Jugular Venous Saturation Research Articles

Effect of hyperventilation on cerebral blood flow in traumatic head injury: clinical relevance and monitoring correlates.

To investigate the effect of hyperventilation on cerebral blood flow in traumatic brain injury. A prospective interventional study. A specialist neurocritical care unit. Fourteen healthy volunteers and 33 patients within 7 days of closed head injury. All subjects underwent positron emission tomography imaging of cerebral blood flow. In patients, PaCO2 was reduced from 36 +/- 1 to 29 +/- 1 torr (4.8 +/- 0.1 to 3.9 +/- 0.1 kPa) and measurements repeated. Jugular venous saturation (SjvO2 ) and arteriovenous oxygen content differences (AVDO2 ) were monitored in 25 patients and values related to positron emission tomography variables. The volumes of critically hypoperfused and hyperperfused brain (HypoBV and HyperBV, in milliliters) were calculated based on thresholds of 10 and 55 mL.100g(-1).min(-1), respectively. Whereas baseline HypoBV was significantly higher in patients ( p<.05), baseline HyperBV was similar to values in healthy volunteers. Hyperventilation resulted in increases in cerebral perfusion pressure (p <.0001) and reductions in intracranial pressure (p <.001), whereas SjvO2 (>50%) and AVDO2 (<9 mL/mL) did not exceed global ischemic thresholds. However, despite these beneficial effects, hyperventilation shifted the cerebral blood flow distribution curve toward the hypoperfused range, with a decrease in global cerebral blood flow (31 +/- 1 to 23 +/- 1 mL.100g(-1).min(-1); p<.0001) and an increase in HypoBV (22 [1-141] to 51 [2-428] mL; p<.0001). Hyperventilation-induced increases in HypoBV were apparently nonlinear, with a threshold value between 34 and 38 torr (4.5-5 kPa). Hyperventilation increases the volume of severely hypoperfused tissue within the injured brain, despite improvements in cerebral perfusion pressure and intracranial pressure. Significant hyperperfusion is uncommon, even at a time when conventional clinical management includes a role for modest hyperventilation. These reductions in regional cerebral perfusion are not associated with ischemia, as defined by global monitors of oxygenation, but may represent regions of potentially ischemic brain tissue.

Increasing Mean Arterial Blood Pressure Has No Effect on Jugular Venous Oxygen Saturation in Insulin-Dependent Patients During Tepid Cardiopulmonary Bypass

Preexisting diabetes mellitus is one of the major factors related to adverse postoperative neurological disorders after cardiac surgery. In previous reports, we found that diabetic patients more often experienced cerebral desaturation than nondiabetic patients during normothermic cardiopulmonary bypass (CPB). The purpose of this study was to examine the effects of increasing mean arterial blood pressure (MAP) by the administration of phenylephrine on internal jugular venous oxygen hemoglobin saturation (Sjvo2) during tepid CPB in diabetic patients. We studied 20 diabetic patients scheduled for elective coronary artery bypass graft surgery and, as a control, 20 age-matched nondiabetic patients. After the induction of anesthesia, a fiberoptic oximetry catheter was inserted into the right jugular bulb to monitor Sjvo2. After measuring the baseline partial pressure of the arterial and jugular venous blood gases and cardiovascular hemodynamic values, MAP was increased by the repeated administration of a 10-μg bolus of phenylephrine until it reached 100% of baseline values. There was a significant difference in Sjvo2 value between the Diabetic and Control groups after the administration of phenylephrine (Diabetic group, 56% ± 6%; Control group: 60% ± 4%) (P < 0.05). There was a significant difference in the arterial-jugular oxygen content difference value between the Diabetic and Control groups after the administration of phenylephrine (diabetic group, 4.9% ± 0.6%; Control group, 4.5% ± 0.4%) (P < 0.05). We subdivided the Diabetic group into three groups (Diet Therapy group [n = 4], Glibenclamide group [n = 10], and Insulin-Dependent group [n = 6]). There was a significant difference in the mean slopes of Sjvo2 versus cerebral perfusion pressure for increasing cerebral perfusion pressure between the Insulin-Dependent group and the other groups (Dunnett test:P = 0.04). Increasing MAP had no effects on the Sjvo2 value in insulin-dependent patients during tepid CPB.

