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PROPOFOL AND ALFENTANIL DURING ONE-LUNG

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Hemodynamic effects of induction, intubation, skin incision, clamping of one lung, and any unwanted side effects such as involuntary movements, stiffness, and postoperative nausea were noted, as were times and dosages of all drugs administered. Special attention was given to the recovery times and such characteristics as the times from the end of operation (last skin suture) to spontaneous breathing, extubation, opening of the eyes on command, and being oriented (defined as knowing name and date of birth). Finally, the anesthesiologist and surgeon independently graded the anesthetic procedure as either satisfactory or unsatisfactory, the anesthesiologist using criteria of smoothness of induction, controllability of depth of anesthesia, movements, unwanted side effects, and awakening characteristics, and the surgeon assessing operating conditions and awakening characteristics. Data are reported as mean values plus standard deviations (SD). Analysis of variance and paired t tests were applied to analyze the data from the consecutive perioperative times. P < 0.05 was considered significant. RESULTS

Demographic data are shown in Table 1. The durations of the operations and infusions and the dosages of the drugs given, with their standard deviations, are shown in Table 2. The mean induction dose of propofol was 2.3 mg/kg, and the infusion rate was 0.12 mg/kg/min (7.2 mg/kg/h). Mean duration of the operation was 151 minutes, and of the propofol infusion, 148 minutes. The mean total dose of alfentanil given (bolus plus infusion) was 8.1 mg over 125 minutes. Changes in blood pressure and pulse rate from preoperative values (baseline) during the procedure are shown in Fig 1. After induction, there was a significant decrease in systolic blood pressure of 28%, returning towards normal after bronchoscopy or intubation. Directly after clamping of the double-lumen tube and collapse of the

Table 1. Demographic

Data (n = 14) 45 + 12

Mean age (yr) Mean

weight (kg)

55 + 9

Male Female ASA classes

9 5

I and

II

ASA class Ill Lobectomy

11 3 12

Pneumonectomy

2

Tuberculosis

B

Echinococcus, aspergillosis

3

Bronchiectasis Bullae Carcinoma NOTE. Data given as means + SD.

195

Table 2. Times and Dosages (n =

14)

Duration of operation (min)

151 + 53

Duration of propofol infusion (min)

140 f 49

Duration of alfentanil infusion (min)

125 & 44

Propofol induction dosage (mg/kg) Total propofol infused (mg) Propofol infusion rate (mg/kg/min) Total alfentanil bolus plus infusion (mg) Total atracurium (ma)

2.3 + 0.3 933

f 343

0.12

+ 0.02

8.1 + 2.70 50*

15

NOTE. Data given as means f SD.

nondependent lung, there was an increase in mean blood pressure of 13% from preoperative baseline value. During the rest of the procedure, the blood pressure remained constant at a level that did not differ significantly from the baseline value. Mean pulse rates did not deviate more than 15% from the preoperative baseline values during the entire procedure. Apart from a slight increase after intubation and clamping, no significant changes from baseline values occurred. Arterial and central venous oxygen tensions are shown in Fig 2, and the oxygen saturations in Fig 3. None of the patients developed hypoxemia during the surgical procedure. Mean PaO, values remained high, showed no significant differences directly after one-lung collapse, and decreased slightly towards the end of the one-lung period. The lowest value for PaO, was 15.6 kPa (117 mm Hg) on an Fro, of 1. During the recovery period the mean PaO, was 14.8 kPa (111 mm Hg), on an Fro, of 0.35, with a lowest value of 9.5 kPa (71 mm Hg). The oxygen saturation never decreased below 98.5%. Both the mixed venous oxygen tension (PVO,) and saturation (S80,) remained above normal levels during the procedure and within normal limits during the recovery period. WO, values showed no significant differences during the one-lung period or during the rest of the operation, The calculated shunt fractions are shown in Fig 4. The mean preoperative shunt value of 8% increased significantly to 23% after induction on an Fro, of 1. The shunt value did not significantly change further during the one-lung phase, decreased to 15% at the end of the operation, and remained at 13.6% during the recovery period. Recovery characteristics and postoperative observations are shown in Tables 3 and 4 respectively. Mean recovery times were short. The majority of the patients (71%) could be extubated within 5 minutes after the end of the

