jugular vein asymmetry

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

jugular vein asymmetry

Postby Cece » Sun Jul 31, 2011 8:16 pm

Anaesthesia. 1998 Jul;53(7):627-33.

Anatomical variation of cerebral venous drainage: the theoretical effect on jugular bulb blood samples.

Beards SC, Yule S, Kassner A, Jackson A.

SourceIntensive Care Unit, Withington Hospital, South Manchester University Hospitals Trust, UK.

Recent studies have demonstrated significant variation in bilateral jugular venous oxygen saturation measurements which may be of clinical significance. We have therefore measured variations in normal dural sinus venous drainage to assess the possible effects of normal anatomical variations on measured jugular venous oxygen saturation. Normal volunteers (n = 25) were imaged using magnetic resonance venography to demonstrate variations in venous anatomy. Flow was measured in the superior sagittal sinus and bilaterally in the transverse sinus, sigmoid sinus proximal to the jugular bulb and proximal jugular vein using phase difference magnetic resonance imaging. Examination of magnetic resonance venogram images showed considerable variability in the symmetry of transverse sinus flow. Complete absence of one transverse sinus was seen in four cases and significant asymmetry in the size of the transverse sinuses was present in 13. Quantitative flow studies demonstrated that the ratio of superior sagittal sinus to combined jugular bulb flow showed remarkably little variation (0.46 +/- 0.06). Measurements of transverse sinus flow showed significant asymmetry (< 40% of superior sagittal sinus flow in one transverse sinus) in 21 of 25 volunteers. The effect of the observed asymmetry on jugular venous oxygen saturation was modelled based on the assumption of either a supratentorial or infratentorial lesion. This model predicted significant asymmetry in jugular venous oxygen saturation measurements (> 10%) in 65% of cases with a supratentorial lesion which is in close agreement with clinical observations. This study suggests that normal variations in venous drainage may account for observed asymmetry in jugular venous oxygen saturation measurements.

I am being dragged away from CCSVI to watch Paranormal Activity 2. Which might be scary. But I am starting this thread for research into any effects of jugular vein asymmetry. The jugular veins vary in size, with the left more commonly but not always being the smaller one.

This article was looking at the effects of 'normal' anatomical variants in the dural sinuses to see how it affected the oxygen saturation in the jugular bulb, which is right where the sinus connects to the jugular.
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Postby Cece » Mon Aug 01, 2011 2:43 pm


Jugular venous oxygen is an indirect assessment of
cerebral oxygen use (see Figure 2). Simplistically,
when demand exceeds supply, the brain extracts
greater oxygen, resulting in decreased jugular bulb
oxygen saturation. If cerebral blood flow (CBF) decreases,
a point is eventually reached at which the
brain can no longer completely compensate for decreased
CBF by a further increase in oxygen extraction.
At this point, oxygen consumption decreases and
anaerobic metabolism with lactate production ensues.
When cerebral oxygen supply exceeds demand, oxygen
saturation of jugular bulb blood is increased.

Our brains can run on anaerobic metabolism with lactate production when oxygen is below a certain point? What are the consequences of this type of metabolism?

While cerebral oxygen consumption (CMRO2) is described
by the equation (CjvO2 5 oxygen content of jugular venous blood):
CMRO2 5 CBF 3 (CaO2 2 CjvO2)
The difference in oxygen content between arterial and
jugular venous blood is expressed by the term (CaO2
2 CjvO2) or AjvDO2. By rearranging the above equation
it is apparent that: AjvDO2 5 CMRO2/CBF
Normally, AjvDO2 is stable at 4–8 mL O2/100 mL
blood (29,30). If CMRO2 remains constant, changes in
AjvDO2 should reflect changes in CBF. If AjvDO2 is
,4 mL O2/100 mL blood, it is assumed that oxygen
supply is greater than demand (i.e., luxuriant). An
AjvO2 .8 mL O2/100 mL blood suggests that demand
is in excess of supply (i.e., ischemia

The = signs and x signs got dropped when I copied this over.
Jugular venous oxygen saturation is normally approximately
55%–75% (1), which is lower than systemic
mixed venous oxygen saturation.
Experimental studies suggest thresholds for jugular
venous oxygen values and neurologic change which are
summarized in Table 1. If the SjVO2 is , 50%, therapy(s)
directed at increasing cerebral oxygen supply and/or
decreasing demand should be initiated as detailed in
Figure 3.

