Acta anaesth. scand. 1978, 22, 145-153

Cardiovascular Effects of Local Adrenaline Infiltration During Neurolept Analgesia and Adrenergic Beta-Receptor Blockade in Man P. J. PONTINEN Department of Anaesthesia, Kainuu Central Hospital, Kajaani, Finland

The adrenergic beta-receptor blocking drug, alprenolol, was given together with atropine to 15 patients during neurolept analgesia (NLA) in order to prevent adrenaline-induced cardiac arrhythmias. Four patients operated on without adrenergic beta-receptor blockade formed the control group. Three of them developed tachyarrhythmias, ventricular tachycardia, multifocal ventricular extrasystoles and supraventricular tachycardia. All these arrhythmias were terminated by the adrenergic beta-receptor blocking drug, propranolol. The fourth patient developed a temporary sinus tachycardia which did not require any treatment. The adrenergic beta-receptor blockade induced a slight increase in pulse rate with almost no change in arterial blood pressure. T h e incidence of arrhythmias due to adrenaline infiltration was much less in this group. There was one supraventricular tachycardia and scattered ventricular extrasystoles in two other patients. NLA alone does not protect the heart against adrenaline-induced arrhythmias. I t does, however, seem to be compatible with a n adrenergic beta-receptor blockade, which in turn provides partial protection against adrenaline-induced arrhythmias. The occasionally developing arrhythmias can then be terminated with specific adrenergic beta blockers.

Received 31 March, acceptedfor publication 2 1 Jw1e 1977

et al. 1974). Circulating The cardiovascular system is known to remain 1971, HEMPELMANN stable during neurolept analgesia (NLA) catecholamines remain low during NLA 1973). The coronary vessels are (PONTINENet al. 1964, BUHR & HENSCHEL(TAMMISTO et al. 1966), although the induction of anaesthesia also dilated during NLA (PATSCHKE may cause some arrhythmias (REINIKAINEN & 1976). For these reasons NLA is particularly PONTINEN1966) and fluctuations in blood well suited for open-heart surgery (RUG1968, pressure (KRONSCHWITZ 1972). Oxygen con- HEIMER 1967, MULLER& DIETZEL et al. 1970, STOELTINC & GIBBS sumption of the myocardium is low and the JACOBSON et al. 1975). heart tolerates hypoxia during NLA well 1973, STOELTINC In spite of these positive properties of NLA, (BRUCKNER et al. 1972, REINECKE et al. 1972, SPIECKERMANN 1973, SONNTAG 1974, PAT- cardiac arrhythmias are common if the 1966, patients are not atropinized ( PONTINEN SCHKE et al. 1976). NLA has no negative & PONTINEN 1966) or if there ionotropic effect on the heart (FISCHER 1972, REINIKAINEN et al. 1973, KETTLER 1973, OSTHEIMER et al. 1975). is carbon dioxide retention (PONTINEN The increased microcirculation and decrease 1966). No published reports concerning the in peripheral resistance may be due to cardiovascular effects of local adrenaline adrenergic alpha-receptor blockade caused infiltration during NLA have been found. by dehydrobenzperidol (WHITWAM & RUSSEL Although there are many reports concernD

