Acta anaesth. scand. 1979, 23, 471-479
Cardiovascular Effects of Neurolept Anaesthesia in Patients with Coronary Artery Disease H. T Y D ~ and N C. J. WESTERHOLM Departments of Anaesthesiology, Thoracic and Cardiovascular Surgery and Clinical Physiology, University Hospital, Uppsala, Sweden
An anaesthetic technique comprising a combination of phenoperidine (0.1 mg . kg-l),diazepam (0.06mg kg-l) and pancuronium bromide (0.1 mg . kg-') with controlled ventilation was evaluated in 12 patients with severe coronary artery disease. The heart rate, cardiac output and mean arterial blood pressure did not change significantly between the preinduction and postinduction measurements. The right atrial pressure and pulmonary capillary wedge pressure decreased significantly by 33% and 36D/,, respectively, probably due to the influence of positive-pressure ventilation. There was no depression of the left ventricular performance. Received 8 February, accepted for publication 2 March 1979
Anaesthesia for the patient with coronary tion after aorto-coronary bypass operations, artery disease is a challenge because of the we found it vital to investigate further the limited reserves regarding the myocardial influence of the specific anaesthetic technique oxygen supply/demand ratio (BUCKBERG used. The present study was therefore des1977). It calls for detailed consideration of igned to elucidate the haemodynamic effects phenoperidine-diazepam-pancuronium the anaesthetic technique to be employed. of bromide anaesthesia during controlled ventiNeurolept anaesthesia has been claimed to lation in patients with coronary artery be well tolerated by poor-risk patients d isease. ' (NILSSON & JANSSEN 196I ) , including those undergoing open-heart surgery (CORSSEN et al. 1965). There has also been accumulating evidence in favour of neurolept anaes- MATERIAL AND M E T H O D S thesia for patients with hypertension and Patients ischaemic heart disease (PRYS-ROBERTS et al. Twelve male patients with severe coronary artery 1971, BILLE-BRAHEet al. 1978). MAU- disease were studied during induction of anaesthesia for aorto-coronary bypass surgery. Patients with NUKSELA (1977), in a comparative haemodynamic study of balanced, neurolept and severe arterial hypertension (24/14 kPa or higher) halothane anaesthesia during open-heart were excluded. The mean age was 52 years (range 38-65). All patients had been treated with betasurgery (including coronary artery bypass receptor blocking agents preoperatively, and these operations), made the case for neurolept were withdrawn 3 days prior to surgery according to the routine in open-heart cases. Four patients were anaesthesia as the best choice. We have been using different modifications having digitalis therapy. Six patients had suffered one of neurolept anaesthesia in open-heart surgery or more previous myocardial infarctions. None was in congestive heart failure. for over a decade, with favourable clinical results (WESTERHOLM 1967). During studies Investigative scheme of the early postoperative circulatory adapta- Haemodynamic measurements were performed im0001-5172/79/050471-09$02.50/0
0 1979 The Scandinavian Society of Anaesthesiologists
472
1-1. T Y ~ A NND
c. 1 .
M'ESTERHOIM
mediately prior to induction of anaesthesia, i.e. about 15 min after the Catheterization, which was carried ont with the patient in a state of heavy sedation. 'The postinduction recordings were made about 30 min after induction of anaesthesia, before surgery was begun and at least 15 min after the discontinuation of nitrous oxide (see Anaesthesia). For comparison, resnlts of the preoperative haemodynamic investigation performed on an average G months earlier have been included in the table and figures. The methods used in the preoperative investigation have been described by KLiNCEN ( I 978). Airaestlresiri
An oral sedative containing 150 mg mcballymal sodium, 50 mg allylmalonyl carbamide and 50 mg hydroxizine chloride (Vesparax,@UCB) was given the night before the operation. Two hours prior to induction of anaesthesia the patient was prernedicated with pentobarbital sodium (Mebumal, AGO), 100 mg orally, and one hour later he was given 10 mg of morphine chloride and 0.4 mg of scopolamine bromide (Morfnskopolamin, AGO) intramuscularly. Anaesthesia was induced with phenoperidine (Lealgin," Leo) 0.1 mg . k g - ' , given intravenously (i.v.), and nitrous oxide/oxygen 1 : 1 administered through a non-rebreathing circuit. After induction of muscle relaxation with pancuronium bromide [Pavulon,o Organon) 0.1 m g . kg-l i.v., oral intubation was performed. The patient was ventilated with an EngstrGm 300 respirator (Engstrom Medical, Sweden), the minute ventilation being set according to the nomogram of E N G S T K & ~M HEKZOG (1959). At least 15 min prior to the postinduction haemodynamic measurements air was substituted for nitrous oxide and the patient was given phenoperidine 0.05 mg . kg-' and diazepam 0.06 m g . kg-l i.v. Nitrous oxide was reinstituted after the haemodynamic recordings.
