Anaesth Intens Care (1992), 20, 479-483

Propofol Induction for Laryngeal Mask Airway Insertion: Dose Requirement and Cardiorespiratory Effects D. W. BLAKE,* P. DAWSON,t G. DONNANt AND A. BJORKSTEN§ Department of Anaesthesia, Royal Melbourne Hospital, Parkville, Victoria SUMMARY The dosage, haemodynamic and respiratory effects ofpropofol for laryngeal mask airway (LMA) insertion were investigated. Fifty patients (ASA I-II) were randomly assigned one offour induction doses ofpropofol (1.5-2.5 mg/kg) delivered over 30 seconds and the first attempt at LMA insertion was made at 90 seconds. The LMA was inserted at 90 seconds in 35 patients and by 300 seconds in 13 others (mean plasma concentration at 90 seconds was 7.7 mcg/ml (no delay) versus 5.2 mcg/ml (insertion delayed), P < 0.01). Insertion was less successful after 1.5 mcg/kg (failed at 90 seconds in 6 of12 patients), but did not vary with the other doses. Additional propofol (0.5 mg/kg/30s) was required in 22 patients for LMA insertion or to prevent movement, resulting in propofol concentrations at 120-180 seconds above 7 mcg/ml. Respiratory effects were minor, but MAP decreased by 18 ± 1.4 mmHg at 90 seconds. Cardiovascular effects did not differ significantly between dosage groups or with the use of additional propofol. Key Words: EQUIPMENT: laryngeal mask airway; ANAESTHETICS, INTRA VENOUS: propofol, haemodynamics, induction, respiratory effects

The laryngeal mask airway (LMA, Intavent, Colgate Medical) may be used as an alternative to a facemask in patients breathing spontaneously during general anaesthesia. I It facilitates the connection of respiratory monitors, may improve airway control, and frees the anaesthetist's hands during the maintenance of anaesthesia. 24 The LMA may also be inserted following intravenous (IV) induction alone, avoiding pollution of the operating theatre with volatile anaesthetics. The LMA is suitable for many 'day-case' procedures where propofol is often chosen as the induction agent due to the need for early recovery.5 Propofol may also facilitate LMA insertion by inducing greater jaw and upper airway relaxation compared with an equivalent dose of thiopentone. 6,7 The consequences of altering the anaesthesia induction to facilitate LMA insertion have not been studied. It has been assumed that a larger dose of IV induction agent will be required than that needed *F.F.A.R.A.C.S., Ph. D., Director of Aoaesthesia. tF.F.A.R.A.C.S., Staff Aoaesthetist. tF.F.A.R.A.C.S., Staff Aoaesthetist. §Ph.D., Scientific Officer. Address for CorrespondencelReprints: Prof. D. Blake, Department of Aoaesthesia, d- Post Office, Tbe Royal Melbourne Hospital, Parkville, Victoria 3050. Accepted for publication June 3, 1992 Anaesthesia and Intensive Care. Vol. 20. No. 4. November. 1992

to produce loss of consciousness. However, large bolus doses of propofol result in significant hypotension, principally due to a reduction in preload.8-1O In the present study we aimed to compare the ease of LMA insertion at a range of propofol doses when this was used as the sole induction agent, to determine the range of arterial propofol concentrations associated with successful LMA insertion and to monitor the haemodynamic and respiratory changes. METHODS Informed consent was obtained from fifty patients, ASA class I and 11, having elective orthopaedic surgery. The project was approved by the Board of Medical Research and Ethics Committees of the Royal Melbourne Hospital. Patients were randomised to receive one of four initial bolus doses of propofol. Groups I to 3 received 1.5, 2.0 or 2.5 mg/kg respectively according to total body weight (TBW). In group 4, lean body mass (LBM) was estimated from TBW and height according to the formula LBM = 1.1 TBW - 128 (TBW/height)2 for males and 1.07 TBW - 148 (TBW/height)2 for females,l1 and received 2.8 mg/kg of LBM. The dose in group 4 was equivalent to 2.0 mg/kg of TBW for a patient

480

D. W.

BLAKE ET AL.

