Br.J. Anaesth. (1975), 47, 977
INTRACRANIAL PRESSURE DURING RECOVERY FROM NITROUS OXIDE AND HALOTHANE ANAESTHESIA IN NEUROSURGICAL PATIENTS P . B . J0RGENSEN AND B . B . MlSFELDT SUMMARY
All inhalation anaesthetic agents increase intracranial pressure (McDowall, Barker and Jennett, 1966; Fitch et al., 1969; Jennett et al., 1969). This increase is the result of cerebral vasodilatation and the consequent increase of cerebral blood volume. The iDtracranial hypertension is most pronounced in patients with intracranial space-occupying lesions, as these patients have less reserve space. Minor changes in blood volume may, therefore, cause major changes in intracranial pressure. Another factor of major importance in anaesthesia for intracranial procedures is arterial carbon dioxide tension. Hypercapnia adds to the vasodilating effect of anaesthetic ngeats, while hypocapnia effectively counteracts it. There are many published reports of intracranial pressure changes during induction of anaesthesia, but there has been little previous interest in the period following surgery. At this time, when artificial hyperventilation is interrupted and spontaneous breathing begins, arterial carbon dioxide tension must increase, probably leading to some degree of hypercapnia. PAUL BALSLEV JORGENSEN, M.D.; BENT B. MISFELDT, M.D.;
Departments of Neurosurgery and Anaesthesia, University Hospital (Rigshospitalet), 9 Blegdamsvej, 2100 Copenhagen, Denmark.
If this occurs, vasodilatation caused by anaesthetic agents will be potentiated and intracranial hypertension will result after operation. Therefore we found it worthwhile to study this period by correlating the clinical state with arterial carbon dioxide tension and intracranial pressure. MATERIAL AND METHODS
Seven patients were studied during recovery from general anaesthesia. The diagnosis, the intracranial pressure during 24 hr after anaesthesia, and the treatment directed against intracranial hypertension are presented in table I. Intracranial pressure, arterial pressure and central venous pressure were recorded continuously via catheters in a lateral ventricle, in the radial artery of the non-dominant hand, and in a subclavian vein (Jorgensen and Henriksen, 1973). All catheters were placed after induction of anaesthesia. Pressures were referred to forehead level. Cerebral perfusion pressure (CPP) was calculated as the difference between mean arterial pressure (MAP) and mean intracranial pressure (ICP). Blood samples were drawn through the arterial catheter for determination of Po2, Pco2 and pH by standard Radiometer equipment. Five patients underwent craniotomy for removal of
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Seven patients with intracranial disorders were studied during recovery from anaesthesia with nitrous oxide and halothane. Arterial, intracranial, and central venous pressure, and arterial carbon dioxide tension were measured and compared with the patient's clinical state. No patient had evidence of increased brain volume when the dura was closed. All had been hyperventilated during the surgical procedure. Cessation of hyperventilation and the continued administration of anaesthetics was followed by a moderate increase in intracranial pressure and a reduction in cerebral perfusion pressure, but critically low values were not seen. Spontaneous respiration returned when the PaCo2 was in the range 33-51 mm Hg. When spontaneous respiration was judged to be normal, anaesthesia was interrupted and the endotracheal tube was removed. In the following minutes, until the patients were awake, the intracranial pressure decreased to normal or near normal values, with minimal change in PaCo2. In these seven patients in whom there were no signs of brain swelling, the skull was closed, the patients were allowed to resume spontaneous respiration, and anaesthesia was terminated without major changes in intracranial pressure or cerebral perfusion pressure. However, hyperventilation is advocated after operation in patients with marked brain swelling.
BRITISH JOURNAL OF ANAESTHESIA
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TABLE I. Details of the patients studied. 24 hr after recovery from anaesthesia Patient no. Sex Age 1
F
Diagnosis
Intracranial pressure Plateau (mm Hg) waves
Clinical state
Treatment
38 hydrocephalus
postencephalitis
20-40
—
alert/papilloedema
F
21 cerebellar angioma
10-35
—
alert/papilloedema
dexamethasone
3
F
57 cerebral metastasis
15-25
—
alert/papilloedema
dexamethasone
4
F
57 acoustic neuroma
5-10
—
alert
dexamethasone
5
F
40 acoustic neuroma
5-10
—
alert
—
6
M
55 cerebral atrophy
5-10
—
alert
—
7
F
20 chiasmatic haematoma
0-20
—
somnolent
dexamethasone
tumours or haematomas, and two patients were studied after ventriculography. Anaesthesia had been induced with barbiturate-relaxant, and, after endotracheal intubation, was maintained with 50% nitrous oxide in oxygen plus 0.5-1.0% halothane. Controlled hyperventilation by means of an Engsrrom ventilator was used throughout the operative procedures to counteract the vasodilator effects of anaesthetic agents and to minimize brain swelling. At the end of the procedure the patients were placed in bed in a supine position. Hyperventilation with 50% nitrous oxide in oxygen and 0.5-1.0% halothane was continued for at least 10 min in order to maintain PaCo2 at an unchanged value. Then a set of control values of MAP, ICP and CVP were measured and an arterial blood sample was drawn for gas analysis (first measurement). Ventilation was then reduced stepwise until the beginning of spontaneous respiratory movements. The next values were obtained at this time (second measurement). The ventilator was then disconnected, and respiration was assisted manually with an anaesthesia bag until spontaneous ventilation was judged clinically to be adequate, whereupon the third measurement was made. The endotracheal tube was now removed and halothane and nitrous oxide administration was discontinued. Oxygen was given by mask until the patient responded to verbal stimulation, and the last set of pressure and gas values was obtained {fourth measuretnent). This sequence was used to
avoid coughing and high intracranial pressure peaks during removal of the tube. The data are shown in figures 1-3. RESULTS
Control measurements during hyperventilation (first measurement), showed PaCo2 values between 20 and 32 mm Hg (mean: 24.1 mm Hg). Perfusion pressures were between 48 and 86 mm Hg (mean: 64.9 mm Hg). Only one patient (no. 1), following a ventriculogram, showed an elevated ICP (15 mm Hg) during hypocapnia. After hyperventilation was discontinued, Pa«>2 increased until spontaneous respiration started, at Pco 3 values in the range 33-51 mm Hg (mean: 40.3 mm Hg) (second measurement). At this time ICP had increased to 2-39 mm Hg (mean: 17.9 mm Hg); thus CPP was reduced to 44-82 mm Hg (mean: 58.2 mm Hg). Four to 28 min (mean: 19 min) passed before spontaneous respiratory movements were seen, and a further period of 3-8 min (mean: 6 min) until respiration was judged clinically to be sufficient. The appearance of adequate spontaneous respiration was associated with only minimal changes in Pco 2 , 35-55 mm Hg (mean: 42.0 mm Hg) and ICP, 11-39 mm Hg (mean: 21.1 mm Hg) (third measurement). CPP decreased slightly in two patients (nos. 2 and 4), but increased in the other five patients because of an increase in arterial pressure. When the patients were awake (fourth measurement) Paco2 was 29-53 mm Hg (mean: 39.0 mm Hg). In
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2
979
INTRACRANIAL PRESSURE AND RECOVERY FROM ANAESTHESIA CPP mm Hg
2.
