Barotrauma may result in pulmonary interstitial emphysema, pneumomediastinum, pneumoperitoneum, pneumothorax, and/or tension pneumothorax. High peak inflation pressures (>40cm water) are associated with an increased incidence of barotrauma. However, note that separating barotrauma from volutrauma is difficult, since increasing barometric pressure is usually accompanied by increasing alveolar volume.
Experimental models of high peak inflation pressures in animals with high extrathoracic pressures have not demonstrated direct alveolar damage from increased pressure without increased volume as well. Thus, the statement that high airway pressures result in alveolar overdistention (volutrauma) and accompanying increased microvascular permeability and parenchimal injury may be more accurate. Alveolar cellular dysfunction occurs with high airway pressures. The resultant surfactant depletion leads to atelectasis, which requires further increases in airway pressure to maintain lung volumes.
High-inspired concentration of oxygen result in free-radical formation and secondary cellular damage. The same high concsntratiom of oxygen can lead to alveolar nitogen washout and secondary absorption atelectasis.
It has been theorized that pulmonary biophysical and biomecahanical injury in the presence of bacterial lung infections contributes to bacterial translocation and bacteremia.
The heart, great vessels, and pulmonary vasculature lie within the chest cavity and are subject to the increased intrathoracic pressures associated with mechanical ventilation. The result is a decrease in cardiac output due to decreased venous return to the right heart (dominant), right ventricular dysfunction and altered left ventricular distensibility.
The decrease in cardiac output from reduction of right ventricular preload is more pronounced in the hypovolemic patient and in those with a low ejection fraction.
Exaggerated respiratory variation on the arterial pressure wave form is a clue that positive-pressure ventilation is significantly affecting venous return and cardiac output. In the absence of an arterial line, a good pulse oxymetri wave form can be equally instructive. A reduction in the variation after volume loading confirm this effect. These effects will most frequently be seen in patients with preload-dependent cardiac function (that is, operating on the right side of the Starling curve) and in hypovolemic patients or in those with otherwise compromised venous return.
Increased alveolar-capillary permeability secondary to pulmonary inflammatory changes may, alternatively, contribute to increased cardiac output.
RENAL, HEPATIC AND GASTROINTESTINAL EFFECTS
Positive-pressure ventilation is responsible for an overall decline in renal function with decreased urine volume and sodium excretion.
Hepatic function is adversely affected by decreased cardiac output, increased hepatic vascular resistance and elevated bile duct pressure.
The gastric mucosa does not have autoregulatory capability. Thus, mucosal ischaemia and secondary bleeding may result from decreased cardiac output and increased gastric venous pressure.