STEEGERS AND BACKX

196

60

,

I

Fig 1. Changes in blood pressure and pulse rate during the different stages of the study. All comparisons made with preoperative values. Abbreviations: ind, 1 minute after induction; int, 1 minute after intubation: inc. 1 minute after incision: maint, 16 minutes af-

ind

int

inc

%f# systolic

maint

a

1 lung

1 lung

diastolic

D

2 lung

end

ter incision; 1 lung, 16 minutes after one-luna collaose and 30 minutes thereafter,‘2 lung, 16 minutes after reinflation in case of lobectomy or 16 minutes after pneumonectomy; end, directly after extubation: racov. 30 minutes postoperatively.

r6cov

pulse rate

One lung trial mean values + SD n = 14

surgical procedure, and were oriented and clearheaded within 27 minutes. Three patients were very sleepy and became oriented only after 45 to 90 minutes. Two of them needed naloxone, 0.4 mg. Two patients showed signs of restlessness and one of stiffness. No patient complained of awareness during surgery. All anesthetics were graded good to satisfactory. DISCUSSION

The decrease in blood pressure after induction is a known feature of propofol.g In this study, it may well have been enhanced by the simultaneous administration of alfentanil.” In retro-

spect, the mean induction dose of propofol, 2.3 mg/kg, was too high for ASA class II and III patients and for some elderly patients; therefore, it is recommended that a smaller dose of up to 2 mg/kg be used for these patients instead.” An often-recommended regimen for an alfentanil infusion is 5 to 10 pg/kg/min for 10 minutes as a loading dose, followed thereafter by an infusion of 1 ~g/kg/min.‘2~13 This protocol was unsuitable for the combined TIVA technique because of the long awakening times and high percentage of patients needing naloxone at the end of the operation (unpublished pilot study). Probably because of the relatively long interval

70

1

60 50 40 30 Fig 2. Arterial and central venous oxygen tensions during the different stages of the study. Abbreviations: preop, preoperative; 2 lung, 16 minutes after induction; 1 lung, 16 minutes after one-lung collapse and 30 minutes thereafter, end op. between 16 minutes postlobectomy or pneumonactomy and skin closure; recov. 30 minutes postoperatively.

20 10 0

preop

2lung

llung

BEI Pa02 One lung trial mean values + SD n = 14

llung

EI

Pv02

end op

recov

PROPOFOL AND ALFENTANIL

DURING ONE-LUNG

197

VENTILATION

100 95 90 P

85

C

80

e n t

75

e r

70 85 80

wm Fig 3. Arterial and central venous oxygen saturations during the different stages of the study. Same measurement times as in Fig 2.

2 lung

1 lung

EBB

SaO2

1 lung

I

end op

recov

SvO2

One lung trial mean values + SD n = 14

between induction and incision times in the current study, it was found that an infusion rate of 3 pg/kg/min for 10 minutes, followed by a rate of 1 pg/kg/ min, providing a loading dose of about 2.25 mg (41 pg/kg) before incision, gave a stable blood pressure and pulse rate, sufficient postoperative analgesia, and short recovery times (Table 3). This protocol, ie, a constant alfentanil dose and a variable propofol infusion, forced the authors to treat sudden signs of light anesthesia with a bolus of propofol and/or with increasing the propofol infusion rate. In practice, however, it may be more appropriate to give an additional

small bolus of alfentanil as well. This will provide sufficient alfentanil blood levels, especially during such painful periods as incision and spreading of the thorax, while avoiding side effects associated with higher levels that would result from a higher initial infusion rate. The decrease in the PaO, from 53 to 46 kPa (397 to 345 mm Hg) after one-lung collapse is not significant. The further decrease towards the end of the one-lung period to 40 kPa (300 mm Hg) is statistically significant (P = 0.02), but of no clinical importance, because all of these values exceed normal physiologic requirements. The high central venous PO, values measured during

25 P ;

20

: n

15

t

10 5

weep

2lung

llung

llung

ES4 shunt One lung trial mean values + SD n = 14

end op

recov Calculated perFig 4. centage of pulmonary shunt during the different stages of the study. Same measurement times as in Fig 2.

