Can pulmonary embolism lead to respiratory acidosis or alkalosis?

Pulmonary Embolism Primarily Causes Respiratory Alkalosis, Not Acidosis

Pulmonary embolism (PE) predominantly leads to respiratory alkalosis due to ventilation-perfusion mismatch and hyperventilation, though in severe cases or with diagnostic delay, a base deficit may develop despite persistent respiratory alkalosis. 1, 2

Pathophysiological Mechanisms of Respiratory Changes in PE

• Respiratory alkalosis is the most common acid-base disturbance in acute PE, characterized by hypocapnia (decreased PaCO2) and increased pH 1, 2

• The primary mechanisms causing respiratory alkalosis in PE include:

  • Ventilation-perfusion mismatch from obstructed pulmonary vessels combined with zones of overflow in non-obstructed vessels 1
  • Hyperventilation triggered by hypoxemia, anxiety, and pain 2
  • Stimulation of pulmonary receptors due to the embolism itself 3

• Hypoxemia in PE results from:

  • Low cardiac output leading to desaturation of mixed venous blood 1
  • Ventilation-perfusion mismatch contributing to arterial hypoxemia 1
  • Right-to-left shunting through a patent foramen ovale in approximately one-third of patients 1

Clinical Presentation and Blood Gas Findings

• Respiratory alkalosis is found in 23-37% of PE patients, with the percentage varying based on whether arterial or capillary blood is analyzed 4
• Hypoxemia is present in 63-100% of patients depending on the sampling method, but approximately 40% of patients may have normal arterial oxygen saturation 2, 4
• Blood gas analysis typically shows:
  • Decreased PaCO2 (hypocapnia) 1, 3
  • Increased pH (alkalemia) 3
  • Decreased PaO2 (hypoxemia) in most but not all cases 4

Development of Base Deficit in PE

• Despite respiratory alkalosis being the primary acid-base disturbance, some PE patients develop a base deficit without overt circulatory failure 3
• This base deficit is associated with:
  • More severe pulmonary vascular obstruction (48±12% vs. 36±17% obstruction index) 3
  • Greater diagnostic delay (fewer patients diagnosed within one week) 3
  • Lower bicarbonate levels (22.5±0.7 vs. 26.1±1.6 mmol/L) 3
  • More pronounced hypocapnia (PaCO2 33±3 vs. 36±5 mmHg) 3

Clinical Implications and Pitfalls

• Normal blood gas values do not rule out PE - approximately 40% of patients may have normal oxygen saturation 2, 4

• The absence of respiratory alkalosis does not exclude PE diagnosis, especially in patients with pre-existing cardiorespiratory disease 2

• The development of a base deficit in a patient with PE suggests:

  • More severe disease 3
  • Longer diagnostic delay 3
  • Possible underlying conditions such as cardiorespiratory disorders or cancer 3
  • Need for closer monitoring and treatment 3

• Respiratory acidosis is not a typical finding in uncomplicated PE and would suggest:

  • Pre-existing pulmonary disease 2
  • Severe respiratory failure requiring mechanical ventilation 5
  • Terminal stages with cardiopulmonary collapse 1

Key Points for Clinical Practice

• Suspect PE in patients with unexplained dyspnea and respiratory alkalosis, even with normal oxygenation 2
• The presence of base deficit in a PE patient with respiratory alkalosis indicates more severe disease and possible diagnostic delay 3
• Risk stratification of PE should be based primarily on hemodynamic stability and right ventricular function rather than solely on oxygenation status 2
• The development of respiratory acidosis in PE is uncommon and suggests either severe respiratory failure or pre-existing pulmonary disease 1, 5