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CUIRASS VENTILATORS
BRITISH JOURNAL OF ANAESTHESIA
1086 NITROUS OXIDE AND INTRACRANIAL PRESSURE
block the alpha-vasoconstrictive reaction to surgical trauma or other forms of adrenergic stress whereas halothane does. Details of the volume-pulse plethysmographic studies of nitrous oxide and halothane have still to be reported. The clinical significance of these observations is a controversial subject. Some anaesthetists regard the vasodilator effect of die inhalational anaesthetics to be a contraindication to dieir use in neurosurgical patients. Other anaesthetists have used them successfully in these circumstances. Obviously, there are other factors to be considered in the protection of patients from the undesirable consequences of sudden increases in intracranial pressure. The placing of the patient in a slightly head-up position during the induction of anaesthesia with these agents will counteract the cerebral hyperaemic effect of alpha-vasodilatation by facilitating the pooling of blood in the dilated alpha vessels of the extremities. The deliberate lowering of the Paooi by passive hyperventilation during the induction of anaesthesia will ensure the rapid onset of cerebral vasoconstriction, and the avoidance of all factors which cause tachycardia will maintain a low cardiac output and a correspondingly low cerebral blood flow. In die study of the effects of anaesthetic agents on die intracranial blood vessels it should be remembered that the majority of die deeper vessels of die brain are autoregulatory and are not directly influenced to any great extent by changes in the activity of the sympathetic nervous system (Csillik et al., 1971). MICHAEL JOHNSTONE
Manchester REFERENCES
Adams, R. W., Gronert, G. A., Sundt, T. M., and Michenfelder, J. D. (1972). Halothane hypocapnia and cerebrospinal fluid pressure in neurosurgery. Anesthesiology, 37, 510. Csillik, B., Jancso, G., Toth, L., Kozma, M., Kalman, G., and Karcsu, S. (1971). Adrenergic innervation of hypothalamic blood vessels: a contribution to the problem of central diermodetectors. Acta anal. (Basel), 80, 142. Green, H. D., and Kepchar, J. H. (1959). Control of peripheral resistance in major systemic vascular beds. Physiol. Rev., 39, 617. Johnstone, M. (1968). Hypocapnic vasoconstriction. during halothane anaesthesia in surgical patients. Brit. J. Anaesth., 40, 607. (1972). The cardiovascular effects of oxytocic drugs. Brit. J. Anaesth., 44, 826.
CORRESPONDENCE CUIRASS VENTILATORS
Sir,—Our department is embarking on a reassessment of the use of the cuirass for assisted ventilation. In this region we have several old polio patients regularly using the cuirass. We are measuring its efficiency on these cases and hope to define its value in other situations, such as early acute or chronic respiratory failure and weaning from IPPR.
Our Electronics department is also attempting to devise a low cost negative/positive power unit based on a domestic vacuum cleaner. I would be most interested to hear from centres who have experience in the use of the cuirass, and grateful for any information or advice on indications, details of apparatus and practical management, cheap power units, etc. A. MARSHALL BARR
Printed In Great Britain br John Sbmtu & SOD Ltd, Pufc Road, Altrlncbam, Chahhc. WA14 SQQ
Reading
Downloaded from http://bja.oxfordjournals.org/ at University of Arizona on July 25, 2015
Sir,—Drs Henriksen and Jorgensen (Brit. J. Anaesth. (1973), 45, 486) observed that nitrous oxide increased the intracranial pressure as judged by intraventricular and epidural measurements in patients with intracranial disorders. Nitrous oxide also decreased the cerebral perfusion pressure. The intracranial hypertension caused by the nitrous oxide was counteracted efficiendy either by hyperventilation (moderate hypocapnia) or by the withdrawal of the nitrous oxide. They concluded that the most likely mechanism for the pressure elevation is vasodilatation with an increase in intracranial blood volume. I should like to confirm Drs Henriksen and Jorgensen's suggestion that nitrous oxide dilates at least some of the intracranial blood vessels. An extensive study of the effects of nitrous oxide on peripheral vascular behaviour by means of volume-pulse plethysmography has shown that nitrous oxide dilates the alpha-adrenoceptive (finger) blood vessels and constricts the betaadrenoceptive (forearm muscle) vessels in most patients. As the pial or meningeal vessels are alpha-adrenoceptive (Green and Kcpchar, 1959), their behaviour in patients anaesthetized with nitrous oxide will be similar to that of the blood vessels of the finger. The combination of effects, alpha-vasodilatation and beta-vasoconstriction, is characteristic of blockage or depression of the sympathetic innervation of the vascular beds and excludes the possibility of a direct depression of the vascular smooth muscle. Vasodilator drugs which depress the vascular smooth muscle directly are not selectively adrenoceptive and affect equally the alpha and the beta blood vessels Qohnstone, 1972). The alpha-vasodilatation of nitrous oxide anaesthesia is transient and is man'mnl in most patients for only a short time after the induction of anaesthesia. The initial surgical incision of the skip usually causes reflex alpha-vasoconstriction. This indicates that the depression of sympathetic activity caused by the nitrous oxide is not sufficient to control the adrenergic reactions to surgical trauma. The initial effects of nitrous oxide and of halothane on peripheral vascular behaviour are similar. Both cause alpha-vasodilatation and beta-vasoconstriction (Johnstone, 1972). Neither blocks the vasoconstrictive reaction of the cerebral and other blood vessels to hypocapnia induced by passive hyperventilation (Adams et al., 1972; Johnstone, 1968). The important difference between the two drugs, so far as their effects on peripheral vascular behaviour are concerned, is that nitrous oxide does not