STEEGERS AND BACKX

198

Table 3. Recovery

Characteristics

Table 4. Postoperative

(n = 14) Times in Minutes 14 * (6.6)

Stop infusion-end operation End operation-spontaneous

breathing

1 * (3.3)

End operation-extubation

4 zt (3.2)

End operation-eyes open

10 f (16.8)

End operation-orientation

26 f (21.7)

End operation-first analgesic given

47 f (23.8)

Data (n = 14)

No. clear-headed within 30 min

10

No. sleepy after 30 min

3

No. nauseated

0

No. restless

2 1

No. stiff No. with good reaction to anesthetic

13

No. with satisfactory reaction to anesthetic

1

NOTE. Data given as means k SD.

the procedure can be explained by the high arterial saturations and a lower oxygen consumption during anesthesia.i4 Because there was no absolute indication for the insertion of a pulmonary artery catheter in every patient, central venous blood was used for the calculation of the shunt fractions. Although gases obtained from the right atrium should not be regarded as truly mixed venous samples, previous studies have indicated that central venous PO, does correlate reasonably well with mixed venous PO,.15,16An increase in the shunt fraction after induction and before any surgery, on an FtO, of 1, has been observed by several investigators.“*” A further increase can be expected during one-lung ventilation. Capan et all9 used 100% oxygen and 0.75% to 1.5% halothane and found an initial shunt of 26%, increasing to 38% during one-lung ventilation. Hatting and Coetzee,20 using enflurane, 1% to 1.5% and 100% oxygen, found shunts of 31% and 45%, respectively. Some of the reasons for these increases, like a decrease in functional residual capacity after the induction of anesthesia, airway closure, and microatelectases caused by the loss of alveolar support by N,, all causing V/Q mismatch, are well described.‘7*18*2’ Changes in WO, or in cardiac output affect shunt as we11.22 Drugs may also affect the hypoxic pulmonary vasoconstriction (HPV). Intravenous opiates have no effect, whereas inhalational agents do depress HPV and cardiac output.23*24Propofol can de-

press cardiac output,25 but its effect on HPV has not yet been studied. In the present study, a similar initial increase in calculated shunt (to 23%) was found, but, most remarkably, no significant further increase was seen during one-lung ventilation. The role of propofol in this regard, especially its effect on HPV, warrants further investigation. Towards the end of the procedure, the shunt value decreased, but remained 14% in the recovery phase. This value is significantly higher (P = 0.03) than the preoperative one. Because the patients received only 35% oxygen via an oxygen mask during this period, this is probably not a direct effect of the higher FtO,, but a residual effect of the 100% oxygen administered during the operation. Further investigation in this area, with propofol and lower FtO, values, would be interesting. In conclusion, it is believed that this TIVA technique with propofol and alfentanil is suitable for major thoracic surgery. It provided a smooth and easily controllable anesthetic with stable blood pressure and pulse rate even during the period of one-lung ventilation. The majority of the patients awoke quickly, were oriented and clear-headed within 30 minutes, and were able to cough and sigh on command. Postoperative analgesia was good and lasted for an average of 47 minutes. ACKNOWLEDGMENT The authors thank A. R. Coetzee for his advice.

