Teresa S. Mayberg

Comparison of flow and velocity during dynamic autoregulation testing in humans.

Background and Purpose We compared relative changes in middle cerebral artery velocity and internal carotid artery flow during autoregulation testing to test the validity of using transcranial Doppler recordings of middle cerebral artery velocity to evaluate cerebral autoregulation in humans. Methods Seven human volunteers had dynamic autoregulation tested during surgical procedures that included exposure of the internal carotid artery. The mean arterial blood pressure and middle cerebral artery velocity spectral outline (Vmax), using transcranial Doppler, and ipsilateral internal carotid artery flow, using an electromagnetic flowmeter, were continuously and simultaneously recorded during transient sharp decreases in blood pressure that were induced by rapid deflation of thigh blood pressure cuffs. The resulting responses of velocity in the middle cerebral artery and flow in the internal carotid artery were compared. Results Moderate decreases in blood pressure evoked responses in cerebral autoregulation. There were no significant (P=.97) differences between the responses in middle cerebral artery velocity and internal carotid artery flow to the blood pressure decreases. Conclusions Relative changes in Vmax accurately reflect relative changes in internal carotid artery flow during dynamic autoregulation testing in humans. Therefore, alterations in middle cerebral artery diameter do not occur to the extent that they introduce a significant error in making these comparisons. (Stroke. 1994;25:793‐797.)

Dynamic and Static Cerebral Autoregulation during Isoflurane, Desflurane, and Propofol Anesthesia

Background Although inhalation anesthetic agents are thought to impair cerebral autoregulation more than intravenous agents, there are few controlled studies in humans. Methods In the first group (n = 24), dynamic autoregulation was assessed from the response of middle cerebral artery blood flow velocity (Vmca) to a transient step decrease in mean arterial blood pressure (MABP). The transient hypotension was induced by rapid deflation of thigh cuffs after inflation for 3 min. In the second group (n = 18), static autoregulation was studied by observing Vmca in response to a phenylephrine-induced increase in MABP. All patients were studied during fentanyl (3 micrograms.kg-1.h-1)/nitrous oxide (70%) anesthesia, followed by, in a randomized manner, isoflurane, desflurane, or propofol in a low dose (0.5 MAC or 100 micrograms.kg-1.min-1) and a high dose (1.5 MAC or 200 micrograms.kg-1.min-1). The dynamic rate of regulation (dROR) was assessed from the rate of change in cerebrovascular resistance (MABP/Vmca) with the blood pressure decreases using computer modeling, whereas the static rate of regulation (sROR) was assessed from the change in Vmca with the change in MABP. Results Low-dose isoflurane delayed (dROR decreased) but did not reduce the autoregulatory response (sROR intact). Low-dose desflurane decreased both dROR and sROR. During 1.5 MAC isoflurane or desflurane, autoregulation was ablated (both dROR and sROR impaired). Neither dROR nor sROR changed with low- or high-dose propofol. Conclusions At 1.5 MAC, isoflurane and desflurane impaired autoregulation whereas propofol (200 micrograms.kg-1.min-1) preserved it.

Ketamine Does Not Increase Cerebral Blood Flow Velocity or Intracranial Pressure During Isoflurane/Nitrous Oxide Anesthesia in Patients Undergoing Craniotomy

Ketamines effect on cerebral hemodynamics is controversial.We hypothesized that ketamine would not increase intracranial pressure (ICP) and cerebral blood flow (CBF) velocity in anesthetized, ventilated patients. Twenty patients requiring craniotomy for brain tumor or cerebral aneurysm were studied. After induction with thiopental, anesthesia was maintained with isoflurane and nitrous oxide in oxygen. During controlled ventilation (PaCO2 34 +/- 1 mm Hg); middle cerebral artery blood flow velocity (VMCA), mean arterial blood pressure (MAP), bilateral frontooccipital processed electroencephalogram (EEG), and ICP were measured before and for 10 min after intravenous ketamine 1.0 mg/kg. Cerebral arteriovenous oxygen content difference (AVDO2) and cerebral perfusion pressure (CPP) were calculated. After ketamine, MAP, CPP, PaCO2, and AVDO2 were unchanged. ICP decreased from 16 +/- 1 mm Hg to 14 +/- 1 mm Hg (mean +/- SE; P < 0.001) and VMCA decreased from 44 +/- 4 cm/s to 39 +/- 4 cm/s (P < 0.001). Total EEG power decreased (P < 0.02). These results suggest that ketamine can be used in anesthetized, mechanically ventilated patients with mildly increased ICP without adversely altering cerebral hemodynamics. (Anesth Analg 1995;81:84-9)