In figure 3, it shows that if SJVO2 is less than 90%, measures should be taken to correct the hypoxia.
Despite the limitations of SjVO2 monitoring, there is
no better, commercially available, continuous, relatively
low-cost, bedside monitor to assess the adequacy
of cerebral oxygenation. Jugular venous oxygenation
provides information on global brain
oxygenation and is recommended in the treatment of
patients with head injury, especially those receiving
hyperventilation therapy.
Jugular venous oxygen monitoring is often performed
in conjunction with other monitoring and imaging
techniques and provides early detection of cerebral
ischemia that might otherwise go unrecognized.
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Postby Cece » Mon Aug 01, 2011 3:42 pm

Anaesthesiol Reanim. 2000;25(3):68-73.
[Effect of normobaric hyperoxia on parameters of brain metabolism].
[Article in German]
Schaffranietz L, Heinke W, Rudolph C, Olthoff D.
SourceKlinik und Poliklinik für Anästhesiologie und Intensivtherapie, Universität Leipzig. schal@medizin.uni-leipzig.de

In the literature there is only little information about the influence of hyperoxia on cerebral metabolic parameters. The aim of our study was to examine the effect of increased inspiratory oxygen concentrations on parameters of brain metabolism in elective neurosurgical patients. Ten patients undergoing an elective craniotomy for brain tumour resection were included in the study. The inspiratory oxygen concentration was raised at intervals of 15 minutes from 0.4 to 0.6 to 1.0 before opening the skull under "relative steady state conditions". At five defined measuring points, a blood gas analysis and an analysis of lactate and glucose levels were performed from arterial and jugularvenous blood. The lactate oxygen index (LOI), the arterio-jugularvenous lactate difference (AJDL) and the oxygen content of the arterial (caO2) and jugularvenous (cjO2) blood were calculated. Under increasing levels of FiO2, one can see an increase in sjO2, of jugularvenous oxygen tension (pjO2) and in oxygen content (cjO2). The most important result is the significant decrease (10% from baseline) in jugularvenous lactate at FiO2 1.0, while arterial lactate did not change significantly nor did the following parameters: paCO2, pjCO2, LOI, modified LOI, arterial and jugularvenous glucose. Hyperoxia causes a possible shift to aerobic metabolic situation in the brain reflected by decreased jugularvenous lactate.
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Anaesthesiol Reanim. 2001;26(5):123-32.
[Hyperoxia-induced liberation of big-endothelin into jugular venous blood of electric neurosurgical patients].
[Article in German]
Schaffranietz L, Vetter B, Rudolph C, König F.
SourceKlinik und Poliklinik für Anästhesiologie und Intensivtherapie am Universitätsklinikum Leipzig (AöR). schal@medizin.uni-leipzig.de

The use of hyperoxia in emergency situations is generally accepted, but the routine and uncritical application of higher oxygen concentrations is criticized. The influence of short-term application of hyperoxia on cerebral oxygenation, cerebral lactate and BIG-endothelin (BIG-ET) was studied. After approval by the Ethics Committee of the University of Leipzig, 22 patients (hyperoxia group n = 16, normoxia, control group n = 6) undergoing an elective craniotomy were included in the study. After induction of a total intravenous anaesthesia (sufentanil and propofol), a fibre-optic catheter was inserted into the bulb of the jugular vein. The inspiratory concentration of oxygen was raised from 0.4 to 1.0 for 15 minutes. Before, during and after hyperoxia, a blood gas analysis and analysis of lactate and BIG-ET were performed from arterial and jugularvenous blood. Hyperoxia caused a significant increase in jugularvenous oxygen saturation (sjO2) from 60.4 +/- 8.8% to 68.6 +/- 10.4% and jugularvenous oxygen content (cjvO2) from 10.27 +/- 2.06 vol% to 11.76 +/- 2.16 vol%. These changes were reversible after the end of hyperoxia. The jugularvenous lactate decreased significantly (9%) from 1.20 +/- 0.48 mmol/l to 1.10 +/- 0.45 mmol/l after the end of hyperoxia. Hyperoxia led to a significant increase in jugularvenous BIG-ET from 3.35 +/- 0.61 pg/ml to a maximum of 3.82 +/- 0.95 pg/ml and a decrease in the arterio-jugularvenous difference of BIG-ET from 0.19 +/- 0.53 pg/ml to a minimum -0.11 +/- 0.32 pg/ml. The changes in lactate and BIG-ET were also seen after the end of the hyperoxia. In the control group (normoxia, FiO2 0.4), no significant changes in sjO2, oxygen content, lactate and BIG-ET were observed. The increase in jugularvenous BIG-ET and the decrease in the arterio-jugularvenous difference of BIG-ET following hyperoxia indicate a higher cerebral release of BIG-ET.


I think an oxygen tank would be of use.

This addressed the shift from aerobic to anaerobic metabolism in the brain, with the generation of lactate.
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