Open heart surgery (OHS) is a major procedure, and patients often worry about complications like a “collapsed lung,” which describes a loss of lung volume. Experiencing some degree of lung volume loss is extremely likely, though the specific type and severity vary significantly among patients. Understanding the difference between the expected and the rare complications is important for managing expectations during recovery.
Understanding the Likelihood of Post-Surgical Lung Collapse
The question of whether a collapsed lung is common after open heart surgery requires distinguishing between two distinct medical conditions: atelectasis and pneumothorax. Atelectasis is a partial collapse of the tiny air sacs (alveoli) and is the most frequent pulmonary complication after OHS. Studies show a significant degree of atelectasis in the majority of patients, with incidence ranging from 30% to over 70% based on post-operative chest imaging.
This partial collapse is considered an expected consequence of general anesthesia and the surgery itself, often causing temporary breathing difficulties and reduced oxygen levels. However, a true pneumothorax—a complete collapse where air leaks into the pleural space between the lung and the chest wall—is a far less common event. The incidence of pneumothorax is low, typically around 1.4% of patients, and is usually related to specific procedural events, such as the insertion or removal of chest tubes.
Specific Mechanisms Leading to Post-Operative Lung Issues
The physiological changes induced by OHS promote lung volume loss, starting with general anesthesia and mechanical ventilation. Anesthesia suppresses the natural drive to take deep breaths, and the use of muscle relaxants causes the diaphragm to move upward, compressing the lower portions of the lung. This combination rapidly leads to the formation of atelectasis in the dependent regions of the lungs, often within minutes of inducing anesthesia.
The physical trauma of the surgery further complicates lung function due to the proximity of the heart, lungs, and diaphragm. Manipulation of the chest cavity or procedures like harvesting the internal thoracic artery can irritate or temporarily injure the phrenic nerve, which controls the diaphragm muscle. When the diaphragm is weakened or paralyzed, the ability to fully expand the lung is significantly reduced, directly contributing to collapse and impaired gas exchange.
Post-operatively, the sternal incision causes considerable pain, leading patients to take rapid, shallow breaths, a phenomenon known as “splinting.” This restricted breathing prevents small airways from re-expanding fully, prolonging atelectasis and hindering secretion clearance. Additionally, fluid accumulation, known as a pleural effusion, is common after OHS and can exert external pressure on the lung tissue, physically compressing it.
Identifying Symptoms and Clinical Management
Post-operative lung compromise can manifest through several recognizable symptoms, though the severity depends on the extent of the collapse. Patients may experience shortness of breath, rapid and shallow breathing, and a persistent cough. A drop in the body’s oxygen saturation levels is a key clinical sign, and patients may also report chest pain, particularly when attempting to take a deep breath.
Doctors confirm the presence and extent of lung issues primarily through a chest X-ray, which is a standard procedure in the immediate post-operative period. For the common atelectasis, management focuses heavily on non-invasive techniques that require active patient participation. The cornerstone of this recovery is the use of an incentive spirometer, a device that encourages patients to take slow, maximal deep breaths to re-inflate the collapsed air sacs. Early and frequent ambulation also plays a significant role in improving lung function and clearing secretions.
In the event of a true, severe pneumothorax, a more direct intervention is necessary to re-establish normal lung volume. This typically involves inserting a temporary chest tube into the pleural space to drain the trapped air, allowing the lung to fully re-inflate and ensuring the patient’s respiratory stability.