Lung Function: Splinting Effects

Introduction

• In the context of lung function, splinting refers to taking shallow breaths to prevent lung expansion and reduce pain.1 This is typically seen in patients with blunt thoracic trauma from falls, assault, motor vehicle injuries, or sports.
• Additionally, postoperative pleuritic or incisional pain is one of the most common settings in which respiratory splinting occurs. Postoperative atelectasis is more common after cardiac surgeries, especially those with cardiopulmonary bypass or needing mechanical ventilation.
• Other high-risk surgeries include thoracic, upper abdominal, bariatric, or spinal surgeries. This hypoventilation can lead to atelectasis and a higher risk of pneumonia due to decreased mucociliary clearance.

Anatomy and Physiology

• Quiet inspiration, or respiration at rest, depends on diaphragmatic contraction with descent of the diaphragm and expansion of the lower rib cage, increasing thoracic volume and decreasing intrathoracic pressure. The external intercostals and accessory muscles contribute to deeper breaths or forced inspiration.
• At end-expiration, FRC represents the balance point between lung elastic recoil and chest wall outward recoil. FRC is important for maintaining alveolar patency and preventing lung collapse.
• Please see the OA summary on Lung Mechanics for more details. Link
• Pain inhibits deep inspiration as the expanded lungs and chest wall tend to increase the pain. In response, the patient instinctively will reduce diaphragmatic excursion to avoid worsening the pain.
• Shallow breathing decreases tidal volume, thereby lowering FRC and promoting airway closure. Early airway closure promotes alveolar instability and increases the likelihood of atelectasis.
• Pulmonary atelectasis can cause various consequences, including respiratory insufficiency/hypoxemia, pneumonia, and worse overall outcomes, such as increased risk of postoperative pulmonary complications, delayed recovery and mobilization, or increased length of hospital stay.²
• Additionally, patients will have an ineffective cough due to guarding and pain, which impairs mucus clearance and causes airway plugging, thereby increasing the risk of pneumonia.⁶
• A meta-analysis from 2017 reported that postoperative pulmonary complications, such as respiratory infection, acute respiratory distress syndrome, pleural effusion, atelectasis, and others, increase postoperative mortality. 14-30% of patients will die from a postoperative pulmonary complication within 30 days of surgery, compared to 0.2-3% of patients without a postoperative pulmonary complication.³

Risk Factors for Atelectasis and Hypoxemia

Several risk factors are associated with pulmonary atelectasis.²

• Age: The susceptibility to airway closure is strongly age-dependent and is typically evaluated by the relationship between FRC and closing capacity (CC). CC represents the lung volume at which small airways begin to close, while FRC is the end-expiratory resting lung volume. When CC approaches or exceeds FRC, small airways close during normal tidal breathing, promoting regional hypoventilation and atelectasis. In young adults (aged 20 years), the FRC exceeds the CC, making airway closure unlikely.

• Obesity: Obesity increases the mechanical load on the respiratory system. The increased mass of thoracic and abdominal adipose tissue adds significant weight to the chest wall and increases the intra-abdominal pressure. This increases the compressive forces on the lungs and displaces the diaphragm upward, particularly in the supine position. As a result, greater pressure is required to achieve the same lung volumes, leading to lower respiratory system compliance and reduced baseline FRC. As discussed before, when FRC falls below the CC, small airways close during tidal breathing, leading to atelectasis. Obesity also changes the transpulmonary pressures needed during general anesthesia. Obese patients are at a greater risk for airway closure and atelectasis, and often require increased positive end-expiratory pressure maintain adequate positive end-expiratory transpulmonary pressure. Please see the OA summary on obesity: pulmonary manifestations for more details. Link
• Abdominal hypertension: Conditions such as ascites, portal hypertension, or even pregnancy increase the abdominal pressure that compresses the diaphragm. This limits the area available for diaphragmatic expansion, further reducing lung volumes. Higher abdominal pressure also increases pleural pressure, thereby reducing transpulmonary pressure. This increases the pressure required for the alveoli to remain open, thereby increasing the likelihood of airway closure and dependent atelectasis.
• Pulmonary disease: Pulmonary inflammation or fibrosis increases the risk of atelectasis and subsequent hypoxemia due to reduced surfactant production and reduced lung compliance. Chronic obstructive pulmonary disease (COPD) also increases the risk of atelectasis due to loss of elastic recoil. Patients with chronic lung disease have reduced reserve and impaired ability to reopen collapsed alveoli. Please see the OA summary on COPD for more details. Link
• Smoking: Smoking increases airway secretions that can cause bronchial obstruction and atelectasis. Chronic smoke exposure also impairs mucociliary clearance by damaging the ciliated respiratory epithelium, thereby increasing the likelihood of postoperative mucus retention. The airway epithelium produces more mucus as it becomes more inflamed and hyperreactive to normal airway constituents. Further, smoking increases the risk of chronic pulmonary disease and can cause COPD, which further compounds the risks of atelectasis. Please see the OA summary on cigarette smoking and anesthesia for more details. Link
• General anesthesia medications:
  • Opioids: Opioids decrease the neural stimulation for respiratory muscles and reduce the sensitivity of the osmoreceptors to hypercapnia. This results in reduced respiratory effort and cough production. Opioids also impair the generation of an effective cough by reducing respiratory muscle activation and expiratory force. This further increases the risk of hypoventilation and atelectasis.
  • Neuromuscular blocking agents: These agents can increase intra-abdominal pressure on the lungs and cause overall respiratory dysfunction by impairing muscle coordination and strength.⁴
• General anesthesia: General anesthesia decreases the diaphragmatic tone and decreases the FRC by 15-20%. 5 Using a high FiO₂ also promotes absorption atelectasis, in which oxygen diffuses out of the alveoli quickly, causing them to collapse. Longer surgery increases exposure to reduced FRC, impaired muscle tone, and high FiO₂, thereby increasing cumulative atelectasis. Please see the OA summary on effects of anesthesia on the respiratory system. Link
• Nature of surgery: Thoracic and upper abdominal surgeries are associated with the greatest diaphragmatic inhibition and postoperative pain, which increases splinting and risk of atelectasis compared to minimally invasive surgery.⁶ This could be caused by direct diaphragmatic injury, such as from surgical retraction; impaired cough, leading to limited mucus clearance; and reduced mobility.

Pain Regimens and Treatment for Respiratory Splinting

• Proper analgesia reduces splinting, thereby improving patient outcomes and reducing the risk of atelectasis. ERAS outlines a multimodal, opioid sparing pain control regimen that includes a combination of acetaminophen, nonsteroidal anti-inflammatory drugs or COX-2 inhibitors, gabapentin, ketamine, tramadol, or regional techniques such as peripheral nerve blocks.⁷ Opioid containing regimens can cause respiratory depression, drowsiness, and delayed mobilization. This increases the risk of atelectasis and hypoxemia.
• An enhanced recovery after thoracic surgery review noted that the ERAS pain regimen improved outcomes, reduced complications, and helped to preserve pulmonary function.⁶ It allows patients to take deeper breaths and preserve tidal volume as well as produce a cough if necessary to clear mucus buildup. It also enables early mobilization, which further increases lung volumes and clearance of secretions.
• Targeted, multimodal analgesia is therefore a core strategy in preventing splinting-related pulmonary complications, including atelectasis, hypoxemia, and progression to respiratory failure.