Hypoxemia

Basic Science

This section provides an abbreviated overview of oxygen physiology. For an in-depth discussion of oxygen physiology, please visit the dedicated OA summary. Link

Hypoxia can be defined as:

• ↓ SpO₂ greater than 5% from baseline or
• SpO₂ less than 90% or
• PaO₂ less than 60 mmHg3

Gas Exchange

• Oxygen is perfusion-limited, meaning it diffuses quickly and fully equilibrates between the alveoli and capillaries during the time the blood is in the pulmonary capillaries.²
• The alveolar-arterial oxygen gradient (A-a O₂ gradient) is the difference between the alveolar oxygen concentration (PAO2) and the arterial oxygen concentration (PaO2).²
• The PaO₂ can be measured, and the PAO₂ can be derived from the alveolar gas equation.²

• The normal A-a gradient: 5-10 mmHg. This can increase with age and lung pathology.
• The most common cause of hypoxemia is an increased alveolar-arterial gradient, which is influenced by right-to-left shunting, ventilation-perfusion mismatch, and mixed venous oxygen tension.¹

Ventilation and Perfusion

• In order for oxygen to cross the alveoli-capillary interface, both ventilation and perfusion must occur.²
  • Ventilation refers to the movement of air into and out of the alveoli.²
  • Perfusion is the movement of blood through the capillaries.²
• The V/Q ratio represents the relation between ventilation and perfusion in gas exchange.²
  • Normal V/Q  ≈  0.8-1
  • i.e., (4L/min ⁡ventilation⁡)/(5L/min⁡ cardiac output⁡)=0.8
• Failure of ventilation or perfusion can lead to shunt or dead-space physiology.2

• The poorly oxygenated blood from shunt physiology mixes with appropriately oxygenated blood, resulting in a decrease in the overall oxygen content of the pulmonary venous blood.²
• Anesthesia can commonly lead to V/Q mismatch via multiple mechanisms
  • Atelectasis is a common cause of shunt physiology and thus hypoxemia during general anesthesia.²
    • This can be treated with recruitment maneuvers and increasing PEEP, which restores end-expiratory lung volume.2
  • The breathing circuit is a common cause of increased dead space during anesthesia.²
• Please see the OA summary on Effects of Anesthesia on the Respiratory System. Link
• When hypoxia occurs, the pulmonary arteries will selectively vasoconstrict to improve V/Q mismatching. This is called hypoxic pulmonary vasoconstriction and is especially relevant in managing patients requiring one-lung ventilation for surgical exposure.²
• Please see the OA summary on hypoxia during one-lung ventilation for more details. Link

Oxygen Transport

• Oxygen travels through the blood in two forms: dissolved or carried by hemoglobin.¹
• The total oxygen content of the blood can be calculated by the following equation:

• The oxyhemoglobin dissociation curve describes the partial pressure of oxygen at which oxygen dissociates from hemoglobin.
• The P₅₀ is the O₂ tension at which hemoglobin is 50% saturation.¹

• Many factors influence the partial pressure of oxygen at which oxygen dissociates from hemoglobin.

Normal P₅₀ in adults is 27 mmHg
P₅₀ in a term pregnant person is 30 mmHg
P₅₀ in an infant is 19 mm Hg
*Bohr effect: acidosis ↓ Hb affinity for O₂

Oxygen Delivery

• Oxygen delivery depends on arterial oxygen content and cardiac output, as represented by the oxygen delivery equation.¹

DO₂ = O₂ delivery
CaO₂ = arterial O₂ content
QT = Cardiac output

• Inadequate oxygen delivery can result from low PaO₂, low hemoglobin concentration, or poor cardiac output.
• Mixed venous oxygen is a helpful measure of the body’s balance of oxygen supply and demand.¹
• Normal mixed venous oxygen is about 40 mmHg and represents a balance between oxygen supply and demand.¹
  • High mixed venous O₂: hyperoxia, polycythemia, hypothermia
  • Low mixed venous O₂: lung disease, anemia, high metabolic state, cardiogenic shock
• Mixed venous oxygen tension depends on cardiac output, oxygen consumption, and hemoglobin concentration.¹
• The Fick equation expresses the relationship between O₂ consumption, O₂ content, and cardiac output.¹

• • • VO₂ = O₂ consumption
    • QT = cardiac output
    • CaO₂ = arterial O₂ content
    • CvO₂ = venous O₂ content
• Oxygen consumption can be grossly estimated 3-5 mL/kg/min for adults

Closing Capacity

• Small airways rely on radial traction from surrounding tissue and on lung volume to remain open. The volume at which these airways begin to close is called the closing capacity.¹
• The collapse of small airways leads to shunt physiology.
• Closing capacity increases with age and obesity to the point where it can equal or exceed functional residual capacity.¹

Ventilatory Response to Hypoxemia

• Low PaO₂ triggers peripheral chemoreceptors, causing an increased minute ventilation.⁴
  • The only chemoreceptors that respond to hypoxemia are the aortic and carotid bodies.⁴
  • Notably, these receptors respond only to low arterial oxygen tension, not to low oxygen content (i.e., anemia or CO poisoning).⁴
  • Unlike the CO2 response curve (see OA summary on hypercarbia Link), the ventilatory response to hypoxia curve is far from linear and only really rises when the PaO₂ is 60 mmHg (depending on the PaCO₂) (Figure 2). The response is amplified in the setting of hypercapnia.⁴
• Prolonged hypoxia, however, can cause apnea.⁴

Clinical Applications

• Hypoxia is feared by medical providers because if not corrected quickly, it can have devastating outcomes, including neurologic injury, arrhythmias, hypotension, bradycardia, and cardiac arrest.³

Etiology of Hypoxia

• The etiologies of hypoxemia can be broken up into four categories: hypoventilation, diffusion limitation, shunt, and V/Q mismatch⁴ (Table 2).

Hypoxia Prevention

• Complete a careful equipment and machine check prior to induction.³
• Preoxygenate for 3 minutes or 10 deep breaths until the end tidal O2 is greater than 80%.³
• Optimize ventilation parameters: increase FiO₂ and PEEP.³
• Improve cardiopulmonary mechanics with positioning when possible.³

Management

• Assume low SpO₂ is hypoxemia (rather than a monitor error) until proven otherwise.³
• Increase FiO₂ to 1.0 and increase gas flows.³
• If hemodynamically stable, consider a recruitment maneuver and increasing PEEP.³
• Check for adequate ventilation:³
  • Ensure adequate ETCO₂
  • Verify ETT position
  • Check peak inspiratory pressure (PIP)
    • High PIP: Hand ventilate to check compliance, try recruitment if hemodynamically stable, auscultate and assess chest movement to evaluate for bronchospasm, endobronchial intubation, pneumothorax
    • Low PIP: check for a leak
  • Draw an ABG
• Confirm pulse oximeter function.³
• Work through a differential diagnosis:³
  • Aspiration, atelectasis, pulmonary embolism, bronchospasm, anaphylaxis, pleural effusion, cardiac dysfunction, pneumothorax, anemia, etc.
  • Consider hypoventilation, over narcotization, and residual neuromuscular blockade in extubated patients.
• Abort surgery if hypoxia persists, and consider transferring to the intensive care unit.³