3.
A.
17.9 76.1 58.3 40.3 -1.3
21.1 86.3 65.1 42.0 -1.5
91.1 65.0 39.0
100 90 80-
60 5040;
MEAN VALUES
ICP MAP CPP Pa C02 CVP
MEAN VALUES
MAP ICP
69.0
761
86.3
91.1
4.1
17.9
21.1
6.1
FIG. 1. Intracranial pressure (ICP) and arterial pressure (MAP) in seven patients during recovery from anaesthesia. (1) 50% nitrous oxide in oxygen and 0.5% halothane and controlled hyperventilation. (2) 50% nitrous oxide in oxygen and 0.5 % halothane at onset of spontaneous respiration. (3) 50 % nitrous oxide in oxygen and 0.5 % halothane, when spontaneous respiration is judged to be adequate. (4) 100% oxygen after removal of the endotracheal tube, when the patients are responding to verbal stimulation.
all but one patient (no. 1) ICP was normal, ranging from 0 to 23 mm Hg (mean: 6.1 mm Hg), and CPP was in excess of 70 mm Hg (mean: 85.0 mm Hg) in all patients. From 9 to 31 min elapsed between removal of the endotracheal tube and awakening. CVP was virtually unchanged throughout the study. DISCUSSION
Patients with intracrardal disorders who receive general anaesthesia during operations or neuroradiological examinations risk secondary brain damage as a result of a decrease in the cerebral perfusion pressure with local or global ischaemia, or compression and distortion of brain tissue from the shifting of masses.
4.1
69.0 64.9 25.0 -2.7
6.1
-2.7
FIG. 2. Cerebral perfusion pressure (CPP) in seven patients during recovery from anaesthesia. (1) 50 % nitrous oxide in oxygen and 0.5% halothane and controlled hyperventilation. (2) 50 % nitrous oxide in oxygen and 0.5 % halothane at onset of spontaneous respiration. (3) 50 % nitrous oxide in oxygen and 0.5 % halothane, when spontaneous respiration is judged to be adequate. (4) 100 % oxygen after removal of the endotracheal tube, when the patients are responding to verbal stimulation.
The autoregulatory mechanisms of cerebral arterioles will keep blood flow constant at perfusion pressures of as little as 40 mm Hg in normal brain (Haggendal et al., 1970; Zwetnow, 1970), whether this reduction is a result of an increase in intracranial pressure or of decrease in arterial pressure. However, in patients with intracranial disease, autoregulation may be impaired locally or globally. Thus blood flow may decrease in these patients when a decrease in perfusion pressure is only moderate. Several factors may contribute to the reduction in cerebral perfusion pressure during general anaesthesia : (1) An increase in intracranial pressure resulting from an increase in blood volume caused by hypercapnia and anaesthetic agents. (2) A reduction in arterial pressure because of the cardiovascular effects of hypocapnia and anaesthetics. (3) An increase in venous pressure as a result of inappropriate positioning of the head with compression of jugular veins.
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70-
980
BRITISH JOURNAL OF ANAESTHESIA
Pa
CO 2 mmHg
2.. T
3. T
T
25.0
40.3
42.0
39.0
6050-
302010-
MEAN VALUES
FIG. 3. Arterial carbon dioxide tension (Pacoz) in seven patients during recovery from anaesthesia. (1) 50 % nitrous oxide in oxygen and 0.5 % halothane with controlled hyperventilation. (2) 50% nitrous oxide in oxygen and 0.5% halothane at onset of spontaneous respiration. (3) 50% nitrous oxide in oxygen and 0.5% halothane, when spontaneous respiration is judged to be adequate. (4) 100% oxygen after removal of the endotracheal tube, when the patients are responding to verbal stimulation.
