Cerebral blood flow reactivity to changes in carbon dioxide calculated using end-tidal versus arterial tensions.

We retrospectively examined arerial and end-tidal estimations of CO2 tension used to calculate cerebrovascular reactivity in 68 anesthetized patients. CBF was measured using the intravenous 133Xe technique at mean +/- SD PaCO2 values of 28.2 +/- 5.2 and 38.8 +/- 4.8 mm Hg. The correlation between all PaCO2 and end-tidal PCO2 (PetCO2) values was y = 0.85x - 0.49 (r = 0.93, p = 0.0001). There was a moderate correlation between age and the difference between PaCO2 and PetCO2 (y = 0.11x + 0.79; r = 0.73, p = 0.0001). Cerebrovascular reactivity to changes in CO2 (ml 100 g-1 min-1 mm Hg-1) was similar (p = 0.358) when calculated by using either PaCO2 (1.9 +/- 0.8) or PetCO2 (1.8 +/- 0.8) and highly correlated (y = 0.86x + 0.23; r = 0.91, p = 0.0001). The CBF response to changes in CO2 tension can be reliably estimated from noninvasive measurement of PetCO2.

Characterization of arteriovenous malformation feeding vessels by carbon dioxide reactivity.

PURPOSE: To characterize cerebral hemodynamics in patients immediately before microsurgical resection of moderate to large arteriovenous malformations during isoflurane anesthesia. METHODS: In angiographically defined arteriovenous malformation feeding and nonfeeding arteries, transcranial Doppler studies were performed in 25 surgeries on 22 patients. The mean blood flow velocity and pulsatility index were recorded in the middle, anterior, and posterior cerebral arteries. Transcranial Doppler velocities were measured at end-tidal carbon dioxide tensions (PetCO2) of about 25 and 35 mm Hg. Carbon dioxide reactivity was calculated as percentage mean blood flow velocity change per mm Hg PetCO2 change. RESULTS: Patient demographic and clinical data for the arteriovenous malformation group followed the expected strata of a large arteriovenous malformation population. All patients were neurologically stable before surgery. A total of 43 feeding arteries and 55 nonfeeding arteries were studied. Compared with nonfeeders, feeders exhibited higher mean blood flow velocity (68 +/- 5 vs 31 +/- 3 cm/sec, P < 0.0001) and lower pulsatility index (0.64 +/- 0.03 vs 0.88 +/- 0.04, P < 0.001); anterior and middle cerebral artery velocities at normo- and hypocapnia were significantly higher than posterior cerebral arteries for both feeders and nonfeeders (P < 0.001). Carbon dioxide reactivity was 0.2 +/- 0.2%/mm Hg in feeders and 2.1 +/- 0.2%/mm Hg in nonfeeders, with no significant difference between arteries. In four of eight patients with lesions fed by the anterior circulation (middle cerebral artery with or without anterior cerebral artery feeders), posterior cerebral artery nonfeeders exhibited low reactivity. In 2 of 5 patients with ipsilateral posterior cerebral artery feeders, contralateral posterior cerebral artery nonfeeders exhibited impaired reactivity. CONCLUSIONS: Quantitative transcranial Doppler studies are technically feasible in the operating room or interventional suite during anesthesia. Hemodynamic assessment using physiologic challenges of arteriovenous malformation feeders as well as angiographically uninvolved vessels may be useful as criteria in the assessment of malformations and arteriovenous malformation patients may exhibit abnormal vasoreactivity in distant uninvolved perfusion territories, suggesting a deranged neural control mechanism.

The effect of arteriovenous malformation resection on cerebrovascular reactivity to carbon dioxide.

