Tension pneumothorax

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

A one-way-valve effect raises intrapleural pressure, collapses the ipsilateral lung, shifts the mediastinum and impairs venous return. Positive-pressure ventilation can make deterioration extremely rapid.

Tension is diagnosed from cardiorespiratory compromise plus a plausible pleural cause. Stable radiographic mediastinal shift without physiological compromise is not automatically tension and should not trigger an unplanned emergency incision.

Needle decompression can fail because the catheter is too short, kinked, displaced, blocked or valved. Open thoracostomy gives more reliable access in trained hands and must still be followed by a method that maintains pleural drainage.

No response after technically adequate decompression should trigger a structured recheck: wrong side/diagnosis, contralateral tension, haemothorax, tamponade, profound haemorrhage, tube/circuit problem or ongoing bronchial obstruction.

Key points

Tension pneumothorax is pleural air under pressure causing severe respiratory compromise and/or obstructive shock; it is physiology, not simply mediastinal shift on an image.
Suspect it after chest trauma, positive-pressure ventilation/NIV, pleural/lung procedure or spontaneous pneumothorax with abrupt hypoxia, hypotension or peri-arrest deterioration.
Look for unilateral reduced/absent breath sounds and expansion, hyperresonance, rapidly increasing airway pressures, falling tidal volumes, distended neck veins or surgical emphysema; tracheal deviation is late and unreliable.
NICE says decompress before imaging only when haemodynamic instability or severe respiratory compromise is present; in that situation, do not wait for CXR or CT.
In hospital, open thoracostomy followed by chest drain is preferred over needle decompression when appropriately trained expertise is available.
A trained lateral thoracostomy is made in the 4th or 5th intercostal space just anterior to the mid-axillary line; follow the trauma/pleural procedural standard and protect the neurovascular bundle.
If open thoracostomy cannot be delivered immediately, needle thoracostomy with a sufficiently long standard non-valved cannula is a temporary bridge, followed urgently by definitive thoracostomy/chest drain.
Never use a blood-control/closed-system IV cannula for needle decompression unless the specific device and required extra equipment are approved for that use; NHS England issued a national safety alert.
In traumatic cardiac arrest, trained teams should perform immediate bilateral chest decompression while treating haemorrhage, hypoxia and tamponade; POCUS must not delay this or prolong CPR pauses.
After decompression, reassess breath sounds, chest movement, SpO2, BP, airway pressure and clinical response, secure definitive drainage and image only once physiology permits.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Traumatic pleural injury

Penetrating or blunt chest trauma can create a one-way air leak, especially when tissue flaps or dressings prevent pressure release.

Positive-pressure ventilation

Ventilation can force air through injured or fragile lung into the pleural space, causing rapid pressure accumulation and haemodynamic collapse.

Spontaneous pneumothorax

A primary or secondary spontaneous air leak can evolve into tension physiology when pleural gas continues to enter but cannot escape.

Iatrogenic injury

Central venous access, pleural procedures, biopsy or resuscitation may breach pleura and create tension, particularly during subsequent positive-pressure support.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
One-way pleural filling
Air enters the pleural space during inspiration or ventilation but cannot leave effectively, so intrapleural pressure rises breath by breath.
2
Lung collapse
Increasing pressure compresses the affected lung and may displace the mediastinum, producing severe ventilation-perfusion mismatch and hypoxaemia.
3
Venous return obstruction
Raised intrathoracic pressure compresses the venae cavae and right heart, sharply reducing preload and cardiac output.
4
Obstructive shock
Progressive hypoxaemia and circulatory obstruction cause hypotension, altered consciousness and pulseless electrical activity unless pressure is relieved immediately.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Spontaneously breathing patientRed flag

Acute pleuritic pain and severe dyspnoea progressing to unilateral absent breath sounds, hypoxaemia, tachycardia and hypotension; agitation may precede reduced consciousness.

Ventilated patientRed flag

Abrupt desaturation, hypotension, rising peak airway pressure, reduced delivered tidal volume and unilateral reduced breath sounds; arrest can follow within minutes.

Traumatic arrestRed flag

Chest trauma with PEA/near-arrest, hypoxia or difficult ventilation: tension is a reversible cause that is treated by immediate bilateral decompression in the trained trauma pathway.

Procedure-related tensionRed flag

Sudden compromise after central line, lung biopsy, thoracentesis, drain removal or positive-pressure initiation should prompt immediate pleural assessment and decompression when unstable.