The influence ofthese factors upon cerebral vascular dynamics has been examined thoroughly during induction of anaesthesia and before the skull is opened (McDowall, Barker and Jennett, 1966; Fitch et al., 1969; Henriksen and Jergensen, 1973; Jorgensen and Henriksen, 1973). It is generally accepted that patients are treated most safely with a barbiturate-relaxant induction (Pierce et al., 1962) followed by endotracheal intubation and the rapid establishing of controlled hyperventilation to reduce the period of hypercapnia and hypoxia. Inhalation anaesthetic agents should not be administered before hypocapnia can counteract their vasodilator effects (Adams et al., 1972; Misfeldt, Jergensen and Rishoj, 1975). Until now little attention has been paid to intracranial pressure changes in the period immediately after operation. This may be a result of the general belief that, at this time following the removal of space-occupying lesions, the risks of intracranial hypertension and mass shift are much reduced. However, a tumour may not have been removed radically,
and local or diffuse brain swelling may develop or be present because of an increase in blood volume and oedema. Further, in patients who have undergone neuroradiological examinations, the risks of intracranial hypertension and mass shift are still present, since a possible tumour or haematoma has not been removed. Leech, Barker and Fitch (1974) report briefly on the increase in intracranial and systemic pressure in patients brought from the hypocapnic to the normocapnic state, despite the appearance of slackness of the dura when the skull is being closed. However, no information about PaCo2 changes were presented. What factors influence the intracranial pressure changes during recovery from anaesthesia? (1) Concentrations of anaesthetic agents decrease rapidly, and if there are remaining residual effects from these upon cerebral vascularity, ICP must decrease while anaesthetics are exhaled. (2) After hyperventilation during the operative procedures one must allow PaCo2 to increase before the patient will be able to breathe spontaneously. This will increase ICP. (3) While the concentration of anaesthetic agents decreases and Pco2 increases, arterial pressure increases, and thus improves cerebral perfusion pressure. (4) Any oedema or haematoma initiated during operation or during hypoxia by inadequate perfusion pressure will increase ICP and bring about a risk of mass shift and herniation. In the present study of patients, none of whom had evidence of severe brain swelling at closure of the dura, all of whom had received nitrous oxide and halothane during hypocapnia, and had the endotracheal tube removed after a period of hypoventilation and were then awakened, we found the following: (1) The intracranial pressure increased when hyperventilation was discontinued and PaCO2 increased, but from the onset of spontaneous respiration little further increase was observed. (2) The cerebral perfusion pressure did not decrease to less than the critical 40 mm Hg value, because the arterial pressure increased simultaneously, both during hypoventilation and during lightering of anaesthesia. (3) The intracranial pressure decreased in all patients when the administration of anaesthetics was interrupted, despite rearly unchanged Paco2 values. (4; In most patients spontaneous respiration renamed at normocapnia and before severe hypercapr.ia had
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1 •
INTRACRANIAL PRESSURE AND RECOVERY FROM ANAESTHESIA
REFERENCES
Adams, R. W., Gronert, G. A., Sundt, T. M.3 and Michenfelder, J. D. (1972). Halothane, hypocapnia and cerebrospinal fluid pressure in neurosurgery. Anesthesiology, 37, 510. Fitch, W., Barker, J., McDowall, D. G., and Jennett, W. B. (1969). The effect of methoxyflurane on cerebrospinal fluid pressure in patients with and without intracranial space-occupying lesions. Br. J. Anaesth., 41, 554. Haggendal, E., Ldfgren, J., Nilsson, N. J., and Zwetnow, N. N. (1970). Effect of varied cerebrospinal fluid pressure on cerebral blood flow in dogs. Ada Physiol. Scand., 79, 262. Henriksen, H. T., and Jorgensen, P. B. (1973). The effect of nitrous oxide on intracranial pressure in patients with intracranial disorders. Br. J. Anaesth., 45, 486. Jennett, W. B., Barker, J., Fitch, W., and McDowall D. G. (1969). Effect of anaesthesia on intracranial pressure in patients with space-occupying lesions. Lancet, 1, 61. Jorgensen, P. B., and Henriksen, H. T. (1973). The effect of fluoroxene on intracranial pressure in patients with intracranial space-occupying lesions. Br. J. Anaesth., 45, 599. Leech, P., Barker, J., and Fitch, W., (1974). Changes in intracranial pressure and systemic arterial pressure during the termination of anaesthesia (abstract). Br. J. Anaesth., 46, 315. McDowall, D. G., Barker, J., and Jennett, W. B. (1966). Cerebrospinal fluid pressure measurements during anaesthesia. Anaesthesia, 21, 189. Misfeldt, B. B., Jorgensen, P. B., and Rishej, M. (1975). The effect of nitrous oxide and halothane upon the intracranial pressure in hypocapnic patients with intracranial disorders. Br. J. Anaesth., 46, 853. Pierce, E. C , Lambertsen, C. J., Deutsch, S., Chase, P. E., Lunde, H. W., Dripps, P. D., and Price, H. L. (1962). Cerebral circulation and metabolism during thiopental anesthesia and hyperventilation in man. J. Clin. Invest., 41, 1664. Zwetnow, N. N. (1970). Effects of increased cerebrospinal fluid pressure on the cerebral bloodflowand on the energy metabolism of the brain: an experimental study. Ada Physiol. Scand., (Suppl), 339, 1.
