Can pulmonary embolism (PE) cause lactic acidosis?

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Last updated: July 6, 2025View editorial policy

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From the Guidelines

Yes, pulmonary embolism (PE) can cause lactic acidosis, as evidenced by the 2020 ESC guidelines for the diagnosis and management of acute pulmonary embolism 1. This occurs when a blood clot lodges in the pulmonary arteries, obstructing blood flow to the lungs and creating a ventilation-perfusion mismatch. The resulting tissue hypoxia forces cells to switch from aerobic to anaerobic metabolism, producing lactic acid as a byproduct.

Key Points to Consider:

  • In severe PE cases, reduced cardiac output from right heart strain further compromises systemic perfusion, worsening tissue hypoxia and lactic acid production.
  • Clinically, lactic acidosis may manifest as tachypnea, altered mental status, and metabolic acidosis on arterial blood gas analysis, with lactate levels typically above 2 mmol/L, as described in the context of metabolic acidosis 1.
  • The presence of lactic acidosis in PE patients often indicates severe disease and may be associated with higher mortality.
  • Treatment focuses on addressing the underlying PE through anticoagulation (typically with heparin initially, followed by oral anticoagulants), considering thrombolysis in massive PE, and supporting oxygenation and hemodynamics while the body clears the excess lactate once tissue perfusion improves.

Pathophysiological Considerations:

  • The 2020 ESC guidelines highlight that pulmonary arteries, combined with zones of overflow in the capillary bed served by non-obstructed pulmonary vessels, result in ventilation/perfusion mismatch, which contributes to hypoxaemia 1.
  • Right-to-left shunting through a patent foramen ovale can be detected by echocardiography in about one-third of patients, leading to severe hypoxaemia and an increased risk of paradoxical embolization and stroke.
  • Acute RV failure is a critical determinant of clinical severity and outcome in acute PE, with clinical symptoms and signs of overt RV failure and haemodynamic instability indicating a high risk of early mortality.

From the Research

Lactic Acidosis and Pulmonary Embolism

  • Lactic acidosis is a condition characterized by the accumulation of lactate in the body, often due to tissue hypoxia or impaired oxygen utilization 2.
  • Pulmonary embolism (PE) is a condition where a blood clot blocks the flow of blood in the lungs, which can lead to tissue hypoxia and potentially lactic acidosis.
  • Studies have shown that lactic acidosis can occur in critically ill patients, including those with PE, due to reduced oxygen utilization and tissue hypoperfusion 3, 4.
  • The development of acidemia in critically ill patients, including those with PE, is often attributed to reductions in oxygen utilization, leading to anaerobic metabolism and lactic acidosis 4.
  • However, there is no direct evidence in the provided studies that specifically links PE to lactic acidosis as a direct cause-and-effect relationship.
  • Treatment of lactic acidosis typically involves restoring adequate tissue perfusion and oxygenation, which may be achieved through thrombolytic therapy in the case of PE 5, 6.
  • Thrombolytic therapy has been shown to improve right-ventricular function and pulmonary perfusion in patients with PE, which may help to reduce the risk of lactic acidosis 6.

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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