Jugular Bulb Oxygen Saturation Research Articles

Is there a correlation between neurone-specific enolase and jugular venous bulb oxygen saturation during CABG

s: European Association of Cardiothoracic Anaesthesiologists; 17th Annual Meeting; Dublin, Ireland; June 12-15, 2002: Cardiopulmonary Bypass and Surgery

Incidence of intracranial hypertension related to jugular bulb oxygen saturation disturbances in severe traumatic brain injury patients.

To analyze the Intracranial Hypertension (IH) development related to jugular bulb oxygen saturation (SjO2) disturbances in severe traumatic brain injury patients (sTBI). One hundred and thirty-five sTBI patients were reviewed. Those without IH at admission (n = 116) were included. All patients underwent ICP and SjO2 continuous monitoring. Two groups were distinguished according to the SjO2 values during the first 24 hours. Group A: those with abnormal SjO2 (SjO2 more than 75% or less than 55%) and Group B: those with normal SjO2 (55-75%). Differences in IH development and outcome between groups were analyzed. Causes of abnormally low SjO2 were identified. IH developed in 56.9% of patients, between 12 and 48 hours from admission. Group A had a significantly higher incidence of IH than Group B (p < 0.001) and it also had a worse outcome than Group B (GOS 1-2) (p < 0.005). Patients from Group A had a risk of IH 4.5 fold higher than Group B. Considering only patients who developed IH, an abnormal SjO2 value increased 2.3 fold the risk of death compared to those without SjO2 disturbances. Main causes of SjO2 desaturation were hyperventilation (40.7%), hypovolemia (28.4%) and anemia (21%). Early detection of disturbances in oxygen supply-demand relationship and prevention or resolution of the secondary insults which produce these disturbances, might lead to a reduction in the incidence of intracranial hypertension.

Difference of Jugular Bulb Oxygen Saturation under Propofol, Enflurane and Isoflurane Anesthesia with Hydralazine-induced Deliberate Hypotension

Background: Hydralazine produces cerebral vasodilation, which could appear differently according to which kind of anesthetics was used. SjO, CBF and AJDO2 have been studied during general anesthesia with enflurane, isoflurane or propofol in 42 patients undergoing spinal surgery. Methods: Forty-two healthy adult patients were divided into Group P (Propofol-N2O, n = 15), Group E (Enflurane-N2O, n = 15) and Group I (Isoflurane-N2O, n = 12). During the course of the study, the anesthetic concentration was constant. Induced hypotension was provided with hydralazine 20 mg in combination with a continuous infusion of esmolol within 50-100g/kg/min. Arterial blood and jugular bulb blood were obtained and analyzed at normotensive and hypotensive period, respectively. SjO2, was compared within and between groups. Results: SjO values of Group P were 66.2 7.7%, and 81.5 ﾒ 6.1%, those of Group E were 79.5 5.6%, and 78.9 X 4.9% and those of Group I were 82.0 ･ 6.2%, and 84.4 ﾝ 3.7% at normotension and hypotension, respectively (P 0.05 between Group P and Group E, P 0.05 between Group P and Group I, P 0.05 within Group P). Conclusions: When the changes of CBF is assumed with that of SjO, it may be concluded that CBF increased with hydralazine-induced hypotension in propofol-N2O anesthesia. It may be suggested that hydralazine reverses propofol induced cerebral vasoconstriction.