PRESSION INTRA-CRANIENNE AU COURS DE LA RECUPERATION SUIVANT UNE ANESTHESIE PAR L'OXYDE AZOTEUX ET L'HALOTHANE CHEZ DES PATIENTS DE NEUROCHIRURGIE RESUME
Sept patients presentant des troubles intra-craniens ont ete etudies au cours de la recuperation qui a suivi leur anesthesie par Poxyde azoteux et Phalothane. On a mesure la pression veineuse centrale, la tension arterielle et la pression intra-cranienne ainsi que la tension de Panhydride carbonique arteriel et on les a comparees a Petat clinique du patient. On n'a constate sur aucun patient que le volume du cerveau avait augmente au moment ou Pon a ferine la dure-mere. Tous avaient ete surventiles pendant Poperation chirurgicale. L'arret de la surventilation et Padministration continue d'agents anesthesiques a ete suivie d'une augmentation moderee de la pression intracranienne et d'une reduction de la pression de la perfusion cerebrale, mais on n'a constate aucune valeur critiquement basse. Las respiration spontanee est revenue lorsque le Paco2 s'est situi dans la plage des 33-51 mm Hg. Lorsqu'on a estime que la respiration spontanee £tait normale, on a interrompu Panesthesie et enlevi le tube endotracheal. Au cours des minutes suivantes et jusqu'a ce que les patients soient reveilles, la pression intra-cranienne a baisse' jusqu'a des valeurs normles ou presque normales, avec changement minimal dans le Paco2. Sur aucun de ces sept patients on n'a constate de signe d'enflure du cerveau, le crane e'tait ferine et on les a laisse respirer spontanement; Panesthesie a eti interrompue sans qu'il y ait de changements importants dans la pression intra-cranienne ou dans la pression de la perfusion cerebrale. On recommande cependant, apres une operation, une surventilation des malades presentant une enflure marquee du cerveau.
INTRAKRANIALER DRUCK WAHREND DES ERWACHENS AUS EINER STICKOXYDUND HALOTHANNARKOSE NACH NEUROCHIRURGISCHEN EINGRIFFEN ZUSAMMENFASSUNG
7 Patienten mit interkranialen Krankheitserscheinungen wurden wahrend des Erwachens aus einer Stickoxyd- und Halothannarkose studiert. Arterieller, intrakranialer und zentralvenoser Druck wurden gemessen, ebenso die arterielle Kohlendioxydspannung, und mit dem klinischen Zustand des Patienten verglichen. Bei keinem Patienten ergaben sich Beweise fiir ein erhahtes Gehirnvolumen nach SchlieBung der Dura. Alle waren wahrend der Operation hyperbeluftet. Einstellung der Hyperbeliiftung und fortgesetzte Verabreichung von Narkosemittehi waren gefolgt von einem leichten Anstieg des interkranialen Drucks und von einer Verringerung des zerebralen Perfusionsdruckes, doch kam es dabei nicht zu kritisch geringen Werten. Spontane Atmung trat wieder ein, wenn sich das Paco2 im Bereich 33-51 mm Hg befand. Bei normaler spontaner Atmung wurde die Narkose unterbrochen und die Trachealrohre entfernt. In den folgenden Minuten bis zum Erwachen der Patienten sank der intrakraniale Druck auf normal oder fast normal ab, bei minimalen Verandenrngen in Paco2. Bei diesen 7 Patienten, bei denen es zu keiner Gehimschwellung kam, war der Schadel geschlossen, man lieC sie die spontane Atmung wieder aufnehmen und die Narkose wurde unterbrochen, ohne wesentliche Veranderungen des intrakranialen oder des zerebralen Perfusionsdruckes. Hyperbeliitung wird aber doch bei Patienten mit deutlicher Gehimschwellung empfohlen.
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occurred. This indicates that the respiratory depression from nitrous oxide and halothane is without significance during this period. It is concluded that patients without evidence of marked brain swelling may be allowed safely to resume spontaneous respiration, and have the endotracheal tube removed and be awakened from nitrous oxide and halothane anaesthesia. However, even in these patients some degree of intracranial hypertension may occur and a risk of hypercapnia exists. Therefore, if evidence of severe brain swelling is present at the time of closure of a craniotomy, it is likely that hyperventilation is indicated at least until nitrous oxide and halothane have been eliminated and probably for at least the next 24 hr, in order to minimize further brain swelling and to counteract development of secondary hypoxic and ischaemic brain damage.
981
BRITISH JOURNAL OF ANAESTHESIA
982 PRESION INTRACRANEAL DURANTE LA RECUPERACION DE ANESTESIA CON HALOTANE Y OXIDO NITROSO EN PACIENTES NEUROQUIRURGICOS SUMARIO
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Se estudiaron siete pacientes con perrurbaciones intracraneales durante la recuperation de anestesia con halotane y 6xido nitroso. Se midieron la presion arterial, intracraneal y el sistema de venas central asi como la tension arterial provocada por el bioxido de carbono y se compararon con la condici6n clinica del paciente. Ninguno de los pacientes demostro aumento de volumen del craneo cuando estaba cerrada la duramater. Todos habian tenido una gran ventilation durante la operation quinirgica. Despues de pesar la hiperventilacion y la administration continua de anestesicos, se produjo un aumento moderado de presion
intracraneal y una reduction en la presion cerebral por perfusion, pero ne se observaron valores bajos criticos. La respiration espontanea reaparecio cuando el Paco2 se hallaba dentro de los limites de 33-51 mm Hg. Cuando se considero que la respiration espontanea era normal, se interrumpid la anestesia y se extrajo el tubo endotraqueal. Durante los siguientes minutos, hasta que se despertadon los pacientes, disminuyo la presion intracraneal hasta alcanzar valores normales o proximos, con un cambio minimo de Paco2. En estos siete pacientes cuyos cerebros no presentaron senales de hinchazon, el craneo estaba cerrado, se dejo a los pacientes que reanudasen la respiracion espontanea y se interrumpio la anestesia sin cambios importantes en la presion intracraneal o en la presion cerebral por perfusion. Sin embargo se recomienda la hiperventilacion despues de la operation en pacientes con una hinchazon notable del cerebro.