Direct cerebrovasodilatory effects of halothane, isoflurane, and desflurane during propofol-induced isoelectric electroencephalogram in humans

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the agents direct vasodilatory action and the indirect vasoconstrictive action mediated by flow‐metabolism coupling. To compare the intrinsic action of volatile anesthetics, the effect of halothane, isoflurane, and desflurane on flow velocity in the middle cerebral artery during propofol‐induced isoelectricity of the electroencephalogram was examined.

The Influence of Propofol with and without Nitrous Oxide on Cerebral Blood Flow Velocity and CO2 Reactivity in Humans

The cerebrovascular response to CO2 has been reported to be preserved during propofol anesthesia, but no comparison with awake control values has been made, and the additional influence of N2O has not been investigated. Using the noninvasive technique of transcranial Doppler ultrasonography, this study investigated the cerebrovascular response to varying levels of PaCO2 while awake and during anesthesia with propofol and propofol/N2O. Seven adults without systemic diseases undergoing nonneurologic surgery were studied. A pulsed-wave Doppler monitor was used to measure the mean middle cerebral artery flow velocity (Vmca) during varying levels of PaCO2 (25-55 mmHg) under the following conditions: 1) awake; 2) propofol 2.5 mg.kg-1 bolus followed by continuous infusion of 150 micrograms.kg-1.min-1; and 3) propofol as in the condition above plus 70% N2O. During the awake study condition, hypocapnia was induced by voluntary hyperventilation, and hypercapnia was induced with rebreathing of 7% CO2 in a closed circuit. During the anesthetized study conditions, hypocapnia and hypercapnia were induced by adjustment of minute ventilation. A minimum of five to six simultaneous Vmca and PaCO2 measurements were obtained under each of the study conditions. Systemic blood pressure was monitored via a radial arterial catheter, and phenylephrine was administered if mean arterial blood pressure decreased below 60 mmHg (phenylephrine was used in three of five patients in the propofol-N2O group). Linear regression and analysis of covariance were used for statistical analysis of Vmca-PaCO2 relationships.(ABSTRACT TRUNCATED AT 250 WORDS)

A critique of the intraoperative use of jugular venous bulb catheters during neurosurgical procedures.

We examined the intraoperative use of jugular venous bulb catheters in 100 consecutive patients undergoing neurosurgical procedures. The catheters were successfully placed after induction of anesthesia in 99 patients using an aseptic technique. The efforts were abandoned after four attempts in the remaining patient. The mean time of insertion was 94 s (SD 108, range 15-420). Carotid artery puncture on two occasions controlled by firm pressure was the only complication. Arterial blood pressure, PaCO2, PaO2, and jugular venous bulb oxygen saturations (SjVO2) were intermittently measured at set intervals throughout the operation. We defined cerebral venous desaturation as 1) none (SjVO2 > 50%), 2) mild (45% < SjVO2 < 50%), and 3) severe (SjVO2 < 45%). We graded the usefulness of the catheter as 1) not useful (NU), SjVO2 > 50% and PaCO2 > 25 mm Hg; 2) useful (U1), SjVO2 > 50% and PaCO2 < 25 mm Hg; intervention, no increase in PaCO2; 3) useful (U2), SjVO2 < 50% and PaCO2 < 25 mm Hg; intervention, increase PaCO2 to improve SjVO2; 4) useful (U3), SjVO2 < 50% and PaCO2 > 25 mm Hg; intervention, nonventilatory action to increase SjVO2 (e.g., infusion of mannitol). Mild desaturation was detected in 24 patients and severe desaturation was present in 17 patients. We found SjVO2 monitoring to be useful in 60 of 99 patients studied. It was useful for detecting and treating cerebral venous desaturation in 13 of 18 patients with intracranial hematomas (subdural, epidural, and intracerebral hematomas), 9 of 18 patients with intracerebral tumors, 27 of 45 patients with cerebral aneurysms, and 6 of 8 patients with other intracranial pathology.(ABSTRACT TRUNCATED AT 250 WORDS)