A reply

We appreciate the interest of Dr Alston in our review article on jugular bulb oximetry during cardiac surgery [1]. We agree with him that bench oximetry, not fibreoptic catheters, is the gold standard for the measurement of jugular bulb oxygen saturation (Sjo2) during cardiopulmonary bypass (CPB). Dr Alston provides a perfectly valid explanation of why Sjo2 less than 50% occurs during cardiopulmonary bypass and why, postoperatively, hyperventilation leads to reduced arterial carbon dioxide tension (Paco2), cerebral vasoconstriction, decreased cerebral perfusion and hence increase in oxygen extraction and reduced Sjo2. We recently studied the effect of Paco2 on Sjo2[2], but found that it explains only 34% of the variance of Sjo2 during warm CPB. Recently, Robson and colleagues found that cognitive dysfunction at 3 months after CPB was not related to jugular bulb desaturation (Sjo2 < 50%) during or after CPB [3]. In their study, the authors did not report the early cognitive changes in the first week after CPB or its relation to Sjo2, which was reported by Croughwell et al. [4]. It would be very interesting to confirm this finding because it seems that jugular bulb desaturation may affect only short-term cognitive dysfunction. Low Sjo2 is a symptom of reduced oxygen availability to the brain and if values < 50% do not lead to long-term cerebral damage, we must presume that the brain can still function under this condition. However, there must be some lower limit of Sjo2 (20%, 30%, 40%?) below which cerebral damage will occur. Another factor might be cerebral damage arising from embolism, which would be minimised by reduced cerebral perfusion. We have tried to explain in our review article that Sjo2 does reflect global cerebral oxygenation but does not detect regional cerebral oxygenation. This was confirmed in our recent paper [5] where we found that Sjo2 did not reflect impairment of regional cerebral oxygenation detected by near-infrared spectroscopy (NIRS). Therefore, if brain injury is due to regional ischaemia, it may or may not be reflected by Sjo2. Thus, in attempting to optimise cerebral oxygenation during CPB, it is important to determine whether the aim should be to maintain good oxygenation of the brain or to minimise cerebral perfusion and hence the risk of embolism (while still maintaining adequate oxygenation – whatever this may be).

Current issues in spinal anesthesia.

Spinal anesthesia is an old, simple, and popular anesthetic technique, yet much remains unknown regarding pertinent anatomy, physiology, and pharmacology. Investigations into physiologic effects of spinal anesthesia reveal complex actions on multiple organ systems. New local anesthetics, analgesic additives, and techniques are being investigated for different applications as the practice of medicine focuses on outpatient care. Safety of spinal agents and complications from spinal anesthesia continue to be examined and re-examined to improve safety. Further study will be needed to fully resolve these issues and to further understand and improve the clinical use of spinal anesthesia.

Pediatric neurologic emergencies.

Neuroemergencies are life-threatening situations in which, whatever the cause, common pathologic phenomena result in secondary brain lesions. The goal of critical care management is to stop these self-aggravating processes as soon as possible. Initial resuscitation is devoted to control of the airway and hemodynamic and hydroelectrolytic stabilization. With mass lesions, minimal computed tomographic exploration immediately precedes surgical decompression. Further critical care adapted to the child's needs requires multimodal monitoring. Normoventilation, deep sedation, osmotherapy with mannitol or hypertonic saline solutions, and optimization of mean arterial pressure are the basis of management. A purely pressure-driven approach aimed at controlling cerebral perfusion pressure could be potentially harmful, and associated measurement of blood flow velocity with transcranial Doppler and jugular bulb oxygen saturation monitoring allows an approach to cerebral blood flow and metabolism. Outcome can be improved in dangerous situations such as severe brain injuries, cerebral arteriovenous malformation rupture, status epilepticus, and acute hydrocephalus, provided that emergency management could be applied efficiently.

Risk factors for disordered cerebral autoregulation during hypothermic cardiopulmonary bypass

