Can A Pulmonary Embolism (PE) Cause Atelectasis?

Pulmonary embolism is a pathology with a high incidence in our environment. The deleterious, hemodynamic changes that develop once the embolism has been established, determine the serious and acute complications that this event frames.

Can A Pulmonary Embolism (PE) Cause Atelectasis?

Can a Pulmonary Embolism (PE) Cause Atelectasis?

In relation with pulmonary repercussion of pulmonary embolism, the decrease or absence of pulmonary perfusion produces increased alveolar dead space, reflex bronchoconstriction, and atelectasis. The alveolar produced hypoventilation, the existence of zones of pulmonary infarction and alterations in the pulmonary surfactant produce hypoxemia and retention of carbon dioxide.

Mechanism Of Heart Failure

When the obstruction of the pulmonary arteries due to embolism occurs, the following are affected: 1) Pulmonary tissue, 2) The pulmonary circulation, and 3) The function of the right and left the heart. The degree of cardiopulmonary compromise correlates with the severity of the occlusion produced by the embolus and with the degree of the patient’s underlying disease.

Alterations In Gas Exchange

Abnormalities of gas exchange in the lungs are an inevitable consequence of pulmonary embolization. It is likely that the etiology of the gas exchange abnormality is complex and multifactorial, and may differ from one patient to another. Abnormalities of gas exchange in these patients are complex and depend on the size and characteristics of the embolic material, the extent of the occlusion, the patient’s previous cardiopulmonary status, and the time elapsed since embolization.

The right-to-left shunt, an alteration in the ventilation-perfusion relationship and in certain patients, a drop in the oxygen tension of the venous blood, has played a role in the process of abnormal gas exchange leading to hypoxemia (an abnormal decrease in the oxygen partial pressure in the arterial blood) follow the pulmonary embolism. The etiology of these physiological alterations has not been clearly defined, but there are several hypotheses:

  1. Pulmonary areas with a low ventilation-perfusion ratio may develop due to over perfusion of non-embolized lung regions. Low ventilatory/perfusion ratios can develop as a consequence of the redistribution of blood away from the embolized area, resulting in an over-perfusion of the non-embolized lung areas and atelectasis that initially develop distally to the embolic obstruction that still persists after the early dissolution of the embolism and the resulting reperfusion.
  2. Atelectasis can develop in areas distal to embolic obstruction and with subsequent dissolution or with distal migration of the embolic material; there is reperfusion of these pulmonary areas. The reversal of post-embolic hypoxemia with positive pressure ventilation supports the belief in this theory. Atelectasis can have many causes. Hemorrhagic atelectasis appears to be the result of the loss of surfactant that occurs when the blood flow from the pulmonary artery is occluded. A phenomenon of “air movement” can occur in the regional pulmonary hypoperfusion and be the cause of regional hypocapnia (deficiency of carbon dioxide in the arterial blood) which in turn induces bronchiolar constriction and pneumoconstriction and lead to atelectasis, in addition the embolic material is covered with platelets and this has been proposed as a cause of atelectasis promoting pneumoconstriction and loss of surfactant.
  3. In a variety of animal models of experimentation, the post-embolic pulmonary edema has been shown to play an important role in the development of hypoxemia, but these results are difficult to relate to humans. Another possibility that should be considered is that, with the development of pulmonary hypertension, right ventricular overload, and an increase in right atrial pressure follow pulmonary embolism; there, a deviation of the flow can be developed through a persistent foramen ovale. Approximately 15% of the normal population has a persistent foramen ovale, so this mechanism must be taken seriously.

The pulmonary vascular disease is generally defined as an anatomical narrowing of the pulmonary vascularization. In a broader sense, it can also be defined as a change in the pulmonary vascular impedance in certain regions, which comes from anomalies in the lumen or the walls of pulmonary vessels. There are different clinical situations that cause pulmonary vascular disease, where gas exchange can be evaluated using the multiple elimination techniques.

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