Slow Rewarming Has No Effects on the Decrease in Jugular Venous Oxygen Hemoglobin Saturation and Long-Term Cognitive Outcome in Diabetic Patients

The purpose of this study was to examine the effects of rewarming rate on internal jugular venous oxygen hemoglobin saturation (Sjvo2) during the rewarming period, and long-term cognitive outcome in diabetic patients. We studied 30 diabetic patients scheduled for elective coronary artery bypass graft surgery. As a control, 30 age-matched nondiabetic patients were identified. The diabetic patients were randomly divided into two groups: the Slow Rewarming group (n = 15) (mean rewarming speed: 0.22° ± 0.07°C/min, mean ± sd) or the Standard Rewarming group (Standard group) (n = 15) (mean rewarming speed: 0.46° ± 0.09°C/min, mean ± sd). After the induction of anesthesia, a fiberoptic oximetry catheter was inserted into the right jugular bulb to monitor Sjvo2 continuously. Hemodynamic variables and arterial and jugular venous blood gases were measured at nine time points. All patients underwent a battery of neurologic and neuropsychologic tests on the day before the operation and at 4 mo after surgery. The Sjvo2 values in the Standard group were decreased during the rewarming period compared with at the induction of anesthesia (P < 0.05). There was a significant difference in the Sjvo2 value in the Control group between standard rewarming and slow rewarming during rewarming periods (Standard Control group: 51% ± 8%, Slow Control groups: 58% ± 5%) (P < 0.05). However, there was no difference in the Sjvo2 value in diabetic patients between standard rewarming and slow rewarming during the rewarming period. The rewarming rates (odds ratio: 0.8; 95% confidence interval: 0.5–1.3;P = 0.6) had no correlation with cognitive impairment at 4 mo after the surgery. Diabetes (odds ratio: 1.6; 95% confidence interval: 0.9–2.6;P = 0.04) was a factor in relation to cognitive impairment at 4 mo after the surgery. We concluded that a slow rewarming rate had no effects on the reduction in Sjvo2 value and long-term cognitive outcome in diabetic patients.

Effects of Increasing FiO2 on Venous Saturation During Cardiopulmonary Bypass in the Swine Model

Adequacy of perfusion during cardiopulmonary bypass (CPB) is dependent on nutrient delivery and waste removal from the tissue. A recent study showed that over 75% of cardiopulmonary bypass procedures are completed using continuous venous saturation (SvO2) monitoring. The purpose of this study was to determine the effect of changing FiO2 concentration on SvO2. A total of eight mixed gender 45-kg swine were placed on CPB under moderate hypothermic conditions. Animals were divided evenly into two groups: Experimental, where FiO2 was increased to 100% and blood flow decreased to an SvO2 level of prechange in FiO2, and Control, where the same condition was created except no change in blood flow. Variables measured include hemodynamic, blood gas, intramyocardial pH, and lactic acid concentrations. In the experimental group, percentage change of blood flow was decreased from baseline 28.4% ± 12.5% (p &lt; .005) as well as percentage change of oxygen delivery 23.9% ± 14.7% (p &lt; .005). Systemic venous saturation percentage change was increased in both the experimental 14.4% ± 6.8% (p &lt; .05) and control 11.2% ± 7.1% (p &lt; .05) groups. Jugular venous saturation percentage change was decreased in the experimental group 7.8% ± 6.34% (p &lt; .02), but not in the control animals. Myocardial venous saturation percentage change decreased in the experimental group to 3.73% ± 8.34% (p &lt; .004). Experimental manipulation, however, did not significantly change jugular lactic acid concentrations or intramyocardial pH values. In conclusion, these results suggest that decreased blood flow adjusting for increased SvO2associated with high PaO2 did not result in significant reduction of adequacy of perfusion markers for organs studied.

Invited commentary

Invited commentary

Reduction of cerebral hyperemia with anti-hypertensive medication after electroconvulsive therapy.