Disordered cerebral autoregulation during cardiopulmonary bypass (CPB) is regarded as one of the causes of neurological dysfunction after cardiac surgery. However, little documentation of risk factors associated with cerebral autoregulation during CPB has been reported. Sixty consecutive patients undergoing coronary artery bypass were classified into subgroups according to whether they had preoperative cerebrovascular disease (CVD), hypertension (HT), or diabetes (DM). Cerebral oxygenation was monitored by jugular venous bulb oxygen saturation (SjvO2) and near-infrared spectroscopy parameter (%Oxy-Hb) during the operation, and the relationships between these values and intraoperative parameters were evaluated. The results showed that SjvO2 and %Oxy-Hb in the CVD+group were lower than in the CVD-group. Multiple stepwise regression analysis on SjvO2 and %Oxy-Hb in the CVD+ group revealed that only MAP was a predictive factor and that there was a positive correlation between MAP and both SjvO2 and %Oxy-Hb (r=.651,r=.693, respectively,P 0.0001), and the correlation was stronger in patients without any risk factors (r=.671,P=0.0001). The results suggested that patients with CVD, HT, and DM may experience failure of cerebral pressureflow autoregulation and cerebrovascular reactivity during CPB.

Changes in jugular bulb oxygenation in patients undergoing warm coronary artery bypass surgery (34-37oC)

Imbalance between cerebral oxygen supply and demand is thought to play an important role in the development of cerebral injury during cardiac surgery with cardiopulmonary bypass. We studied jugular bulb oxygen saturation, jugular bulb oxygen tension, arterial-jugular bulb oxygen content difference and oxygen extraction ratio in 20 patients undergoing warm coronary artery bypass surgery (34-37 degrees C) with pH-stat blood gas management. Only two patients showed desaturation (jugular bulb oxygen saturation < 50%) at 5 min on bypass, and none from 20 min onwards. Multiple regression models were performed after using bypass temperature, mean arterial pressure, cerebral perfusion pressure, haemoglobin concentration and arterial carbon dioxide tension as independent variables, and arterial-jugular bulb oxygen content difference, jugular bulb oxygen saturation, oxygen extraction ratio and jugular bulb oxygen tension as individual dependent variables. We found that jugular bulb oxygen saturation, jugular bulb oxygen tension and oxygen extraction ratio are mainly dependent on arterial carbon dioxide tension, and arterial-jugular bulb oxygen content difference is dependent on arterial carbon dioxide tension and the bypass temperature. Our results suggest jugular bulb oxygenation is mainly dependent on arterial carbon dioxide tension during warm cardiopulmonary bypass.

Limits of Intermittent Jugular Bulb Oxygen Saturation Monitoring in the Management of Severe Head Trauma Patients

Limits of Intermittent Jugular Bulb Oxygen Saturation Monitoring in the Management of Severe Head Trauma Patients

Limits of Intermittent Jugular Bulb Oxygen Saturation Monitoring in the Management of Severe Head Trauma Patients

Limits of Intermittent Jugular Bulb Oxygen Saturation Monitoring in the Management of Severe Head Trauma Patients

Limits of Intermittent Jugular Bulb Oxygen Saturation Monitoring in the Management of Severe Head Trauma Patients

Limits of Intermittent Jugular Bulb Oxygen Saturation Monitoring in the Management of Severe Head Trauma Patients

Limits of Intermittent Jugular Bulb Oxygen Saturation Monitoring in the Management of Severe Head Trauma Patients

Limits of Intermittent Jugular Bulb Oxygen Saturation Monitoring in the Management of Severe Head Trauma Patients

Arterial and venous contributions to near-infrared cerebral oximetry.