To investigate the cerebral hemodynamic changes associated with obliteration of arteriovenous malformations (AVMs), we studied 26 patients undergoing total microsurgical AVM resection during isoflurane and N2/O2 anesthesia. Detectors were placed 5 to 6 cm from the margin of the lesion and in a homologous contralateral position. Cerebral blood flow (CBF) was measured using the intravenous xenon-133 technique before and after AVM resection, during both hypocapnia and normocapnia at each stage. Intraoperative changes in CBF were related to a risk score system based on the patient's history and preoperative angiograms. Seven otherwise healthy patients undergoing spinal surgery were studied to control for anesthetic effects. Patient demographic and clinical data for the AVM group conformed to the expected strata of a large AVM population. The CBF increased after excision (22 +/- 1 ml/100 g/min before excision to 30 +/- 2 ml/100 g/min after excision; mean +/- SE, n = 25, P less than 0.002) without a hemispheric difference. CO2 reactivity increased slightly after excision (4.2 +/- 0.3% change/mm Hg before excision to 4.7 +/- 0.3% change/mm Hg after excision; n = 14, P less than 0.02). The baseline CBF and CO2 reactivity were not different from the control group. There was a weak correlation between the risk score and the percentage of change in the ipsilateral CBF, with a trend for the patients with the lowest risk to have the lowest CBF changes after resection. There was no relationship between CO2 reactivity and risk grade. None of the patients awoke from anesthesia with unexpected neurological deficits. The highest CBF increases were associated with postoperative brain swelling in one patient and fatal intracerebral hemorrhage in another. Both patients had normal CO2 reactivity before excision. One patient suffered postoperative intracerebral hemorrhage, attributable to technical problems, and had no increase in CBF. We conclude that, with an acute increase in the arteriovenous pressure gradient (and cerebral perfusion pressure) that results from shunt obliteration, there is an immediate global effect of AVM resection to increase CBF. Cerebrovascular reactivity to CO2 remains intact both before and after excision.

Cerebral hyperemia after arteriovenous malformation resection is related to "breakthrough" complications but not to feeding artery pressure. The Columbia University Arteriovenous Malformation Study Project.

To study the pathophysiology of idiopathic postoperative brain swelling or hemorrhage after arteriovenous malformation resection, termed normal perfusion pressure breakthrough (NPPB), we performed cerebral blood flow (CBF) studies during 152 operations in 143 patients, using the xenon-133 intravenous injection method. In the first part of the study, CBF was intraoperatively measured (isoflurane/N2O anesthesia) during relative hypocapnia in 95 patients before and after resection. The NPPB group had a greater increase (P < 0.0001) in mean +/- standard deviation global CBF (28 +/- 6 to 47 +/- 16 ml/100 g/min, n = 5) than did the non-NPPB group (25 +/- 7 to 29 +/- 10 ml/100 g/min, n = 90); both arteriovenous malformation groups showed greater increase (P < 0.05) than did controls undergoing craniotomy for tumor (23 +/- 6 to 23 +/- 6 ml/100 g/min, n = 22). Ipsilateral and contralateral CBF changes were similar. In a second cohort of patients with arteriovenous malformations, CBF was measured at relative normocapnia and it increased (P < 0.002) from pre- to postresection (40 +/- 13 to 49 +/- 15 ml/100 g/min, n = 57). There were no NPPB patients in this latter cohort. The feeding mean arterial pressure was measured intraoperatively before resection or at the last embolization before surgery (n = 64). The feeding mean arterial pressure (44 +/- 16 mm Hg) was 56% of the systemic arterial pressure (78 +/- 12 mm Hg, P < 0.0001) and was not related to changes in CBF from pre- to postresection. There was an association between increases in global CBF from pre- to postresection and NPPB-type complications, but there was no relationship of these CBF changes to preoperative regional arterial hypotension. These data do not support a uniquely hemodynamic mechanism that explains cerebral hyperemia as a consequence of repressurization in hypotensive vascular beds.

Pressure autoregulation is intact after arteriovenous malformation resection.