Several different anti-hypertensive regimens have been introduced for the prevention of systemic hyperdynamic responses after electrically induced seizures. In the present study, the effects of anti-hypertensive medications on cerebral circulation were studied. Systemic blood pressure was controlled by several anti-hypertensive medications, nicardipine, prostaglandin EI, alprenolol and nitroglycerin, in 30 patients (150 electroconvulsive therapy trials). Changes in cerebral blood flow velocity were measured by transcranial Doppler sonography of the right middle cerebral artery from the start of anesthesia to 10 min after the electrical shock. Administration of a Ca2+ antagonist, nicardipine, or prostaglandin EI did not alter the augmented cerebral blood flow velocity after the seizure. However, a beta-adrenergic blocking agent, alprenolol (P<0.05) or nitroglycerin (P<0.01) partially inhibited the increase in cerebral blood flow velocity. Maximal blood flow velocity was 133% larger than the pre-anesthesia value in the control group, 109% in the nicardipine group, 113% in the prostaglandin EI group, 72% in the alprenolol group, and 45% in the nitroglycerin group, respectively. The increase in cerebral blood flow velocity after electrically induced seizure was independent of systemic blood pressure. Internal jugular venous saturation (SjO2) was increased, and difference in arterial and venous concentrations of lactate was not altered in all groups. Cerebral hemodynamics is altered by ECT, even when systemic hemodynamics are stabilized by antihypertensive medication. Although the effects of antihypertensive medicine on cerebral hemodynamics are variable, systemic blood pressure control by these agents does not induce cerebral ischemia after ECT.

Relationship between intracranial pressure, mild hypothermia and temperature-corrected PaCO2 in patients with traumatic brain injury.

To study the effects of mild hypothermia and associated changes in temperature-corrected PaCO2 (cPaCO2) on intracranial pressure (ICP), mean velocity of the middle cerebral artery (Vm), and venous jugular saturation in O2 (SjvO2) in patients with severe traumatic brain injury (TBI). Prospective, observational study. Intensive care unit. Severe TBI patients mechanically ventilated, sedated and paralyzed. Twenty patients were subjected to four consecutive periods: (a) normocapnia-normothermia; (b) hypocapnia-normothermia, where hypocapnia was induced by an increase in minute volume; (c) hypocapnia-hypothermia, where hypocapnia was induced by hypothermia maintaining the ventilatory settings constant; (d) normocapnia-hypothermia, where normocapnia was achieved by a decrease in minute volume. cPaCO2 was 41 +/- 8 mmHg in periods 1 and 4, and 31 +/- 7 mmHg in periods 2 and 3. Core temperature was 37.1 +/- 0.8 degrees C in periods 1 and 2, and 34.1 +/- 1.1 degrees C in periods 3 and 4. End-tidal CO2 and cPaCO2 values showed no difference between periods 1 and 4 and periods 2 and 3. ICP and Vm were dependent on cPaCO2 but independent of core temperature values. SjvO2 was related to cPaCO2 and was significantly higher during period 3 than during period 2 (P < 0.05). The decrease in ICP was similar when hypocapnia was induced by hyperventilation or as a result of hypothermia alone. The relationship between cPaCO2 and ICP might predict variations in ICP during changes in core temperature. Further studies are needed to confirm the cerebral metabolic effects of moderate hypothermia in TBI patients.

Indomethacin: its role in the management of intractable intracranial pressure (ICP) after severe head injury

