Retrograde Catheterization of the Right Internal Jugular Vein for Serial Measurements of Cerebral Venous Oxygen Content

Enevoldsen, E.

doi:10.1038/jcbfm.1989.101

Cited by 90 publications

(36 citation statements)

References 6 publications

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“…For the present study the most crucial assumption is that blood sampled from the catheter in the internal jugular vein represents cerebral venous blood. Even with the optimal catheter placement employed in the present study (Jacobsen and Enevoldsen, 1989), b lood obtained from the bulb of the internal jugular vein contains a slight admixture of blood of extrac ranial origin. Although the amount of extracranial contamination is usually very slight «2.6%) (Shen kin et aI., 1948;Lassen, 1959), an activation induced increase in extracranial contamination would have influenced our results.…”

Section: Technical Considerationsmentioning

confidence: 87%

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Persistent Resetting of the Cerebral Oxygen/Glucose Uptake Ratio by Brain Activation: Evidence Obtained with the Kety—Schmidt Technique

Madsen

Hasselbalch²,

Hagemann³

et al. 1995

J Cereb Blood Flow Metab

243

188

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Summary: Global cerebral blood flow (CBF), global ce rebral metabolic rates for oxygen (CMR02), and for glu cose (CMRglc), and lactate efflux were measured during rest and during cerebral activation induced by the Wis consin card sorting test. Measurements were performed in healthy volunteers using the Kety-Schmidt technique. Global CMR02 was unchanged during cerebral activa tion, whereas global CBF and global CMRglc both in creased by 12%, reducing the molar ratio of oxygen to glucose consumption from 6.0 during baseline conditions to 5.4 during activation. Data obtained in the period fol lowing cerebral activation showed that the activation induced resetting of the relation between CMRglc and CMR02 persisted virtually unaltered for �40 min after the mental activation task was terminated. Address correspondence and reprint requests to Dr. Peter Lund Madsen at Department of Neurology, The National Uni versity Hospital, Rigshopitalet, 9, Blegdamvej, DK-2100 Copen hagen, Denmark.Abbreviations used: CMR1ac, cerebral lactate efflux; LCI, lac tate/glucose index. 485tion-induced increase in cerebral lactate efflux measured over the same time period accounted for only a small fraction of the activation-induced excess glucose uptake. These data confirm earlier reports that brain activation can induce resetting of the cerebral oxygen/glucose con sumption ratio, and indicate that the resetting persists for a long period after cerebral activation has been termi nated and physiologic stress indicators returned to base line values. Activation-induced resetting of the cerebral oxygen/glucose uptake ratio is not necessarily accounted for by increased lactate production from nonoxidative glucose metabolism. Key Words: Cerebral metabolism Cerebral lactate efflux-Cerebral blood flow-Cerebral activation-U ncoupling.from CMR02 observed during activation could be due to errors with the PET models employed to measure CMR02 (Sokoloff, 1992). Moreover, it is surprising that nonoxidative glucose metabolism should be the major energy source for cerebral ac tivation, given the low yield of ATP from this path way compared with that from the oxidative path way. The initial aim of this study was to address this controversy employing the Kety-Schmidt tech nique, which is independent of the assumptions on which the PET models for measurements of

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Section: Technical Considerationsmentioning

confidence: 87%

“…The catheter tip was advanced to the base of the skull, J Cereb Blood Flow Metab, Vol. 15, No.3, 1995 and the correct placement was verified as described else where (Jacobsen and Enevoldsen, 1989). Arterial bloo( was sampled from a catheter in the radial artery.…”

Section: Protocol Imentioning

confidence: 99%

Persistent Resetting of the Cerebral Oxygen/Glucose Uptake Ratio by Brain Activation: Evidence Obtained with the Kety—Schmidt Technique

Madsen

Hasselbalch²,

Hagemann³

et al. 1995

J Cereb Blood Flow Metab

243

188

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“…Correct positioning of the jugular bulb catheter was confirmed with a lateral head-and-neck radiograph. 20 Cerebral venous monitoring via a jugular bulb catheter allows assessment of global oxygen delivery adequacy and does not exacerbate intracranial hypertension. 21 JVOS was monitored continuously via the reverse jugular catheter and was recorded hourly.…”

