Edward H. Stullken

The nonlinear responses of cerebral metabolism to low concentrations of halothane, enflurane, isoflurane, and thiopental.

The relationship between cerebral oxygen consumption (CMRO2) and anesthetic concentration has been assumed (based upon isolated measurements) to be approximately linear at concentrations less than 1 MAC. The shapes of the anesthetic dose-response curves for both CMRO2 and cerebral blood flow (CBF) were examined by multiple measurements made at small, progressive concentration increments from 0 to 2 MAC halothane (six dogs), enflurane (six dogs), and isoflurane (six dogs), and during a constant 23 mg/kg/hr infusion of thiopental (six dogs). The EEG was continuously recorded and changes in EEG patterns from “awake” to “anesthetic” were correlated with changes in anesthetic concentration, CBF, and CMRO2. The significance of changes in the slopes of regression lines for CMRO2, before, during and after changes in EEG patterns from “awake” “anesthetic” were then determined. Contrary to previous inferences, CMRO2, dose–response curves were found to be nonlinear at anesthetic concentrations less than 1 MAC for all anesthetics studied. CMRO2, decreased precipitously until a stable “anesthetic” pattern was observed on the EEG; thereafter, CMRO2, decreased at a markedly reduced rate. The onset of this change occurred at concentrations well below MAC for the inhalational anesthetics. With the thiopental infusion, CMRO2 decreased most rapidly during the first 25 minutes. With halothane and enflurane, CBF was maximal during the period of transition in the EEG from an “awake” to an “anesthetic” pattern. CBF was elevated at all concentrations of isoflurane studied. CBF decreased rapidly during thiopental infusion until the EEG pattern changed from “awake” to “anesthetic” and then more slowly. The results demonstrate that the change in the EEG to an “anesthetic” pattern, which occurs at concentrations well below MAC, is accompanied by an abrupt metabolic depression. It is speculated that these events coincide with the onset of functional depression.

Hemodynamic status following regional and general anesthesia for carotid endarterectomy.

Summary We prospectively studied 23 patients undergoing carotid endarterectomy under regional (n = 13) or general (n = 10) anesthesia to determine the hemodynamic basis of increased frequency in the need for postoperative vasopressor support when regional anesthesia was used. Anesthesia and postoperative care were conducted without reference to hemodynamic data from pulmonary artery catheterization. Although mean arterial pressure was similar in the two groups postoperatively, 11 of the 13 patients undergoing regional anesthesia and 3 of the 10 patients undergoing general anesthesia required phenylephrine postoperatively. No patient required therapy postoperatively to reduce a systolic pressure exceeding 160 mm Hg. Mean arterial pressure remained below the preoperative baseline value in both groups (p < 0.05 with general anesthesia; p = 0.06 with regional anesthesia) during follow-up. In the general anesthesia group, systemic vascular resistance declined significantly below baseline (p < 0.05) following the operation, accompanied by a decline in mean arterial pressure (p < 0.05) and a higher cardiac output. Intraoperative fluid requirements were greater during general anesthesia than during regional anesthesia (p < 0.01). Pulmonary artery occlusion pressure was lower postoperatively than at baseline in both groups (p < 0.05). Pulmonary artery occlusion pressure was higher in the general anesthesia group despite the greater use of phenylephrine in the regional anesthesia group.

Myocardial infarction following regional anaesthesia for carotid endarterectomy

From 1969 through 1982, 185 carotid endarterectomies were performed under regional anaesthesia on 153 patients. Of these patients, 38 (25 per cent) had suffered a previous myocardial infarction, 63 (41 per cent) had documented coronary artery disease, and 115 (75 per cent) had hypertension. Anaesthesia was provided by a superficial cervical plexus block. Monitoring consisted of measurement of direct arterial pressure and continuous display of the electrocardiogram. Oxygen was administered by nasal cannula throughout the procedure. Mean arterial pressure was elevated when necessary by infusion of phenylephrine. No patient in this study suffered an acute myocardial infarction. The only cardiac complications consisted of eight episodes of non-life-threatening dysrhythmias, We conclude that regional anaesthesia for carotid endarterectomy is associated with a low risk of perioperative myocardial infarction.RésuméDe 1969 à 1982,185 endartêrectomies de la carotide ont été faites sous anesthésie regionale chez 153 patients. De ces patients, 38 (25 pour cent) avaient déjà eu un infarctus du myocarde, 63 (41 pour cent) avaient une maladie coronarienne documentée et 115 (75 pour cent) souffraient d’hypertension. On pratiquait chez ces patients un bloc du plexus cervical superficiel. On mesurait de façon directe la pression artérielle et on avait un enregistrement continu de l’élecirocardiogramme, On administrait de l’oxygène par canule nasale pendant toute la procédure. La pression artérielle moyenne était augmentée, si cela était nécessaire, par l’infusion de phényléphrine. Aucun patient pendant cette étude n’a subi un infarctus du myocarde. Les seules complications cardiaques ont été 8 épisodes de dysrythmies non menaçantes. Nous concluons que l’anesthésie régionale pour l’endartérectomie de la carotide est associée à un faible risque d’infarctus péri-operatoire.