Succinylcholine does not change intracranial pressure, cerebral blood flow velocity, or the electroencephalogram in patients with neurologic injury

The effect of succinylcholine (SCh) on intracranial pressure (ICP) was studied in 10 mechanically ventilated patients (Glasgow coma scale score 3-10, median 6) being treated for increased ICP in an intensive care unit. Mean arterial blood pressure (MAP), ICP, processed electroencephalogram (EEG), and mean middle cerebral artery blood flow velocity (V mca) were monitored. Baseline measurements after saline injection were obtained for 5 min. SCh (1 mg/kg) was administered intravenously and the above variables were monitored for 15 min. Neither saline nor SCh cause any significant change in cerebral perfusion pressure, MAP, V mca, EEG, or ICP. We conclude that in brain-injured patients, SCh did not alter cerebral blood flow velocity, cortical electrical activity, or ICP.

Isoflurane compared with nitrous oxide anaesthesia for intraoperative monitoring of somatosensory-evoked potentials

Intraoperative monitoring of somatosensoryevoked potentials is a routine procedure. To determine the depressant effect of nitrous oxide relative to isoflurane, the authors recorded the scalp, cervical and brachial plexusevoked responses to stimulation of the median nerve under different anaesthetic conditions. Eight subjects, age 35 ± 6 (SD) yr, weight 68 ± 12 kg, were studied. Following recording of awake control responses, anaesthesia was induced with thiopentone 5 mg· kg− 1 and fentanyl 3 μg· kg− 1 and was followed by succinylcholine 1 mg· kg− 1. During normocapnia and normothermia, and with a maintenance infusion of fentanyl 3 μg · kg− 1· hr− 1, evoked potential recording was repeated under three different anaesthetic conditions; 0.6 MAC nitrous oxide, 0.6 MAC nitrous oxide ± 0.6 MAC isoflurane, and 0.6 MAC isoflurane. Among the anaesthetic conditions, the combination of nitrous oxide-isoflurane had the most depressant effect on the cortical amplitude (67 ± 4% reduction, P < 0.05). Nitrous oxide decreased the cortical amplitude more than an equipotent dose of isoflurane (60 ± 4% vs 48 ± 7%, P < 0.05). The latency was unchanged by nitrous oxide, but increased slightly by isoflurane and isofluranenitrous oxide anaesthesia (1.0 and 0.9 msec respectively, P < 0.05). We conclude that somatosensory-evoked potential monitoring is feasible both during nitrous oxide anaesthesia and isoflurane anaesthesia, but the cortical amplitude is better preserved during 0.6 MAC of isoflurane alone relative to 0.6 MAC of nitrous oxide alone. The depressant effect is maximal during nitrous oxideisoflurane anaesthesia but less than the predicted additive effect.RésuméLe monitorage des potentiels évoqués somato-sensoriels est une technique utilisée couramment. Pour comparer les effets dépresseurs du protoxyde d’azote à ceux de l’isoflurane, les auteurs ont enregistré sur le scalp et les plexus cervical et brachial, les réponses évoquées à la stimulation du nerf médian sous différentes méthodes d’anesthésie. Il ont étudié huit sujets, âgés de 35 ± 6 (SD) ans, pesant 68 ± 12 kg. Après l’enregistrement des réponses vigiles (contrôle), l’anesthésie a été induite avec du thiopentone 5 mg· kg− 1 et du fentanyl 3 μg· kg− 1 suivi de succinylcholine 1 mg· kg− 1. Sous normocapnie et normothermie avec une perfusion d’entretien de fentanyl 3 μg· kg− 1· hr− 1, ils ont répété l’enregistrement des potentiels évoqués pendant trois méthodes d’anesthésie: protoxyde d’azote 0,6 MAC, protoxyde d’azote 0,6 MAC + isoflurane 0,6 MAC, et isoflurane 0,6 MAC. Parmi ces méthodes, le protoxyde d’azote-isoflurane a l’effet dépresseur le plus marqué sur l’amplitude corticale (baisse de 67 ± 4%, P < 0,05). Le protoxyde l’azote diminue l’amplitude corticale d’une façon plus importante qu’une concentration équipolente d’isoflurane (60 ± 4% vs 48 ± 7%, P < 0,05). Sous protoxyde d’azote, la période de latence demeure inchangée, mais augmente légèrement sous isoflurane et sous isoflurane-protoxyde d’azote (1,0 et 0,9 MAC respectivement, P < 0,05). Les auteurs concluent que le monitorage des potentiels somato-sensoriels évoqués est réalisable pendant l’anesthésie au protoxyde d’azote et à l’isoflurane, mais que l’amplitude est mieux préservée pendant 0,6 MAC d’isoflurane seul comparativement à 0,6 MAC de protoxyde d’azote. L’effet dépresseur est maximal pendant l’anesthésie au protoxyde-isoflurane mais il est moindre que la somme arithmétique des effets de chacune des substances.