with 25% fat. The study was continued until 12 patients were completed for each dosage group. An oral premedication of temazepam 10 mg was given one to two hours prior to surgery and all patients fasted for six hours. A cubital fossa venous cannula and radial artery cannula were inserted using 0.5% lignocaine local anaesthesia. Blood pressure (BP), heart rate (HR), arterial oxygen saturation (Sp02) and ECG were monitored for 5 to 10 minutes prior to induction and during two minutes of pre-oxygenation. The initial propofol dose was given over 30 seconds and LMA insertion was attempted at 90 seconds. The level of anaesthesia and the ease of LMA insertion at 90 seconds were scored by the anaesthetist on a scale of 1-3: I: patient suitably relaxed; 2: some movement or coughing, difficulty with mouth opening; 3: inadequate anaesthesia to attempt LMA insertion. If LMA insertion was unsuccessful at 90 seconds, or if the patient moved following insertion further 0.5 mg/kg bolus doses of propofol were given at 30 second intervals to a maximum of 3.5 mg/kg. BP, HR and Sa02 were monitored continuously and recorded for each 30 seconds. A single positive pressure breath and endtidal carbon dioxide (EtC0 2) was used to confirm LMA position. EtC0 2 and respiratory rate were monitored and recorded at 30 second intervals. After insertion of the LMA the patients were allowed to breathe spontaneously on a mixture of 70% nitrous oxide in oxygen and 2-5% enflurane. The time at which regular respiration commenced via the LMA was recorded. The anaesthetist was instructed to use positive pressure ventilation if the Sp02 fell below 90%. The study was continued for 15 minutes or until the start of surgery. The LMA was introduced according to the technique described by Brain;2 that is, placed on the hard palate with cuff deflated and aperture anterior and then advanced in a smooth movement. Ifthe level of anaesthesia was judged to be inadequate (score: 3) LMA insertion was not attempted. The LMAs were inserted by four anaesthetists, each of whom had used this technique for over 50 procedures in the preceding six months. The same anaesthetists judged the scores for anaesthesia and ease of insertion of the LMA. Arterial blood samples (2 ml) were taken for measurement of propofol concentration at 1.5, 2, 3, 4 and 5 minutes following induction. Flushing of the arterial line was avoided to mlDlmlse interruption of BP measurement. Propofol concentrations were measured using a modification of Plummer's method l2 and HPLC. The standard curve was linear from 0.2-10 mg/l (r = 0.9996, n = 4). The within-day coefficient of variation was 4.1 % at 2 mg/I (n = 6).

Variables were analysed by a repeated measures analysis of variance using either dosage group or dose number as categories. The Bonferroni correction was applied to multiple comparisons. Scores for anaesthesia and LMA insertion were analysed by the Kruskal-W allis test. RESULTS

Insertion ofthe LMA was not attempted in two of the 50 patients enrolled for study. One patient developed laryngospasm on induction due to regurgitation of stomach contents. The other patient was intubated because of altered surgical requirements. LMA insertion failed in one other patient, when loss of consciousness was delayed despite a total of 190 mg of propofol and was associated with muscle rigidity and laryngospasm. The LMA was inserted at first attempt (90 seconds after the start of propofol injection) in 35 of 48 patients. Extra propofol (0.5 mg/kg/30s) was required in 13 patients to obtain adequate anaesthesia for LMA insertion, and in a further nine patients to prevent movement afterwards. However, there was no significant difference in the number of extra bolus doses required for LMA insertion between the dosage groups (Table I). The average total dose of propofol administered was least in Group I (144 mg, P < 0.01), similar in Groups 2 and 4 (157 and 166 mg respectively) and greatest in Group 3 (181 mg, P < 0.05). The arterial propofol concentration at 90 seconds was significantly lower in Group I (5.0 ± I mcg/ml) but did not differ significantly between Groups 2, 3 and 4 (mean 7.5 ± 1.0 mcg/ml). The duration of apnoea prior to respiration via the LMA was not correlated with initial propofol dose or with the number of bolus doses given. The anaesthesia score was lower (indicating better conditions for LMA insertion) in Groups 2 and 3 than in Groups I and 4 (P= 0.02). No significant differences were found in the respiratory effects of propofol between the four dosage groups, although oxygen saturation tended to be lower in Group I where insertion of the mask was delayed (P = 0.06). In the first five minutes oxygen saturation was below 90% in only two patients and the maximum end-tidal C02 observed was 59 mmHg, being > 50 mmHg in five patients. The average respiratory rate in the two minutes after LMA insertion was 18 breaths/minute (Table I). The average propofol concentration at 90 seconds in the 35 patients in whom the LMA was inserted at first attempt was 48% higher than that of the 13 patients where repeated attempts were necessary (P = 0.0 I, Table 2). Extra propofol doses in those 13 patients increased the mean total dose by 7% (P= 0.04). When repeated attempts were necessary, insertion was delayed to a mean of 190 Anaesthesia and Intensive Care. Vol. 20. No. 4. November. 1992

