Basil F. Matta

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.

Effects of the Valsalva Maneuver on Cerebral Circulation in Healthy Adults: A Transcranial Doppler Study

BACKGROUND AND PURPOSEnKnowledge is limited about the effects of the Valsalva maneuver on cerebral circulation because of the poor temporal resolution of traditional cerebral blood flow measurements. The purpose of this study was to investigate changes in cerebral blood flow during the Valsalva maneuver and to explore its potential use for the evaluation of cerebral autoregulation.nnnMETHODSnUsing transcranial Doppler ultrasonography, we simultaneously recorded systemic arterial blood pressure in the radial artery and flow velocities in both middle cerebral arteries in 10 healthy adults during the Valsalva maneuver. Goslings pulsatility index was calculated for all phases of the Valsalva maneuver. Autoregulatory capacities were estimated from the change in cerebrovascular resistance (flow velocity in relationship to blood pressure) during phase II and changes in the velocity-pressure relationship in phase IV relative to phase I.nnnRESULTSnThe characteristic changes in blood pressure (phases I to IV) were seen in all subjects, accompanying distinct changes in cerebral blood flow velocity. The relative changes in mean velocity during phases II and IV were significantly greater than those in mean blood pressure. Compared with the baseline value, velocity decreased by 35% in phase IIa, then rose by 56.5% in phase IV (corresponding changes in blood pressure were -10.2% and +29.8%, respectively). During phase II, the pulsatility and cerebrovascular resistance decreased by 19.9%. The increase in cerebral blood flow velocity in phase IV was significantly higher than in phase I (P < .0004), and there was no corresponding significant difference in blood pressure.nnnCONCLUSIONSnThese results demonstrated that in healthy humans the Valsalva maneuver causes characteristic changes in systemic blood pressure as well as in flow velocity in the middle cerebral artery, reflecting the sympathetic and cerebral autoregulatory responses, respectively. Analysis of these changes may provide an estimate of autoregulatory capacity.

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.

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)

Nitrous Oxide Increases Cerebral Blood Flow Velocity During Pharmacologically Induced Eeg Silence in Humans

We examined the effect of nitrous oxide on cerebral blood flow velocity (Vmca), arteriovenous oxygen content difference and cerebral use of glucose during propofol-induced electrical silence of the electroencephalogram (EEG) in 10 patients undergoing anesthesia for nonneurosurgical procedures. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 3 micrograms/kg (followed by an infusion of 2 micrograms/kg/h), vecuronium 0.1 mg/kg, and maintained with a propofol infusion (250-300 micrograms/kg/min) sufficient to induce EEG silence. A transcranial Doppler was used to measure the Vmca and a jugular bulb catheter was inserted for oxygen saturation and glucose use measurements. After a 15-period of isoelectric EEG and normocapnia (PaCO2 38 +/- 1 mm Hg), baseline arterial and jugular bulb venous blood gases were drawn, and mean arterial pressure (MAP), heart rate (HR), and Vmca were recorded. Nitrous oxide was then introduced and equilibrated to an end-tidal concentration of 70% for 15 min, after which MAP, HR, Vmca, arterial and jugular bulb venous blood gases were measured again. Nitrous oxide increased Vmca (29 +/- 4 to 35 +/- 4 cm/s, p < 0.01), cerebral use of oxygen (166 +/- 13 to 190 +/- 12 vol%-cm/s, p < 0.05) and glucose (245 +/- 38 to 290 +/- 48 g%-cm/s, p < 0.05) by approximately 20%. Occasional bursts of EEG activity were observed in eight patients studied during the N2O stage. We conclude that in patients with propofol-induced isoelectric EEG, the increase seen in Vmca with the introduction of N2O is mainly due to cerebral stimulation and increase in cerebral metabolic rate.

