Oxygen Delivery and Consumption

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Oxygen delivery and consumption

Authors: Ilene M Rosen, MD, MSCE, Scott Manaker, MD, PhD
Section Editor: Polly E Parsons, MD
Deputy Editor: Geraldine Finlay, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2022. | This topic last updated: Apr 13, 2021.
INTRODUCTION
Inspired oxygen from the environment moves across the alveolar-capillary membrane into
the blood. Most of the oxygen binds to hemoglobin in red blood cells, although a small
amount dissolves into the plasma. The oxygen is then transported from the lungs to the
peripheral tissues, where it is removed from the blood and used to fuel aerobic cellular
metabolism. This process can be conceptualized as three steps: oxygenation, oxygen
delivery, and oxygen consumption. In this topic review, oxygen delivery and consumption are
reviewed. Oxygenation is discussed separately. (See "Measures of oxygenation and
mechanisms of hypoxemia".)
DEFINITIONS
Oxygen content — The arterial oxygen content (CaO2) is the amount of oxygen bound to
hemoglobin plus the amount of oxygen dissolved in arterial blood:
CaO2 (mL O2/dL) = (1.34 x hemoglobin concentration x SaO2) + (0.0031 x PaO2)
where SaO2 is the arterial oxyhemoglobin saturation and PaO2 is the arterial oxygen tension.
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In dyshemoglobinemias, the oxygen content is calculated with the same equation, although
the saturations (and therefore the oxygen content) will be different for a specific PaO2 [1].
Normal CaO2 is approximately 20 mL O2/dL.
Similarly, the mixed venous blood oxygen content (CvO2) is the amount of oxygen bound to
hemoglobin plus the amount of oxygen dissolved in mixed venous blood:
CvO2 (mL O2/dL) = (1.34 x hemoglobin concentration x SvO2) + (0.0031 x PvO2)
where SvO2 is the mixed venous oxyhemoglobin saturation and PvO2 is the mixed venous
oxygen tension. Normal CvO2 is approximately 15 mL O2/dL. Mixed venous blood is drawn
from the right atrium. Peripheral venous blood should not be substituted because it tends to
overestimate venous oxygen content.
Oxygen delivery — Oxygen delivery (DO2) is the rate at which oxygen is transported from
the lungs to the microcirculation:
DO2 (mL/min) = Q x CaO2
where Q is the cardiac output. Normal DO2 is approximately 1000 mL/min. Normal DO2 is
approximately 500 mL/min/m2 if cardiac index is substituted for cardiac output.
Realize, cardiac output can be measured by thermodilution using a pulmonary artery

catheter, or calculated using the Fick equation:
Q (L/min) = Oxygen consumption ÷ (10 x arteriovenous oxygen difference)
where oxygen consumption is either measured by respirometry (discussed below) or

estimated using a nomogram, and the arteriovenous (AV) oxygen difference is calculated:
AV oxygen difference (mL O2/dL) = CaO2 - CvO2
Oxygen consumption — Oxygen consumption (VO2) is the rate at which oxygen is removed
from the blood for use by the tissues. It can be measured directly or calculated. Both
approaches assume that all unused oxygen passes from the arterial to the venous
circulation.
Direct measurement of VO2 is performed by respirometry. During respirometry, the patient

breathes through a chamber that receives continuous air flow. Measurement of the oxygen
depleted from the chamber, as well as the carbon dioxide and water vapor produced in the
chamber, is used to determine VO2. Respirometry can be used in mechanically ventilated
patients, but the accuracy of direct measurement of VO2 diminishes at high oxygen
concentrations (eg, >80 percent) [2-7]. Normal VO2 in a conscious, resting person is
approximately 250 mL O2/min.
Calculation of VO2 can be performed by rearranging the Fick equation:
VO2 (mL O2/min) = Q x (CaO2 - CvO2)
When calculating VO2, cardiac output should be measured and not calculated from the Fick
equation or a mathematical coupling error may be introduced.
Oxygen extraction — Oxygen extraction is the slope of the relationship between oxygen
delivery (DO2) and oxygen consumption (VO2). It is most commonly expressed as the oxygen
extraction ratio, which is the proportion of arterial oxygen that is removed from the blood as
it passes through the microcirculation:
O2 Extraction Ratio = (CaO2 - CvO2)/CaO2
Normal O2 extraction ratios range from 0.25 to 0.3.
NORMAL PHYSIOLOGY
Under normal circumstances:
● Oxygen consumption (VO2) is proportional to oxygen delivery (DO2) and oxygen

