Elevated Jugular Venous Oxygen Saturation
Elevated Jugular Venous Oxygen Saturation
Object. The aim of this study was to investigate the incidence of elevated (
75%) jugular venous oxygen saturation (SjvO 2) and its relationship to cerebral hemodynamic and metabolic parameters and to outcome after severe head injury.
Methods. Data from 450 severely head injured patients admitted to the Neurosurgical Intensive Care Unit of Ben Taub General Hospital were analyzed retrospectively. The SjvO 2 was measured in blood obtained from indwelling jugular bulb catheters. Patients were classified into the following categories: high (Group I), normal (Group II), or low SjvO 2 (Group III) if their mean SjvO 2 over the duration of monitoring was 75% or higher, 74 to 56%, or 55% or lower, respectively. A high SjvO 2 occurred in 19.1% of patients. There was no consistent relationship between SjvO 2 and simultaneous cerebral blood flow (CBF) or cerebral perfusion pressure measurements. Compared with Groups II and III, the patients in Group I had a significantly higher CBF and lower cerebral metabolic rate of oxygen (CMRO 2). In Group I, the outcomes were death or persistent vegetative state in 48.8% of patients and severe disability in 25.6%. These outcomes were significantly worse than for patients in Group II. Within Group I, the patients with a poor neurological outcome were older and more likely to have suffered a focal head injury; they demonstrated a lower CMRO 2 and a greater rate of cerebral lactate production than the patients who attained a favorable outcome.
Conclusions. Posttraumatic elevation of SjvO 2 is common but cannot be automatically equated with hyperemia. Instead, elevated SjvO 2 is a heterogeneous condition that is associated with poor outcome after head injury and may carry important implications for the management of comatose patients.
JUGULAR venous oxygen saturation (SjvO2) reflects the balance between cerebral oxygen delivery and the cerebral metabolic rate of oxygen (CMRO2), if arterial oxyhemoglobin saturation, hemoglobin concentration, and the hemoglobin dissociation curve remain constant. Any disturbance that increases CMRO2 or decreases oxygen delivery may decrease SjvO2. Conversely, a disorder that decreases CMRO2 or increases oxygen delivery may increase SjvO2.
Low SjvO2 reliably indicates cerebral hypoperfusion or ischemia. In contrast, there are several possible causes of elevated SjvO2, the elucidation of which may be difficult without concomitant measurements of regional and/or global cerebral blood flow (CBF). Focal cerebral ischemia may occur in the presence of a normal or elevated SjvO2 if the involved area of the brain is small or if the reduced oxygen saturation from the ischemic brain is offset by a high oxygen saturation from surrounding hyperemic brain. Dysoxia (defined as oxygen-limited cytochrome turnover) and/or restricted oxygen diffusion from the erythrocytes to the mitochondria can also result in a normal or elevated SjvO2. In some cases, measured values of cerebral oxygen extraction and CMRO2 do not accurately reflect neural metabolic demands, and cerebral ischemic damage could occur despite a superabundant supply of oxygen to the brain. Although oxygen delivery and oxygen consumption are measurable, the true metabolic requirements of the cells, the "oxygen demand," cannot be determined.
The anatomy of the jugular venous system may also play a role in generating high SjvO2 values. The internal jugular vein chosen for monitoring (right or left) may affect the values obtained for SjvO2. More important, when CBF is globally low, extracerebral contamination of blood in the jugular bulb may be significant and may contribute to an increase in the value obtained for SjvO2. Rapid drawing of the blood sample through the catheter (rates . 2 ml/minute) has been another source of artifactual increases in SjvO2.
The purpose of this study was to investigate the incidence of SjvO2 values above the upper limit of normal (
75%) in severely head injured patients and to relate these elevated values to measurements of global CBF and metabolism and also to clinical outcome.
Object. The aim of this study was to investigate the incidence of elevated (
75%) jugular venous oxygen saturation (SjvO 2) and its relationship to cerebral hemodynamic and metabolic parameters and to outcome after severe head injury.
Methods. Data from 450 severely head injured patients admitted to the Neurosurgical Intensive Care Unit of Ben Taub General Hospital were analyzed retrospectively. The SjvO 2 was measured in blood obtained from indwelling jugular bulb catheters. Patients were classified into the following categories: high (Group I), normal (Group II), or low SjvO 2 (Group III) if their mean SjvO 2 over the duration of monitoring was 75% or higher, 74 to 56%, or 55% or lower, respectively. A high SjvO 2 occurred in 19.1% of patients. There was no consistent relationship between SjvO 2 and simultaneous cerebral blood flow (CBF) or cerebral perfusion pressure measurements. Compared with Groups II and III, the patients in Group I had a significantly higher CBF and lower cerebral metabolic rate of oxygen (CMRO 2). In Group I, the outcomes were death or persistent vegetative state in 48.8% of patients and severe disability in 25.6%. These outcomes were significantly worse than for patients in Group II. Within Group I, the patients with a poor neurological outcome were older and more likely to have suffered a focal head injury; they demonstrated a lower CMRO 2 and a greater rate of cerebral lactate production than the patients who attained a favorable outcome.
Conclusions. Posttraumatic elevation of SjvO 2 is common but cannot be automatically equated with hyperemia. Instead, elevated SjvO 2 is a heterogeneous condition that is associated with poor outcome after head injury and may carry important implications for the management of comatose patients.
JUGULAR venous oxygen saturation (SjvO2) reflects the balance between cerebral oxygen delivery and the cerebral metabolic rate of oxygen (CMRO2), if arterial oxyhemoglobin saturation, hemoglobin concentration, and the hemoglobin dissociation curve remain constant. Any disturbance that increases CMRO2 or decreases oxygen delivery may decrease SjvO2. Conversely, a disorder that decreases CMRO2 or increases oxygen delivery may increase SjvO2.
Low SjvO2 reliably indicates cerebral hypoperfusion or ischemia. In contrast, there are several possible causes of elevated SjvO2, the elucidation of which may be difficult without concomitant measurements of regional and/or global cerebral blood flow (CBF). Focal cerebral ischemia may occur in the presence of a normal or elevated SjvO2 if the involved area of the brain is small or if the reduced oxygen saturation from the ischemic brain is offset by a high oxygen saturation from surrounding hyperemic brain. Dysoxia (defined as oxygen-limited cytochrome turnover) and/or restricted oxygen diffusion from the erythrocytes to the mitochondria can also result in a normal or elevated SjvO2. In some cases, measured values of cerebral oxygen extraction and CMRO2 do not accurately reflect neural metabolic demands, and cerebral ischemic damage could occur despite a superabundant supply of oxygen to the brain. Although oxygen delivery and oxygen consumption are measurable, the true metabolic requirements of the cells, the "oxygen demand," cannot be determined.
The anatomy of the jugular venous system may also play a role in generating high SjvO2 values. The internal jugular vein chosen for monitoring (right or left) may affect the values obtained for SjvO2. More important, when CBF is globally low, extracerebral contamination of blood in the jugular bulb may be significant and may contribute to an increase in the value obtained for SjvO2. Rapid drawing of the blood sample through the catheter (rates . 2 ml/minute) has been another source of artifactual increases in SjvO2.
The purpose of this study was to investigate the incidence of SjvO2 values above the upper limit of normal (
75%) in severely head injured patients and to relate these elevated values to measurements of global CBF and metabolism and also to clinical outcome.
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