481

PROPOFOL AND LARYNGEAL MASK AIRWAY TABLE

1 Propofol dose (mg/kg) Total dose (mg) Extra bolus (no. of patients) Propofol concentration at 90 seconds (mcglrol) LMA insertion (sec) End apnoea (sec) Anaesthesia score (1-3) Minimum O 2 saturation (%) 0-5 min Maximum EtC0 2 (mmHg) 0-5 min Respiratory rate 3-5 min (breath/min)

1

Patient groups (n = 12) 2 3

4

p (ANOVA)

Comparisons (1,44 df)

(Gp 1 v 2, 3, 4) (Gp 3 v 2, 4)

1.5 (TBW) 144

2.0 (TBW)

2.5 (TBW)

157

181

2.8 (TBW) 166

8

5

5

4

0.01 0.05 NS

5.0

8.2

6.8

7.4

0.04

(Gp 1 v 2, 3, 4)

130 160 1.9 95

98 180 1.5 98

100 140 1.4 99

104 136 1.9 98

0.01 0.03 0.02 0.06

(Gp (Gp (Gp (Gp

45

47

47

48

NS

19

20

17

18

NS

seconds after commencement of the initial propofol bolus. The success of LMA insertion was not associated with differences in mean age or weight (Table 2). Average propofol concentrations from 1.5-5 minutes after the initial bolus are shown in Figure lA for the four dosage groups. Although the concentration in Group 1 was lower at 90 seconds, subsequent use of extra propofol boluses to achieve the desired level of anaesthesia abolished any difference in propofol concentrations between the groups. However, Group 1 showed a delayed peak at 3 minutes after receiving the greatest number of additional boluses (in 8 of the 12 patients). Concentrations were below 4 mcg/ml in all groups at 4 and 5 minutes. The effect of the additional 0.5 mg/kg boluses is illustrated in Figure 1B. These maintained arterial propofol concentrations at 7 mcg/ml for 3 minutes to facilitate LMA insertion.

Total dose (mg) Propofol concentration at 90 seconds (mcglrol) Average age (yrs) Weight (kg) End apnoea LMA inserted Anaesthesia and Intensive Care. Vol. 20. No. 4. November. 1992

3, 4) 3,4) 2, 3) 3, 4)

Mean arterial pressure (MAP) changed significantly with time after the initial propofol bolus (p= 0.001), but did not differ between the four dosage groups (Figure 2A). MAP decreased an average 18 mmHg (SD = 1.4) at 1 minute, then increased in response to LMA insertion to average 11 mmHg (SD = 2.4) below control at 3 minutes. With nitrous oxide and enflurane anaesthesia at 10 and 15 minutes MAP averaged 29 mmHg (SD = 2.5) below the pre-induction value. The use of additional propofol boluses did not alter the MAP response (Figure 2B). Mean heart rate increased by 8 (SD = 2) beats/min after LMA insertion, but again the heart rate response did not differ between groups or according to the number of bolus doses of propofol. DISCUSSION

Propofol provides a rapid and satisfactory induction of anaesthesia for LMA insertion in the

TABLE

LMA insertion

1 v 2, 2 v 1, 1,4 v 1 v 2,

2

First attempt (n = 35)