extraction
● DO2 and oxygen extraction are inversely proportional to one another
At rest, VO2 remains constant over a wide range of oxygen delivery (DO2) because changes in
DO2 are balanced by reciprocal changes in oxygen extraction ( figure 1). VO2 decreases if
DO2 declines to such a degree that it cannot be balanced by increasing oxygen extraction.
The threshold value of DO2 below which VO2 will fall is called the "critical DO2" ( figure 2).
When metabolic demand increases (eg, exercise, pregnancy), VO2 also increases because
more oxygen is required to maintain aerobic cellular metabolism. This is normally achieved
by increasing both DO2 and oxygen extraction [8,9]. VO2 is disproportionately impacted by
the increased oxygen extraction, with the increased DO2 contributing little [10]. Enhanced
extraction of oxygen is probably mediated at the capillary level [8]. Recent studies suggest
dysregulation of peripheral extraction may play an important role in limiting exercise
capacity in some disorders such as heart failure with preserved ejection fraction [11]
ABNORMALITIES OF OXYGEN DELIVERY AND DEMAND
Decreased oxygen delivery or increased metabolic demand are common sequelae of medical
illness.
Decreased oxygen delivery — Oxygen delivery (DO2) will decrease if cardiac output falls or
arterial oxygen content (CaO2) declines.
● Cardiac output can decrease due to cardiac disease or hypovolemia.
● CaO2 can decrease due to anemia or poor oxygenation. The latter can be caused by
lung disease (eg, ventilation-perfusion mismatch, diffusion limitation), a right-to-left
shunt, diminished inspired oxygen, or hypoventilation. (See "Measures of oxygenation
and mechanisms of hypoxemia".)
In the setting of diminished DO2, maintenance of a normal oxygen consumption (VO2) can be
accomplished by a compensatory increase in oxygen extraction [12]. If increased oxygen
extraction is insufficient to maintain VO2, cardiac output will increase in an effort to improve
DO2. VO2 will fall if these actions are insufficient and DO2 is below the critical DO2 [13].
Increased metabolic demand — Metabolic demand is elevated in critically ill patients (eg,
acute respiratory distress syndrome, sepsis, or septic shock) [3,6,14-21]. VO2 increases
because more oxygen is required to maintain aerobic cellular metabolism. In critically ill
patients, VO2 elevation may be disproportionately accomplished by increasing the DO2. This
is different from healthy individuals in whom VO2 elevation is disproportionately
accomplished by increasing the oxygen extraction, with DO2 contributing little [10]. Whether
such a difference exists between healthy and critically ill individuals is controversial:
● Proponents believe that VO2 is disproportionately affected by DO2 because oxygen

