Johnny E. Brian

Cerebrovascular Responsiveness to Carbon Dioxide in Dogs with 1.4% and 2.8% Isoflurane

Cerebral blood flow (CBF) responsiveness to alterations in arterial CO2 tensions (PaCO2) during 1.4% and 2.8% isoflurane anesthesia was assessed. Dogs were initially anesthetized with thiopental (12 mg/kg, iv bolus), their tracheae intubated, after which anesthesia was maintained with 1.4% isoflurane. In eight animals three levels of PaCO2 (25, 40, and 60 mmHg) were studied during 1.4% and 2.8% isoflurane. Mean arterial blood pressure, sagittal sinus pressure, and cerebrospinal fluid pressure were measured and CBF was determined using radiolabeled microspheres. Cerebral perfusion pressure (CPP) was maintained constant at approximately 80 mmHg by inflation of a balloon in the midthoracic aorta. CBF during normocapnia was 70 +/- 14 and 118 +/- 18 ml.min-1.100 g-1 with 1.4% and 2.8% isoflurane, respectively. As PaCO2 was decreased and increased, CBF decreased and increased to 42 +/- 7% and 185 +/- 16% of control, respectively, during 1.4% isoflurane. During 2.8% isoflurane, hypocapnia decreased CBF to 39 +/- 6% of control, but CBF did not increase with hypercapnia. In a second group of animals (n = 8), the effects of changes in CPP during hypercapnia with 1.4% and 2.8% isoflurane were assessed. Increasing CPP approximately 25 mmHg with both 1.4% and 2.8% isoflurane increased CBF but did not change CVR from control. With 1.4% isoflurane, the cerebral vasculature constricts with hypocapnia and dilates with hypercapnia, whereas with 2.8% isoflurane, vasoconstriction to hypocapnia is retained but vasodilation to hypercapnia is absent.(ABSTRACT TRUNCATED AT 250 WORDS)

Management of cerebral hemispherectomy in children

Surgical removal of a cerebral hemisphere may be undertaken in patients with intractable seizure disorders. Anesthetic management of such patients has not been reviewed in detail before. This study retrospectively analyzed hospital records of ten patients undergoing cerebral hemispherectomy at the Johns Hopkins Hospital between July 1983 and February 1988. Patient records were reviewed for diagnosis, physical characteristics, preoperative medications, anesthetic management, and postoperative course in the intensive care unit (ICU). Massive and sudden blood loss was a common finding in these patients, and during the intraoperative and postoperative periods, fluid resuscitation frequently was an ongoing process. In some patients, the blood loss exceeded one blood volume and was associated with coagulopathy, hypokalemia, and hypothermia. Urine output was elevated by a glucose-induced diuresis in some patients, giving misleading information as to intravascular volume status. Seizures and hemorrhage into the hemispherectomy cavity were management problems in the ICU. From this review, the authors conclude that blood loss may be marked and precipitous during surgical removal of a cerebral hemisphere. Monitoring of intra-arterial pressure and central venous pressure (CVP) is necessary for patient management during the intraoperative and postoperative periods. Intravenous (IV) access should allow rapid intravascular volume administration as it becomes necessary. Patients should remain intubated and observed closely during the immediate postoperative period due to difficulties with hemodynamic stability, seizures, and hemorrhage.

Changes in cerebral blood flow over time during isoflurane anesthesia in dogs.

The present study assessed the impact of time (6 h) on cerebral blood flow (CBF) during isoflurane anesthesia with and without vasopressor administration. All animals were prepared for measurement of CBF by the radiolabeled microsphere method under 1.4% end-tidal (1.0 MAC) isoflurane anesthesia. Surgery required 45 min and was followed by a 15 min stabilization period. In group 1 (n = 6), isoflurane 1.4% was administered for 6 h. CBF after 1 h of isoflurane was 92 +/- 9 ml/min/100 g (mean +/- SEM) and declined to 61 +/- 5 ml/min/100 g at 2 h and further declined to 37 +/- 5 ml/min/100 g at 6 hr. In group 2 (n = 6), isoflurane 1.4% was administered during the first hour. Thereafter, isoflurane 1.4% was continued, angiotensin II (0.3 mug/kg/min) was administered intravenously, and blood was withdrawn to maintain CPP constant for an additional 5 h, with hourly CBF determination. In this group, control CBF was 95 +/- 16 ml/min/100 g and flow was maintained at the control level through 4 h and then declined to 50 +/- 5 ml/min/100 g at 5 and 6 h. In group 3 (n = 6), 1.4% isoflurane was administered and phenylephrine (2.0 mug/kg/min) infusion was combined with hemorrhage to maintain control CPP in an identical sequence to group 2. In group 3, control CBF was 88 +/- 14 ml/min/100 g. As in group 1, CBF decreased significantly at 2 h (p < 0.05) to 68 +/- 13 ml/min/100 g and further declined to 49 +/- 7 ml/min/100 g at 6 h. In all three groups, CMRO2 remained at control levels and there were no changes in arterial carbon dioxide or CPP for the duration of the study. These data demonstrate that the hyperemia caused by isoflurane resolves over time during stable 1 MAC isoflurane anesthesia. The unanticipated interaction of angiotensin II and isoflurane producing a sustained cerebral hyperemia suggests that previous studies that used angiotensin II to support MABP during isoflurane may have reported the effects of angiotensin II in addition to or rather than the effects of isoflurane.

Immediate hemodynamic management following subarachnoid hemorrhage during embolization of cerebral vascular abnormalities.

Three patients are reported who suffered intracranial hemmorrhage during interventionally neuroradiology procedures. All had severe hypertension, cardiac arrhythmias and loss of consciousness. Immediate CT scan showed small amounts of blood in all patients. Arrhythmias were controlled with lidocaine. In two patients, the hypertension was treated only with barbiturates plus fentanyl and in the third with labetol and nitroprusside. In the patient treated with nitroprusside and one patient with barbiturate plus fentanyl a 14-20 min period of hemodynamic stability was followed by vasomotor collapse requiring intravenous vasopressor support. The patient initially treated with nitroprusside suffered irreversibly brain injury whereas the other two improved neurologically following their intracranial bleed. These patients suggest that nitroprusside is detrimental in the acute treatment of malignant hypertension following intracranial hemorrhage.