Index
It is used to help recognize when a patient’s body is drawing more oxygen than usual.
The mixed venous oxygen saturation (SvO2) is the percentage of oxygen bound to hemoglobin in the blood returning to the right side of the heart.
This reflects the amount of oxygen “leftover” after the tissues remove what they need.
An increase in extraction is how bodies meet the oxygen needs of the tissue when the amount of oxygen reaching the tissues is more minor than necessary.
Measurement of mixed venous blood oxygen saturation (SvO2) in the pulmonary artery. It requires the insertion of a pulmonary artery catheter in most clinical settings.
A proper mixed venous sample (called SvO2) is drawn from the tip of the pulmonary artery catheter. It includes all venous blood returning from the head and arms (through the superior vena cava), intestine, and lower extremities.
By the time the blood reaches the pulmonary artery, all of the venous blood has “mixed” to reflect the average amount of oxygen remaining after all tissues in the body have removed oxygen from the hemoglobin.
The mixed venous sample also captures the blood before re-oxygenating in the pulmonary capillary.
Because pulmonary artery catheter use has drastically decreased, continuous measurements of central venous oxygen saturation (ScvO2) obtained from the internal jugular or subclavian catheters are used and interpreted in the same way.
A continuous central venous oxygen saturation (ScvO2) refers to a primary venous sample.
Continuous measurement of central venous oxygen saturation (ScvO2) is a surrogate for mixed venous oxygen saturation (SvO2). It can be used to identify changes in oxygen extraction in a patient’s tissues.
We generally assume (possibly incorrectly at times) that a blood gas sample obtained from the jugular or internal subclavian (reflecting only the head and upper extremities) will have the same meaning as mixed venous oxygen saturation (SvO2).
What does this tell us?
Mixed venous oxygen saturation (SvO2) can help determine if cardiac output and oxygen delivery are high enough to meet patients’ needs.
It can be beneficial if measured before and after changing cardiac medications or mechanical ventilation, especially in unstable patients.
It can be used as a marker for how oxygen is delivered to peripheral tissues by extrapolation.
If mixed venous oxygen saturation (SvO2) is low and the patient has multi-organ failure, an inotrope can be added to help increase cardiac output, i.e., in severe sepsis.
Its central venous oxygen saturation (ScvO2) has been used as a treatment goal in severe sepsis and has been shown to decrease mortality and morbidity (Rivers study).
The continuous measurement obtained once data is entered about the patient (thus trends can be seen with changes in therapy: fluids, inotropes, vasodilators, dialysis) generates good information quickly.
What are the average values?
- Normal mixed venous oxygen saturation (SvO2) 60-80%.
- Normal continuous central venous oxygen saturation (ScvO2) (from an internal jugular or subclavian vein) is> 70%.
How do I use this information clinically?
Adenosine triphosphate (ATP) (energy) is necessary for all cell functions and survival. Tissues require oxygen to produce adenosine triphosphate (energy).
If the amount of oxygen received by the tissues falls below the amount of oxygen required (due to increased need or decreased supply), the body tries to compensate for the following:
First compensation: increases cardiac output.
Cardiac output increases to increase the amount of oxygen delivered to the tissues, as shown below.
The oxygen supply is the amount of oxygen that is delivered to the tissues and is determined by the following:
Oxygen supply (DO2) = Cardiac output (HR X trace volume) X Oxygen content (Hb X SaO2)
If this is not enough to meet the tissue’s energy needs, we move on to our second compensation.
Second compensation: increases tissue oxygen extraction.
The tissues begin to extract or extract a more significant percentage of oxygen from the arterial blood.
This reduces the amount of oxygen that remains in the blood when it returns to the right side of the heart (decreased SvO2).
If this is not enough to meet the energy needs of the tissue, we move on to our second compensation.
Third compensation: increases anaerobic metabolism.
If the tissues do not receive an adequate oxygen supply, anaerobic metabolism becomes the only mechanism to produce adenosine triphosphate tissue.
Anaerobic metabolism is inefficient and produces a large amount of metabolic waste (for example, lactic acid) that is difficult for the body to eliminate quickly.
It also produces a relatively poor supply of adenosine triphosphate. Prolonged anaerobic metabolism leads to energy depletion and metabolic acidosis.
Why measure it?
