[The effect of sedation on pulmonary function]

Opioids, benzodiazepines and hypnotics all affect central respiratory drive, muscular activity of the oropharynx, thoracic wall and diaphragm, bronchomotor tone and pulmonary vascular resistance (PVR), and may thus influence respiratory function during sedation and weaning. Opioids and benzodiazepines will attenuate hypercapnic and hypoxic stimulation of the respiratory centres. Compromise of respiratory drive must also be anticipated with ketamine, in view of recent evidence contradicting earlier findings of central respiratory stimulation. Coordinated muscular activity of the oropharynx is important for airway patency. Since this mechanism is impaired more by benzodiazepines than by ketamine the latter may be advantageous during weaning. Respiratory frequency and tidal volume are both diminished by opioids, benzodiazepines and propofol. The differential impact on intercostal and diaphragmatic muscle activity may prove important in COPD and emphysema. With ketamine spontaneous respiration is increased. Gas distribution and airway pressures are influenced by bronchomotor tone. Bronchodilator effects are well known to arise with ketamine, but have also been demonstrated with benzodiazepines, propofol and some opioids. PVR is a critical factor in respiratory insufficiency. An increase in PVR with ketamine has been found during spontaneous respiration. Since evidence for pulmonary vasodilation during controlled ventilation has been recorded in humans and in vitro experiments, sedation regimens applied in respiratory insufficiency can also include ketamine.