1086 NITROUS OXIDE AND INTRACRANIAL PRESSURE
block the alpha-vasoconstrictive reaction to surgical trauma or other forms of adrenergic stress whereas halothane does. Details of the volume-pulse plethysmographic studies of nitrous oxide and halothane have still to be reported. The clinical significance of these observations is a controversial subject. Some anaesthetists regard the vasodilator effect of die inhalational anaesthetics to be a contraindication to dieir use in neurosurgical patients. Other anaesthetists have used them successfully in these circumstances. Obviously, there are other factors to be considered in the protection of patients from the undesirable consequences of sudden increases in intracranial pressure. The placing of the patient in a slightly head-up position during the induction of anaesthesia with these agents will counteract the cerebral hyperaemic effect of alpha-vasodilatation by facilitating the pooling of blood in the dilated alpha vessels of the extremities. The deliberate lowering of the Paooi by passive hyperventilation during the induction of anaesthesia will ensure the rapid onset of cerebral vasoconstriction, and the avoidance of all factors which cause tachycardia will maintain a low cardiac output and a correspondingly low cerebral blood flow. In die study of the effects of anaesthetic agents on die intracranial blood vessels it should be remembered that the majority of die deeper vessels of die brain are autoregulatory and are not directly influenced to any great extent by changes in the activity of the sympathetic nervous system (Csillik et al., 1971). MICHAEL JOHNSTONE
Manchester REFERENCES
Adams, R. W., Gronert, G. A., Sundt, T. M., and Michenfelder, J. D. (1972). Halothane hypocapnia and cerebrospinal fluid pressure in neurosurgery. Anesthesiology, 37, 510. Csillik, B., Jancso, G., Toth, L., Kozma, M., Kalman, G., and Karcsu, S. (1971). Adrenergic innervation of hypothalamic blood vessels: a contribution to the problem of central diermodetectors. Acta anal. (Basel), 80, 142. Green, H. D., and Kepchar, J. H. (1959). Control of peripheral resistance in major systemic vascular beds. Physiol. Rev., 39, 617. Johnstone, M. (1968). Hypocapnic vasoconstriction. during halothane anaesthesia in surgical patients. Brit. J. Anaesth., 40, 607. (1972). The cardiovascular effects of oxytocic drugs. Brit. J. Anaesth., 44, 826.
CORRESPONDENCE CUIRASS VENTILATORS
Sir,—Our department is embarking on a reassessment of the use of the cuirass for assisted ventilation. In this region we have several old polio patients regularly using the cuirass. We are measuring its efficiency on these cases and hope to define its value in other situations, such as early acute or chronic respiratory failure and weaning from IPPR.
Our Electronics department is also attempting to devise a low cost negative/positive power unit based on a domestic vacuum cleaner. I would be most interested to hear from centres who have experience in the use of the cuirass, and grateful for any information or advice on indications, details of apparatus and practical management, cheap power units, etc. A. MARSHALL BARR
Printed In Great Britain br John Sbmtu & SOD Ltd, Pufc Road, Altrlncbam, Chahhc. WA14 SQQ
Reading
Downloaded from http://bja.oxfordjournals.org/ at University of Arizona on July 25, 2015
Sir,—Drs Henriksen and Jorgensen (Brit. J. Anaesth. (1973), 45, 486) observed that nitrous oxide increased the intracranial pressure as judged by intraventricular and epidural measurements in patients with intracranial disorders. Nitrous oxide also decreased the cerebral perfusion pressure. The intracranial hypertension caused by the nitrous oxide was counteracted efficiendy either by hyperventilation (moderate hypocapnia) or by the withdrawal of the nitrous oxide. They concluded that the most likely mechanism for the pressure elevation is vasodilatation with an increase in intracranial blood volume. I should like to confirm Drs Henriksen and Jorgensen's suggestion that nitrous oxide dilates at least some of the intracranial blood vessels. An extensive study of the effects of nitrous oxide on peripheral vascular behaviour by means of volume-pulse plethysmography has shown that nitrous oxide dilates the alpha-adrenoceptive (finger) blood vessels and constricts the betaadrenoceptive (forearm muscle) vessels in most patients. As the pial or meningeal vessels are alpha-adrenoceptive (Green and Kcpchar, 1959), their behaviour in patients anaesthetized with nitrous oxide will be similar to that of the blood vessels of the finger. The combination of effects, alpha-vasodilatation and beta-vasoconstriction, is characteristic of blockage or depression of the sympathetic innervation of the vascular beds and excludes the possibility of a direct depression of the vascular smooth muscle. Vasodilator drugs which depress the vascular smooth muscle directly are not selectively adrenoceptive and affect equally the alpha and the beta blood vessels Qohnstone, 1972). The alpha-vasodilatation of nitrous oxide anaesthesia is transient and is man'mnl in most patients for only a short time after the induction of anaesthesia. The initial surgical incision of the skip usually causes reflex alpha-vasoconstriction. This indicates that the depression of sympathetic activity caused by the nitrous oxide is not sufficient to control the adrenergic reactions to surgical trauma. The initial effects of nitrous oxide and of halothane on peripheral vascular behaviour are similar. Both cause alpha-vasodilatation and beta-vasoconstriction (Johnstone, 1972). Neither blocks the vasoconstrictive reaction of the cerebral and other blood vessels to hypocapnia induced by passive hyperventilation (Adams et al., 1972; Johnstone, 1968). The important difference between the two drugs, so far as their effects on peripheral vascular behaviour are concerned, is that nitrous oxide does not