Library

Notes: There is a variable delay between a reduction in alveolar Po2 and the decrease in arterial oxygen saturation recorded on a pulse oximeter. The decrease in arterial oxygen saturation in response to disconnexion of a paralysed patient from the breathing system, oxygen supply failure with continued mechanical ventilation and disconnexion of the fresh gas supply to Mapleson D and circle absorption breathing systems were studied by simulations on the MacPuf computer model of the cardiorespiratory system. The simulations revealed that there were marked differences between the rate of arterial desaturation which resulted from each of the three types of oxygen supply failure and that arterial oxygen saturation may reach dangerous levels before a pulse oximeter alarm is activated.

Notes: Noninvasive methods of determining cardiac output (by thoracic electrical bioimpedance) and arterial pressure (by intermittent oscillometry) were used to record minute-by-minute changes in heart rate, mean arterial pressure, stroke volume, cardiac output and systemic vascular resistance following induction of general anaesthesia and laryngoscopy and intubation in 60 healthy female patients who were either unpremedicated, or premedicated with temazepam or papaveretum-hyoscine. Anaesthesia was induced with a sleep dose (3–5 mg.kg−1) of thiopentone and maintained with 70% nitrous oxide in oxygen with 0.5–1% enflurane. Tracheal intubation was facilitated by administration of vecuronium 0.1 mg.kg−1. Mean arterial pressure and cardiac output decreased maximally 5 min after induction in all premedication groups by mean estimates of 21–25% and 14–22% respectively. Heart rate increased initially one minute after induction, but decreased to less than the baseline value 5 min after induction. Systemic vascular resistance was unchanged. The stimulus of laryngoscopy and tracheal intubation was accompanied by a significant pressor response and tachycardia one minute after intubation (with mean increases in mean arterial pressure and heart rate of 29–34% and 22–33% respectively). The increase in mean arterial pressure was secondary to an increase in systemic vascular resistance (36–57%), and was accompanied by a decrease in stroke volume (– 25 to –31%). These changes were significant in all three groups. Cardiac output decreased only in unpremedicated patients. There were wide variations in the different haemodynamic indices. The 5th and 95th centiles for the decreases in mean arterial pressure and cardiac output during induction were –17 to –26, –21 to –33, and –21 to –35mmHg, and –0.7 to –2.0, –0.7 to –2.3, and –0.2 to –1.31.min−1 respectively in unpremedicated patients and those premedicated with papaveretum-hyoscine, or temazepam. Corresponding values for increases in mean arterial pressure and systemic vascular resistance, and decreases in stroke volume following laryngoscopy and intubation, were 16 to 33, 16 to 31.5, and 15 to 31 mmHg; 5.0 to 8.6, 3.5 to 10.2, and 4.3 to 7.8 mmffg.min.−1; and –19 to –31, –11 to –32.5, and –9 to –21 ml respectively.