Pulmonary Embolism and Acid-Base Status
No, pulmonary embolism typically causes respiratory alkalosis, not respiratory acidosis. Respiratory acidosis in the setting of PE would be atypical and should raise concern for pre-existing pulmonary disease, severe respiratory failure, or impending cardiopulmonary collapse. 1
The Typical Acid-Base Pattern in PE
Respiratory alkalosis is the most common acid-base disturbance in acute pulmonary embolism, characterized by hypocapnia (decreased PaCO2) and increased pH. 1 This occurs through the following mechanism:
Hyperventilation drives the alkalosis: Patients with PE typically develop tachypnea and increased minute ventilation in response to hypoxemia, V/Q mismatch, and stimulation of pulmonary receptors, leading to excessive CO2 elimination 1
Decreased PaCO2 is a common finding: The ventilation-perfusion mismatch from obstructed pulmonary vessels combined with overflow in non-obstructed vessels contributes to this respiratory alkalosis 1
Why Respiratory Acidosis Would Be Atypical
Respiratory acidosis is NOT a typical finding in uncomplicated pulmonary embolism. 1 The presence of respiratory acidosis (elevated PaCO2 with decreased pH) in a patient with suspected or confirmed PE suggests one of the following concerning scenarios:
Pre-existing Pulmonary Disease
- Patients with chronic obstructive pulmonary disease, severe asthma, or other conditions causing baseline hypoventilation may develop respiratory acidosis when PE occurs 1, 2
- The underlying lung disease prevents the normal compensatory hyperventilation response 2
Severe Respiratory Failure
- In advanced PE with profound respiratory compromise, the patient may become unable to maintain adequate ventilation 1
- This represents a critical deterioration requiring immediate intervention 2
Terminal Stages with Cardiopulmonary Collapse
- Respiratory acidosis in PE may indicate impending or actual cardiopulmonary arrest 1
- This occurs when right ventricular failure becomes so severe that cardiac output collapses, leading to inadequate tissue perfusion and ventilatory failure 3
The Pathophysiology of Gas Exchange in PE
Understanding why PE causes alkalosis rather than acidosis requires recognizing that respiratory symptoms in PE are predominantly consequences of hemodynamic disturbances rather than direct impairment of gas exchange. 1
- Low cardiac output from right ventricular failure leads to desaturation of mixed venous blood 1
- Ventilation-perfusion mismatch occurs from zones of reduced flow in obstructed arteries combined with overflow in non-obstructed vessels 3, 1
- Right-to-left shunting through a patent foramen ovale (present in about one-third of patients) can cause severe hypoxemia 3
- Despite these mechanisms causing hypoxemia, the intact ventilatory response produces hyperventilation and alkalosis 1, 4
Clinical Implications and Pitfalls
If you encounter a patient with suspected PE who has respiratory acidosis, consider the following:
- Reassess the diagnosis: Could this be another condition causing hypoventilation? 2
- Evaluate for pre-existing lung disease: Does the patient have COPD, severe asthma, or neuromuscular disease affecting ventilation? 1, 2
- Recognize severity: Respiratory acidosis in confirmed PE may indicate critical illness requiring immediate advanced support including possible mechanical ventilation or extracorporeal support 1, 5
- Don't be falsely reassured by normal oxygenation: Approximately 40% of PE patients have normal arterial oxygen saturation, yet they still typically have respiratory alkalosis 1
The development of a base deficit in PE suggests more severe disease with longer diagnostic delay, and is associated with more pronounced hypocapnia and metabolic compensation, not respiratory acidosis. 1