Catheterization Under local analgesia, a catheter was introduced percutaneously via the right femoral artery into the common iliac artery or lowcr abdominal aorta for arterial pressure recording. A three-lumen Swan-Ganz thermodilution catheter (mod. 93~-133%7F,Edwards Lab., USA) waq advanced under fluoroscopic control through an antecubital vein until its tip was located in a main branch of the pulmonary artery. No complications occurred.
Laborntog) methods f'ressures. Mean arterial blood pressure (MABP), mean
right arterial pressure (MRAP), mean pulmonary arterial pressure (MPAP) and mean pulmonary capillary wedge pressure (MPCM'P) were registered simultaneously by means of four pressure transducers ( E M T 746, Siemens-Elema, Sweden), amplified ( E M T 311, Siemens-Elema) and recorded on an eight-channel ink-jet recorder (Mingograf 81, Siemens-
Elema) . Mean pressures were obtained by electronic dampening of the signal. All measurements were performed in apnoea with the patient in a supine position, and the mid-thoracic line was taken as the zero reference point. Cardiac output (CO) was determined by the thermodilution technique (FEGLER1954, FORKESTER et al. 1972), using a computer (Devices 3750, Cardiovascular Instruments Ltd, U.K.) as describcd by BRANTIIWAITE 8z BRADLEY (1968). T h e curves were recorded on the Mingograf recorder. Saline at room temperature was used as indicator. The cardiac output was estimated as the mean of at least three well-formed curves. 'The error of a single determination was 7.8%. Heart rate ( H R ) was derived from the electrocardiogram.
Blood gas airalyszs (pH, Pol, Pcol) was performed i n an ABL I blood gas analyser (Radiometer, Denmark) in duplicate. The errors of a single determination were: p H f l.O%, Po, t- 2.3%, Pcol f I .8%. Temperature correction was made according to the method of' KEL.MAN & NUNN(1966). Oxygen saturation ( S o l ) and haemoglobin concentration (Hb) of arterial and mixed venous blood were read on an 11. 182 oximeter (Instrumentation Lab. Inc., USA). Calculatiotu c o x 1000 (ml) HR Systemic vascular resistance (SVR) = MABP MRAP xG0 ( 1 0 6 . N s m - 5 ) CO Pulmonary vascular resistance (PVR) = M PA P - MPCW P x 60 (10' . N s ~ - ~ ) CO Left ventricular stroke work (LVSM') = MABP x SV (mJ) The pressures are given in kPa, C O in 1 . miri-' and H R in beats . min-I. T h e oxygen contents of arterial and mixed venous blood were calculated from the following formula : H b x 0.062 x Sol +PolxO.O1 (mmol. I - ' ) , Stroke volume (SV) =
~
I00
where H b is given in g . 1 - I, Sol in % and Po, in kPa. The arterio-venous oxygen content difference (AVDo ) was calculated by subtracting the mixed venous from the arterial oxygen content. Oxygen uptake (Val) = AVDo, x CO x I /GO (mmol . s - I ) . Statistics
Means, standard deviations (s.d.) and standard errors of the mean (s.e. mean) were calculated according to standard formulae. Student's t-test for paired observations was used. A P value< 0.05 was taken ar, significant.