The loss of autoregulatory control of cerebral perfusion to changes in perfusion pressure in tissue remote from an arteriovenous malformation (AVM) has been proposed as the mechanism underlying "normal perfusion pressure breakthrough." This study is the first direct test of this mechanism. Studies were performed during the resection of moderate to large AVMs in 25 patients undergoing 28 procedures under isoflurane anesthesia. Cerebral blood flow (CBF) was measured (xenon-133 method) in the hemisphere adjacent to the nidus before resection after dural exposure (pre), after AVM removal before dural closure at spontaneous systemic blood pressure (post), and, finally, with the mean arterial pressure increased by 20 mm Hg, using phenylephrine (post-BP). AVM resection resulted in a significant enhancement of perfusion in the adjacent hemisphere (30 +/- 2 vs. 25 +/- 1 ml/100g/min, P < 0.01), but no further increase of CBF occurred during increased perfusion pressure (30 +/- 2 ml/100g/min). One patient suffered a postoperative hemorrhage and another developed intraoperative brain swelling during the course of the resection that necessitated staging the procedure. These two patients had the highest increases in CBF, but intact pressure autoregulation. Preserved autoregulation to increased mean arterial pressure after resection does not support a hemodynamic mechanism for the observed increase in CBF from before the resection to after the resection. Pathological events, however, do appear to be related to increases in hemispheric perfusion.

Adenosine-induced cardiac pause for endovascular embolization of cerebral arteriovenous malformations: technical case report.

OBJECTIVE: Extremely high flow through arteriovenous malformations (AVMs) may limit the safety and effectiveness of endovascular glue therapy. To achieve a more controlled deposition of glue, we used transient but profound systemic hypotension afforded by an intravenously administered bolus of adenosine to induce rapidly reversible high-degree atrioventricular block. METHODS AND CASE REPORT: A patient with a large high-flow occipital AVM fed primarily by the posterior cerebral artery underwent n-butyl cyanoacrylate glue embolization. Nitroprusside-induced systemic hypotension did not adequately reduce flow through the nidus, as determined by contrast injection in the feeding artery. In a dose-escalation fashion, boluses of adenosine were administered to optimize the dose and verify that there was no flow reversal in the AVM and no other unexpected hemodynamic abnormalities by arterial pressure measurements and transcranial Doppler monitoring of the posterior cerebral artery feeding the AVM. Thereafter, 64 mg of adenosine was rapidly injected as a bolus to provide 10 to 15 seconds of systemic hypotension (approximately 20 mm Hg). Although there were conducted beats and some residual forward flow through the AVM during this time, the mean systemic and feeding artery pressures were roughly similar and remained relatively constant. A slow controlled injection of n-butyl cyanoacrylate glue was then performed, with excellent filling of the nidus. CONCLUSION: Adenosine-induced cardiac pause may be a viable method of partial flow arrest in the treatment of cerebral AVMs. Safe, deep, and complete embolization with a permanent agent may increase the likelihood of endovascular therapy's being curative or may further improve the safety of microsurgical resection.

Superselective intraarterial papaverine administration: effect on regional cerebral blood flow in patients with arteriovenous malformations.

In this study the authors determined the effect of papaverine on regional cerebral blood flow (rCBF) in the angiographically normal arteriolar beds of patients with arteriovenous malformations (AVMs) who underwent transfemoral superselective angiography. Middle cerebral artery (MCA) branch vessels were catheterized during 10 procedures performed in nine patients. The mean (+/- standard deviation) largest AVM diameter was 4.4 +/- 1 cm. Regional CBF was measured by recording the washout of a bolus of xenon-133 injected through the microcatheter. In a dose-ranging study. rCBF and MCA pressure in two patients were repeatedly measured after 3-minute infusions of papaverine at 0.07, 0.7, and 7 mg/minute. In a single-dose study, an additional eight patients received only the highest dose of papaverine administered over a 3-minute period. In the dose-ranging study, CBF increased from baseline in a dose-dependent fashion. In the single-dose study, papaverine increased in rCBF 103%, from 48 +/- 11 to 95 +/- 23 ml/100 g/minute at an MCA pressure of 55 +/- 23 mm Hg. Increase in rCBF was linearly related (y = 2.2x - 17, r2 = 0.84; p = 0.001) to baseline MCA pressure (range 22-84 mm Hg). Papaverine increases rCBF in a direct proportion to baseline MCA pressure, even at low baseline pressures. Selective infusion of vasodilators should be investigated in acute cerebral hypotension to facilitate either primary or collateral recruitment of CBF by aiding spontaneous autoregulatory vasodilation. In addition, rCBF monitoring may be useful in determining the most effective intraarterial dose of papaverine while minimizing complications due to hyperemia.

