Definition of Acute Hypoxic Respiratory Failure
Acute hypoxic respiratory failure is defined as severe arterial hypoxemia (PaO₂/FiO₂ ≤ 300 mmHg) developing within one week of a known clinical insult, representing Type 1 respiratory failure where oxygenation fails despite normal or increased ventilatory effort. 1
Core Diagnostic Criteria
Physiological Definition:
- PaO₂ < 60 mmHg or SpO₂ < 90% despite supplemental oxygen delivered via face mask with reservoir bag at flows of 10-15 L/min (FiO₂ 0.60-0.95) 1
- Normal or low PaCO₂ distinguishes this from Type 2 (hypercapnic) respiratory failure 2
- Increased respiratory rate > 30 breaths/min commonly accompanies the hypoxemia 1
Temporal Classification:
- Acute onset with rapid deterioration of arterial blood gases, distinguishing it from chronic respiratory failure which develops gradually with compensatory mechanisms 2
- Symptoms develop within 1 week of a known clinical insult in ARDS cases 1
Underlying Pathophysiological Mechanisms
The hypoxemia results from four primary mechanisms, with intrapulmonary shunting being the dominant cause 2, 3:
- Ventilation-perfusion (V/Q) mismatch: Blood flows to poorly ventilated lung regions 2
- Intrapulmonary shunt: Blood bypasses ventilated alveoli entirely, flowing through completely unventilated or fluid-filled lung units 2, 3
- Diffusion impairment: Thickened alveolar-capillary membrane impedes oxygen transfer 2
- Alveolar hypoventilation: Though this typically causes Type 2 failure, it can contribute to hypoxemia 2
Spectrum of Severity: ARDS Classification
When acute hypoxic respiratory failure progresses to bilateral radiographic opacities not explained by cardiac failure or fluid overload, it meets criteria for ARDS 1. The Berlin Definition stratifies severity based on oxygenation with minimum PEEP of 5 cmH₂O 1, 4:
- Mild ARDS: PaO₂/FiO₂ 200-300 mmHg 1, 4
- Moderate ARDS: PaO₂/FiO₂ 100-200 mmHg 1, 4
- Severe ARDS: PaO₂/FiO₂ ≤ 100 mmHg 1, 4
Mortality increases with severity: ICU mortality rates remain 35-40% overall, with higher rates in severe ARDS despite advances in supportive care 1
Common Clinical Causes
Direct lung injury causes include 2:
- Pneumonia (bacterial, viral, aspiration)
- Pulmonary contusion from trauma
- Inhalation injury
Indirect causes include 2:
- Sepsis (most common trigger for ARDS)
- Pancreatitis
- Multiple transfusions
- Non-pulmonary trauma
Other important causes 2:
- Cardiogenic pulmonary edema (fills alveoli creating shunt physiology)
- Pulmonary embolism (causes V/Q mismatch through increased dead space)
Critical Distinction from Type 2 Respiratory Failure
Type 2 (hypercapnic) respiratory failure is fundamentally different, characterized by 2:
- Elevated PaCO₂ > 45 mmHg (6.0 kPa) from alveolar hypoventilation
- Ventilatory pump failure rather than oxygenation failure
- Common causes: COPD exacerbations, neuromuscular disorders, chest wall deformities
- Target SpO₂ 88-92% to avoid worsening hypercapnia, versus 94-98% in Type 1 failure 2
Key Clinical Pitfalls to Avoid
Do not confuse improved oxygenation with improved survival: Multiple studies show that treatments improving PaO₂ do not necessarily reduce mortality, as patients more commonly die from sepsis or multi-organ failure rather than refractory hypoxemia 5, 6
Recognize that standard chest radiographs poorly predict severity: Classic ARDS findings may be asymmetric, patchy, or focal, and radiographic appearance correlates poorly with oxygenation defect severity 2
Monitor for rapid deterioration: When noninvasive support is attempted, patients must be monitored closely as deterioration can occur abruptly, and delayed intubation increases mortality 1
Calculate PaO₂/FiO₂ ratio correctly: This must be done with patients receiving at least 5 cmH₂O PEEP to properly classify ARDS severity 4