Can lactic acid be elevated in Acute Respiratory Distress Syndrome (ARDS)?

Lactic Acid Elevation in ARDS

Yes, lactic acid can be significantly elevated in Acute Respiratory Distress Syndrome (ARDS) due to tissue hypoperfusion, hypoxemia, and increased work of breathing, with levels often correlating with disease severity and prognosis.

Mechanisms of Lactate Elevation in ARDS

• Tissue Hypoxia and Hypoperfusion: ARDS is characterized by extensive right-to-left intrapulmonary shunting (>25% of cardiac output vs normal <5%), leading to hypoxemia and tissue hypoxia 1

• Increased Work of Breathing: Patients with ARDS experience significantly increased work of breathing due to:

  • Decreased lung compliance (often <25% of normal)
  • Increased dead space ventilation
  • Ventilation-perfusion mismatching
  • Respiratory muscle dysfunction 1

• Inflammatory Response: The inflammatory cascade in ARDS activates neutrophils and macrophages, producing cytokines and reactive oxygen species that can impair cellular metabolism 1

Clinical Significance of Lactate in ARDS

• Prognostic Value: Elevated lactate levels in ARDS with septic shock correlate with disease severity and can serve as a non-invasive prognostic marker 2

• Oxygen Delivery-Consumption Relationship: Patients with ARDS who have lactic acidosis (>2.4 mmol/L) show significant dependence of oxygen consumption (VO₂) on oxygen delivery (DO₂), indicating tissue hypoxia 3

• Mortality Correlation: Oxygen delivery below 8 ml/kg/min in critically ill ARDS patients correlates with markedly increased lactate levels and poor survival (14% vs 55% with higher oxygen delivery) 4

Management Implications

• Resuscitation Guidance: The Surviving Sepsis Campaign recommends guiding resuscitation to normalize lactate in patients with elevated levels as a marker of tissue hypoperfusion (weak recommendation, low quality of evidence) 1

• Lactate Clearance: Targeting at least 10% lactate clearance within 2-4 hours is associated with improved outcomes 5

• Fluid Management: Careful fluid administration is crucial as excessive fluids may worsen oxygenation by increasing pulmonary edema and potentially precipitating cor pulmonale 1

Important Considerations

• Non-Hypoxic Causes: Not all lactate elevation in ARDS is due to tissue hypoxia:

  • β-adrenergic medications (including bronchodilators used in management) can cause lactic acidosis even without hypoxemia 6
  • Type B lactic acidosis (without evidence of inadequate oxygen delivery) should be considered in persistent elevations 7

• Bicarbonate Therapy: The Surviving Sepsis Campaign suggests against sodium bicarbonate therapy for hypoperfusion-induced lactic acidemia with pH ≥7.15 1

• Monitoring Parameters: Beyond lactate, monitoring should include clinical examination, hemodynamic assessment, and evaluation of other physiologic variables (heart rate, blood pressure, oxygen saturation, respiratory rate, temperature, urine output) 1

Remember that while lactate elevation is common in ARDS, its interpretation should consider the clinical context, medication effects, and other potential causes beyond tissue hypoxia.