Thiopental effect on cerebral blood flow during carotid endarterectomy.

To investigate the effect of thiopental on cerebral blood flow (CBF) during carotid endarterectomy, five patients receiving isoflurane-N2O anesthesia were studied. During the period of temporary bypass shunting, a baseline CBF was measured using i.v. Xe washout, and global CBF was calculated from the mean of 10 detectors. Thiopental was given in a dose sufficient (mean 4.5, range 2.6-5.8 mg/kg) to result in burst-suppression on the electroencephalogram (EEG) of approximately 1:1 duration and CBF was measured again. Data were compared using repeated measures analysis of variance. Thiopental significantly reduced mean (+/-SE) CBF (ml/100 g/min) from 37 +/- 6 to 18 +/- 2 (p <0.02). Corresponding PaCO2 (mm Hg) values were 42.8 +/- 1.2 and 41.2 +/- 1.6 and mean systemic blood pressure (mm Hg) was 101 +/- 3 and 100 +/- 6, respectively (NS). Mean % change in CBF was 48 +/- 5 (range 32-62%). There was no relationship between the dose administered and the change in CBF. During steady-state anesthesia, a small dose of thiopental capable of suppressing EEG resulted in a profound reduction in CBF.

The equivalence of anesthetic regimens with respect to plasma glucose elevation during cerebrovascular surgery.

Hyperglycemia, even if mild, is known to aggravate neuronal damage from cerebral ischemia. In order better to define the influence of currently used anesthetic techniques on plasma glucose levels during cerebrovascular surgery, we examined serial plasma glucose values during 43 carotid endarterectomies (CEA) and 19 intracranial arteriovenous malformation (AVM) resections. CEA patients (aged 67.6 +/- 1.4 years and weighing 76.4 +/- 2.3 kg, mean +/- SEM) received N2O in O2 and either isoflurane (ISO) (n = 14), halothane (n = 8), fentanyl (n = 10), or sufentanil (n = 11). Plasma glucose was compared at 1.12 +/- 0.05 h (stage 1), 2.08 +/- 0.07 h (stage 2), and 3.12 +/- 0.1 h (stage 3) after induction of anesthesia. AVM patients received ISO and N2O in O2. Plasma glucose was compared 2.32 +/- 0.14 h (stage 1) and 6.25 +/- 0.34 h (stage 2) after induction of anesthesia (surgical stage). Glucose was determined by the hexokinase method. In the CEA cases, progressively elevated plasma glucose levels were associated with successive surgical stage (114 +/- 6, 122 +/- 6, and 138 +/- 6 mg/dl). The seven CEA patients that carried the diagnosis of diabetes mellitus tended to have higher glucose levels but they did not differ significantly from nondiabetic patients. The AVM patients (aged 35.7 +/- 2.3 years and weighing 71.1 +/- 2.9 kg) were all nondiabetic. They were significantly younger than the CEA patients and each received dexamethasone intraoperatively. In these patients, there was a significant effect (p <0.04) of surgical stage to increase plasma glucose (115 +/- 10 vs. 126 +/- 10 mg/dl). For CEA, the anesthetic techniques examined do not differ significantly in their influence on plasma glucose levels, but all techniques were associated with a gradual increase in plasma glucose levels intraoperatively, even in nondiabetic patients. Compared to the group of younger AVM patients, glucose elevation was more pronounced in the elderly CEA patients. We conclude that intraoperative monitoring of plasma glucose may be useful in elderly patients during prolonged neurovascular procedures.

Intact cerebral blood flow reactivity during remifentanil/nitrous oxide anesthesia.