REFERENCES 1. MacKenzie N, Grant IS: Propofol (“Diprivan”) for continuous intravenous anesthesia: A comparison with methohexitone. Postgrad Med J 61:70, 1985 (suppl3) 2. De Grood PMRM, Ruys AHC, Van Egmond J, et al: Propcfol (“Diprivan”) for total intravenous anaesthesia. Postgrad Med J 61:65,1985 3. Steegers PA, Booij LHDJ, Pelgrom R: Continuous infusion of alfentanil. Acta Anaesth Belg 33:81-87, 1982 4. Kay, B: Propofol and alfentanil infusion. A compar-

ison with methohexitone and alfentanil for major surgery: Anaesthesia 41589-595.1986 5. Steegers, PA, Foster, PA: Propofol in total intravenous anaesthesia without nitrous oxide: Anaesthesia 42:9497, 1988 (suppl) 6. Du Grbs B: Use of propofol in anesthesia for cardiac surgery. Preliminary results. Ann Fr Anesth Reanim 6~240-242, 1987 7. Du Toit, SHC: The choice of an appropriate

PROPOFOL AND ALFENTANIL DURING ONE-LUNG

VENTILATION

nonlinear model for the relationship between certain variables in respiratory physiology. S Afr Statist J 18:161-176, 1984 8. Berggren SM: The oxygen deficit of arterial blood caused by nonventilating parts of the lung. Acta Physiol Stand 1 l:l-45, 1942 (suppl) 9. Coates DP, Monk CR, Prys-Roberts C, et al: Hemodynamic effects of infusion of the emulsion formulation of propofol during nitrous oxide anesthesia in man. Anesth Analg 66:64-70, 1987 10. Gepts E, Jonckheer K, Maes V, et al: Disposition kinetics of propofol during alfentanil anaesthesia. Anaesthesia43:8-13, 1988 (suppl) 11. Robinson FP, Dundee JW, Halliday NJ: Age affects the induction dose of propofol (“Diprivan”). Postgrad Med J 61:157,1985 (suppl3) 12. Fragen RJ: Pharmacokinetics of the infusion of alfentanil in man. Br J Anaest 55:1077-1081, 1983 13. Norman J: The IV administration of drugs. Br J Anaest 55:1049, 1983 14. Theye RA, Michenfelder JD: Individual organ contributions to the decrease in whole-body VO, with isoflurane. Anesthesiology 42:35-40, 1975 15. Lipman J, Roos CP, Eidelman J, Plit M: A comparison between right atria1 and pulmonary arterial oxygen tensions. S Afr Med J 70:351-357,1986 16. Chiarla C, Giovannini I, Siegel JH, et al: A simple method for rapid estimate of pulmonary venous admixture. Angiology 39:1030-1035, 1988

199 17. Rehder K, Knopp TJ, Sessler AD, et al: Ventilation-perfusion relationship in young healthy awake and anesthetized-paralyzed man. J App Physiol47:745, 1979 18. Bindslev L, Hedenstierna G, Santesson J, et al: Ventilation-perfusion distribution during inhalation anaesthesia. Acta Anaestesiol Stand 25:360, 198 1 19. Capan LM, Turndorf H, Pate1 C, et al: Optimization of arterial oxygenation during one-lung anesthesia. Anesth Analg 59:847-851, 1980 20. Hatting PW, Coetzee AR: Special preoperative investigations and intraoperative oxygen tensions during one-lung anaesthesia. S Afr Med J (in press) 21. Benumof JL: Physiology of the open chest and one-lung ventilation, in Kaplan JA (ed): Thoracic Anesthesia. New York, NY, Churchill Livingstone, 1983, pp 287-316 22. Benomof JL, Pirlo AF, Tronsdale FR: Inhibition of hypoxic pulmonary vasoconstriction by decreased PvOi A new direct mechanism. J Appl Physiol51:871-874, 1981 23. Sykes MK: in Altura BM, Halevy S (eds): Cardiovascular Actions of Anesthetics and Drugs Used in Anaesthesia. Basel, Switzerland, Karger, 1986 24. Marshall BE, Marshall C: In Covino BG, Fozzard HW, Rehder K, et al (eds): Effects of Anesthesia. American Physiological Society, 1985 25. Claeys MA: Haemodynamic changes during anaesthesia induced and maintained with propofol. Br J Anaesth 60:109-111, 1988