NElJROLEPT ANAESTHESIA IN CORONARY ARTERY DISEASE
RESULTS The results are summarized in Table 1. There were no significant differences between the preoperative haemodynamic data obtained in the catheterization laboratory and the preinduction values. The arterial carbon diovide tension (Pa,,,) fell from 5.0 to 3.7 kPa after induction of anaesthesia and institution of artificial ventilation. This change was significant ( P < 0.01). MABP did not change significantly after induction of anaesthesia, compared with the preinduction level. During anaesthesia MPAP fell by 25;/, (P
Cardiovascular Effects of Neurolept Anaesthesia in Patients with Coronary Artery Disease H. T Y D ~ and N C. J. WESTERHOLM Departments of Anaesthesiology, Thoracic and Cardiovascular Surgery and Clinical Physiology, University Hospital, Uppsala, Sweden
An anaesthetic technique comprising a combination of phenoperidine (0.1 mg . kg-l),diazepam (0.06mg kg-l) and pancuronium bromide (0.1 mg . kg-') with controlled ventilation was evaluated in 12 patients with severe coronary artery disease. The heart rate, cardiac output and mean arterial blood pressure did not change significantly between the preinduction and postinduction measurements. The right atrial pressure and pulmonary capillary wedge pressure decreased significantly by 33% and 36D/,, respectively, probably due to the influence of positive-pressure ventilation. There was no depression of the left ventricular performance. Received 8 February, accepted for publication 2 March 1979
Anaesthesia for the patient with coronary tion after aorto-coronary bypass operations, artery disease is a challenge because of the we found it vital to investigate further the limited reserves regarding the myocardial influence of the specific anaesthetic technique oxygen supply/demand ratio (BUCKBERG used. The present study was therefore des1977). It calls for detailed consideration of igned to elucidate the haemodynamic effects phenoperidine-diazepam-pancuronium the anaesthetic technique to be employed. of bromide anaesthesia during controlled ventiNeurolept anaesthesia has been claimed to lation in patients with coronary artery be well tolerated by poor-risk patients d isease. ' (NILSSON & JANSSEN 196I ) , including those undergoing open-heart surgery (CORSSEN et al. 1965). There has also been accumulating evidence in favour of neurolept anaes- MATERIAL AND M E T H O D S thesia for patients with hypertension and Patients ischaemic heart disease (PRYS-ROBERTS et al. Twelve male patients with severe coronary artery 1971, BILLE-BRAHEet al. 1978). MAU- disease were studied during induction of anaesthesia for aorto-coronary bypass surgery. Patients with NUKSELA (1977), in a comparative haemodynamic study of balanced, neurolept and severe arterial hypertension (24/14 kPa or higher) halothane anaesthesia during open-heart were excluded. The mean age was 52 years (range 38-65). All patients had been treated with betasurgery (including coronary artery bypass receptor blocking agents preoperatively, and these operations), made the case for neurolept were withdrawn 3 days prior to surgery according to the routine in open-heart cases. Four patients were anaesthesia as the best choice. We have been using different modifications having digitalis therapy. Six patients had suffered one of neurolept anaesthesia in open-heart surgery or more previous myocardial infarctions. None was in congestive heart failure. for over a decade, with favourable clinical results (WESTERHOLM 1967). During studies Investigative scheme of the early postoperative circulatory adapta- Haemodynamic measurements were performed im0001-5172/79/050471-09$02.50/0
0 1979 The Scandinavian Society of Anaesthesiologists
472
1-1. T Y ~ A NND
c. 1 .
M'ESTERHOIM
mediately prior to induction of anaesthesia, i.e. about 15 min after the Catheterization, which was carried ont with the patient in a state of heavy sedation. 'The postinduction recordings were made about 30 min after induction of anaesthesia, before surgery was begun and at least 15 min after the discontinuation of nitrous oxide (see Anaesthesia). For comparison, resnlts of the preoperative haemodynamic investigation performed on an average G months earlier have been included in the table and figures. The methods used in the preoperative investigation have been described by KLiNCEN ( I 978). Airaestlresiri
An oral sedative containing 150 mg mcballymal sodium, 50 mg allylmalonyl carbamide and 50 mg hydroxizine chloride (Vesparax,@UCB) was given the night before the operation. Two hours prior to induction of anaesthesia the patient was prernedicated with pentobarbital sodium (Mebumal, AGO), 100 mg orally, and one hour later he was given 10 mg of morphine chloride and 0.4 mg of scopolamine bromide (Morfnskopolamin, AGO) intramuscularly. Anaesthesia was induced with phenoperidine (Lealgin," Leo) 0.1 mg . k g - ' , given intravenously (i.v.), and nitrous oxide/oxygen 1 : 1 administered through a non-rebreathing circuit. After induction of muscle relaxation with pancuronium bromide [Pavulon,o Organon) 0.1 m g . kg-l i.v., oral intubation was performed. The patient was ventilated with an EngstrGm 300 respirator (Engstrom Medical, Sweden), the minute ventilation being set according to the nomogram of E N G S T K & ~M HEKZOG (1959). At least 15 min prior to the postinduction haemodynamic measurements air was substituted for nitrous oxide and the patient was given phenoperidine 0.05 mg . kg-' and diazepam 0.06 m g . kg-l i.v. Nitrous oxide was reinstituted after the haemodynamic recordings.
