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Biomedical subjects

D J Sapsford

Publications and source records attributed to D J Sapsford.

10 recordsLinked to original sources
PubMed1992

Continuous measurements of oxygen saturation during haemodialysis.

A new technique for recording and analysing continuous measurements of oxygen saturation (SpO2) by pulse oximeter during haemodialysis was used to compare changes in SpO2 in eight patients during two 4 h periods of dialysis using a cuprophane membrane, once using an acetate dialysate, and once using bicarbonate. The computer-derived patterns of SpO2 show whether hypoxaemia was caused mainly by extrapulmonary abnormalities (ventilatory control) or intrapulmonary abnormalities (V/Q distribution). The patterns of oxygen saturation were analysed for (i) stability, (ii) the lower median 20th centile of SpO2, and (iii) time below a SpO2 of 90%. Not all patients had reduced oxygenation during acetate dialysis. Three of eight patients had a stable pattern with acetate dialysis and six of eight were stable with bicarbonate. Five of eight patients had a lower SpO2 with acetate but one patient had a lower SpO2 with bicarbonate. Four patients had prolonged, clinically significant periods of oxygen desaturation with SpO2 less than 90%; two of these had particularly prolonged periods during acetate (62 min and 12 min), but one patient showed a longer period during bicarbonate than acetate dialysis (7 min). In two patients the SpO2 declined to less than 84%. The patterns of SpO2 suggested that the decrease in oxygen saturation was due more to extrapulmonary abnormalities causing an instability in ventilatory control rather than to venous admixture. It is recommended that pulse oximetry is used to identify patients at risk of hypoxaemia, to monitor these patients during haemodialysis, and to administer oxygen to those whose SpO2 falls below 90%, particularly if they have anaemia or cardiovascular disease.

Acetates↗
PubMed1992

A study to compare the effectiveness of temazepam and a chloral hydrate/hydroxyzine combination in sedating paediatric dental patients.

The study compared the effectiveness of temazepam and a mixture of chloral hydrate and hydroxyzine in sedating 20 young children aged 20 to 60 months (mean age 38.7 months). All the children exhibited negative behaviour during a screening visit and required at least two visits for restorative treatment with the use of sedation. The children were assigned randomly to receive either 50 mg/kg of chloral hydrate with 25 mg of hydroxyzine or 0.3 mg/kg of temazepam for the first visit, and the alternate regimen for the second visit, in a double-blind manner. Pulse rate and blood oxygen saturation levels were monitored before, during and after the operative procedures. All the treatment sessions were video-recorded and evaluated independently by three paediatric dentists for the degree of crying, movement, sleep and overall behaviour during specific procedures and at specific time intervals. The results showed no statistically significant differences between the two pharmacologic regimens with regard to crying, movement, sleep and overall behaviour. No significant difference in behaviour was found related to either the order of administration of the drugs or to the sex of the patients. It was concluded that 0.3 mg/kg temazepam and a mixture of 50 mg/kg chloral hydrate with 25 mg hydroxyzine had similar sedative effects on the children receiving dental treatment.

Anesthesia, Dental↗
PubMed1991

Nitrous oxide sedation causes post-hyperventilation apnoea.

We have studied, in six normal subjects, the effect of nitrous oxide sedation on the ventilatory pattern and oxygen saturation using pulse oximetry (SpO2) after hyperventilation to an end-tidal carbon dioxide partial pressure (PE'CO2) of 3 kPa. This value of PE'CO2 was shown to be less than the apnoeic threshold of all these subjects when their ventilation vs PE'CO2 response curves were plotted. All subjects became apnoeic when told to relax following hyperventilation while breathing 75% nitrous oxide for 90 s. Apnoea was defined as cessation of breathing for 20 s or more. The mean duration of apnoea was 78 s (range 29-130 s). All subjects demonstrated arterial desaturation (mean SpO2 75%, range 44-87%). In contrast, following hyperventilation with air, no apnoea was seen in any subject, although there was some evidence of desaturation (mean SpO2 92.5%, range 88-98%). It was concluded that subjects who are sedated with nitrous oxide behave similarly to those who are anaesthetized rather than to those who were fully conscious, in that they become apnoeic below the apnoeic threshold point. The reduction in SpO2 after hyperventilation was explained almost entirely by apnoea and may explain abnormalities of respiratory control and hypoxaemia in patients recovering from general anaesthesia or sedation accompanied by hypocapnia. This mechanism may be of importance in obstetric patients after breathing Entonox, when apnoea and hypoxaemia may reduce oxygen delivery to the fetus.

Adult↗
PubMed1991

Changes in amplitude and latency of the P300 component of the auditory evoked potential with sedative and anaesthetic concentrations of nitrous oxide.