If the mixed venous oxygen saturation (SvO2) decreases, the tissues extract a higher percentage of oxygen from the blood than usual.
In other words, a decrease in mixed venous oxygen saturation (SvO2) indicates that cardiac output is not high enough to meet the oxygen needs of the tissue.
Therefore, mixed venous oxygen saturation (SvO2) can indicate whether an individual’s cardiac output is high enough to meet their needs.
An increase in mixed venous oxygen saturation (SvO2) demonstrates a decrease in oxygen extraction and generally indicates that cardiac output meets the tissue’s need for oxygen.
A return of mixed venous oxygen saturation (SvO2) to normal suggests an improvement in the patient.
However, an increase in mixed venous oxygen saturation (SvO2) in an increase in lactate is inappropriate: the patient who has resorted to anaerobic metabolism (third compensation) must have evidence of high cardiac output and increased blood pressure. Extraction.
This is a sinister finding, suggesting that the tissues cannot extract. It can be seen in late septic shock or cell poisoning such as cyanide. Cardiac output is routinely measured to assess the effectiveness of the drug.
Unfortunately, the measurement of cardiac output only gives us a value; it does not indicate whether the measured cardiac output meets the patient’s needs.
For some individuals, a cardiac output that falls below the normal range may be adequate, while for others, a standard or elevated cardiac output value may be too low.
A mixed venous oxygen saturation (SvO2) in the normal range, together with normal lactate, suggests that cardiac output is adequate.
Mixed venous oxygen saturation (SvO2) can be very helpful when determining whether a change in therapy is beneficial.
Measuring mixed venous oxygen saturation (SvO2) before and after a change can help determine whether therapy made the patient better or worse.
Mixed venous oxygen saturation (SvO2) may also help evaluate changes in ventilator therapy, especially in unstable patients.
Changes can be made to the ventilator to increase the oxygen content of the blood, which is essential for the total oxygen supply (oxygen content of cardiac output X).
An increase in positive end-expiratory pressure (PEEP) may be required to increase oxygen content; however, increasing levels of positive end-expiratory pressure (PEEP) can decrease cardiac output.
By measuring mixed venous oxygen saturation (SvO2) before and after a change in positive end-expiratory pressure (PEEP), the optimal level of positive end-expiratory pressure (PEEP) can be determined.
The “best” positive end-expiratory pressure (PEEP) is the level that improves arterial oxygen saturation (SaO2) without causing mixed venous oxygen saturation (SvO2).
The need for oxygen in tissues is satisfied when the amount of oxygen delivered to the tissues is sufficient to meet the amount of oxygen consumed (VO2).
When the oxygen supply falls below the oxygen consumption needs, lactic acidosis develops.
Possible problems
It must be measured from a pulmonary artery catheter (PAC). Therefore the patient is exposed to the risks associated with pulmonary artery catheterization (arrhythmia, pulmonary infarction, embolism, bleeding, pneumothorax, line sepsis).
Blood taken from a standard central line to estimate mixed venous oxygen saturation (SvO2) is not an actual result. It is not as accurate and maybe mainly superior to vena cava (SVC) blood which has a different effect.
Oxygen saturation than mixed venous oxygen saturation (SvO2) -> used as a treatment target in severe sepsis and has decreased mortality and morbidity.
It can be high in various situations (sepsis, liver failure, embedded pulmonary artery catheter, administration of a high fraction of inspired oxygen (FiO2)). It can be low in several situations (multi-organ failure, cardiac arrest).
Requires calibration to change hematocrit. Gattinoni RCT did not benefit from monitoring mixed venous oxygen saturation (SvO2).
Real-time monitoring of mixed venous oxygen saturation (SvO2) or central venous oxygen saturation is often used during resuscitation from septic shock.
However, the meaning of these parameters is far from straightforward.
In some patients with septic shock, mixed venous oxygen saturation (SvO2) may be low due to profound hypovolemia or myocardial dysfunction. Still, it obviously cannot alone indicate whether a fluid attack would increase cardiac output.
Due to profound impairment of oxygen extraction capabilities in other patients, mixed venous blood oxygen saturation (SvO2) may be abnormally high even in patients who may still respond positively to fluid infusion.
In either case, other reliable dynamic parameters can help address the critical issue of responsiveness and unresponsiveness.