Not all absent sliding is tension

Mainstem intubation, pleurodesis, fibrosis and apnoea can alter ultrasound/lung findings; physiology and the whole airway/chest assessment determine the emergency action.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Immediate clinical ABCDE assessmentFirst step
Why
Establish severe respiratory compromise or obstructive shock and choose emergency decompression.
Interpretation and limitations
Instability plus unilateral chest findings is sufficient to act; repeated examination after intervention tests the working diagnosis.
02
Airway and ventilator/circuit check
Why
Exclude tube displacement, obstruction, disconnection and severe dynamic hyperinflation.
Interpretation and limitations
Pass a suction catheter, check tube depth and circuit while another trained clinician prepares chest decompression; do not allow sequential checks to delay treatment in peri-arrest tension.
03
Point-of-care thoracic ultrasound
Why
Support the diagnosis and identify side when immediately available in skilled hands.
Interpretation and limitations
Absent sliding/B-lines and lung point support pneumothorax; in arrest, RCUK says POCUS must not prolong pauses or delay treatment.
04
Chest X-ray
Why
Confirm a stable suspected pneumothorax and check definitive drain/complications after stabilisation.
Interpretation and limitations
Do not obtain before decompression when tension causes haemodynamic instability or severe respiratory compromise.
05
Response to decompression
Why
Confirm restoration of pleural pressure and guide further action.
Interpretation and limitations
Improved BP, ventilation, SpO2 and chest movement supports diagnosis; absent response requires immediate site/patency/contralateral and alternative-cause reassessment.
06
Blood gas, FBC, coagulation and group-and-save
Why
Assess respiratory failure, bleeding and trauma/procedure consequences after immediate treatment.
Interpretation and limitations
Do not wait for laboratory results before emergency decompression.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Massive haemothorax

Trauma with shock and unilateral reduced breath sounds also suggests intrapleural blood; percussion, ultrasound and the response to drainage help discriminate.

Cardiac tamponade

Obstructive shock with raised venous pressure but no unilateral pleural signs, plus pericardial fluid on focused ultrasound, favours tamponade.

Massive pulmonary embolism

Sudden shock, hypoxaemia and right-heart strain without unilateral pleural air indicate high-risk PE, but unstable patients may have more than one cause.

Endotracheal tube malposition

After intubation, unilateral breath sounds and hypoxaemia may reflect endobronchial placement; tube depth and imaging distinguish it from tension while rapid assessment continues.

Severe dynamic hyperinflation

In ventilated obstructive disease, breath stacking can cause hypotension and high airway pressures bilaterally, improving when expiratory time and circuit pressure are addressed.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01UnstableDecompress before imagingFirst stepSuspected tension pneumothorax with haemodynamic instability or severe respiratory compromise.

1Call resuscitation/trauma and airway help, give high-concentration oxygen, monitor and expose the chest; if on NIV/ventilation, temporarily release positive pressure as clinically safe while immediate decompression is prepared.
2Use open thoracostomy in hospital when an appropriately trained operator is immediately available; enter at the 4th/5th intercostal space just anterior to the mid-axillary line using the approved sterile trauma technique.
3If that cannot happen immediately, perform trained needle decompression with a long standard non-valved cannula as a bridge; never use an incompatible closed blood-control cannula.
4DefinitiveInsert/secure a definitive chest drain or maintain the thoracostomy according to the resuscitation pathway, then reassess physiology and obtain imaging when stable.

02Traumatic arrestBilateral decompressionTraumatic cardiac arrest or peri-arrest where tension pneumothorax is possible.

1Run the traumatic-arrest pathway, correcting catastrophic haemorrhage, oxygenation, tension pneumothorax and tamponade in parallel; these reversible causes take priority over routine sequential ALS tasks.
2Appropriately trained clinicians perform immediate bilateral finger thoracostomies at the lateral 4th/5th intercostal spaces; place drains as required to keep tracts patent.
3DefinitiveContinue blood-product resuscitation, airway/ventilation and definitive trauma transfer; use POCUS only if it does not interrupt or delay these actions.

03No responseRecheck the decompression and diagnosisShock or ventilation failure persists immediately after attempted decompression.

1DefinitiveCheck correct side/site and whether a needle is long enough, non-valved, patent and still in the pleural space; convert a needle to open thoracostomy/definitive drain promptly.
2Assess the contralateral chest and decompress bilaterally in traumatic arrest; check endotracheal tube, obstruction and dynamic hyperinflation.
3Search for major haemorrhage/haemothorax, tamponade, embolism and other 4H/4T causes while continuing resuscitation.