146

P. J. PONTINEN

ing the adrenergic beta-receptor blockade Motiitorittg technique during halothane anaesthesia in man (PAYNE ECG and peripheral pulse wave (through a n earpiece & SENFIELD 1964, PONTINEN & EKHOLM 1964, photocell (Hewlett-Packard 780-16) ) were both continuously monitored on an oscilloscope (H-P 7803A) JOHNSTONE 1966, 1968, 1969, STEPHEN and recorded on paper (Sanborn 322T). The same et al. 1971), reports about the compatibility was true for the radial artery (H-P 1280B) and the of adrenergic beta-receptor blockade during right ventricular or pulmonary artery (H-P 1280C) NLA are rare (PONTINEN & EKHOLM 1964, pressures (Sanborn 764+ 7702). CVP was monitored with a simple water manometer (Fenwal) from the PONTINEN et al. 1965, P ~ N T I N E1969). N superior vena cava (Cardioflex, Vygon). Arterial Preliminary results concerning the cardio- blood samples were taken during the steady state of vascular effects of adrenergic beta-receptor NLA, 15 min after the injection of beta blocker and blockade and adrenaline infiltration during 15 min after the adrenaline infiltration for blood gas NLA are presented here, for it is often an analysis and for acid-base balance ( I L 113 Blood gas alternative to halothane anaesthesia in analyzer) and electrolyte measurements (IL 127 Flame Photometer + IL 144 Automatic dilutor, Instrumentaelderly people undergoing prolonged ENT tion Laboratories). surgery, where deliberate use of local adrenaBeta blockade line infiltration is common.

MATERIAL AND METHODS The series comprised 19 patients, 12 men and 7 women between the ages of 17 and 68 years, none of whom showed signs or symptoms of respiratory or cardiovascular disease. The subjects were fully informed of the nature of the experiments and agreed to participate. All patients were to undergo middle-ear microsurgery, where surgical trauma is minimal but the operation field is infiltrated with adrenaline to reduce bleeding.

Alprenolol, a specific beta-receptor blocking agent with some intrinsic sympathomimetic activity and membrane-stabilizing properties (ABLADet al. 1967) was given intravenously 15-25 min before the adrenaline infiltration to 15 patients. T h e dose was 0.04 mg/kg body weight given together with atropine 0.01 mg/kg. The other four patients were operated on without a prophylactic beta-receptor blockade. If persisting tachyarrhythmias occurred, these patients were then treated with another specific adrenergic beta-receptor blocker, propranolol (0.04 mg/kg i.v. with atropine 0.01 mg/kg).

RESULTS Anaesthetic technique Patients were premedicated with 10 mg of diazepam orally the night before and on the morning of the operation day. Atropine 0.01 mg/kg body weight was injected intravenously immediately before the induction of NLA. Anaesthesia was induced with a sleep dose of thiopentone (200400 mg) given immediately after an intravenous injection of 5 to 10 ml of thalamonal@, a 1:50 mixture of a powerful analgetic, fentanyl, and a neuroleptic, dehydrobenzperidol. Intubation was facilitated by suxamethonium (50-100 mg) and anaesthesia maintained with fractional doses of thalamonal up to 10-15 ml; it was then replaced by fentanyl to avoid an overdose of dehydrobenzperidol. Patients were relaxed with alcuronium and ventilated with 2 : 1 nitrous oxide/oxygen mixture using a Bird 4/8 anaesthesia ventilator. Vasoconstriction was achieved locally by infiltrating the skin of the posterior meatal wall with Rosen's solution (2% mepivacaine 3 ml+O.lo% adrenaline 0.6 ml). The site of the incision, either endaural or retroauricular, as well as the site of the fascia1 graft were infiltrated with 0.25% bupivacaine containing 1 :200.000 adrenaline.

Adrenaline infiltration induced ventricular arrhythmias in two of the four patients operated without adrenergic beta-receptor blockade. These were bursts of ventricular tachycardia and multifocal ventricular extrasystoles in one patient and multifocal ventricular extrasystoles in the other (Figs. 1 and 2). They were terminated by an intravenous injection of propranolol (0.04 mg/kg) with atropine (0.01 mg/kg). The doses of infiltrated adrenaline were, respectively, 2.3 and 4.8 pg/kg. Supraventricular tachycardia occurred in one patient. This, too, was terminated by an intravenous injection of propranolol and atropine using the same dose as above. Temporary sinus tachycardia not requiring antiarrhythmic therapy was recorded in the fourth patient. In all four patients, the radial artery

BETA BLOCKADE AND ADRENALINE DURING NLA

147

+-I

1 sec HR 1 2 0 l m i n

Fig. 1. Bursts of ventricular tachycardia (upper tracing) and reflections on peripheral pulse wave (lower tracing) during NLA due to adrenaline infiltration (2.3pg/kg).