Intracranial hypertension that fails to respond to first line medical and surgical treatment after head injury is associated with a 92% mortality overall.1 The addition of barbiturates will result in a good or moderate neurological outcome in 35% of patients,2 but those with hyperaemia do significantly worse. However barbiturates may not be a logical choice for those patients whose intracranial hypertension is secondary to hyperaemia, and may be associated with significant complications. In these patients cerebral vasoconstrictors such as indomethacin may be more appropriate and possibly associated with fewer unwanted effects. In one study six out of 10 patients who received indomethacin for intracranial hypertension unresponsive to barbiturates survived.3 However it is unclear how many were hyperaemic since jugular venous saturation (SjO2) was not monitored. We report our experience with indomethacin in 10 severely head-injured patients. Our protocol aims to maintain a target cerebral perfusion pressure (CPP) and ICP through the application of sedation, diuretics, CSF drainage, mild hypothermia, muscle relaxation and control of arterial carbon dioxide (PaCO2). If the ICP remains elevated thenSjO2 is monitored. The combination of raised ICP andSjO2 is taken to indicate hyperaemia (absolute or relative). In these circumstances the patient is hyperventilated to aPaCO2 of 28 mmHg and if necessary an intravenous infusion of thiopentone commenced. We used indomethacin infusions in 10 patients fulfilling these criteria of hyperaemia. In seven patients the hyperaemia was confirmed as absolute by demonstrating a raised middle cerebral artery velocity (MCAV) with transcranial Doppler. The mean age of the patients was 21.2 yr (range 8–55). Indomethacin was infused for a mean of 3.8 days (1–11) at a rate of 3–11 mg h−1. The effect of indomethacin on mean (SD) ICP, CPP andSjO2 is shown in Table 4. At 6-month follow up there were seven survivors (three good recovery, three moderate recovery, one severely disabled). Three patients died with intractable ICP and septic shock. Two of these patients had associated renal failure. There were no episodes of gastrointestinal bleeding. Two of the three patients who died did not have MCAV measured, and therefore indomethacin may not have been strictly indicated. These results achieved in this subgroup of head injured patients is much better than that expected, and matches the outcome achieved in the overall ICU head injury population. Indomethacin may have a role in the management of raised ICP associated with hyperaemia after severe head injury. We recommend however that it should only be used with monitoring of bothSjO2 and MCAV.

Biologically variable pulsation improves jugular venous oxygen saturation during rewarming

Background. Conventional pulsatile (CP) roller pump cardiopulmonary bypass (CPB) was compared to computer controlled biologically variable pulsatile (BVP) bypass designed to return beat-to-beat variability in rate and pressure with superimposed respiratory rhythms. Jugular venous O2 saturation (SjvO2) below 50% during rewarming from hypothermia was compared for the two bypass techniques. A SjvO2 less than 50% during rewarming is correlated with cognitive dysfunction in humans.Methods. Pigs were placed on CPB for 3 hours using a membrane oxygenator with α-stat acid base management and arterial filtration. After apulsatile normothermic CPB was initiated, animals were randomized to CP (n = 8) or BVP (roller pump speed adjusted by an average of 2.9 voltage output modulations/second; n = 8), then cooled to a nasopharyngeal temperature of 28°C. During rewarming to stable normothermia, SjvO2 was measured at 5 minute intervals. The mean and cumulative area for SjvO2 less than 50% was determined.Results. No between group difference in temperature existed during hypothermic CPB or during rewarming. Mean arterial pressure, arterial partial pressure O2, and arterial partial pressure CO2 did not differ between groups. The hemoglobin concentration was within 0.4 g/dL between groups at all time periods. The range of systolic pressure was greater with BVP (41 ± 18 mm Hg) than with CP (12 ± 4 mm Hg). A greater mean and cumulative area under the curve for SjvO2 less than 50% was seen with CP (82 ± 96 versus 3.6% ± 7.3% · min, p = 0.004; and 983 ± 1158 versus 42% ± 87% · min; p = 0.004, Wilcoxon 2-sample test).Conclusions. Computer-controlled BVP resulted in significantly greater SjvO2 during rewarming from hypothermic CPB. Both mean and cumulative area under the curve for SjvO2 less than 50% exceeded a ratio of 20 to 1 for CP versus BVP. Cerebral oxygenation is better preserved during rewarming from moderate hypothermia with bypass that returns biological variability to the flow pattern.

Estimation of jugular venous O2 saturation from cerebral oximetry or arterial O2 saturation during isocapnic hypoxia.