INTRACRANIAL PRESSURE DURING RECOVERY FROM NITROUS OXIDE AND HALOTHANE ANAESTHESIA IN NEUROSURGICAL PATIENTS P . B . J0RGENSEN AND B . B . MlSFELDT SUMMARY
All inhalation anaesthetic agents increase intracranial pressure (McDowall, Barker and Jennett, 1966; Fitch et al., 1969; Jennett et al., 1969). This increase is the result of cerebral vasodilatation and the consequent increase of cerebral blood volume. The iDtracranial hypertension is most pronounced in patients with intracranial space-occupying lesions, as these patients have less reserve space. Minor changes in blood volume may, therefore, cause major changes in intracranial pressure. Another factor of major importance in anaesthesia for intracranial procedures is arterial carbon dioxide tension. Hypercapnia adds to the vasodilating effect of anaesthetic ngeats, while hypocapnia effectively counteracts it. There are many published reports of intracranial pressure changes during induction of anaesthesia, but there has been little previous interest in the period following surgery. At this time, when artificial hyperventilation is interrupted and spontaneous breathing begins, arterial carbon dioxide tension must increase, probably leading to some degree of hypercapnia. PAUL BALSLEV JORGENSEN, M.D.; BENT B. MISFELDT, M.D.;
Departments of Neurosurgery and Anaesthesia, University Hospital (Rigshospitalet), 9 Blegdamsvej, 2100 Copenhagen, Denmark.
If this occurs, vasodilatation caused by anaesthetic agents will be potentiated and intracranial hypertension will result after operation. Therefore we found it worthwhile to study this period by correlating the clinical state with arterial carbon dioxide tension and intracranial pressure. MATERIAL AND METHODS
Seven patients were studied during recovery from general anaesthesia. The diagnosis, the intracranial pressure during 24 hr after anaesthesia, and the treatment directed against intracranial hypertension are presented in table I. Intracranial pressure, arterial pressure and central venous pressure were recorded continuously via catheters in a lateral ventricle, in the radial artery of the non-dominant hand, and in a subclavian vein (Jorgensen and Henriksen, 1973). All catheters were placed after induction of anaesthesia. Pressures were referred to forehead level. Cerebral perfusion pressure (CPP) was calculated as the difference between mean arterial pressure (MAP) and mean intracranial pressure (ICP). Blood samples were drawn through the arterial catheter for determination of Po2, Pco2 and pH by standard Radiometer equipment. Five patients underwent craniotomy for removal of
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on June 21, 2015
Seven patients with intracranial disorders were studied during recovery from anaesthesia with nitrous oxide and halothane. Arterial, intracranial, and central venous pressure, and arterial carbon dioxide tension were measured and compared with the patient's clinical state. No patient had evidence of increased brain volume when the dura was closed. All had been hyperventilated during the surgical procedure. Cessation of hyperventilation and the continued administration of anaesthetics was followed by a moderate increase in intracranial pressure and a reduction in cerebral perfusion pressure, but critically low values were not seen. Spontaneous respiration returned when the PaCo2 was in the range 33-51 mm Hg. When spontaneous respiration was judged to be normal, anaesthesia was interrupted and the endotracheal tube was removed. In the following minutes, until the patients were awake, the intracranial pressure decreased to normal or near normal values, with minimal change in PaCo2. In these seven patients in whom there were no signs of brain swelling, the skull was closed, the patients were allowed to resume spontaneous respiration, and anaesthesia was terminated without major changes in intracranial pressure or cerebral perfusion pressure. However, hyperventilation is advocated after operation in patients with marked brain swelling.
BRITISH JOURNAL OF ANAESTHESIA
978
TABLE I. Details of the patients studied. 24 hr after recovery from anaesthesia Patient no. Sex Age 1
F
Diagnosis
Intracranial pressure Plateau (mm Hg) waves
Clinical state
Treatment
38 hydrocephalus
postencephalitis
20-40
—
alert/papilloedema
F
21 cerebellar angioma
10-35
—
alert/papilloedema
dexamethasone
3
F
57 cerebral metastasis
15-25
—
alert/papilloedema
dexamethasone
4
F
57 acoustic neuroma
5-10
—
alert
dexamethasone
5
F
40 acoustic neuroma
5-10
—
alert
—
6
M
55 cerebral atrophy
5-10
—
alert
—
7
F
20 chiasmatic haematoma
0-20
—
somnolent
dexamethasone
tumours or haematomas, and two patients were studied after ventriculography. Anaesthesia had been induced with barbiturate-relaxant, and, after endotracheal intubation, was maintained with 50% nitrous oxide in oxygen plus 0.5-1.0% halothane. Controlled hyperventilation by means of an Engsrrom ventilator was used throughout the operative procedures to counteract the vasodilator effects of anaesthetic agents and to minimize brain swelling. At the end of the procedure the patients were placed in bed in a supine position. Hyperventilation with 50% nitrous oxide in oxygen and 0.5-1.0% halothane was continued for at least 10 min in order to maintain PaCo2 at an unchanged value. Then a set of control values of MAP, ICP and CVP were measured and an arterial blood sample was drawn for gas analysis (first measurement). Ventilation was then reduced stepwise until the beginning of spontaneous respiratory movements. The next values were obtained at this time (second measurement). The ventilator was then disconnected, and respiration was assisted manually with an anaesthesia bag until spontaneous ventilation was judged clinically to be adequate, whereupon the third measurement was made. The endotracheal tube was now removed and halothane and nitrous oxide administration was discontinued. Oxygen was given by mask until the patient responded to verbal stimulation, and the last set of pressure and gas values was obtained {fourth measuretnent). This sequence was used to
