot be predicted.

Finally, PPV does not increase ITP by similar amounts in all regions of the thorax. Diaphragmatic ITP increases least, while juxtacardiac ITP increases most. Dependent regional ITP exceeds non-dependent ITP by an amount equal to the vertical hydrostatic pressure gradient. Thus, where ITP is measured, if at all, determines both the mean ITP and its swings during pPv.

When tidal volume is kept constant, changes in peak and mean airway pressure reflect changes in the mechanical properties of the lungs and the degree of patient co-operation, but may not reflect changes in ITP. Accordingly, changes in airway pressure should not be used to assess changes in global cardiovascular dynamics in response to PPV under conditions in which lung mechanics vary rapidly.

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