Cerebral oximetry is a noninvasive bedside technology using near-infrared light to monitor cerebral oxygen saturation (Sco2) in an uncertain mixture of arteries, capillaries, and veins. The present study used frequency domain near-infrared spectroscopy to determine the ratio of arterial and venous blood monitored by cerebral oximetry during normoxia, hypoxia, and hypocapnia. Twenty anesthetized children aged < 8 yr with congenital heart disease of varying arterial oxygen saturation (Sao2) were studied during cardiac catheterization. Sco2, Sao2, and jugular bulb oxygen saturation (Sjo2) were measured by frequency domain near-infrared spectroscopy and blood oximetry at normocapnia room air, normocapnia 100% inspired O2, and hypocapnia room air. Among subject conditions, Sao2 ranged from 68% to 100%, Sjo2 from 27% to 96%, and Sco2 from 29% to 92%. Sco2 was significantly related to Sao2 (y = 0. 85 x -17, r = 0.47), Sjo2 (y = 0.77 x +13, r = 0.70), and the combination (Sco2 = 0.46 Sao2 + 0.56 Sjo2 - 17, R = 0.71). The arterial and venous contribution to cerebral oximetry was 16 +/- 21% and 84 +/- 21%, respectively (where Sco2 = alpha Sao2 + beta Sjo2 with alpha and beta being arterial and venous contributions). The contribution was similar among conditions but differed significantly among subjects (range, approximately 40:60 to approximately 0:100, arterial:venous). Cerebral oximetry monitors an arterial/venous ratio of 16:84, similar in normoxia, hypoxia, and hypocapnia. Because of biologic variation in cerebral arterial/venous ratios, use of a fixed ratio is not a good method to validate the technology.

Management of raised intracranial pressure in children.

Children suffer a significant number of head injuries as a result of their high activity levels, immature developmental skills and increased head-to-body mass ratio. Primary brain injury is irreversible, but secondary insults can be limited. Central to this is the management of raised intracranial pressure (ICP). The pathophysiology of head injury can explain some of the causes of raised ICP. Monitoring of ICP is important and this is closely linked to the maintenance of an adequate cerebral perfusion pressure and the importance of normovolaemia. Other interventions that have been shown to limit rises in ICP are appropriate use of positioning, mechanical ventilation and drug therapy. Less common therapies include jugular venous bulb oxygen saturation monitoring and the use of trometamol (THAM). Most nursing interventions do not actively reduce ICP, but they are central to its management. Reducing stimuli, avoiding cluster care, manual hyperinflation and limiting routine endotracheal suction may prevent an accumulative rise in ICP. Based on this literature review, it is possible to divide these interventions into first and second tier treatments, as shown in the protocol. Much of the suggested management will occur simultaneously, but it is important to assess the child's own response to each intervention and thus tailor treatment to minimize secondary brain injury.

Intracerebral steal phenomenon associated with global hyperemia in moyamoya disease during revascularization surgery.

The collateral vessels in moyamoya disease appear to retain their ability to constrict during hypocapnia but not to dilate during hypercapnia. It has been claimed that hypercapnia, as well as hypocapnia, decreases the blood flow in regions perfused by collateral vessels, presumably because of intracerebral steal. If this holds true, the decrease in blood flow may be proportional to the global hyperemia in the brain. To establish appropriate hemodynamic control during revascularization surgery, the authors monitored the jugular bulb oxygen saturation (SjO2) intraoperatively, a method that could sensitively detect global hyperemia. A total of 17 patients, most of whom presented with transient ischemic attacks or fluctuating neurological deficits, underwent intraoperative monitoring of their SjO2 and end-tidal carbon dioxide (ETCO2) after a state of anesthesia had been induced with isoflurane (Group 1) or propofol (Group 2). In eight of these patients, the regional cerebral blood flow (rCBF) of the collateral vessel territory was also monitored by laser Doppler flowmetry during the period of cortical exposure, and a total of 113 data sets (averaged values during 2.5-minute intervals) was collected. There was fluctuation in the ETCO2 levels ranging from 36 to 44 mm Hg. The mean SjO2 level was clearly greater (p < 0.01) in Group 1 (71.8 +/- 2.2%) than in Group 2 (63.3 +/- 2.1%). An episodic fall in rCBF was observed in association with a transient increase in SjO2. Such an event was not uncommon in Group 1 and there was a greater risk of rCBF decreasing when SjO2 exceeded a cutoff level of 76% (p < 0.01). This level could sometimes be reached at a broad range of ETCO2 readings (37-44 mm Hg). In Group 2, similar events sometimes occurred when SjO2 increased beyond 70%. However, this level could be reached only with a higher ETCO2 (42-44 mm Hg). The rCBF level was negatively correlated to SjO2 (p < 0.01), but not always to ETCO2, indicating that the episodic fall in rCBF was closely related to global hyperemia rather than the absolute level of hypercapnia. The observed association between a fall in rCBF and global hyperemia supports the intracerebral steal hypothesis and indicates that it is prudent to avoid excessive global hyperemia. The optimal range of CO2 for isoflurane is more restricted than that for propofol, presumably because isoflurane induces hyperemia by itself. Monitoring of SjO2 appears to represent the most practical technique for detecting global hyperemia as well as global ischemia, both of which may cause ischemic complications in moyamoya disease.