Remifentanil hydrochloride is a new opioid rapidly metabolized by blood and tissue esterases. The swift degradation accounts for the elimination half-life (t1/2 beta) of < 10 min. An anesthetic agent allowing more rapid postoperative assessment of the neurosurgical patient would be beneficial. This study examined the effect of remifentanil on cerebral blood flow (CBF) reactivity to changes in the arterial pressure of carbon dioxide (PaCO2). Cerebral blood flow was measured with intravenous 133-Xenon during remifentanil/ nitrous oxide (N2O) anesthesia in 10 patients undergoing craniotomy. Cerebrovascular reactivity was determined by repeating CBF measurements after the addition of carbon dioxide (CO2) to the inspired gas mixture. The CBF increased from 21 +/- 6 to 31 +/- 7 ml/100 g/min as the PaCO2 increased from 27 +/- 4 to 36 +/- 3 mm Hg. The relative CBF reactivity was 3.6 +/- 1.2%/mm Hg CO2. During the CBF determinations, the doses of remifentanil administered were not significantly different (0.38 +/- 0.18 microgram/kg/min at hypocapnia vs. 0.34 +/- 0.16 microgram/kg/min at normocapnia). Electroencephalographic monitoring showed a spectral edge frequency of 26 +/- 1 Hz before induction, 25 +/- 1 Hz during maintenance of the remifentanil/N2O anesthetic (0.32 +/- 0.15 microgram/kg/ min), 24 +/- 1 Hz during hypocapnic CBF determination, and 24 +/- 2 Hz during normocapnic CBF determination. At the completion of the procedure, the patients responded to commands within 3.6 +/- 2.5 min and were extubated 7.2 +/- 4.5 min after the remifentanil/N2O was discontinued. In conclusion, absolute CBF values during remifentanil/N2O are similar to previously reported CBF values during fentanyl/N2O and isoflurane/N2O anesthesia, and cerebrovascular reactivity to CO2 remains intact.

Effect of intracarotid papaverine on human cerebral blood flow and vascular resistance during acute hemispheric arterial hypotension.

This study assessed the feasibility of augmenting cerebral blood flow (CBF) and decreasing hemispheric cerebrovascular resistance (CVR) by intracarotid papaverine during acute cerebral hypotension. Awake patients (n = 10) undergoing transfemoral balloon occlusion of an internal carotid artery (ICA) with nitroprusside (SNP)-induced systemic hypotension (10% reduction of mean arterial pressure) were studied. We measured mean femoral artery pressure (MAP), mean distal ICA pressure (P(ica)), and CBF (intracarotid 133Xe) at two time points: before and after intracarotid papaverine infusion (1 or 7 mg/min). Two patients became symptomatic immediately after ICA occlusion and were excluded. One patient developed a focal seizure during papaverine infusion. In another, the occlusion balloon deflated prematurely. Of the remaining six patients, two of the three patients who received high-dose papaverine (7 mg/min) developed transient obtundation. The remaining three patients, who received low-dose papaverine (1 mg/min), did not develop any neurologic symptoms. There was a trend for intracarotid papaverine to increase hemispheric CBF by 36% (33 +/- 10 versus 45 +/- 22 ml x 100 g(-1) x min(-1), P = .084, n = 6); papaverine decreased CVR from 1.3 +/- 0.4 to 1.0 +/- 0.3 mm Hg x ml(-1) x 100 g(-1) x min(-1) (P = .049). There was no significant change in heart rate, MAP, or P(ica) during experimental protocol. Manipulation of CVR by intracarotid papaverine during acute hemispheric arterial hypotension appears to be feasible. Further studies are needed to establish safety and efficacy.

Fever after subarachnoid hemorrhage: risk factors and impact on outcome.

