IPPV - complications of ventilation

Haemodynamic complications

Venous return depends on passive flow from central veins to right atrium. An increase in intrathoracic pressure is transmitted across compliant lungs to increase right atrial pressure and reduce venous return. This is less of a problem with stiff lungs (e.g. ARDS), but will be exacerbated by inverse I:E ratio and high PEEP. As lung volume is increased by IPPV, the pulmonary vasculature is constricted. Pulmonary vascular resistance and diastolic volume of the right ventricle rise and, by septal shift, left ventricular filling is impeded. These effects all contribute to a reduced stroke volume. This can be minimised by reducing airway pressure, avoiding prolonged inspiratory time, and maintaining blood volume.

Ventilator trauma

Barotrauma relates to gas escape into cavities and interstitial tissues during IPPV. Distending volume and high shear stress are probably responsible rather than high pressures. It is most likely to occur with high VT. It occurs in IPPV and conditions associated with lung overinflation (e.g. asthma). Tension pneumothorax is life-threatening and should be suspected in any patient on IPPV who becomes suddenly agitated, tachycardic, hypotensive, or exhibits sudden deterioration in their blood gases. An immediate chest drainage tube should be inserted if tension pneumothorax develops. Prevention of ventilator trauma relies on avoidance of high VT and high airway pressures.

Nosocomial infection

Endotracheal intubation bypasses normal defence mechanisms. Ciliary activity and cellular morphology in the tracheobronchial tree are altered. The requirement for endotracheal suction further increases susceptibility to infection. In addition, the normal heat and moisture exchanging mechanisms are bypassed, requiring artificial humidification of inspired gases. Failure to provide adequate humidification increases the risk of sputum retention and infection. Maintaining ventilated patients at 30* upright, head tilt reduces the incidence of nosocomial pneumonia.

Acid–base disturbance

Over-ventilating patients with chronic respiratory failure may, by rapid correction of hypercapnia, cause respiratory alkalosis. This reduces pulmonary blood fl ow and may contribute to hypoxaemia. Respiratory acidosis due to hypercapnia may be due to inappropriate ventilator settings or may be desired to avoid high VT and ventilator trauma.

Water retention

Vasopressin released from the anterior pituitary is increased due to a reduction in intrathoracic blood volume and psychological stress. Reduced urine flow thus contributes to water retention. In addition, the use of PEEP reduces lymphatic flow with consequent peripheral oedema, especially affecting the upper body. High airway pressure reduces venous return, again contributing to oedema.

Respiratory muscle wasting

Prolonged ventilation may lead to disuse atrophy of the respiratory muscles with subsequent weaning difficulty.