-

1 sec HR 1261min

Fig. 2. Multifocal ventricular extrasystoles (upper tracing) and reflections on peripheral pulse wave (lower tracing) during NLA due to adrenaline infiltration (4.8pg/kg).

k Pa

2or OL

* 10 sec

Fig. 3. A typical pressure response (upper tracing) and reflections on peripheral pulse wave (lower tracing) due to adrenaline infiltration (4.8 ,ug/kg) during NLA.

148

P. J. PONTINEN

Table 1 Cardiac arrhythmias and the doses of infiltrated adrenaline (pg/kg).

burst of ventricular tachycardia multifocal ventricular extrasystoles supraventricular tachycardia sinus tachycardia

1.

male

34

2.

male

57

3.

male

48

4.

female

68

5.

female

52

6.

male

17

7.

female

17

8.

female

53

9.

male

GO

10.

female

52

alprenolol+ atropine

11.

male

33

12.

male

52

13.

male

34

14.

male

41

15.

female

62

16.

male

22

17.

male

34

18.

male

48

19.

female

45

alprenolol atropine alprenolol + atropine alprenolol + atropine aIprenolol+ atropine alprenolol+ atropine alprenolol + atropine alprcnolol + atropine alprenolol + atropine aprenolol + atropine

+

alprenolol atropine alprenolol+ atropine alprenolol atropine alprenolol atropiric alprenolol+ atropine

+

4.8

3.5 2.2 4.4

3.4 supraventricular tachycardia

+

+

2.3

3.6 3.0

scattered ventricular extrasystoles scattered ventricular ext rasystoles

3.3

7.6

3.7 2.7 2.7 2.9 3.1

2.9 2.6

3.7 3.5

BETA BLOCKADE AND ADRENALINE DURING NLA

kPo

L4

1 I

I

0

+S

I

I

L

10

15

20

min

Fig. 4. Fluctuations of mean systolic (-0-) and diastolic pressures (-o-) in radial artery due to adrenaline infiltration during NLA (fs.d., N = 4).

pressure changes were typical of adrenaline, i.e. an initial pressure fall due to peripheral vasodilatation before the pressure response (Figs. 3 and 4). Adrenergic beta-receptor blockade induced with alprenolol (0.04 mg/kg with atropine 0.01 mg/kg) during the steady state of NLA caused minimal changes in pulse rate, radial artery pressure, right ventricular pressure and CVP (as seen in Fig. 5). Adrenaline infiltration induced a pressure response without an initial pressure fall (Fig. 6). The pulse rate decreased in 12 patients during this adrenaline-induced pressure rise. Scattered premature ventricular contractions were recorded in two of these patients. There was an increase in pulse rate in two patients and supraventricular tachycardia in one. Cardiac arrhythmias and the doses of infiltrated adrenaline are presented in Table 1.

Table 2 Acid-base balance and levels of blood gases (kPa) and serum potassium and sodium concentrations (mM) in arterial blood during neurolept analgesia after adrenaline infiltration without (A) and with alprenolol blocking (B). (Meansf s.d.) A. NLA Adrenaline (n = 4)

I

NLA

pH Paco, Paoz BE K Na

7.380 f 0.000 5.5f 0.3 12.4f2.2 -].Of 1.0

15 min after adrenaline 7.383 k 0.023 5.5 k 0.3 12.4k2.5 +0.3& 1.5 3.7 k 0.0 136.5k 2.1

B. NLA Alprenolol Adrenaline (n = 15)

NLA pH Pacoz Pao2 BE K Na

I

15 min after adrenaline

15 min after alprenolol I

I

7.400* 0.036 4.8 2 0.4 15.0 2.6 --1.9+2.6

149

7.409 k 0.026 4.7 0.6 14.4k 3.0 -1.8k3.3 3.7k0.2 131.2 f 4.8

7.421 & 0.028 4.8 0.5 15.3f 2.9 -0.7k2.6

150

P. J. PONTINEN

Acid base status, blood gas values and electrolytes were within the normal range throughout the procedure (Table 2). When a beta-blocking drug was not given before adrenaline infiltration, an initial increase in the amplitude of the peripheral pulse wave was seen. This was soon replaced by a decrease in amplitude. With beta blockade, this initial increase in pulse wave due to the vasodilating effect of adrenaline was recorded in six patients. The response was vasoconstriction from the very beginning in eight patients.