OBJECTIVE: To identify risk factors for refractory fever after subarachnoid hemorrhage (SAH), and to determine the impact of temperature elevation on outcome. METHODS: We studied a consecutive cohort of 353 patients with SAH with a maximum daily temperature (T(max)) recorded on at least 7 days between SAH days 0 and 10. Fever (>38.3 degrees C) was routinely treated with acetaminophen and conventional water-circulating cooling blankets. We calculated daily T(max) above 37.0 degrees C, and defined extreme T(max) as daily excess above 38.3 degrees C. Global outcome at 90 days was evaluated with the modified Rankin Scale (mRS), instrumental activities of daily living (IADLs) with the Lawton scale, and cognitive functioning with the Telephone Interview of Cognitive Status. Mixed-effects models were used to identify predictors of T(max), and logistic regression models to evaluate the impact of T(max) on outcome. RESULTS: Average daily T(max) was 1.15 degrees C (range 0.04 to 2.74 degrees C). The strongest predictors of fever were poor Hunt-Hess grade and intraventricular hemorrhage (IVH) (both p < 0.001). After controlling for baseline outcome predictors, daily T(max) was associated with an increased risk of death or severe disability (mRS > or = 4, adjusted OR 3.0 per degrees C, 95% CI 1.6 to 5.8), loss of independence in IADLs (OR 2.6, 95% CI 1.2 to 5.6), and cognitive impairment (OR 2.5, 95% CI 1.2 to 5.1, all p < or = 0.02). These associations were even stronger when extreme T(max) was analyzed. CONCLUSION: Treatment-refractory fever during the first 10 days after subarachnoid hemorrhage (SAH) is predicted by poor clinical grade and intraventricular hemorrhage, and is associated with increased mortality and more functional disability and cognitive impairment among survivors. Clinical trials are needed to evaluate the impact of prophylactic fever control on outcome after SAH.

Three-minute blood flow index for assessment of cerebrovascular reserve.

Regional cerebral blood flow studies with xenon-133 are useful in the functional assessment of cerebrovascular diseases. Conventional models for cerebral blood flow calculation employ 11 minutes of data collection. However, in many circumstances it is not possible to maintain steady-state physiologic conditions for 11 minutes. We compared a monocompartmental model that requires only 3 minutes of data collection with the bicompartmental model that requires 11 minutes of data collection. The correlation between the absolute values for global cerebral blood flow (initial slope index, intravenous method) in 72 anesthetized patients was r = 0.88; for 54 awake patients inhaling xenon-133, the correlation was r = 0.77. Cerebral blood flow was determined with intravenous xenon-133 at baseline and during a CO2 challenge in 50 patients during cerebrovascular surgery under general anesthesia. Reactivity to a 10-mm Hg rise in PaCO2 was calculated in absolute terms and as a percentage change from baseline using both the 3-minute and the 11-minute models. The correlation of CO2 reactivity calculated with the two models was r = 0.9 for the absolute values and r = 0.8 for the relative change. Cerebral blood flow calculated with the two models correlated well in both awake and anesthetized patients. In addition, there was a good correlation between CO2 reactivity calculated with the two models. In situations in which physiologic conditions cannot be held stable for 11 minutes, the 3-minute initial slope index may be used to quantitatively assess cerebrovascular reserve with a CO2 challenge.

Deliberate hypotension in patients with intracranial arteriovenous malformations: esmolol compared with isoflurane and sodium nitroprusside.

Thirty patients undergoing resection of arteriovenous malformations with deliberate hypotension were randomized to receive 1 of 3 hypotensive agents. Anesthesia was maintained with isoflurane and nitrous oxide in all patients. Mean arterial pressure was reduced 20% to 60-65 mm Hg with use of either isoflurane (less than or equal to 4%), sodium nitroprusside (less than or equal to 8 micrograms.kg-1.min-1), or esmolol (less than or equal to 24 mg/min). Esmolol was associated with a decrease in cardiac output from 6.2 +/- 1.3 to 3.8 +/- 0.8 L/min, which, because of a 22% increase in systemic vascular resistance, far exceeded the reduction in mean arterial pressure. Systemic vascular resistance increased despite a 32% decrease in plasma renin activity. In contrast, with sodium nitroprusside or isoflurane, the decrease in mean arterial pressure was associated with decreases in systemic vascular resistance of similar magnitude, with no change in cardiac output. Plasma renin activity levels increased 48% with sodium nitroprusside and 126% with isoflurane. Heart rate increased 13% with sodium nitroprusside, remained unchanged with isoflurane, and decreased 23% with esmolol. Although esmolol may be used as a primary hypotensive agent, the potential for marked myocardial depression must be recognized. The differences in pharmacologic properties for the different hypotensive agents suggest that combinations of these agents may provide a pharmacologic profile superior to either agent alone.