Near-infrared spectroscopy (NIRS) has the potential for providing valuable information about oxygen delivery to the brain. However, questions have been raised about the accuracy of these measurements. This study was undertaken to compare noninvasive cerebral saturation measurements to jugular venous saturation under conditions of hypoxia and hypercapnia. Data was obtain on forty-two subjects. Cerebral oxygenation was measured with a Somanetics INVOS 4100-SSA placed on the forehead of the subjects. PETCO2 was controlled to approximately 2 and 7 mmHg above resting values and PETO2 was controlled to 80, 45, 60 and 41 mmHg consecutively for four of five minutes each. Internal jugular blood gas measurements were made via a retrograde catheter. Both the cerebral oximetry measured saturation (rSO2) and the jugular venous saturation (SjvO2) were significantly increased by increasing the PETCO2 at all levels of hypoxia. The increase in the rSO2 was less than the increase in SjvO2. The rSO2 had a bias of 5.2% and a precision of 10.7% compared to the measured SjvO2. Cerebral oxygen saturation measured by cerebral oximetry compares well to the measured SjvO2 in normal subjects, despite multiple physiological reasons for differences. The closer relationship of SjvO2 to rSO2 than SaO2 under the conditions of these experiments indicates that the measurement reflects primarily intracranial saturation. However, outcome studies under clinical conditions are needed to determine the clinical utility of cerebral oximetry.

Influence of cardiopulmonary bypass temperature on circulatory pathophysiology and clinical outcomes.

This study was designed to investigate the effects of cardiopulmonary bypass (CPB) perfusion temperature. Forty-four patients who had undergone elective coronary bypass surgery were randomly divided into 2 groups (22 patients each) according to their perfusion temperature (N group=36 degrees C; L group=30 degrees C). The concentrations of endogenous catecholamines, complements, elastase, serotonin, arachidonic acid metabolites and endothelin underwent various changes throughout the CPB but did not exhibit any statistical differences in either group. None of the substances measured correlated with systemic vascular resistance at any time. The temperature of the perfusion appears to be a major determinant of vascular tone. The postoperative PO2 was better, and postoperative pulmonary vascular resistance lower in the N group (p<0.05), most likely because of a much larger water balance during hypothermic CPB (p<0.01). The postoperative blood loss was statistically less in the N group (p<0.05). Although apparent brain damage, evidenced by the leakage of creatine kinase-BB, was not seen, the jugular bulb venous hemoglobin saturation levels (<50% in 27% of the N group, p<0.05) and higher lactate levels suggested that normothermic perfusion was relatively disadvantageous. It is concluded that normothermic CPB was relatively safe and advantageous with regard to hemostasis and pulmonary function.

Burst suppression or isoelectric encephalogram for cerebral protection: evidence from metabolic suppression studies

Metabolic suppression may have a role in cerebral protection. It is often assumed that the cerebral metabolic and protective effects of qualitative burst suppression are similar to those of the isoelectric encephalogram (EEG). We have examined the effect of different degrees of EEG suppression on blood flow and oxygen difference during general anaesthesia. We studied 11 patients undergoing general anaesthesia for resection of acoustic neuromas. The study was performed after surgery with propofol and remifentanil anaesthesia. Transcranial Doppler ultrasonography and jugular bulb venous saturations were measured at values of EEG suppression: 0%, 50% and 100% (isoelectric EEG). Data from nine patients were suitable for analysis. There were no significant differences in mean arterial pressure, heart rate or PaCO2 during EEG activity, 50% burst suppression ratio or isoelectric EEG. There was a significant decrease in middle cerebral artery flow velocity (vmca) with increasing EEG suppression (0% suppression, mean 38 (SEM 4) cm s-1; 50% suppression, 29 (3) cm s-1; and 100% suppression, 24 (2) cm s-1; P < 0.05). Jugular bulb venous saturations did not change consistently with the change in EEG activity, indicating intact flow-metabolism coupling. We conclude that the degree of EEG suppression had a significant effect on blood flow. If flow-metabolism coupling is maintained, the assumption that cerebral metabolism during 50% EEG burst suppression is equivalent to isoelectric EEG may not be justified. If cerebral protection is related to brain metabolism, then an isoelectric EEG may give more cerebral protection than 50% burst suppression.