extraction is impaired during critical illness. Supporting this hypothesis, lactic acidosis is
often present despite increased DO2 [22,23]. In other words, anaerobic metabolism is
required despite an increased supply of oxygen. Ineffective oxygen extraction may be
due to poor oxygen uptake or poor utilization by the cells [15].
● Opponents argue that both VO2 and DO2 were calculated in most of the studies that
suggest that DO2 has a disproportionate impact on VO2 during critical illness [24]. This
could introduce mathematical coupling errors, which would falsely increase the
strength of the relationship between VO2 and DO2. In addition, VO2 was not
disproportionately affected by DO2 in the few studies that directly measured VO2 [3,25-
28].
We believe that the relationship between DO2 and VO2 in critically ill patients is similar to that
in healthy patients during increased metabolic demand (eg, exercise, pregnancy). In other
words, we believe that increased oxygen extraction, and not increased DO2, has the greatest
impact on increasing the VO2 in critically ill patients. We base this belief on the following:
● Numerous studies have evaluated the impact of augmenting DO2 on VO2 with
conflicting results [3,7,9,25-44]. Methods of augmenting DO2 have included inotropic
agents, saline loading, and vasodilators to improve cardiac output, as well as red blood
cell transfusions to increase arterial oxygen content (CaO2). Regardless of the
intervention, DO2 and VO2 were strongly correlated when VO2 and DO2 were both
calculated, but not when VO2 was directly measured.
● A few studies have evaluated the impact of augmenting DO2 and patient-centered
outcomes, such as survival, organ failure, length of ICU stay, and length of
hospitalization [35,37-39,45-51]. While some of the studies found an improvement in
morbidity or mortality, others found no effect or potential harm. Those that
demonstrated improvement had significant methodologic problems, such as baseline
differences between the treatment and control groups, and failure to use an intention-
to-treat analysis.
Taken together, we believe there are insufficient data to warrant the routine augmentation of
DO2 in critically ill patients if there is no evidence of ongoing tissue hypoxia.
SUMMARY AND RECOMMENDATIONS
● Inspired oxygen from the environment moves across the alveolar-capillary membrane
into the blood and is then transported to the peripheral tissues. There, it is removed
from the blood and used to fuel aerobic cellular metabolism. This process can be
conceptualized as three steps: oxygenation, oxygen delivery, and oxygen consumption.
(See 'Introduction' above.)
● The arterial oxygen content (CaO2) is the amount of oxygen bound to hemoglobin plus
the amount of oxygen dissolved in arterial blood, while the mixed venous blood oxygen
content (CvO2) is the amount of oxygen bound to hemoglobin plus the amount of
oxygen dissolved in mixed venous blood. (See 'Oxygen content' above.)
● Oxygen delivery (DO2) is the rate at which oxygen is transported from the lungs to the
microcirculation, oxygen consumption (VO2) is the rate at which oxygen is removed
from the blood for use by the tissues, and oxygen extraction is the proportion of arterial
oxygen that is removed from the blood as it passes through the microcirculation. (See
'Oxygen delivery' above and 'Oxygen consumption' above and 'Oxygen extraction'
above.)
● VO2 normally remains constant over a wide range of DO2 because changes in DO2 are
balanced by reciprocal changes in oxygen extraction. VO2 will decrease only if DO2
declines to such a degree that it cannot be balanced by increasing oxygen extraction.
(See 'Normal physiology' above.)
● VO2 increases when metabolic demand increases (eg, exercise, pregnancy). This is
disproportionately accomplished by increasing the oxygen extraction, with DO2
contributing little. (See 'Normal physiology' above.)
● Decreased oxygen delivery or increased metabolic demand are common sequelae of

medical illness.
• When DO2 is decreased (eg, heart failure), a compensatory increase in oxygen

extraction may allow VO2 to remain normal. If increased oxygen extraction is
insufficient to maintain VO2, cardiac output will increase in an effort to improve DO2.
VO2 will fall if these compensatory mechanisms are inadequate. (See 'Decreased
oxygen delivery' above.)
• When metabolic demand increases (eg, sepsis), VO2 also increases. This may be
disproportionately accomplished by increasing the DO2, rather than enhancing the
oxygen extraction. (See 'Increased metabolic demand' above.)
● In critically ill patients in whom there is no evidence of ongoing tissue hypoxia, we

suggest that DO2 should NOT be routinely augmented (Grade 2B). (See 'Increased
metabolic demand' above.)
Use of UpToDate is subject to the Terms of Use.
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Topic 1623 Version 14.0
GRAPHICS
The relationship between oxygen consumption