avoid coughing and high intracranial pressure peaks during removal of the tube. The data are shown in figures 1-3. RESULTS
Control measurements during hyperventilation (first measurement), showed PaCo2 values between 20 and 32 mm Hg (mean: 24.1 mm Hg). Perfusion pressures were between 48 and 86 mm Hg (mean: 64.9 mm Hg). Only one patient (no. 1), following a ventriculogram, showed an elevated ICP (15 mm Hg) during hypocapnia. After hyperventilation was discontinued, Pa«>2 increased until spontaneous respiration started, at Pco 3 values in the range 33-51 mm Hg (mean: 40.3 mm Hg) (second measurement). At this time ICP had increased to 2-39 mm Hg (mean: 17.9 mm Hg); thus CPP was reduced to 44-82 mm Hg (mean: 58.2 mm Hg). Four to 28 min (mean: 19 min) passed before spontaneous respiratory movements were seen, and a further period of 3-8 min (mean: 6 min) until respiration was judged clinically to be sufficient. The appearance of adequate spontaneous respiration was associated with only minimal changes in Pco 2 , 35-55 mm Hg (mean: 42.0 mm Hg) and ICP, 11-39 mm Hg (mean: 21.1 mm Hg) (third measurement). CPP decreased slightly in two patients (nos. 2 and 4), but increased in the other five patients because of an increase in arterial pressure. When the patients were awake (fourth measurement) Paco2 was 29-53 mm Hg (mean: 39.0 mm Hg). In
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on June 21, 2015
2
979
INTRACRANIAL PRESSURE AND RECOVERY FROM ANAESTHESIA CPP mm Hg
2.
3.
A.
17.9 76.1 58.3 40.3 -1.3
21.1 86.3 65.1 42.0 -1.5
91.1 65.0 39.0
100 90 80-
60 5040;
MEAN VALUES
ICP MAP CPP Pa C02 CVP
MEAN VALUES
MAP ICP
69.0
761
86.3
91.1
4.1
17.9
21.1
6.1
FIG. 1. Intracranial pressure (ICP) and arterial pressure (MAP) in seven patients during recovery from anaesthesia. (1) 50% nitrous oxide in oxygen and 0.5% halothane and controlled hyperventilation. (2) 50% nitrous oxide in oxygen and 0.5 % halothane at onset of spontaneous respiration. (3) 50 % nitrous oxide in oxygen and 0.5 % halothane, when spontaneous respiration is judged to be adequate. (4) 100% oxygen after removal of the endotracheal tube, when the patients are responding to verbal stimulation.
all but one patient (no. 1) ICP was normal, ranging from 0 to 23 mm Hg (mean: 6.1 mm Hg), and CPP was in excess of 70 mm Hg (mean: 85.0 mm Hg) in all patients. From 9 to 31 min elapsed between removal of the endotracheal tube and awakening. CVP was virtually unchanged throughout the study. DISCUSSION
Patients with intracrardal disorders who receive general anaesthesia during operations or neuroradiological examinations risk secondary brain damage as a result of a decrease in the cerebral perfusion pressure with local or global ischaemia, or compression and distortion of brain tissue from the shifting of masses.
4.1
69.0 64.9 25.0 -2.7
6.1
-2.7
FIG. 2. Cerebral perfusion pressure (CPP) in seven patients during recovery from anaesthesia. (1) 50 % nitrous oxide in oxygen and 0.5% halothane and controlled hyperventilation. (2) 50 % nitrous oxide in oxygen and 0.5 % halothane at onset of spontaneous respiration. (3) 50 % nitrous oxide in oxygen and 0.5 % halothane, when spontaneous respiration is judged to be adequate. (4) 100 % oxygen after removal of the endotracheal tube, when the patients are responding to verbal stimulation.
The autoregulatory mechanisms of cerebral arterioles will keep blood flow constant at perfusion pressures of as little as 40 mm Hg in normal brain (Haggendal et al., 1970; Zwetnow, 1970), whether this reduction is a result of an increase in intracranial pressure or of decrease in arterial pressure. However, in patients with intracranial disease, autoregulation may be impaired locally or globally. Thus blood flow may decrease in these patients when a decrease in perfusion pressure is only moderate. Several factors may contribute to the reduction in cerebral perfusion pressure during general anaesthesia : (1) An increase in intracranial pressure resulting from an increase in blood volume caused by hypercapnia and anaesthetic agents. (2) A reduction in arterial pressure because of the cardiovascular effects of hypocapnia and anaesthetics. (3) An increase in venous pressure as a result of inappropriate positioning of the head with compression of jugular veins.
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Pa
CO 2 mmHg
2.. T
3. T
T
25.0
40.3
42.0
39.0
6050-
302010-
MEAN VALUES
FIG. 3. Arterial carbon dioxide tension (Pacoz) in seven patients during recovery from anaesthesia. (1) 50 % nitrous oxide in oxygen and 0.5 % halothane with controlled hyperventilation. (2) 50% nitrous oxide in oxygen and 0.5% halothane at onset of spontaneous respiration. (3) 50% nitrous oxide in oxygen and 0.5% halothane, when spontaneous respiration is judged to be adequate. (4) 100% oxygen after removal of the endotracheal tube, when the patients are responding to verbal stimulation.