Balloon pump–induced pulsatile perfusion during cardiopulmonary bypass does not improve brain oxygenation

Background: Whether pulsatile flow offers substantial advantages for brain protection during cardiopulmonary bypass is controversial. The purpose of this study is to determine whether differences exist between pulsatile and nonpulsatile bypass concerning the effects on internal jugular venous saturation and on the state of regional cerebral oxygenation during normothermia. Methods: Twenty-two patients undergoing elective coronary artery bypass grafting were randomly divided into 2 groups: group 1 (n = 11) received nonpulsatile perfusion during cardiopulmonary bypass and group 2 (n = 11) received pulsatile perfusion during bypass. We used an intra-aortic balloon pump to generate pulsatility. A spectrophotometric probe (INVOS 3100R, Somanetics, Troy, Mich) was used to assess the state of regional cerebral oxygenation. A 4F fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to monitor jugular venous oxygen saturation. Hemodynamic variables, arterial and jugular venous blood gases, and regional cerebral oxygenation were measured at 7 times points. Results: In both groups, jugular venous oxygen saturation decreased at the early stage of the cardiopulmonary bypass ( P = .03). Five patients in group 1 and 6 in group 2 had a jugular venous oxygen saturation of less than 50%. In both groups, the regional cerebral oxygenation value decreased during cardiopulmonary bypass ( P = .04). Conclusions: The present results showed that pulsatility generated through the use of intra-aortic balloon pumping did not produce any beneficial effects on jugular venous oxygen saturation and regional cerebral oxygenation at normothermia. (J Thorac Cardiovasc Surg 1999;118:361-6)

Jugular Bulb Oxygen Saturation During Propofol and Isoflurane/Nitrous Oxide Anesthesia in Patients Undergoing Brain Tumor Surgery

We investigated, in brain tumor patients, the jugular bulb venous oxygen partial pressure (PjO2) and hemoglobin saturation (SjO2), the arterial to jugular bulb venous oxygen content difference (AJDO2), and middle cerebral artery blood flow velocity (Vmca) during anesthesia, and the effect of hyperventilation on these variables.Twenty patients were randomized to receive either isoflurane/nitrous oxide/fentanyl (Group 1) or propofol/fentanyl (Group 2). At normoventilation (PaCO2 35 +/- 2 mm Hg in Group 1 and 33 +/- 3 mm Hg in Group 2), SjO2 and PjO2 were significantly higher in Group 1 than in Group 2 (SjO2 60% +/- 6% and 49% +/- 13%, respectively; P = 0.019) (PjO2 32 +/- 3 and 27 +/- 5 mm Hg, respectively; P = 0.027). In Group 2, 5 of 10 patients had SjO2 <50%, and 3 of these patients had SjO2 <40% and AJDO2 >9 mL/dL. All patients in Group 1 had SjO2 >50%. During hyperventilation, there were no differences in SjO2, PjO2, or AJDO2 between the two groups. On hyperventilation, there was no correlation between the relative decreases of Vmca and 1/AJDO2 (r = 0.21, P = 0.41). The results indicate during propofol anesthesia, half of the brain tumor patients showed signs of cerebral hypoperfusion, but not during isoflurane/nitrous oxide anesthesia. Furthermore, during PaCO2 manipulations, shifts in Vmca are inadequate to evaluate brain oxygen delivery in these patients. Implications: During propofol anesthesia at normoventilation, 50% of brain tumor patients showed signs suggesting cerebral hypoperfusion, but this could not be demonstrated during isoflurane/nitrous oxide anesthesia. During PaCO (2) manipulations, consecutive measurements of the cerebral blood flow velocity may be inadequate to assess cerebral oxygenation. (Anesth Analg 1999;89:358-63)