Impaired cerebral autoregulation after mild brain injury

BACKGROUNDnSevere head injury may impair cerebral autoregulation, which can increase the risk of secondary neuronal injury. The likelihood of impairment in autoregulation is assumed to be low with mild head injury. We report here the absence of cerebral autoregulation in a patient who suffered a concussion from an automobile accident 6 days earlier.nnnMETHODSnThe patient participated in a clinical study approved by the institutional human subjects review committee, investigating the dose-effect relationship of anesthetics on cerebral autoregulation. The patient was scheduled to undergo repair of a knee injury suffered during a motor vehicle accident, during which she had a concussion. The screening evaluation revealed no evidence of neurologic disease. The test was to be performed three times in each patient: baseline autoregulation measurements during stable fentanyl-nitrous oxide anesthesia, second and third measurements during low dose and high dose of the anesthetic to which the patient was assigned. Autoregulation was tested by increasing the mean systemic blood pressure from 80 mm Hg-100 mm Hg using a phenylephrine infusion while simultaneously recording flow velocity from a middle cerebral artery using transcranial Doppler ultrasonography.nnnRESULTSnStatic autoregulation testing during baseline testing demonstrated complete absence of this homeostatic mechanism and the study was canceled. Repeated testing in the recovery unit after the patient awoke showed identical results.nnnCONCLUSIONSnTrivial mild head injury may result in loss of cerebral autoregulation. A clinical study of a larger series to document the incidence is warranted.

Propofol anesthesia for craniotomy: a double-blind comparison of remifentanil, alfentanil, and fentanyl.

For patients undergoing craniotomy, it is desirable to have stable and easily controllable hemodynamics during intense surgical stimulation. However, rapid postoperative recovery is essential to assess neurologic function. Remifentanil, an ultra-short-acting mu-opioid receptor agonist, may be the ideal agent to confer the above characteristics. In this prospective randomized study, we compared the hemodynamic stability, recovery characteristics, and the dose of propofol required for maintaining anesthesia supplemented with an infusion of remifentanil, alfentanil, or fentanyl in 34 patients scheduled for supratentorial craniotomy. With routine monitors in place, anesthesia was induced with propofol (2-3 mg/kg), atracurium (0.5 mg/kg), and either remifentanil (1 microg/kg), alfentanil (10 microg/kg), or fentanyl (2 micro/kg). The lungs were ventilated with O2/air to mild hypocapnia. Anesthesia was maintained with infusions of propofol (50-100 microg/kg/min) and either remifentanil (0.2 microg/kg/min), alfentanil (20 microg/kg/h), or fentanyl (2 microg/kg/h). There were no significant differences among the groups in the dose of propofol maintenance required, heart rate, or mean arterial pressure. However, the time to eye opening (minutes) was significantly shorter in the remifentanil compared to the alfentanil group (6+/-3; 21+/-14; P = 0.0027) but not the fentanyl group (15+/-9). We conclude that remifentanil is an appropriate opioid to use in combination with propofol during anesthesia for supratentorial craniotomy.

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.

The effects of sevoflurane on cerebral hemodynamics during propofol anesthesia

We investigated the cerebral hemodynamic effects of 0.5 and 1.5 minimum alveolar anesthetic concentration (MAC) sevoflurane during propofol anesthesia in 10 patients undergoing supratentorial tumor resection. All patients received a standardized anesthetic, and their lungs were ventilated with a mixture of air and oxygen to produce mild hypocapnia. Anesthesia was then maintained with a propofol infusion. Muscle relaxation was obtained by infusion of atracurium. A transcranial Doppler probe was used to measure red cell flow velocity in the right middle cerebral artery (Vmca). A right-sided jugular bulb catheter was inserted for sampling of jugular bulb blood. After a 30-min period of stabilization and before the start of surgery, baseline arterial and jugular bulb blood samples were drawn to define the arterial-venous oxygen content difference (AVDO2). Mean arterial pressure and Vmca were recorded. Sevoflurane (0.5 and 1.5 MAC) in oxygen/air was then administered, and all measurements were repeated. Administration of sevoflurane at 0.5 MAC did not change Vmca or AVDO2. Sevoflurane (1.5 MAC) did not change Vmca. There was an approximately 25% reduction in AVDO2 (P < 0.05). This suggests that during propofol anesthesia, although 1.5 MAC sevoflurane does not increase red blood cell velocity, there is a relative increase in flow with respect to metabolism. Administration of large-dose sevoflurane may be associated with a degree of luxury perfusion. Implications: We investigated the cerebral hemodynamic effects of sevoflurane in patients undergoing neurosurgery. Small-dose sevoflurane (1%) did not change brain blood flow or oxygen consumption. Large-dose sevoflurane (3%) did not change flow velocity but reduced brain oxygen consumption by 25%. Sevoflurane may provide a degree of luxury perfusion. (Anesth Analg 1997;85:1284-7)