684 Correspondence

In the next half hour she pressed the button three more times and succeeded in giving herself two more boluses. One hour later the PCA was discontinued because the respiratory rate had decreased to 10 breaths/minute and further to 7 breaths/minute half an hour later. No naloxone or oxygen was administrered. Pain and sedation scores were recorded half hourly. Not surprisingly, these indicate that the patient was asleep and pain free for the first 4 hours after operation.

Arterial oxygen saturation (Spo,) was monitored using a Nellcorr NlOO pulse oximeter interfaced with a BBC computer, and the Spo, was digitally recorded every 5 seconds. The results were stored on floppy disk and analysed later. The lowest Spo, was 81% during the first hour after operation. The total number of recordings of Spo, below 90% in the first hour was 32, the number below 85% was six. Moderate hypoxaemia has been defined as Spo, < 90%; severe hypoxaemia as Spo, < 85%., Moderate hypoxaemia occurred in this patient for 160 seconds in the first hour (32 x 5 seconds) and severe hypox- aemia for 30 seconds. The-lowest Spo, recording was 86% after the first hour. Mean time per hour for Spo, < 90% was 83 seconds (range 20-175) over the next 3 hours.

A diamorphine infusion (20 mg in 48 ml 0.9% saline) at 1-2 ml/hour) was commenced 4 hours after operation. There were no further problems apparent clinically. Over the following 14 hours, the lowest Spo, recorded was 8170, mean time per hour for Spo, < 90% was 28 seconds (range 0-90), mean time per hour for Spo, < 85% was 1 second (range 0-1 5 seconds) after which time Spo, recording was abandoned. The diamorphine infusion was discontinued 60 hours after operation. The patient made an otherwise uneventful recovery. Two days later, pain free on a diamor- phine infusion and wide awake, the patient could not recall pressing the button more than once after operation.

PCA was reported as safe in children,, although respira- tory depression occurred in one patient whose analgesia was assisted by the staff. Respiratory depression in adults, was caused by patient self-overdose after b~prenorphine,~ alfentanil,4 and with pethidine' when it was associated with hypovolaemia. Apnoea has also been reported in adults due to incorrect setting up of the pump.'

This case illustrates that a child may develop significant respiratory depression, even when only the patient has control over the patient-controlled analgesia pump button, both bolus dose and lockout time are reasonable and the drug is delivered into a dedicated intravenous line. This is the first time that this is reported in a child.

Wheatley et af.' suggest that Spo, monitoring should be used in high-risk adult patients who receive opiates after operation because bradypnoea is a much less sensitive index of respiratory depression. Further work needs to be done to assess the consequences of the arterial oxygen desaturation we have noted, but in the meantime we believe that Spo, monitoring should be considered in children who have PCA on a general ward, in addition to routine respira- tory rate monitoring.

University Hospital, Nottingham NG7 2UH

C.G. STACK N.J. MASSEY

References 1. WHEATLEY RG, SOMERVILLE ID, SAPSFORD DJ, JONES JG.

Postoperative hypoxaemia: comparison of extradural, im and patient-controlled opioid analgesia. British Journal of Anaesthesia 1990; 64: 267-75. GAUKROGER PB, TOMKINS DP, VAN DER WALT JH. Patient- controlled analgesia in children. Anaesthesia and Intensive Care 1989; 17: 264-8. Gless JM, JOHNSON HD, DAVIS FM. Patient administration of i.v. buprenorphine for postoperative pain relief using the 'Cardiff demand analgesia appaI'dtuS. British Journal of Anaesthesia 1982; 5 4 279-84. CuRRiE J, OWEN H, MATHER LE. Patient controlled analgesia with alfentanil: analgesic blood concentrations in the postoperative period. Proceedings of the Anaesthetic Research Society, London meeting, 10-1 I , November 1989.

5 . TAMSEN A, HARTVIG P, FAGERLUND C, DAHSTROM B, BONDESSON U. Patient-controlled analgesic therapy: clinical experience. Acta Anaesthesiologica Scandinavicu 1982; 26

6. WHITE PF. Mishaps with patient-controkd analgesia.

2.

3.

4.

SUPPI 7 4 157-60.

Anesthesiology 1987; 66: 81-3.

Admission blood pressure and anaesthesia

A diastolic blood pressure consistently greater than 110 mmHg is often considered a contraindication to elective surgery,' while labile pressure after admission is a known predictor of a potentially excessive pressor response to intubation., Anaesthetists expect a patient's blood pressure to be recorded in every ward pre-operative evaluation but another measurement is not always taken before induction of anaesthesia.

We prospectively reviewed, during a 4-week period, all patients who attended our small theatre complex. Ward data were extracted from the patient's chart (usually manual BP measurement by the nursing staff) and determined by automated noninvasive BP monitors during anaesthesia, recording at 2.5-minute intervals until surgery commenced; the BP on admission to the anaesthetic room, together with the highest and lowest pressures after induction were noted.

A diastolic of (or greater than) 90 mmHg on the ward, was not a good predictor of an elevated diastolic on admission to the anaesthetic room, having a sensitivity of only 68% (25/24+ 12); while the specificity of this screening

test was 80% (125/124+ 12), (Table I.) The power of the test was not improved if the criterion was a diastolic of (or greater than) 100 mmHg.

Patients with a diastolic of (or greater than) 90 mmHg in the anaesthetic room showed significantly (p < 0.001) greater blood pressure lability after induction of general

Table 1. Number of patients with the defined diastolic blood pressure.