The P300 component of the auditory evoked response was recorded from six subjects whilst they listened via headphones to a series of clicks which were interrupted unpredictably by a tone burst. They were instructed to press a button as quickly as possible after hearing the tone whilst breathing first air and then a series of increasing concentrations of nitrous oxide. Both the amplitude and the latency of the P300 changed in a dose-dependent manner with nitrous oxide, as did minimum reaction time. At nitrous oxide concentrations which prevented recall of any events that occurred whilst breathing the gas, four subjects continued to respond to the tone by pressing the button. In three subjects, the P300 wave was still detectable with a nitrous oxide concentration at which the task was no longer performed. These results show that there is retention of the ability to perform a reaction time task when there is a complete loss of recall of the task. There may be some recognition of an auditory stimulus, as manifest by a P300 wave, albeit reduced greatly in amplitude, in the absence of a motor response to it. The P300, therefore, merits investigation as a tool for studying conscious awareness under anaesthesia.

Anesthesia Recovery Period↗
PubMed1991

Patterns of oxygenation after thoracotomy.

We have studied patterns of oxygen saturation (SpO2) before and after thoracotomy in 20 patients monitored nightly from the preoperative night to the fourth postoperative night. After operation, 10 patients received paravertebral bupivacaine (PVB) infusion and 10 received paravertebral saline (PVS) infusion. Papaveretum was given as required. Before operation the SpO2 profiles formed two groups: stable with SpO2 greater than 94% and stable with a median SpO2 less than 94% (hypoxaemia). During the first night after operation SpO2 profiles formed four groups: stable, not hypoxaemic (2/20); stable, hypoxaemic but improving (8/20); stable and constant hypoxaemia (5/20); unstable, hypoxaemic and deteriorating (5/20). Eleven patients remained hypoxaemic as late as the fourth night after operation. All patients who were hypoxaemic before operation were hypoxaemic after operation. Postoperative hypoxaemia was predicted in only 50% of cases. Papaveretum requirement was reduced in the PVB group, but regional analgesia did not affect the proportion of patients showing each SpO2 profile. Papaveretum caused a decrease in SpO2 in both analgesic groups.

Adult↗
PubMed1990

Postoperative hypoxaemia: comparison of extradural, i.m. and patient-controlled opioid analgesia.

Arterial oxygen saturation (SaO2) was analysed continuously before and for 24 h after lower abdominal surgery in 30 patients breathing air using one of three postoperative analgesic regimens: i.v. diamorphine using a patient-controlled analgesia system (PCAS), extradural diamorphine or i.m. morphine. Hypoxaemia was defined as SaO2 less than 94% for more than 6 min h-1. Before operation there was no difference between the three analgesia groups assessed by the duration when SaO2 was less than 94%. After operation the pattern of SaO2 vs time distribution was either stable, with little variation from hour to hour with no hypoxaemia, or unstable with large variation with 30% of patients hypoxaemic. Thus three patterns of SaO2 distribution were seen in the postoperative period: stable without hypoxaemia (4/10 PCAS, 0/10 extradural, and 1/10 i.m. patients), unstable without hypoxaemia (4/10 PCAS, 5/10 extradural and 7/10 i.m. patients) and unstable with prolonged nocturnal periods with SaO2 less than 94% for a mean of 17.7 min h-1, 95% confidence limits (CL) 10-25 min h-1, (2/10 PCAS, 2/10 i.m. and 5/10 extradural patients). Before operation, the unstable group with hypoxaemia spent longer at less than 94% SaO2 (mean 4.8 min h-1, 95% CL 1.0-8.6 min h-1) than the stable group (mean 0.4 min h-1, 95% CL 0.17-0.61 min h-1) and this was a predictor of postoperative hypoxaemia. Hypoxaemia occurred in all analgesia groups, but extradural diamorphine tended to cause longer periods. Some patients at risk of postoperative hypoxaemia may be predicted by preoperative monitoring of SaO2 although extradural diamorphine boluses were associated with hypoxaemia in patients with normal preoperative values.

Abdomen↗
PubMed1990

Postoperative hypoxaemia: mechanisms and time course.

Postoperative hypoxaemia results predominantly from two mechanisms. Gas exchange is impaired during anaesthesia as a result of reduced tone in the muscles of the chest wall and probably alterations in bronchomotor and vascular tone, and the resulting changes persist into the postoperative period. In addition, there is an abnormality of control of breathing, which results in episodic obstructive apnoea. These episodes continue for several days after operation and are related to sleep pattern and analgesic administration, although the precise effects of different analgesic regimens have not been evaluated. Oxygen administration is effect in reducing the degree of hypoxaemia.

Anesthesia, General↗