Improving Neurologic Outcome after Cardiac Surgery

Improving Neurologic Outcome after Cardiac Surgery

Central Nervous System Metabolic and Physiologic Effects of Laparoscopy

We set out to determine whether the increases in intracranial pressure (ICP) associated with CO2 insufflation had any metabolic effect on the central nervous system in a head injury when compared with gasless laparoscopy (GL). To test this hypothesis, we looked at both the ICP and jugular bulb venous saturation (JVS), with and without a coexisting cerebral mass lesion. Twenty-five kilogram male pigs had tracheostomy, epidural balloon, pulmonary arterial catheter, arterial line, and jugular bulb catheter placed. Intravenous Pentobarbital was used for anesthesia. Either CO2 laparoscopy (CL; n=7) or GL (n=7) were performed both with and without an epidural balloon inflated to a baseline ICP of 25. Data were analyzed using the Student's t test with a P value <0.05 being significant. Cerebral perfusion pressure and most hemodynamic values did not differ. Both central venous pressure and peak inspiratory pressure were significantly elevated whenever CO2 insufflation took place, reflecting an increased intrathoracic pressure. When comparing both study groups, the partial pressure of CO2 did not differ. CL increases ICP significantly above the gasless group in our head injury model. This is most likely secondary to increased intrathoracic pressure. The question still remains whether these changes are clinically significant. We could not demonstrate significant metabolic effects secondary to laparoscopy. In patients suffering head injury, GL rather than CL might be safer to avoid ICP elevation. Additional studies looking at central nervous system metabolic and objective histopathologic effects should be undertaken with larger numbers of study animals.

A lesson learned from jugular venous oximetry

The authors describe the case of a severely head injured patient whose profound cerebral infarction was clearly indicated by prolonged desaturation on jugular venous oximetry. Shortly thereafter jugular venous oxygen saturation returned to normal stable values and measured within normal limits for the next 24 h. As demonstrated by a computed tomography (CT) scan, these values appear to have represented a jugular mixture of significant amount of cerebral blood that had passed through infarcted tissue and remained highly saturated. This is a very graphic example of the misleading influence that regional flow-metabolic inhomogeneities can have on jugular venous saturation and it emphasizes that cerebral ischemia can be easily missed if no information on cerebral blood flow or regional metabolism is available.

Should Induced Hypertension Be Beneficial After Traumatic Brain Injury?

Should Induced Hypertension Be Beneficial After Traumatic Brain Injury?

The Calibration and Validation of a Phase-modulated Near-infrared Cerebral Oximeter

Objective. This study was undertaken to compare the cerebral oxygenation measured by an experimental phase-modulated near-infrared (NIR) spectroscopy system with capillary saturation estimated from jugular venous oxygen saturation. Methods. Jugular venous catheters were placed in 30 patients undergoing carotid endarterectomy and 194 measurements of venous oxygen saturation were obtained intra operatively. Simultaneous measurement of optical path length at 754, 785, and 816 nm was performed using a phase-modulated near-infrared spectroscopy system. Optical calibration was performed using both an optical bench and a scattering mold. Hemoglobin saturation was calculated from NIR measurements using equations derived from diffusion theory. Capillary saturation was calculated from the arterial and venous saturations. Results. Jugular venous saturations ranged from 41 to 92%. When calibrated using the optical bench, the NIR estimates of hemoglobin saturation deviated from estimated capillary values by an average of 2.6% bias and 4.3% deviation. No systematic bias was noted. NIR values derived from mold calibration were less accurate and precise (4.6% bias and 6.9% deviation.) Use of the initial venous sample as an in vivocalibration improved the accuracy of the mold calibration but did not alter the performance of the bench calibration. Conclusions. Under the conditions tested, an experimental phase-modulated near-infrared spectroscopy system calibrated using an optical bench agreed with capillary saturation estimated from jugular venous samples. Further work is necessary to demonstrate valid performance of the system under other conditions.

Jugular venous desaturation following cardiac surgery

Twenty-two patients undergoing coronary artery bypass surgery underwent postoperative measurement and recording of jugular venous oxyhaemoglobin saturation (SjO2) with desaturation defined as a value of less than 50% for 5 min or longer. Fifteen of the 22 patients monitored experienced desaturations. An average of four episodes were experienced by those 15 patients (range 1-14). The mean duration of a single episode was 46 (range 5-212) min whilst mean total duration of desaturation was 175 (range 5-570) min. The mean duration of desaturation in the 15 patients, expressed as a percentage of monitored time, was 21.1% (range 0.58%-61.96%). SjO2 desaturation, possibly indicating cerebral hypoperfusion, occurs in the early post-operative period following cardiac surgery.