Are all effects of esmolol equally rapid in onset?

The purpose of this study was to compare the time course of the bradycardic and hypotensive effects of esmolol. Ten patients undergoing craniotomy requiring hypotension were anesthetized with nitrous oxide and isoflurane. During steady state anesthesia, the response to an infusion of esmolol 500 micrograms.kg-1.min-1 for 90 s followed by 300 micrograms.kg-1.min-1 was measured over 60 min. Heart rate (HR), mean arterial pressure (MAP), and plasma renin activity (PRA) responses did not occur with equal rapidity. The half-time for the 14% decrease in HR (81 +/- 13 bpm to 70 +/- 9 bpm) was 1.2 min. MAP decreased by 26% (85 +/- 7 mm Hg to 63 +/- 6 mm Hg) with a 17.8 min half-time. This delay in MAP response may, in part, be related to the gradual 44% decline in PRA (9.5 +/- 4.5 ng.mL-1.h-1 to 5.3 +/- 2.5 ng.mL-1.h-1) occurring with a half-time of 11.9 min. The times to attainment of 90% maximum decreases were 4.8 +/- 3.0 min for HR, 42.5 +/- 8.9 min for MAP, and 32.1 +/- 15.0 min for PRA. Thus although esmolol has an ultrashort kinetic half-life, only the HR effect can be considered to have an ultrashort onset.

Intraoperative 133Xe cerebral blood flow measurements by intravenous versus intracarotid methods.

To document the comparability of cerebral blood flow (CBF) values determined by quantification of 133Xe washout after either intravenous or intracarotid administration, 12 patients undergoing elective carotid endarterectomy anesthetized with N2O/O2 and either isoflurane or halothane were studied. Scintillation counters were placed over the middle cerebral artery territory ipsilateral to the operated carotid artery. CBF was measured by the intravenous method during dissection of the carotid sheath and was calculated as the initial slope index from head washout curves collected for 11 min after injection of 10-20 mCi 133Xe in saline into a large vein. Immediately prior to carotid occlusion, CBF was determined by direct injection of 1 mCi 133Xe in saline into either the internal carotid artery or the common carotid artery with the external carotid artery occluded. For the intracarotid injections, the initial slope was calculated from the 1st min of washout. Data were analyzed by linear regression and analysis of variance. Values are expressed as mean +/- SD. The mean CBF for intravenous and intracarotid methods were both 29 +/- 10 ml.100 g-1.min-1. The correlation between CBF measured by intravenous and intracarotid methods was excellent and was described by the line y = x + 0.6, r = 0.92. We conclude that in the flow range studied, the intravenous technique may be applied to measure CBF in physiologically stable situations in which direct intracarotid injection is not feasible.

Desflurane and isoflurane have similar effects on cerebral blood flow in patients with intracranial mass lesions.