DISCUSSION

arrhythmogenic dose of adrenaline during relatively light levels of halothane anaesthesia in dogs has been reported to be 4.6 pg/kg (MUNSON & TUCKER 1975), as compared to 36 pg/kg in dogs awake (JOAS & STEVENS 1971). In man, it has been shown that ventricular arrhythmias occur in all patients where the dose of infiltrated adrenaline exceeds 6.9 pg/kg (IKEZONO et al. 1969). Ventricular arrhythmias were common also in the group receiving adrenaline from 0.5 to 3.5pg/kg (IKEZONO et al. 1969). In the present study, ventricular arrhythmias occurred in patients receiving only 2.3 and 4.8 pg/kg adrenaline. Although their ventilation was controlled and their acid base status, blood

effect and concomitant tachycardia does not exceed 10 min, serious tachycardias interfering with the circulation must be terminated immediately. Propranolol was effective in

92

88

'I

12

-LL1

-2

'

0

+10

+5

+15

min

Fig. 5. The effects of alprenolol (0.04 mgjkg) given together with atropine (0.01 rng/kg) during NLA on (from top to bottom) heart rate (beatslmin), radial artery pressure (kPa) (systolic and diastolic), mean right ventricle pressure (kPa) and central venous pressure (cmH20).

I

.S

10

15

20

min

Fig. 6. The effects of' alprenolol on adrenaline-induced changes in mean systolic (-0-) and diastolic (-0-) pressures in radial artery during NLA ( & s.d., N = 15).

BETA BLOCKADE AND ADRENALINE DURING NLA

terminating ventricular arrhythmias, and also supraventricular tachycardia, without undue depression of the circulation. The circulatory changes due to the adrenergic beta-receptor blockade were minimal and compared favourably with those seen during halothane anaesthesia (PONTINEN 1978). These findings confirm earlier reports where beta-receptor blockers were used to combat ventricular tachyarrhythmias during NLA (PONTINEN & EKHOLM 1964, PONTINEN et al. 1965). The stable pulse rate may have been due to atropine, which was always given as a safety measure on the basis of previous experience (PONTINEN 1969). The conclusion to be drawn from these results is that adrenergic beta-receptor blockade is compatible with NLA, provided that general safety measures, atropinization and normal acid base status are taken care of. Beta-receptor blockade provides only partial protection against adrenaline-induced arrhythmias. The time interval between alprenolol injection and adrenaline infiltration was rather long, up to 25 min. As the effective half-life of intravenous alprenolol is approx. 40 min (JOHNSTONE 1968), the actual serum concentration of alpreno101 during adrenaline infiltration was far less than immediately after the injection. This might have been at least a partial reason for the arrhythmias noticed. The pressure response to infiltrated adrenaline altered during adrenergic beta-receptor blockade. Instead of an initial fall in blood pressure, there was a steady rise starting immediately after the infiltration. The pressure response seems to have been more pronounced and prolonged during beta-receptor blockade, although the results are difficult to compare. This may be due to the beta,receptor blocking effect of alprenolol. This peripheral vasoconstriction is seen in the diminution of the peripheral pulse wave during the adrenaline-induced pressure rise.

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151

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Cardiovascular effects of local adrenaline infiltration during neurolept analgesia and adrenergic beta-receptor blockade in man.

Acta anaesth. scand. 1978, 22, 145-153 Cardiovascular Effects of Local Adrenaline Infiltration During Neurolept Analgesia and Adrenergic Beta-Recepto...
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