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Anesthesiology Core Review: Part Two Advanced Exam

Chapter 4: Mixed Venous Oxygen Saturation

Hannah Schobel

INTRODUCTION
Mixed venous oxygen saturation (SvO2) is a measurement of whole body oxygenation. Mixed venous blood in measured in the pulmonary artery to
sample deoxygenated blood entering the pulmonary artery before passing through the lungs. The pulmonary artery receives a mixture of blood from
the superior vena cava, inferior vena cava, and coronary sinus. It serves as a sample of whole body oxygen utilization. Pulmonary artery blood can be
sampled periodically by withdrawing blood through a pulmonary artery catheter or continuously with an oximetric Swan–Ganz catheter.

The normal mixed venous oxygen saturation is about 70%–75%. This value reflects the fact that the body normally extracts only 25%–30% of oxygen
carried in the blood.

Mixed venous oxygen saturation can be explained using the modified Fick equation:

where SaO2 is the arterial Hgb saturation (%),VO2 is the oxygen consumption (mL/min), Q is the cardiac output (L/min), and Hgb is hemoglobin (g/dL).

The majority of oxygen in blood in bound to hemoglobin. A very small amount in dissolved in the blood as indicated by the arterial oxygen content
equation

The Fick equation can be rewritten to express the relationship between oxygen consumption, oxygen content, and cardiac output. The difference
between CaO2 and CvO2 is the amount of oxygen utilized by the tissues:

where CaO2 is the arterial oxygen content (mL/dL) and CvO2 is the mixed venous oxygen content (mL/dL).

When oxygen delivery is reduced, oxygen consumption remains constant by increasing oxygen extraction as well as cardiac output. This mechanism is
protective until tissues extract about 50%–60% of oxygen from the blood. Once oxygen extraction reaches this maximum, oxygen consumption is
supply-dependent and lactic acidosis due to cellular hypoxia develops. SvO2 can be used as an indirect indicator of cardiac output in the presence of
constant SaO2, VO2, and Hgb.

DECREASED MIXED VENOUS OXYGEN SATURATION

A decrease in SvO2 signifies insufficient oxygen delivery or increased oxygen consumption (Table 4-1). This problem occurs in low cardiac output,
anemia, hypoxemia, or hypermetabolic states. The body compensates to maintain aerobic respiration by increasing oxygen extraction from
hemoglobin. The body can maximally extract 50%–60% of oxygen carried in the blood, decreasing SvO2 to 40%–50%. Once the tissues reach maximal
oxygen extraction, further reduction in oxygen delivery results in anaerobic metabolism, acidosis, and multiorgan failure.

TABLE 4-1
Cause of Decreased SvO2

Decreased Oxygen Delivery Increased Oxygen Consumption

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Hypoxia Fever
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Decreased cardiac output Shivering

Anemia Exercise
A decrease in SvO2 signifies insufficient oxygen delivery or increased oxygen consumption (Table 4-1). This problem occurs in low cardiac output,
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anemia, hypoxemia, or hypermetabolic states. The body compensates to maintain aerobic respiration by increasing oxygen extraction from
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hemoglobin. The body can maximally extract 50%–60% of oxygen carried in the blood, decreasing SvO2 to 40%–50%. Once the tissues reach maximal
oxygen extraction, further reduction in oxygen delivery results in anaerobic metabolism, acidosis, and multiorgan failure.

TABLE 4-1
Cause of Decreased SvO2

Decreased Oxygen Delivery Increased Oxygen Consumption

Hypoxia Fever

Decreased cardiac output Shivering

Anemia Exercise

Abnormal Hgb (e.g., CO) Hyperthyroid/thyroid storm

Malignant hyperthermia

INCREASED MIXED VENOUS OXYGEN SATURATION

An increase in SvO2 signifies decreased oxygen consumption (Table 4-2). This situation occurs commonly in vasodilatory shock. The oxygenated blood
is not circulating normally throughout the body. The majority of oxygenated blood is diverted away from the core to the periphery. The blood supply
and oxygen carried to vital organs such as the brain, heart, and kidneys is insufficient. Though the mechanism is different from those in states of low
SvO2, the result of anaerobic respiration and multiorgan failure is the same.

TABLE 4-2
Causes of Increased SvO2

Decreased oxygen consumption

Left to right shunt
Impaired tissue uptake, e.g., CN and CO
Hypothermia
Sepsis
Increased cardiac output
Sampling error, e.g., wedged PA catheter

Severe hypotension and shock are the clinical scenarios where O2 is most commonly measured in the critical care setting. Shock is defined as a
condition where oxygen delivery does not meet the demands for aerobic metabolism of the tissues.

There are three commonly defined types of shock:

Shock CVP CI/CO SVR SvO2

Cardiogenic High Low High Low

Hypovolemic Low Low High Low

Vasodilatory Low High Low High

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SvO2 can be measured to help guide resuscitation. It is used as one variable in addition to blood pressure, pulse pressure variation, labs, urine output,
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as well as physical exam in diagnosing and treating the unstable patient.
Severe hypotension and shock are the clinical scenarios where O2 is most commonly measured in the critical care setting. Shock University of Michigan
is defined as a
condition where oxygen delivery does not meet the demands for aerobic metabolism of the tissues. Access Provided by:

There are three commonly defined types of shock:

Shock CVP CI/CO SVR SvO2

Cardiogenic High Low High Low

Hypovolemic Low Low High Low

Vasodilatory Low High Low High

SvO2 can be measured to help guide resuscitation. It is used as one variable in addition to blood pressure, pulse pressure variation, labs, urine output,
as well as physical exam in diagnosing and treating the unstable patient.

SUMMARY
Mixed venous oxygen saturation needs to be used as one monitor in a larger assessment of tissue oxygen and hemodynamic stability. SvO2 measures
global oxygenation and may not reflect tissue hypoxia of individual organs and extremities. In these cases, a patient may exhibit lactic acidosis in the
presence of normal SvO2. In addition, increased cardiac output can compensate for decreased Hgb or increased VO2, rendering a normal SvO2.

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