Nitrous oxide-isoflurane anesthesia causes more cerebral vasodilation than an equipotent dose of isoflurane in humans

To compare the cerebral vascular and metabolic effect of an isoflurane-nitrous oxide mixture to an equipotent dose of isoflurane at 1.1 minimum alveolar anesthetic concentration (MAC), and to study the interaction between nitrous oxide and isoflurane anesthesia, we measured right middle cerebral artery blood flow velocity (V mca) and cerebral arteriovenous oxygen content difference (AVDO2) in six healthy patients during normocapnia and normothermia under the following sequence of steady-state anesthetic conditions: Condition A, 0.5 MAC of isoflurane, Condition B, 0.5 MAC of isoflurane + 0.6 MAC of N2O, Condition C, 1.1 MAC of isoflurane + 0.6 MAC of N2O, and Condition D, 1.1 MAC of isoflurane. The study entry sequence was randomized. V mca and AVDO2 during 1.1 MAC of isoflurane (Condition D) was 48 +/- 7 cm/s and 3.9 +/- 0.6 vol%, respectively. Substituting 0.6 MAC of isoflurane with an equipotent concentration of N2O (Condition B) resulted in an increase in both V mca and AVDO2 of approximately 20% (P < 0.05). These findings suggest that the increase in flow was accompanied by an even greater increase in metabolic rate. Adding 0.6 MAC of N2O to 1.1 MAC of isoflurane (Condition C) also increased V mca (P < 0.05). We conclude that N2O is a more potent cerebral vasodilator than an equipotent dose of isoflurane alone in humans.

The influence of arterial oxygenation on cerebral venous oxygen saturation during hyperventilation

