Pneumothorax and Chest Tube Management

Overview

A pneumothorax is the accumulation of air in the pleural space, separating the visceral and parietal pleura and causing partial or complete lung collapse. The degree of respiratory impairment depends on the size of the pneumothorax, how quickly it develops, and — critically — whether the patient has pre-existing lung disease. At one end of the spectrum is the small primary spontaneous pneumothorax in a healthy young adult that may resolve with observation alone; at the other end is tension pneumothorax, a medical emergency requiring immediate decompression.

This guide covers the disease spectrum, the indications and techniques for pleural drainage, and the respiratory therapist’s role in managing chest tubes and closed drainage systems. The immediate resuscitation of a tension pneumothorax — including needle decompression — is covered in depth in the tension pneumothorax emergency guide; cross-reference it when managing the unstable patient.

Key Concepts

Pneumothoraces are classified by etiology, and the distinction drives management decisions:

• Primary spontaneous pneumothorax— occurs in the absence of underlying lung disease, most commonly in tall, thin young men who smoke. The mechanism is rupture of apical subpleural blebs. Because the remaining lung is healthy, these patients typically tolerate the event better than those with pre-existing disease.
• Secondary spontaneous pneumothorax— complicates existing lung pathology: emphysema and COPD (the most common cause), cystic fibrosis, interstitial lung disease, and pulmonary infections including Pneumocystis jirovecii pneumonia. Even a small pneumothorax can cause life-threatening decompensation when lung reserve is already limited.
• Iatrogenic pneumothorax— results from procedures that violate the pleural space or raise intrathoracic pressures: central venous catheter placement (subclavian or internal jugular), thoracentesis, transbronchial or percutaneous lung biopsy, and barotrauma from high airway pressures or excessive PEEP during mechanical ventilation.
• Tension pneumothorax— a one-way valve mechanism allows air to enter the pleural space with each breath but prevents it from escaping. Pressure builds, compressing the ipsilateral lung, shifting the mediastinum to the contralateral side, kinking the great veins, and reducing venous return. The result is obstructive shock. This is a clinical diagnosis treated with immediate needle decompression followed by definitive chest tube insertion; a chest X-ray should not delay treatment. Full management is covered in the tension pneumothorax emergency guide.

Three-chamber closed drainage system

Understanding the drainage unit is central to chest tube management. The three chambers serve distinct functions:

• Collection chamber— collects blood, fluid, or exudate draining from the pleural space. Volume and character are documented on every assessment.
• Water-seal chamber— acts as a one-way valve, allowing air to exit the pleural space while preventing atmospheric air from entering. Normal respiratory pressure swings produce tidaling: the fluid level rises with inspiration (negative pleural pressure) and falls with expiration. Continuous bubbling in this chamber indicates an ongoing air leak and must be assessed systematically. Once the lung re-expands and the leak seals, both tidaling and bubbling cease.
• Suction-control chamber— governs the amount of negative pressure applied to the pleural space. In a wet-suction system, the water column height determines the suction level (commonly −20 cmH₂O); gentle continuous bubbling in this chamber confirms that suction is active. Dry-suction systems use a calibrated dial instead of a water column. The suction source pressure is set higher than the desired level — the chamber limits what reaches the patient.

Assessment & Findings

Clinical presentation ranges from mild dyspnea to cardiovascular collapse. Severity correlates with the size of the pneumothorax and the patient’s underlying reserve.

• Symptoms— sudden-onset pleuritic chest pain (sharp, worsening with inspiration) and dyspnea are the hallmarks. Small pneumothoraces in healthy patients may produce only mild discomfort; secondary pneumothoraces can cause severe respiratory distress with minimal air accumulation.
• Physical exam (affected side)— decreased or absent breath sounds, hyperresonance to percussion, and decreased tactile fremitus. In tension pneumothorax, the trachea deviates away from the affected side as mediastinal structures are pushed toward the contralateral hemithorax. Neck vein distension and hypotension may also be present.
• Chest X-ray— the upright CXR shows a thin visceral pleural line with absent peripheral lung markings beyond it. On a supine film (common in ICU patients), the air rises anteriorly and may appear only as a “deep sulcus sign” — an abnormally deep and lucent costophrenic angle.
• Lung ultrasound— absent lung sliding (the normal shimmering motion of the visceral pleura) at the affected side, with a “barcode” or “stratosphere” sign on M-mode, is a fast and highly sensitive bedside finding. Ultrasound is particularly valuable in unstable patients who cannot be transported for imaging.
• Ventilated patients— a sudden rise in peak inspiratory pressure and plateau pressure, accompanied by hypoxemia and hemodynamic instability, should immediately raise suspicion for tension pneumothorax. SpO₂ and blood pressure may deteriorate rapidly; do not wait for confirmatory imaging if the clinical picture is convincing.

RT Priorities / Interventions

The respiratory therapist’s priorities span supplemental oxygen delivery, assistance with drainage procedures, ongoing chest tube and system management, and ventilator optimization to prevent worsening.

