From the Guidelines
In pulmonary embolism, ventilation remains normal in affected lung areas, but perfusion is significantly decreased, creating a ventilation-perfusion mismatch, with airway resistance typically normal, lung compliance slightly decreased, minute ventilation increased, and pO2 decreased with pCO2 normal or decreased on ABG, as supported by the 2014 ESC guidelines 1. In pulmonary embolism (PE), there are characteristic changes in respiratory physiology and blood gases.
- Ventilation remains normal in affected lung areas, but perfusion is significantly decreased due to blood vessel obstruction by the embolus, creating a ventilation-perfusion (V/Q) mismatch.
- Airway resistance typically remains normal since PE affects blood vessels rather than airways.
- Lung compliance may decrease slightly due to compensatory vasoconstriction in non-affected areas and potential atelectasis.
- Minute ventilation often increases as the body attempts to compensate for hypoxemia.
- On arterial blood gas (ABG), pO2 is usually decreased (hypoxemia) due to the V/Q mismatch, while pCO2 is often normal or decreased (hypocapnia) due to compensatory hyperventilation. The goal is to maintain an oxygen saturation of 94–98% (or 88–92% if the patient is at risk of hypercapnic respiratory failure) as recommended by the BTS guideline for oxygen use in adults 1. In severe PE, respiratory failure may develop with rising pCO2 levels, and mechanical ventilation may be required, with careful consideration of tidal volumes and positive end-expiratory pressure (PEEP) to avoid worsening RV failure, as suggested by the 2014 ESC guidelines 1. These physiological changes reflect the body's attempt to maintain oxygenation despite blocked pulmonary blood flow, with the severity of abnormalities correlating with the size and extent of the embolism.
From the Research
Pulmonary Embolism: Ventilation, Perfusion, and Gas Exchange
- In pulmonary embolism, there is typically an increase in ventilation rate as a response to the condition, prior to cardiac failure, which is at least in part due to systemic hypoxemia 2.
- The increase in ventilation and cardiac output can improve overall gas exchange in pulmonary embolism, but this comes at the cost of an increased pulmonary blood pressure, which may contribute to pulmonary hypertension as a result of the condition 2.
- Acute pulmonary thromboembolism produces a number of pathophysiologic derangements of pulmonary function, including increased pulmonary vascular resistance, and disturbs matching of ventilation and blood flow, resulting in some lung units being overventilated relative to perfusion and others being underventilated relative to perfusion 3.
Airway Resistance and Compliance
- Abnormalities of pulmonary compliance and airway resistance may accompany pulmonary embolism 3.
- However, the exact changes in airway resistance and compliance in pulmonary embolism are not well-defined in the provided studies.
Minute Ventilation
- Minute ventilation may increase in response to pulmonary embolism, as the body attempts to compensate for the decreased gas exchange and hypoxemia 2.
- However, the exact changes in minute ventilation in pulmonary embolism are not well-defined in the provided studies.
pCO2 and pO2 on ABG
- Pulmonary embolism can lead to abnormalities in gas exchange, resulting in changes in pCO2 and pO2 on arterial blood gas (ABG) analysis 3, 4.
- However, the exact changes in pCO2 and pO2 in pulmonary embolism are not well-defined in the provided studies, and would depend on the severity of the condition and the individual patient's response.