Section: Methodsmentioning

confidence: 99%

Worsening of cerebral hyperemia by the administration of terlipressin in acute liver failure with severe encephalopathy

et al. 2004

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There is increasing evidence that terlipressin is useful in patients with cirrhosis and hepatorenal syndrome, but there are no data of its use in patients with acute liver failure (ALF) in whom hepatorenal syndrome is common. Although terlipressin produces systemic vasoconstriction, it produces cerebral vasodilatation and may increase cerebral blood flow (CBF). Increased CBF contributes to intracranial hypertension in patients with ALF. The aim of this study was to evaluate the safety of terlipressin in patients with ALF with respect to cerebral hemodynamics. Six successive patients with ALF were ventilated electively for grade IV hepatic encephalopathy. Patients were monitored invasively and CBF was measured (KetySchmidt technique). Measurements were made before and at 1, 3, and 5 hours after intravenous (single bolus) administration of terlipressin (0.005 mg/kg), median, 0.25 mg (range, 0.2-0.3 mg). There was no significant change in heart rate, mean arterial pressure, or cardiac output. CBF and jugular venous oxygen saturation both increased significantly at 1 hour (P ‫؍‬ 0.016). Intracranial pressure increased significantly at 1 hour (P ‫؍‬ 0.031), returning back to baseline values at 2 hours. In conclusion, administration of terlipressin, at a dose that did not alter systemic hemodynamics, resulted in worsening of cerebral hyperemia and intracranial hypertension in patients with ALF and severe hepatic encephalopathy. These data suggest the need to exercise extreme caution in the use of terlipressin in these patients in view of its potentially deleterious consequences on cerebral hemodynamics. (HEPATOLOGY 2004;39:471-475.)

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“…The proximal port was used for drug administration and the distal port for blood sampling. A 20 cm, 20 gauge JVB catheter (Cook, Bloomington, IN, U.S.A.) was percutaneously placed via a retrograde an terior jugular vein approach above the thoracic inlet (Grif fith and Greenbaum, 1973;Jakobsen and Enevoldsen, 1989). A 60 cm 5.8F catheter (Bunegin-Albin, Cook, IN, U.S.A.) was placed in the aortic arch, either percutane ously or by cut down via the femoral artery.…”

Section: Methodsmentioning

confidence: 99%

Cerebral Lactate Uptake during Cardiopulmonary Resuscitation in Humans

Rivers

Paradis

Martin

et al. 1991

J Cereb Blood Flow Metab

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Animal studies have shown cerebral lactate uptake under conditions of anoxia and ischemia. Cerebral lactate uptake in humans during cardiopulmonary resuscitation (CPR) has not been previously reported in the literature. Forty-five patients receiving CPR underwent simultaneous sampling through jugular venous bulb, right atrial, and central aortic catheterization. The mean net cerebral lactate uptake (central aortic minus jugular venous bulb) was 0.76 ± 1.86 and 0.80 ± 2.03 m M on initial measurement and 10 min later, respectively. Both measurements were statistically significant (p = 0.01) compared to normal controls who have net cerebral output of lactate of −0.18 ± 0.1 m M. Seventy-one percent of all patients had a cerebral uptake on initial sampling and this gradient persisted upon sampling 10 min later in 68% of the remaining 40 patients who did not have a return of spontaneous circulation. Among multiple variables measured, patients who exhibited a cerebral lactate uptake were 13.2 years younger (p = 0.004), received an additional 7.6 min of CPR (p = 0.05), and had a mean arterial lactate concentration of 4.8 m M higher (p = 0.005) than the nonuptake group. The pathophysiologic explanation of cerebral lactate uptake during CPR is multifactorial and includes utilization and/or diffusion.

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Retrograde Catheterization of the Right Internal Jugular Vein for Serial Measurements of Cerebral Venous Oxygen Content

Cited by 90 publications

References 6 publications

Persistent Resetting of the Cerebral Oxygen/Glucose Uptake Ratio by Brain Activation: Evidence Obtained with the Kety—Schmidt Technique

Persistent Resetting of the Cerebral Oxygen/Glucose Uptake Ratio by Brain Activation: Evidence Obtained with the Kety—Schmidt Technique

Worsening of cerebral hyperemia by the administration of terlipressin in acute liver failure with severe encephalopathy

Cerebral Lactate Uptake during Cardiopulmonary Resuscitation in Humans

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