(VO2), oxygen delivery (DO2), and the extraction
ratio
(A) An inverse relationship exists between oxygen delivery (DO 2 ) and

the extraction raio (ER), with no correlation between oxygen
consumption (VO 2 ) and the ER.
(B) An improved ability to extract oxygen during exercise exists at all

levels of DO 2 .
Graphic 52578 Version 2.0
Oxygen delivery (DO2) and consumption (VO2)
In the normal state (blue line), oxygen consumption is constant over

a range of DO2, and decreases only when DO2 falls below a critical
level (critical DO2). Pathologic changes caused by sepsis or systemic
inflammatory responses (red line) cause increased VO2 and
impaired peripheral oxygen utilization, resulting in an elevation in
critical DO2.
Graphic 54410 Version 1.0
Contributor Disclosures
Ilene M Rosen, MD, MSCE No relevant financial relationship(s) with ineligible companies to
disclose. Scott Manaker, MD, PhD Other Financial Interest: National Board for Respiratory Care
[Director]; Expert witness in workers' compensation and in medical negligence matters [General
pulmonary and critical care medicine]. All of the relevant financial relationships listed have been
mitigated. Polly E Parsons, MD No relevant financial relationship(s) with ineligible companies to
disclose. Geraldine Finlay, MD No relevant financial relationship(s) with ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy

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Oxygen delivery and consumption - UpToDate 05/24/22 8:14 p. m.

Official reprint from UpToDate®

CaO2 (mL O2/dL) = (1.34 x hemoglobin concentration x SaO2) + (0.0031 x PaO2)

CvO2 (mL O2/dL) = (1.34 x hemoglobin concentration x SvO2) + (0.0031 x PvO2)

DO2 (mL/min) = Q x CaO2

Realize, cardiac output can be measured by thermodilution using a pulmonary artery

Q (L/min) = Oxygen consumption ÷ (10 x arteriovenous oxygen difference)

where oxygen consumption is either measured by respirometry (discussed below) or

AV oxygen difference (mL O2/dL) = CaO2 - CvO2

Direct measurement of VO2 is performed by respirometry. During respirometry, the patient

Calculation of VO2 can be performed by rearranging the Fick equation:

VO2 (mL O2/min) = Q x (CaO2 - CvO2)

O2 Extraction Ratio = (CaO2 - CvO2)/CaO2

Normal O2 extraction ratios range from 0.25 to 0.3.

Under normal circumstances:

● Oxygen consumption (VO2) is proportional to oxygen delivery (DO2) and oxygen

● DO2 and oxygen extraction are inversely proportional to one another

ABNORMALITIES OF OXYGEN DELIVERY AND DEMAND

● Cardiac output can decrease due to cardiac disease or hypovolemia.

● Proponents believe that VO2 is disproportionately affected by DO2 because oxygen

SUMMARY AND RECOMMENDATIONS

● Decreased oxygen delivery or increased metabolic demand are common sequelae of

• When DO2 is decreased (eg, heart failure), a compensatory increase in oxygen

● In critically ill patients in whom there is no evidence of ongoing tissue hypoxia, we

Use of UpToDate is subject to the Terms of Use.

1. Needleman JP, Setty BN, Varlotta L, et al. Measurement of hemoglobin saturation by

dobutamine. Chest 1994; 106:1524.

6. Dantzker DR, Foresman B, Gutierrez G. Oxygen supply and utilization relationships. A

28. Boyd O, Grounds M, Bennett D. The dependency of oxygen consumption on oxygen

50. Gattinoni L, Brazzi L, Pelosi P, et al. A trial of goal-oriented hemodynamic therapy in

The relationship between oxygen consumption

(A) An inverse relationship exists between oxygen delivery (DO 2 ) and

(B) An improved ability to extract oxygen during exercise exists at all

Graphic 52578 Version 2.0

Oxygen delivery (DO2) and consumption (VO2)

In the normal state (blue line), oxygen consumption is constant over

Graphic 54410 Version 1.0

Conflict of interest policy

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