The influence ofthese factors upon cerebral vascular dynamics has been examined thoroughly during induction of anaesthesia and before the skull is opened (McDowall, Barker and Jennett, 1966; Fitch et al., 1969; Henriksen and Jergensen, 1973; Jorgensen and Henriksen, 1973). It is generally accepted that patients are treated most safely with a barbiturate-relaxant induction (Pierce et al., 1962) followed by endotracheal intubation and the rapid establishing of controlled hyperventilation to reduce the period of hypercapnia and hypoxia. Inhalation anaesthetic agents should not be administered before hypocapnia can counteract their vasodilator effects (Adams et al., 1972; Misfeldt, Jergensen and Rishoj, 1975). Until now little attention has been paid to intracranial pressure changes in the period immediately after operation. This may be a result of the general belief that, at this time following the removal of space-occupying lesions, the risks of intracranial hypertension and mass shift are much reduced. However, a tumour may not have been removed radically,
and local or diffuse brain swelling may develop or be present because of an increase in blood volume and oedema. Further, in patients who have undergone neuroradiological examinations, the risks of intracranial hypertension and mass shift are still present, since a possible tumour or haematoma has not been removed. Leech, Barker and Fitch (1974) report briefly on the increase in intracranial and systemic pressure in patients brought from the hypocapnic to the normocapnic state, despite the appearance of slackness of the dura when the skull is being closed. However, no information about PaCo2 changes were presented. What factors influence the intracranial pressure changes during recovery from anaesthesia? (1) Concentrations of anaesthetic agents decrease rapidly, and if there are remaining residual effects from these upon cerebral vascularity, ICP must decrease while anaesthetics are exhaled. (2) After hyperventilation during the operative procedures one must allow PaCo2 to increase before the patient will be able to breathe spontaneously. This will increase ICP. (3) While the concentration of anaesthetic agents decreases and Pco2 increases, arterial pressure increases, and thus improves cerebral perfusion pressure. (4) Any oedema or haematoma initiated during operation or during hypoxia by inadequate perfusion pressure will increase ICP and bring about a risk of mass shift and herniation. In the present study of patients, none of whom had evidence of severe brain swelling at closure of the dura, all of whom had received nitrous oxide and halothane during hypocapnia, and had the endotracheal tube removed after a period of hypoventilation and were then awakened, we found the following: (1) The intracranial pressure increased when hyperventilation was discontinued and PaCO2 increased, but from the onset of spontaneous respiration little further increase was observed. (2) The cerebral perfusion pressure did not decrease to less than the critical 40 mm Hg value, because the arterial pressure increased simultaneously, both during hypoventilation and during lightering of anaesthesia. (3) The intracranial pressure decreased in all patients when the administration of anaesthetics was interrupted, despite rearly unchanged Paco2 values. (4; In most patients spontaneous respiration renamed at normocapnia and before severe hypercapr.ia had
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INTRACRANIAL PRESSURE AND RECOVERY FROM ANAESTHESIA
REFERENCES
Adams, R. W., Gronert, G. A., Sundt, T. M.3 and Michenfelder, J. D. (1972). Halothane, hypocapnia and cerebrospinal fluid pressure in neurosurgery. Anesthesiology, 37, 510. Fitch, W., Barker, J., McDowall, D. G., and Jennett, W. B. (1969). The effect of methoxyflurane on cerebrospinal fluid pressure in patients with and without intracranial space-occupying lesions. Br. J. Anaesth., 41, 554. Haggendal, E., Ldfgren, J., Nilsson, N. J., and Zwetnow, N. N. (1970). Effect of varied cerebrospinal fluid pressure on cerebral blood flow in dogs. Ada Physiol. Scand., 79, 262. Henriksen, H. T., and Jorgensen, P. B. (1973). The effect of nitrous oxide on intracranial pressure in patients with intracranial disorders. Br. J. Anaesth., 45, 486. Jennett, W. B., Barker, J., Fitch, W., and McDowall D. G. (1969). Effect of anaesthesia on intracranial pressure in patients with space-occupying lesions. Lancet, 1, 61. Jorgensen, P. B., and Henriksen, H. T. (1973). The effect of fluoroxene on intracranial pressure in patients with intracranial space-occupying lesions. Br. J. Anaesth., 45, 599. Leech, P., Barker, J., and Fitch, W., (1974). Changes in intracranial pressure and systemic arterial pressure during the termination of anaesthesia (abstract). Br. J. Anaesth., 46, 315. McDowall, D. G., Barker, J., and Jennett, W. B. (1966). Cerebrospinal fluid pressure measurements during anaesthesia. Anaesthesia, 21, 189. Misfeldt, B. B., Jorgensen, P. B., and Rishej, M. (1975). The effect of nitrous oxide and halothane upon the intracranial pressure in hypocapnic patients with intracranial disorders. Br. J. Anaesth., 46, 853. Pierce, E. C , Lambertsen, C. J., Deutsch, S., Chase, P. E., Lunde, H. W., Dripps, P. D., and Price, H. L. (1962). Cerebral circulation and metabolism during thiopental anesthesia and hyperventilation in man. J. Clin. Invest., 41, 1664. Zwetnow, N. N. (1970). Effects of increased cerebrospinal fluid pressure on the cerebral bloodflowand on the energy metabolism of the brain: an experimental study. Ada Physiol. Scand., (Suppl), 339, 1.