Jugular venous bulb oxygen saturation in patients with preexisting diabetes mellitus or stroke during normothermic cardiopulmonary bypass.

The authors hypothesized that patients with cerebrovascular abnormalities or metabolic disorders may experience abnormality in cerebral circulation more frequently than patients without these risks. The current study attempted to assess jugular venous bulb oxygen saturation (SjvO2) in patients with preexisting diabetes mellitus or stroke undergoing normothermic cardiopulmonary bypass. Thirty-nine patients undergoing elective coronary artery bypass graft surgery were studied, including 19 age-matched control patients, 10 diabetic patients, and 9 patients with preexisting stroke A 4.0-French fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to continuously monitor internal SjvO2. Hemodynamic parameters and arterial and jugular venous blood gases were measured at seven time points: (1) after the induction of anesthesia and before the start of surgery, (2) just after the beginning of cardiopulmonary bypass, (3) 20 min after the beginning of bypass, (4) 40 min after the beginning of bypass, (5) 60 min after the beginning of bypass, (6) just after the cessation of bypass, and (7) at the end of the operation. No significant differences were seen in mean arterial pressure, arterial carbon dioxide tension (PaCO2), or hemoglobin concentration among the three groups during the study. The SjvO2 value did not differ among the three groups after anesthesia induction and before surgery, just after the beginning of cardiopulmonary bypass, 60 min after the beginning of bypass, just after the end of bypass, or at the end of the operation. Significant differences between the control group and the diabetic and stroke groups were observed, however, at 20 min and 40 min after the beginning of bypass (at 20 min: control group 62.2 +/- 6.8%, diabetes group 48.4 +/- 5.1%, stroke group 45.9 +/- 6.3%; at 40 min: control group 62.6 +/- 5.2%, diabetes group 47.1 +/- 5.2%, stroke group 48.8 +/- 4.1% [values expressed as the mean +/- SD]; P < 0.05). Also, values in the diabetes and stroke groups were decreased at 20 min and 40 min after the beginning of bypass compared with before the start of surgery. A reduced SjvO2 value was observed more frequently in patients with preexisting diabetes mellitus or stroke during normothermic cardiopulmonary bypass. It is possible that cerebral circulation during normothermic bypass is altered in patients with risk factors for cerebrovascular disorder.

Effects of isoflurane, sevoflurane and propofol anaesthesia on jugular venous oxygen saturation in patients undergoing coronary artery bypass surgery

We investigated the effect of sevoflurane, isoflurane and propofol on jugular venous bulb oxygen saturation (SjO2) in 21 patients undergoing coronary artery bypass graft surgery (CABG) during and after normothermic cardiopulmonary bypass (CPB). Patients received a standardized anaesthetic consisting of fentanyl, midazolam and were then randomly allocated to receive either isoflurane, sevoflurane or propofol for maintenance. SjO2 values were significantly lower than baseline 1 h after CPB in the propofol but not the isoflurane or the sevoflurane groups. Furthermore, SjO2 values were significantly higher during CPB in the isoflurane group (P = 0.0081) and significantly lower 6 h after CPB in the sevoflurane group (P = 0.0447) when compared to the propofol group. We conclude that jugular venous desaturation during and after normothermic CPB is more likely during propofol anaesthesia.