• Supplemental oxygen for reabsorption— in a small, stable, conservatively managed pneumothorax, administering high-flow or 100% oxygen accelerates pleural air reabsorption via nitrogen washout. Because the pleural air is predominantly nitrogen, delivering high fractional inspired O₂ reduces blood nitrogen partial pressure, steepening the diffusion gradient and drawing nitrogen out of the pleural space up to four times faster than on room air.
• Intervention thresholds— small or asymptomatic primary spontaneous pneumothoraces in hemodynamically stable patients may be managed with observation and supplemental oxygen. Larger pneumothoraces, symptomatic presentations, secondary spontaneous pneumothorax, and all iatrogenic pneumothoraces in ventilated patients typically require needle aspiration or insertion of a small-bore (pigtail) or large-bore chest tube.
• Chest tube and drainage system management— keep the drainage unit below the level of the patient’s chest at all times to prevent back-flow of fluid into the pleural space. On every assessment: confirm tidaling (normal swings with breathing), check for continuous bubbling (air leak), document drainage volume and character, and inspect the insertion-site dressing for occlusion and subcutaneous emphysema. Ensure all connections are secure and tubing is free of dependent loops that trap fluid.
• Troubleshooting an air leak— if continuous bubbling is present, localize the source before attributing it to the patient. Inspect the tubing and connections for breaks; briefly occlude the tubing close to the insertion site with a padded clamp — if bubbling stops, the leak is from the patient or insertion site; if it continues, the leak is in the system distal to the clamp. Never leave the tube clamped.
• Ventilator management for barotrauma prevention— in mechanically ventilated patients at risk for or with an existing pneumothorax, minimize plateau pressure (target ≤28–30 cmH₂O), use the lowest effective PEEP, and consider lung-protective tidal volumes (6 mL/kg ideal body weight). Elevated peak pressures with stable plateaus suggest tube obstruction or secretions; elevated plateaus suggest reduced compliance, which can signal a new pneumothorax.

Common Pitfalls

• Clamping a tube with an active air leak— the most dangerous error. Clamping a chest tube that is actively bubbling traps air in the pleural space and can rapidly convert a simple pneumothorax into a fatal tension pneumothorax. Never clamp a chest tube without physician order and only when there is no active air leak.
• Elevating the drainage unit above the chest— gravity-dependent drainage requires the unit to remain below the insertion site. Lifting the unit during patient transport allows fluid to flow back into the pleural space, risking empyema and loss of drainage.
• Confusing tidaling with an air leak— tidaling is the rhythmic fluid swing in the water-seal chamber synchronized with breathing; it is normal and indicates a patent tube. An air leak is identified by continuous bubbling, independent of respiratory phase. Misidentifying one for the other leads either to unnecessary intervention or to a missed leak.
• Waiting for imaging before treating tension pneumothorax— tension pneumothorax is a clinical diagnosis. Sending a hemodynamically unstable patient to radiology for confirmatory imaging can be fatal. When the clinical picture is consistent — absent breath sounds, tracheal deviation, hypotension, distended neck veins — immediate needle decompression is indicated.
• Aggressive positive-pressure ventilation worsening barotrauma— high tidal volumes, excessive PEEP, and prolonged inspiratory times increase mean and peak alveolar pressures, raising the risk of alveolar rupture and pneumothorax extension or recurrence. Adopt lung-protective settings early in at-risk patients.

Board Exam Pearls

• Tracheal deviation in tension pneumothorax is away from the affected side. Treat immediately with needle decompression; do not wait for imaging.
• Continuous bubbling in the water-seal chamber = air leak. Tidaling = normal respiratory pressure swings. Know the difference; the TMC exam tests both.
• Never clamp a chest tube with an active air leak — this is a high-yield safety rule that appears frequently on respiratory therapy board exams.
• 100% oxygen speeds reabsorption of a small spontaneous pneumothorax through nitrogen washout, not by increasing O₂ delivery to the collapsed lung.
• Classic triad on the affected side: hyperresonant percussion + absent breath sounds + decreased tactile fremitus. In tension, add tracheal deviation, distended neck veins, and hemodynamic compromise.
• In a ventilated patient, a sudden rise in both peak and plateau pressures with hemodynamic instability should prompt evaluation for tension pneumothorax.
• Secondary spontaneous pneumothorax (e.g., in severe COPD) is less well tolerated than primary and almost always requires drainage regardless of size.

FAQ

Related Resources

Sources

1. Kacmarek RM, Stoller JK, Heuer AJ. Egan's Fundamentals of Respiratory Care. 12th ed. Elsevier; 2021.
2. MacDuff A, Arnold A, Harvey J; BTS Pleural Disease Guideline Group. Management of spontaneous pneumothorax: British Thoracic Society Pleural Disease Guideline 2010. Thorax. 2010;65 Suppl 2:ii18-ii31.
3. Cairo JM. Mosby's Respiratory Care Equipment. 11th ed. Elsevier; 2022.