PRESSION INTRA-CRANIENNE AU COURS DE LA RECUPERATION SUIVANT UNE ANESTHESIE PAR L'OXYDE AZOTEUX ET L'HALOTHANE CHEZ DES PATIENTS DE NEUROCHIRURGIE RESUME
Sept patients presentant des troubles intra-craniens ont ete etudies au cours de la recuperation qui a suivi leur anesthesie par Poxyde azoteux et Phalothane. On a mesure la pression veineuse centrale, la tension arterielle et la pression intra-cranienne ainsi que la tension de Panhydride carbonique arteriel et on les a comparees a Petat clinique du patient. On n'a constate sur aucun patient que le volume du cerveau avait augmente au moment ou Pon a ferine la dure-mere. Tous avaient ete surventiles pendant Poperation chirurgicale. L'arret de la surventilation et Padministration continue d'agents anesthesiques a ete suivie d'une augmentation moderee de la pression intracranienne et d'une reduction de la pression de la perfusion cerebrale, mais on n'a constate aucune valeur critiquement basse. Las respiration spontanee est revenue lorsque le Paco2 s'est situi dans la plage des 33-51 mm Hg. Lorsqu'on a estime que la respiration spontanee £tait normale, on a interrompu Panesthesie et enlevi le tube endotracheal. Au cours des minutes suivantes et jusqu'a ce que les patients soient reveilles, la pression intra-cranienne a baisse' jusqu'a des valeurs normles ou presque normales, avec changement minimal dans le Paco2. Sur aucun de ces sept patients on n'a constate de signe d'enflure du cerveau, le crane e'tait ferine et on les a laisse respirer spontanement; Panesthesie a eti interrompue sans qu'il y ait de changements importants dans la pression intra-cranienne ou dans la pression de la perfusion cerebrale. On recommande cependant, apres une operation, une surventilation des malades presentant une enflure marquee du cerveau.
INTRAKRANIALER DRUCK WAHREND DES ERWACHENS AUS EINER STICKOXYDUND HALOTHANNARKOSE NACH NEUROCHIRURGISCHEN EINGRIFFEN ZUSAMMENFASSUNG
7 Patienten mit interkranialen Krankheitserscheinungen wurden wahrend des Erwachens aus einer Stickoxyd- und Halothannarkose studiert. Arterieller, intrakranialer und zentralvenoser Druck wurden gemessen, ebenso die arterielle Kohlendioxydspannung, und mit dem klinischen Zustand des Patienten verglichen. Bei keinem Patienten ergaben sich Beweise fiir ein erhahtes Gehirnvolumen nach SchlieBung der Dura. Alle waren wahrend der Operation hyperbeluftet. Einstellung der Hyperbeliiftung und fortgesetzte Verabreichung von Narkosemittehi waren gefolgt von einem leichten Anstieg des interkranialen Drucks und von einer Verringerung des zerebralen Perfusionsdruckes, doch kam es dabei nicht zu kritisch geringen Werten. Spontane Atmung trat wieder ein, wenn sich das Paco2 im Bereich 33-51 mm Hg befand. Bei normaler spontaner Atmung wurde die Narkose unterbrochen und die Trachealrohre entfernt. In den folgenden Minuten bis zum Erwachen der Patienten sank der intrakraniale Druck auf normal oder fast normal ab, bei minimalen Verandenrngen in Paco2. Bei diesen 7 Patienten, bei denen es zu keiner Gehimschwellung kam, war der Schadel geschlossen, man lieC sie die spontane Atmung wieder aufnehmen und die Narkose wurde unterbrochen, ohne wesentliche Veranderungen des intrakranialen oder des zerebralen Perfusionsdruckes. Hyperbeliitung wird aber doch bei Patienten mit deutlicher Gehimschwellung empfohlen.
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occurred. This indicates that the respiratory depression from nitrous oxide and halothane is without significance during this period. It is concluded that patients without evidence of marked brain swelling may be allowed safely to resume spontaneous respiration, and have the endotracheal tube removed and be awakened from nitrous oxide and halothane anaesthesia. However, even in these patients some degree of intracranial hypertension may occur and a risk of hypercapnia exists. Therefore, if evidence of severe brain swelling is present at the time of closure of a craniotomy, it is likely that hyperventilation is indicated at least until nitrous oxide and halothane have been eliminated and probably for at least the next 24 hr, in order to minimize further brain swelling and to counteract development of secondary hypoxic and ischaemic brain damage.
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982 PRESION INTRACRANEAL DURANTE LA RECUPERACION DE ANESTESIA CON HALOTANE Y OXIDO NITROSO EN PACIENTES NEUROQUIRURGICOS SUMARIO
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Se estudiaron siete pacientes con perrurbaciones intracraneales durante la recuperation de anestesia con halotane y 6xido nitroso. Se midieron la presion arterial, intracraneal y el sistema de venas central asi como la tension arterial provocada por el bioxido de carbono y se compararon con la condici6n clinica del paciente. Ninguno de los pacientes demostro aumento de volumen del craneo cuando estaba cerrada la duramater. Todos habian tenido una gran ventilation durante la operation quinirgica. Despues de pesar la hiperventilacion y la administration continua de anestesicos, se produjo un aumento moderado de presion
intracraneal y una reduction en la presion cerebral por perfusion, pero ne se observaron valores bajos criticos. La respiration espontanea reaparecio cuando el Paco2 se hallaba dentro de los limites de 33-51 mm Hg. Cuando se considero que la respiration espontanea era normal, se interrumpid la anestesia y se extrajo el tubo endotraqueal. Durante los siguientes minutos, hasta que se despertadon los pacientes, disminuyo la presion intracraneal hasta alcanzar valores normales o proximos, con un cambio minimo de Paco2. En estos siete pacientes cuyos cerebros no presentaron senales de hinchazon, el craneo estaba cerrado, se dejo a los pacientes que reanudasen la respiracion espontanea y se interrumpio la anestesia sin cambios importantes en la presion intracraneal o en la presion cerebral por perfusion. Sin embargo se recomienda la hiperventilacion despues de la operation en pacientes con una hinchazon notable del cerebro.