Repeated attempts (n = 13)

P

159 7.7

170 5.2

0.04 0.01

43

39 69 161 190

NS NS NS 0.001

68 153 92

482

D. W. BLAKE ET AL.

ARTERIAL PROPOFOL (mcg/ml) 10,------------------------------------,

MAP CHANGE (mmHg)

O __Tn~~~~~norn,_--__~----~~

T

B

A

A

I

-10 -20 -30

-40

1.5

2 3 4 TIME AFTER INITIAL BOLUS (min)

DOSE GROUP mg/Kg

•

1.5

C

2.0

-50 '--______________________________- - - 1 2 3 4 5 10 15 TIME AFTER INITIAL BOLUS (min)

5

tz:l 2.5 I2'l 2.B(LBM)

10,------------------------------------,

•

B

1.5 L I 2.0 [S; 2.5 Cl 2.8(LBM)

MAP CHANGE (mmHg)

. .rT~~~"..,_--__~----,._"

O,.~

-10 -20 -30

-40

o

1.5

2 3 4 TIME AFTER INITIAL BOLUS (min) •

SINGLE BOLUS

5

[J REPEATED DOSES

-~'--------------------------------~

2

3 4 10 TIME AFTER INITIAL BOLUS (min)

• SINGLE BOLUS

15

0 REPEATED DOSES

FIGURE I.-Mean arterial propofol concentrations (mcg/ ml) at 1.5 - 5 minutes after the start of the initial IV bolus. Top (A) - 4 dosage groups (n = 12): 1.5, 2.0 and 2.5 mglkg body weight and 2.8 mg/kg estimated lean body weight. Below (B) - patients requiring a single bolus only (n = 26, solid bars), patients receiving more than one bolus (n = 22, open bars). Error bars indicate standard deviations (in A derived from error mean square of the between groups analysis of variance).

FIGURE 2.-Mean arterial pressure (MAP) change from control prior to injection of propofol. Above (A) - 4 dosage groups (n = 12). Below (B) - patients requiring a single propofol bolus only (n = 26, solid bars), patients receiving more than one bolus (n = 22, open bars). Error bars indicate standard deviations as in Figure I.

majority of patients. A success rate of94% for LMA insertion was achieved with propofol alone, suggesting that the routine addition of other drugs during induction is unnecessary. The use of preoxygenation and a slow injection of the initial bolus over 30 seconds were important features of the technique used. 13 Significant arterial desaturation was avoided in all patients, the apnoeic interval was short and the total dose of propofol required was often smaller than that used in other studies. 9,14 The technique failed in two patients in this study, highlighting the limitations of the laryngeal mask when regurgitation or airway problems occur on induction and preclude its use. A dose of 2.0 mg/kg propofol was more effective than 1.5 mg/kg, but increasing the initial bolus to 2.5 mg/kg or calculating the dose according to an estimated lean body mass did not improve

conditions for LMA insertion. Greater variability in the propofol dose needed for loss of consciousness compared with thiopentone has previously been described. 15 This suggests that propofol should be slowly titrated to effect in order to avoid overdosage and increased side-effects. The LMA can often be inserted when anaesthesia is not considered to be ideal, as in 52% of our patients when the anaesthetist's score was greater than I. If the dosage of propofol is only just adequate to induce loss of consciousness, as with our lowest dose, LMA insertion can be achieved at first attempt in only about 40% of cases. Further O. 5 mg/kg doses at a 30 second interval were effective in maintaining the required arterial propofol concentration of 7-8 mcg/ml. The absence of any difference in magnitude of the initial MAP reduction between the dosage Anaesthesia and Intensive Care. Vol. 20. No. 4. November. 1992