BACKGROUND: Before desflurane is advocated for patients undergoing neurosurgical procedures, it is necessary to determine the effect of desflurane on cerebral blood flow (CBF). In this study, CBF values are compared between desflurane and isoflurane at two doses. In addition, CBF reactivity to CO2 and the effect of prolonged exposure were compared between the two agents. METHODS: Cerebral blood flow measurements with intravenous 133Xe were performed in 24 patients undergoing craniotomy for mass lesions, randomized to receive either isoflurane or desflurane in oxygen and air. Cerebral blood flow was determined at 1 and 1.5 MAC concentrations at PaCO2 of 25 mmHg in the absence of surgical stimulation. Intraoperatively, with 1.25 MAC anesthesia, CBF was determined at target PaCO2 of 25 and 35 mmHg. In 15 patients, an additional measurement at 1.25 MAC was made before closure. RESULTS: At 1.0 MAC, mean +/- SD CBF values for the desflurane and isoflurane groups were 18 +/- 2 and 20 +/- 3 ml x 100 g-1 x min-1, respectively. At 1.5 MAC, CBF values were the same for the two anesthetics; 17 +/- 3 ml x 100 g-1 x min-1 for isoflurane and 19 +/- 4 ml.100 g-1 x min-1 for desflurane. During 1.25 MAC anesthesia, there were no differences between groups, with CO2 reactivity 1.3 +/- 1.2 ml x 100 g-1 x min-1 x mmHg-1 for desflurane and 1.6 +/- 0.6 ml.100 g-1 x min-1 x mmHg-1 for isoflurane. There was no demonstrable decrease in CBF with prolonged exposure to either agent. CONCLUSIONS: Desflurane and isoflurane are similar in terms of absolute CBF, the response to increasing doses, and the preservation of CO2 reactivity.

Pharmacokinetics and pharmacodynamics of rocuronium (Org 9426) in elderly surgical patients.

The effects of age on the pharmacokinetic and pharmacodynamic responses to rocuronium (Org 9426) were studied in 20 elderly (> 70 yr) and 20 younger control patients (< 60 yr) during N2O/O2, fentanyl anesthesia. The onset times were the same for both the elderly and younger control group, but the duration of action of rocuronium was significantly prolonged in the elderly patients. Elderly patients, when compared with the younger, also exhibited a significant decrease in plasma clearance (3.67 +/- 1.0 vs 5.03 +/- 1.5 mL.kg-1.min-1, mean +/- SD) and volume of distribution (399 +/- 122 vs 553 +/- 279 mL/kg, mean +/- SD). During the recovery phase of paralysis, no significant difference was seen in the log plasma concentration versus twitch tension response relationship between 20% and 80% paralysis in young and elderly patients receiving rocuronium. The differences in action of rocuronium between the elderly and younger groups can be fully explained by the observed differences in the distribution and elimination of rocuronium between the two groups. The decreased total body water and decreased liver mass which normally accompany aging are likely explanations for the pharmacokinetic changes found in the elderly in this study. We conclude that the action of rocuronium is prolonged in patients aged more than 70 yr because of decreased elimination of the drug.

Adenosine-induced ventricular asystole to induce transient profound systemic hypotension in patients undergoing endovascular therapy. Dose-response characteristics.

BACKGROUND: Adenosine-induced asystole has been used to induce transient systemic hypotension for various vascular procedures. Dose-response characteristics of adenosine-induced ventricular asystole have not been determined. METHODS: During endovascular embolization of cerebral arteriovenous malformations, the authors performed a series of adenosine test injections to establish a dose-response relation in each patient. After an interval of 3-10 min, the dose was escalated by 10-20 mg for each injection to achieve an end point of 20-30 s of stable mean arterial pressure (MAP) reduction to 25-30 mmHg. All patients received constant infusion of nitroprusside (approximately 1 microgram. kg-1. min-1) throughout the procedure. RESULTS: The authors studied four adult patients (age, 22-44 yr; two patients had two separate procedures) and one pediatric patient (age, 4 yr). Twenty-three adenosine injections resulted in measurable asystole. The adenosine dose was 0. 98 +/- 0.40 mg/kg (mean +/- SD), and the dose range was 0.24-1.76 mg/kg (6-90 mg). The duration of asystole, MAP < 30 mmHg, and MAP < 50 mmHg, were 8 +/- 3 s, 18 +/- 12 s, and 50 +/- 29 s, respectively. The minimum MAP and the MAP for the first 20 s were 16 +/- 3 mmHg and 30 +/- 9 mmHg, respectively. There was a linear relation between adenosine dose and the duration of hypotension with MAP < 30 mmHg and MAP < 50 mmHg. CONCLUSIONS: In the dose range studied, a series of adenosine test injections can be used to determine optimal adenosine dose for induction of transient profound hypotension.