Electroencephalographic Evidence of Arousal in Dogs from Halothane after Doxapram, Physostigmine, or Naloxone

: The clinical impressions of enhanced arousal from halothane anesthesia and improvement of postanesthesia recovery scores after doxapram, physostigmine, or naloxone have not been verified in laboratory studies based on the effect of these drugs on MAC. With induction of anesthesia, a shift in the amplitude of the EEG from low to high occurs at anesthetic concentrations well below MAC and appears to coincide with the loss of consciousness. The authors examined the effect of arousal agents on the end-tidal halothane concentration required to produce this shifting EEG. In 24 unmedicated dogs, the end-tidal halothane concentration was elevated to 20 per cent above the shift point concentration (from 0.61 +/- 0.03 to 0.73 +/- 0.03 per cent) and maintained at this level for 30 min. Doxapram, 1 mg/kg, iv, and physostigmine, 0.03 mg/kg, iv, converted the EEG from a high amplitude to a low amplitude tracing in 22 +/- 3 s in eight of eight, and 225 +/- 37 s in seven of eight dogs, respectively. The end-tidal halothane concentration required to restore the shifting EEG was elevated above control for 50 +/- 7 min and 109 +/- 7 min, respectively. Naloxone, 0.06 mg/kg, iv, produced an awake EEG in two of eight dogs in 233 +/- 18 s which persisted for 22 +/- 4 min, and a transiently shifting EEG in three of eight dogs between 200 and 240 s. Naloxone 0.006, mg/kv, iv, produced an awake EEG in 80 +/- 8 s in four of four dogs who had previously received doxapram 3 h earlier. In this model doxapram and physostigmine paralleled the clinically observed onset and duration of arousal. The inconstant arousal from halothane anesthesia induced by naloxone was interpreted in terms of an opiate receptor independent action.

Intracranial Pressure during Hypotension and Subsequent Vasopressor Therapy in Anesthetized Cats

The effects of vasopressor therapy on intracranial pressure (ICP) during hypotension were evaluated in 45 adult cats anesthetized with pentobarbital and hyperventilated via an endotracheal tube with nitrous oxide, 70 per cent, and oxygen, 30 per cent, to maintain Paco225 ± 5 torr. Hypotension was induced by intravenous administration of trimethaphan camsylate or sodium nitroferricyanide and by hemorrhage. Vasopressor (norepinephrine, ephedrine, or isoproterenol) administration in the absence of hypotension caused slight transient increase: in ICP. Trimethaphan produced increases in ICP averaging 4.3 mm Hg, while sodium nitroferricyanide caused no change and hemorrhage decreased ICP by 3.9 mm Hg. After hypotension was established, vasopressors caused increases in ICP of 1–21 mm Hg. The greatest increase was seen with norepinephrine administration during sodium nitroferricyanide-induced hypotension. Increases in ICP were pronounced in absolute magnitude and rapidity of rise but were of short duration (2 to 5 minutes). The elevation of pressure might be of clinical significance in patients who have pre-existing intracranial hypertension or space-occupying lesions.

Anesthesia and subarachnoid intracranial pressure.

&NA; Intracranial pressure (ICP) was continuously monitored by the Richmond technic of Vries and Becker in 17 patients undergoing elective craniotomy. This method entails the placement, under local anesthesia, of a hollow screw through the cranium into the subarachnoid space. The screw was connected to a Statham P23Db pressure transducer with heavy vinyl tubing and with pressures recorded on a Beckman Dynograph®. The effects of 3 anesthetic technics—halothane, enflurane, and nitrous oxide‐narcotic‐relaxant—on ICP during induction and maintenance were compared with preinduction control pressures. Control ICP in awake, lightly premedicated patients was 15 ± 10 torr. Mask inductions with halothane and enflurane consistently caused significant increases in ICP from preinduction levels in the absence of excitement or airway obstruction. Induction with nitrous oxide‐narcotic‐relaxant did not increase ICP. Decreases in ICP following barbiturate administration were noted. Addition of halothane and enflurane to the inspired mixture of patients controlled and hyperventilated with nitrous oxide and oxygen caused consistent increases in ICP. With control hyperventilation (Paco2 25 ± 5 torr), the ICP did not return toward preinduction values within 5 minutes with enflurane and halothane.