PROPOFOL AND LARYNGEAL MASK AIRWAY

groups was surprising. If the predominant effect of propofol is direct myocardial depression, this should be dose-related. Alternatively propofol may reduce MAP due to reduction in sympathetic tone l6 or by a direct venodilator effect to reduce cardiac output. 8 The response to these changes would depend more on the resting state of the circulation than on the propofol dose. The addition of nitrous oxide exaggerates the hypotensive effect of propofol 17 in spontaneously breathing patients, but this was avoided until after the LMA was inserted in the present study. The mean propofol concentration measured at 5 minutes after the initial bolus fell below 3 mcglml, less than that required for anaesthesia. IS The hypotension at 10 and 15 minutes was therefore primarily due to the effects of nitrous oxide and enflurane. The haemodynamic response to LMA insertion was minor with only a slight increase in MAP towards control at 3 minutes and no increase in heart rate. When opioids or other supplements are avoided during induction, the cardiovascular and respiratory depressant effects of propofol are minor in patients classified ASA I or n. We suggest that, after pre-oxygenation, if propofol is titrated over three to four minutes, good conditions are provided for LMA insertion. This is associated with transient plasma concentrations of 7 to 8 mcg/ml, cardiovascular responses are masked and spontaneous respiration is rapidly resumed. REFERENCES

1. Brodrick PM, Webster MR, N unn JF. The laryngeal mask airway. A study of 100 patients during spontaneous breathing. Anaesthesia 1989; 44:238-241. 2. Brain AIJ. The laryngeal mask - a new concept in airway management. Br J Anaesth 1983; 55:801-804. 3. Alexander CA, Leach AB, Thompson AR, Lister JB. Use your brain! Anaesthesia 1988; 43:893-894. 4. Maltby JR, Watson Ne. The laryngeal mask airway: clinical appraisal in 250 patients. Can J Anaesth 1990; 37:509-513.

Anaesthesia and Intensive Care. Vol. 20. No. 4. November. 1992

483

5. Heath PJ, Ogg TW, Gilks WR. Recovery after daycase anaesthesia. Anaesthesia 1990; 45:911-915. 6. McKeating K, Bali M, Dundee JW. The effects of thiopentone and propofol on upper airway integrity. Anaesthesia 1988; 43:638-640. 7. Keaveny JP, Knell PJ. Intubation under induction doses of propofol. Anaesthesia 1988; 43(Supp):80-81. 8. Goodchild CS, Serrao JM. Cardiovascular effects of propofol in the anaesthetized dog. Br J Anaesth 1989; 63:87-92. 9. Grounds RM, Twigley AJ, Carli F, Whitwam JG, Morgan M. The haemodynamic effects of intravenous induction. Comparison of the effects of thiopentone and propofol. Anaesthesia 1985; 40:735-740. 10. Claeys MA, Gepts E, Camu F. Haemodynamic changes during anaesthesia induced and maintained with propofol. Br J Anaesth 1988; 60:3-9. 11. Crankshaw DP, Beemer GH. How should we administer intravenous drugs? Bailliere's Clinical Anaesthesiology 1991; 5:327-351. 12. Plum mer GF. Improved method for the determination of propofol in blood by high performance liquid chromatography with fluorescence detection. J Chromatography 1987; 421:171-176. 13. Stokes DN, Hutton P. Rate dependent induction phenomena with propofol: implications for the relative potency of intravenous anaesthetics. Anesth Analg 1991; 72:578-583. 14. Hickey S, Cameron AE, Asbury AJ. Cardiovascular response to insertion of Brain's laryngeal mask. Anaesthesia 1990; 45:629-633. 15. Leslie K, Crankshaw DP. Potency of propofol for loss of consciousness after a single dose. Br J Anaesth 1990; 64:734-736. 16. Patrick MR, Blair IJ, Feneck RO, Sebel PS. A comparison of the haemodynamic effects of propofol (Diprivan) and thiopentone in patients with coronary artery disease. Postgrad Med J 1985; 61(Supp1 3):23-27. 17. Monk CR, Coates DP, Prys-Roberts C, Turtle MJ, Spelina K. Haemodynamic effects of a prolonged infusion ofpropofol as a supplement to nitrous oxide anaesthesia. Br J Anaesth 1987; 59:954-960. 18. Richards MJ, Skues MA, Jarvis AP, Prys-Roberts C. Total IV anaesthesia with propofol and alfentanil. Br J Anaesth 1990; 65:157-163.