Anaesthetic room

< 90 mmHg 2 90 mmHg Ward

2 90 mmHg 2s 32 Sl* < 90 mmHg 12 125 137t

37** 157tt

Mean diastolic blood pressures (mmHg) * 96 (1.5 SEM), ** 99 (1.4 SEM), 775 (0.6 SEM), t t 74 (0.8 SEM).

Correspondence 685

Table 2. Mean absolute change (mmHg) in systolic blood pressure after induction of general anaesthesia.

Anaesthetic room diastolic pressure

3 90 mmHg* < 90 mmHgt

Highest - 18 (SEM 4.3) - 1 (SEM 2.0) p < 0.001 Lowest -50 (SEM 5.7) -31 (SEM 1.5) p < 0.0001

*n = 37 patients, 46% with tracheal intubation; t n = 157 patients, 50% with tracheal intubation.

anaesthesia (Table 2). Similar trends existed if the groups were separated by ward blood pressure, although they failed to reach statistical significance.

A ward admission diastolic pressure of (or greater than) 90 mmHg in our hospital was a relatively insensitive predictor of similar hypertension in the anaesthetic room.

The pressure returned to normal levels in 56% of the patients who were hypertensive on admission despite the absence of blood pressure-modifying therapy, while almost one third of patients with an elevated diastolic in the anaesthetic room had normal ward pressures. If therefore we want an accurate baseline pressure for management of anaesthetics we should measure it ourselves!

Leicester Royal Injrmary, A.D. COLQUHOUN Leicester LEI 5 WW P.C. RABEY

References 1. GOLDMAN L, CALDERA DL. Risks of general anaesthesia and

elective operation in the hypertensive patient. Anesthesiology

BEDFORD RF, FEINSTEIN B. Hospital admission blood pressure: a predictor for hyertension following endotracheal intubation. Anesthesia and Analgesia 1980; 5 9 367-70.

1979; 50: 285-92. 2.

Severe bradycardia and cardiac arrest

Several subjects developed severe bradycardia during a study that compared halothane and isoflurane for rapid inhalational induction. Two patients had a brief asystolic cardiac arrest. A heart rate of less then 30 beats per minute occurred in six of the 25 patients. All of these patients were in the halothane group and anaesthesia was induced with a single vital capacity breath of 4.5 MAC halothane. Once surgical anaesthesia was achieved (central pupils and regular breathing), the patients were given 10 pg/kg alfentanil intravenously. followed 30 seconds later by 1 mg/kg suxamethonium. Anaesthesia was maintained with 2% halothane in 100% oxygen at 100 ml/kg/minute between the onset of surgical anaesthesia and intubation. The two patients who developed asystolic cardiac arrest both reverted to sinus rhythm rapidly after the administration of atropine 20 pg/kg and ventilation with oxygen via a tracheal tube.

All the patients in the study group were ASA 1, young (mean age, 26 years), unpremedicated patients who were to have dental surgery. No episodes of bradycardia were precipitated during the induction sequence in the patients who received isoflurane, with a technique identical to that described for the halothane group. We consider the anti- adrenergic effect of halothane,’ the vagotonic effect of alfentani12 and the parasympathomimetic effect of

~uxamethonium~ to be additive or synergistic in the aetiology of the bradycardia.

The bradycardias in our series occurred during the performance of a research project, where monitoring was optimal, vigilance maximal (two anaesthetists present) and treatment immediate. The outcome for the patients who had asystolic arrests was therefore good. Our concern is that severe bradycardia may occur in less than optimal circumstances.

Area 361, P.V. VAN HEERDEN Johannesburg Hospital, M. BUKOFZER Private Bag X39, K.R. EDGE 2000 Johannesburg, South Africa

References 1. WOOD M. Inhalational anaesthetic agents. In: WOOD M,

WOOD AJJ, eds. Drugs and anesthesia. Baltimore: Williams and Wilkins, 1982: 262.

2. MARYNIAK JK, BISHOP VA. Sinus arrest after alfentanil. British Journal of Anaesthesia 1987; 59: 390-1.

3. WOOD M. Neuromuscular blocking agents. In: WOOD M, WOOD AJJ, eds. Drugs and Anesthesia. Baltimore: Williams and Wilkins, 1982: 307-8.

Oropharyngeal volumes

We read Newcombe and Russell’s article (Anaesthesia 1989; 44: 982-3) with great interest.

We disagree with them that ‘A search of the literature failed to provide any information, . . . ’. Indeed, J.F. Nunn and colleagues studied the anatomical subdivisions of the volume of respiratory deadspace and effect of position of the jaw’ in six cadavers with a method very similar to that of Newcombe and Russell. However, in this study, the nasal part of the deadspace was closed off, so as to measure extrathoracic deadspace only, that is, the real oropharyngeal volume. Mean water volumes were 48 (SD 21.5) ml with the jaw depressed, 72 (SD 32) ml with the jaw in the normal position, and 119 (SD 42) ml when the jaw was protruded.

These figures were confirmed in anaesthetised and conscious subjects, using other techniques of course, and they were in agreement with other similar published data. There was considerable interpersonal variation, just as Newcombe and Russell noted. The slightly larger values obtained by Newcombe and Russell were certainly due to the fact that the nasopharynx was not excluded. Did not Newcombe and Russell, in fact, measure ‘oronasopharyngeal volumes’, and not just ‘oropharyngeal volumes’? Vomitus does not just fill the oropharynx, but the nasal cavities as well. So, the right volume was measured, but its name was not quite right.

Moreover, as Nunn et al. pointed out, the position of the jaw alters these volumes, but Newcombe and Russell made