Limits of Intermittent Jugular Bulb Oxygen Saturation Monitoring in the Management of Severe Head Trauma Patients

To evaluate, in a prospective, observational study, whether bilateral monitoring of jugular bulb oxyhemoglobin saturation (SjO2), in addition to standard monitoring, results in modification of the management of severe head trauma. The patients underwent bilateral jugular bulb cannulation and observation at 8-hour intervals, during which SjO2 was measured and the neurological condition and physiological variables were assessed. The study group was responsible for evaluating whether the physician's decision-making process was influenced by the detection of SjO2 abnormalities. The SjO2 discrepancy in simultaneous bilateral samples was also evaluated to determine whether it interfered with the interpretation of data and with clinical decision-making. The SjO2-related complications were monitored. Thirty patients underwent 319 observations. In 96% of patients, SjO2 was normal or high and had no influence on the diagnostic or therapeutic strategies. Treatment decisions were dictated by changes in clinical status and in intracranial and cerebral perfusion pressure. When these parameters were abnormal, treatment was administered, even if SjO2 was normal (101 observations). Conversely, when SjO2 was the only detected abnormality (34 observations), no treatment was administered. Abnormally low SjO2 values, caused by hypovolemia and hypocapnia, were detected in 3.4% of observations and actually modified the management. The discrepancies in simultaneous bilateral samples were substantial and gave rise to relevant interpretation problems. Fifteen percent of jugular catheters showed evidence of bacterial colonization. Intermittent SjO2 monitoring did not substantially influence the management of severe head trauma. Therefore, recommendation for its routine use in all patients seems inadvisable, and indications for this invasive method should no longer be defined on the basis of experts' opinions, but rather on randomized, prospective studies.

Cerebral blood flow and metabolism in severe brain injury: the role of pressure autoregulation during cerebral perfusion pressure management.

To ascertain if norepinephrine can be used as part of the cerebral perfusion pressure (CPP) management to increase arterial blood pressure (MAP) without causing cerebral hyperemia after severe head injury (HI). Prospective, interventional study. Intensive care unit in a university hospital. Twelve severely HI patients; median Glasgow Coma Scale was 6 (range 3-8). CPP management ( = 70 mmHg). Pressure autoregulation (assessed by norepinephrine infusion) was defined intact if % CPP/%CVR < or = 2. Cerebral blood flow (CBF: Xe133 inhalation technique), jugular bulb oxygen saturation (SjO2) and transcranial Doppler (TCD) were recorded during the test. Norepinephrine increased CPP by 33 % (+/- 4). Autoregulation was found to be intact in ten patients and defective in two. In the ten patients with preserved autoregulation, CBF decreased from 31 +/- 3 to 28 +/- 3 ml/ 100 g/min; in the two patients with impaired autoregulation CBF increased respectively from 16 to 35 and from 21 to 70 ml/100 g/min. SjO2 did not change significantly from baseline. TCD remained within the normal range. During CPP management norepinephrine can be used to increase MAP without potentiating hyperemia if pressure autoregulation is preserved. The assessment of pressure autoregulation should be considered as a guide for arterial pressure-oriented therapy after HI.

Monitorage de la saturation veineuse jugulaire en oxygène au cours d'un vasospasme cérébral sévère après hémorragie sous-arachnoïdienne

Jugular venous oximetry in a patient with severe cerebral vasospasm after subarachnoid haemorrhage. Cerebral arterial vasospasm is a major complication of aneurysmal subarachnoid haemorrhage. The conventional treatment of this complication includes haemodilution, hypervolaemia, arterial hypertension and nimodipine. Some patients do not respond to this therapy and require an intra-arterial infusion of papaverine and/or a cerebral angioplasty. Transcranial Doppler detects cerebral vasospasm. However it does not provide an accurate metabolic information on the ischaemic status of the cerebral tissue. This article describes the monitoring of jugular venous bulb oxygen saturation to obtain a real time information on the metabolic effect of cerebral vasospasm and its variations after intra-arterial infusion of papaverine.