Hyperventilation accelerates the rise of arterial blood concentrations of desflurane in gynecologic patients

OBJECTIVES: Under a constant inspired concentration, the uptake of a volatile anesthetic into the arterial blood should mainly be governed by alveolar ventilation, according to the assumption that the patient's cardiac output remains stable during anesthesia. We investigated whether ventilation volume affects the rate of desflurane uptake by examining arterial blood concentrations. METHOD: Thirty female patients were randomly allocated into the following three groups: hyperventilation, normal ventilation and hypoventilation. Hemodynamic variables were measured using a Finometer, inspiratory and end-tidal concentrations of desflurane were measured by infrared analysis, and the desflurane concentration in the arterial blood (Ades) was analyzed by gas chromatography. RESULTS: During the first 10 minutes after the administration of desflurane, the Ades was highest in the hyperventilation group, and this value was significantly different from those obtained for the normal and hypoventilation groups. In addition, hyperventilation significantly increased the slope of Ades-over-time during the first 5 minutes compared with patients experiencing normal ventilation and hypoventilation, but there were no differences in these slopes during the periods from 5-10, 10-20 and 20-40 minutes after the administration of desflurane. This finding indicates that there were no differences in desflurane uptake between the three groups after the first 5 minutes within desflurane administration. CONCLUSIONS: Hyperventilation accelerated the rate of the rise in Ades following desflurane administration, which was time-dependent with respect to different alveolar ventilations levels.

Effect of venous hypercarbia and hyperventilation on myocardial contractility in canine haemorrhagic shock.

To study the effect of venous hypercarbia on myocardial contractility, haemorrhagic shock was produced in six healthy mongrel dogs by ex-sanguination of 15 ml of blood/kg body weight every 20 minutes till a loss of 45 ml/kg was achieved. After recording haemodynamic and respiratory parameters, the dogs were hyperventilated by positive pressure ventilation for 30 minutes and haemodynamic and blood gas parameters reassessed. During haemorrhagic shock, mean cardiac output decreased from 4.23 l min to 0.98 l min (p < 0.01), stroke index from 2.25 to 0.35 ml/kg (p < 0.05) and left ventricular stroke work index from 3.72 to 0.19 g. m/kg. The mean mixed venous pCO2 increased from 35 mmHg to 56.7 mmHg (p < 0.05). During hypoventilation, mixed venous pCO2 decreased to 40 mmHg (p < 0.05) and without any volume replacement, mean cardiac output increased 2.5 l min (P < 0.05), stroke index to 1.13 ml/kg (p < 0.05) and left ventricular stroke work index, and index of myocardial contractility, increased to 0.78 g.m/kg (p < 0.05). Thus, although hypovolaemia is the major cause of low cardiac output in haemorrhagic shock, this study shows that venous hypercarbia (which probably indicates tissue respiratory acidosis) further worsens circulatory failure by decreasing myocardial contractility. Hyperventilation improves cardiac functions and increases output by relieving tissue hypercarbia in spite of persistent hypovolaemia.