What is DO2 (Oxygen Delivery)?
DO2 is the total amount of oxygen delivered to the tissues per minute, calculated as the product of arterial oxygen content (CaO2) and cardiac output (Q), expressed by the equation: DO2 = CaO2 × Q. 1
Core Components of the DO2 Equation
The formula breaks down into two essential elements 1:
- CaO2 (arterial oxygen content): The sum of oxygen dissolved in blood plus oxygen bound to hemoglobin 1
- Q (cardiac output): The volume of blood pumped by the heart per minute 1
Determinants of Arterial Oxygen Content
CaO2 is predominantly determined by total hemoglobin and its oxygen saturation, since oxygen solubility in blood is very low 1. The components include:
- Oxygen bound to hemoglobin (calculated as: Hemoglobin × 1.36 × SaO2) 2
- Oxygen dissolved in plasma (calculated as: PaO2 × 0.0031) 2
- The dissolved component contributes minimally under normal conditions 1
Clinical Calculation and Units
During cardiopulmonary bypass, DO2 is calculated as: DO2 (mL/min/m²) = Pump Flow (L/min) × Arterial Oxygen Content (mL O2/L) × 10 / BSA (m²) 2. This indexed value normalizes delivery to body surface area for comparison across patients.
Target Values in Clinical Practice
During Cardiopulmonary Bypass
Maintain DO2 between 280-300 mL/min/m² during normothermic CPB to optimize clinical outcomes and reduce acute kidney injury (Class IIa, Level B recommendation) 1, 2. This threshold represents a Class I, Level A recommendation for preventing early-stage AKI 1.
General Critical Care
The British Thoracic Society guidelines emphasize that optimizing DO2 requires addressing three key factors: arterial oxygen content, hemoglobin concentration, and cardiac output 1. Simply increasing oxygen saturation from 90% to 100% produces at most a 10% rise in delivery, whereas correcting low cardiac output or severe anemia improves DO2 much more substantially 1.
Physiological Context
The neurocardiopulmonary axis is designed to optimize global oxygen delivery, with local tissue vascular beds responsible for distributing blood flow 1. When PaO2 falls, peripheral chemoreceptors in the carotid body drive increased ventilation to increase PaO2, though this mechanism senses PaO2 rather than CaO2 to prevent ineffective hyperventilation in response to anemia 1.
Common Clinical Pitfalls
Administering supplemental oxygen to a patient with saturation of 90% will produce minimal improvement in DO2 compared to correcting underlying cardiac output or hemoglobin deficits 1. The purpose of oxygen therapy is to increase oxygen delivery to tissues, not merely to increase oxygen carried by the blood 1.
Remember the ABC approach: In addition to optimizing DO2 from lungs to tissues, treat problems impairing oxygen delivery to the lungs themselves, including upper airway obstruction, bronchoconstriction, and pulmonary edema 1.
Monitoring Adequacy of DO2
Mixed venous oxygen saturation (SvO2) serves as an excellent monitor of DO2 adequacy in relation to oxygen consumption, with a target >70% in general critical care 3, 4 and >75% during cardiopulmonary bypass 2. However, a normal or high SvO2 does NOT exclude tissue hypoxia, particularly in septic patients where oxygen extraction may be impaired 3.
Additional monitoring parameters include 3, 2:
- Central venous oxygen saturation (ScvO2): target ≥70%
- Arterial lactate: to detect inadequate tissue oxygenation
- pCO2 gap: when ScvO2 <73% and pCO2 gap >6 mmHg together predict oxygen extraction >30% with 100% positive predictive value