Catheterization Under local analgesia, a catheter was introduced percutaneously via the right femoral artery into the common iliac artery or lowcr abdominal aorta for arterial pressure recording. A three-lumen Swan-Ganz thermodilution catheter (mod. 93~-133%7F,Edwards Lab., USA) waq advanced under fluoroscopic control through an antecubital vein until its tip was located in a main branch of the pulmonary artery. No complications occurred.
Laborntog) methods f'ressures. Mean arterial blood pressure (MABP), mean
right arterial pressure (MRAP), mean pulmonary arterial pressure (MPAP) and mean pulmonary capillary wedge pressure (MPCM'P) were registered simultaneously by means of four pressure transducers ( E M T 746, Siemens-Elema, Sweden), amplified ( E M T 311, Siemens-Elema) and recorded on an eight-channel ink-jet recorder (Mingograf 81, Siemens-
Elema) . Mean pressures were obtained by electronic dampening of the signal. All measurements were performed in apnoea with the patient in a supine position, and the mid-thoracic line was taken as the zero reference point. Cardiac output (CO) was determined by the thermodilution technique (FEGLER1954, FORKESTER et al. 1972), using a computer (Devices 3750, Cardiovascular Instruments Ltd, U.K.) as describcd by BRANTIIWAITE 8z BRADLEY (1968). T h e curves were recorded on the Mingograf recorder. Saline at room temperature was used as indicator. The cardiac output was estimated as the mean of at least three well-formed curves. 'The error of a single determination was 7.8%. Heart rate ( H R ) was derived from the electrocardiogram.
Blood gas airalyszs (pH, Pol, Pcol) was performed i n an ABL I blood gas analyser (Radiometer, Denmark) in duplicate. The errors of a single determination were: p H f l.O%, Po, t- 2.3%, Pcol f I .8%. Temperature correction was made according to the method of' KEL.MAN & NUNN(1966). Oxygen saturation ( S o l ) and haemoglobin concentration (Hb) of arterial and mixed venous blood were read on an 11. 182 oximeter (Instrumentation Lab. Inc., USA). Calculatiotu c o x 1000 (ml) HR Systemic vascular resistance (SVR) = MABP MRAP xG0 ( 1 0 6 . N s m - 5 ) CO Pulmonary vascular resistance (PVR) = M PA P - MPCW P x 60 (10' . N s ~ - ~ ) CO Left ventricular stroke work (LVSM') = MABP x SV (mJ) The pressures are given in kPa, C O in 1 . miri-' and H R in beats . min-I. T h e oxygen contents of arterial and mixed venous blood were calculated from the following formula : H b x 0.062 x Sol +PolxO.O1 (mmol. I - ' ) , Stroke volume (SV) =
~
I00
where H b is given in g . 1 - I, Sol in % and Po, in kPa. The arterio-venous oxygen content difference (AVDo ) was calculated by subtracting the mixed venous from the arterial oxygen content. Oxygen uptake (Val) = AVDo, x CO x I /GO (mmol . s - I ) . Statistics
Means, standard deviations (s.d.) and standard errors of the mean (s.e. mean) were calculated according to standard formulae. Student's t-test for paired observations was used. A P value< 0.05 was taken ar, significant.
NElJROLEPT ANAESTHESIA IN CORONARY ARTERY DISEASE
RESULTS The results are summarized in Table 1. There were no significant differences between the preoperative haemodynamic data obtained in the catheterization laboratory and the preinduction values. The arterial carbon diovide tension (Pa,,,) fell from 5.0 to 3.7 kPa after induction of anaesthesia and institution of artificial ventilation. This change was significant ( P < 0.01). MABP did not change significantly after induction of anaesthesia, compared with the preinduction level. During anaesthesia MPAP fell by 25;/, (P