Cerebral venous oxygen desaturation may occur when hyperventilation is employed during neurosurgical procedures. In this study, we examined the effect of arterial hyperoxia (PaO2 > 200 mmHg) on jugular bulb venous oxygen tension (PjvO2), saturation (SjvO2) and content (CjvO2) in 12 patients undergoing anaesthesia for neurosurgical procedures. Under stable anaesthetic conditions, the inspired oxygen fraction (FlO2) was varied to give four different levels of arterial oxygen tension (PaO2 100–200, 201–300, 301–400, and > 400 mmHg), at two levels of controlled hyperventilation (PaCO2 25 and 30 mmHg). In five patients, a transcranial Doppler probe was used to insonate the middle cerebral artery throughout the study period. Regression lines were constructed for each patient for the PjvO2, SjvO2 and the corresponding PaO2 for both levels of PaCO2 (all PjvO2-PaO2 and SjvO2-PaO2 regression lines r2 > 0.85, P < 0.0001). From these lines we calculated the PjvO2, SjvO2 and CjvO2 at PaO2 of 100, 250 and 400 mmHg, at each level of PaCO2 for each patient. At PaCO2 of 25 mmHg, hyperoxaemia increased PjvO2 (from 27.6 ±1.1 mmHg at PaO2 of 100 mmHg to 30.6 ± 1.4 and 33.6 ± 1.8 mmHg at PaO2 of 250 and 400 mmHg respectively) and SjvO2 (from 54 ± 3% at PaO2 of 100 mmHg to 60 ± 3 and 65 ± 3% at PaO2 of 250 and 400 mmHg respectively, P < 0.05). Hyperoxaemia had a similar effect on SjvO2 and PjvO2 at a PaCO2 of 30 mmHg. For a given PaO2, the PjvO2, SjvO2 and CjvO2 were lower at PaCO2 of 25 mmHg than at a PaCO2 of 30 mmHg (P < 0.01). The predicted CjvO2 based on the increased PaO2 and an unchanged cerebral metabolic rate for oxygen was also calculated and was no different from the measured CjvO2 with hyperoxia. Middle cerebral artery flow velocity did not change with hyperoxia, but decreased with hypocapnia (48 ± 7 to 35 ±4 cm· sec−1, P< 0.01). We conclude that hyperoxia during acute hyperventilation in the anaesthetized patient improves oxygen delivery to the cerebral circulation, as measured by a higher cerebral venous oxygen content and saturation. An increased PaO2 should be considered for those patients in whom aggressive hyperventilation is contemplated.AbstractLa désaturation veineuse centrale peut survenir pendant l’hyperventilation réalisée au cours d’interventions neurochirurgicales. Nous avons étudié les répercussions de l’hyperoxémie (PaO2 > 200 mmHg) sur la tension en oxygène du bulbe jugulaire (PjvO2), sa saturation (SjvO2) et son contenu (CjvO2) chez 12 patients soumis à une anesthésie générale pour une intervention neurochirugicale. Sous des conditions stables d’anesthésie, la fraction en oxygène inspiré (FlO2) a été variée pour produire quatre niveaux différents de tension artérielle en oxygène (PaO2 100–200, 201–300, 301–400 et > 400 mmHg) à deux niveaux d’hyperventilation (PaCO2 25 et 30 mmHg). Une sonde de Döppler intracrânienne a été insérée à cinq patients pour explorer l’artère méningée moyenne. A chaque patient, nous avons construit des lignes de régression de la PjvO2, de la SjvO2 pour la PaO2 correspondante, aux deux niveaux de PaCO2 (toutes les lignes de régression PjvO2-PaO2 et SjvO2-PaO2 r2 > 0,85, P < 0,0001). A partir de ces lignes, nous avons calculé chez chaque patient la PjvO2, la SjvO2 et le CjvO2 aux PaO2 de 100, 250 et 400 mmHg, pour chaque niveau de PaCO2. A la PaCO2 de 25 mmHg, l’hyperoxémie a augmenté la PjvO2 (de 27,6 ±1,1 mmHg pour une PaO2 de 100 mmHg à 30 ± 1,4 et 33,6 ± 1,8 mmHg aux PaO2 de 250 et 400 mmHg respectivement, P < 0,05). L’hyperoxémie a eu le même effet sur la SjvO2 et la PjvO2 à la PaCO2 de 30 mmHg. Pour une PaO2 donnée, la PjvO2, la SjvO2 et le CjvO2 ont été plus bas à la PaCO2 de 25 mmHg qu’à celle de 30 mmHg (P < 0,01). La CjvO2 prédite lorsque la PaO2 augmente et que le taux métabolique cérébral demeure inchangé a aussi été calculée et n’a pas été trouvée différente de la CjvO2 mesurée en hyperoxémie. La vélocité du courant sanguin de l’artère cérébrale moyenne n’a pas changé avec l’hyperoxémie mais a diminué avec l’hypocarbie (de 48 ± 7 à 35 ± 4 cm·sec−1, P < 0,01). Nous concluons que chez le sujet anesthésié, l’hyperoxie produite pendant une hyperventilation aiguë améliore l’apport en oxygène de la circulation cérébrale, comme l’ont montré l’augmentation du contenu veineux cérébral et de la saturation en oxygène. On doit envisager d’augmenter la PaO2 des patients qu’il faut ventiler agressivement.