04Stable imaging findingPneumothorax without tension physiologyPneumothorax is suspected or imaged but the patient has no severe respiratory compromise or haemodynamic instability.

1Obtain appropriate imaging and classify spontaneous, traumatic or iatrogenic cause and high-risk features.
2Manage through the relevant pneumothorax pathway—conservative, ambulatory, aspiration or drain—rather than labelling every mediastinal shift as tension.
3Continue close observation; if physiology deteriorates, switch immediately to the unstable decompression pathway.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Treats life-threatening hypoxaemia during decompression and resuscitation.

Medical oxygen

High-concentration oxygen via reservoir mask at 15 L/min in severe compromise/peri-arrest; use 100% oxygen during ALS, then titrate after stabilisation to 94–98% or 88–92% if hypercapnia risk.

Oxygen does not relieve intrapleural pressure and must never delay decompression. Manage fire risk and titrate down after the emergency.

Reduces procedural pain for thoracostomy or definitive drain.

Lidocaine 1%

If the conscious patient's physiology allows seconds for anaesthesia, infiltrate the lateral thoracostomy/drain tract; total lidocaine without adrenaline should not exceed 3 mg/kg (1% = 10 mg/mL), using less in frailty/liver disease.

Do not delay life-saving decompression in peri-arrest. Avoid intravascular injection and record total dose.

Baseline post-procedural analgesia while a fuller multimodal plan is arranged.

Paracetamol after stabilisation

1 g orally/IV every 4–6 hours as needed, maximum 4 g/24 h in a typical adult; reduce in low body weight, liver disease, malnutrition or heavy alcohol use.

IV and oral doses are cumulative. Severe ongoing pain requires reassessment for malposition, bleeding or recurrent tension rather than analgesic escalation alone.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Cardiac arrest

Unrelieved obstructive shock progresses to pulseless electrical activity, compounded by severe hypoxaemia and acidosis, particularly when baseline cardiopulmonary reserve is limited.

Hypoxic brain injury

Prolonged failure of ventilation and circulation can cause irreversible neurological damage even after successful decompression, with severity determined by its extent and the patient's underlying reserve.

Re-expansion injury

Rapid reinflation of a substantially collapsed lung can rarely produce pulmonary oedema and worsening oxygenation after decompression.

Persistent air leak

Ongoing bronchopleural communication may prevent lung expansion and require continued drainage or thoracic specialist intervention, and increasing the burden of otherwise local respiratory disease.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Continuously monitor ECG, SpO2 and BP during resuscitation; in ventilated patients track peak pressure, delivered tidal volume and ETCO2.
Immediately after decompression, document the side, site, technique/device, air release and changes in BP, oxygenation and ventilation.
Inspect thoracostomy/drain patency, underwater-seal movement/bubbling and surgical emphysema; secure the system against dislodgement during transfer.
Obtain post-stabilisation imaging to confirm lung/drain status and identify haemothorax or other injury, but treat recurrent tension clinically.
Repeat blood gas, lactate, haemoglobin and coagulation according to cause; ongoing shock after decompression demands active search for another reversible cause.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Tension is a physiological diagnosis

Pleural pressure becomes life-threatening when it impairs breathing or circulation; radiographic mediastinal shift in a stable patient is not the same emergency.

Positive pressure accelerates tension

Each delivered breath can add pleural air, so ventilated/NIV patients may progress from desaturation to arrest faster than spontaneous breathers.

Open access is more reliable than a plastic catheter

Needles can be too short, kink or valve shut. NICE favours open thoracostomy where trained expertise is available, followed by definitive drainage.

No hiss does not prove failure

Air release may be subtle in a noisy resuscitation room. Judge decompression from direct tract/device assessment and physiological response.

Bilateral treatment is a trauma-arrest rule

In traumatic arrest the cost of missing contralateral tension is high, so trained algorithms use bilateral thoracostomies even without classic unilateral signs.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for a chest X-ray in an unstable patient with severe respiratory compromise and convincing tension physiology.
02
Waiting for tracheal deviation, which is a late and insensitive sign.
03
Using a short or blood-control/closed-system IV cannula for needle thoracostomy.
04
Treating needle decompression as definitive and failing to place/maintain pleural drainage.
05
Assuming no response disproves tension without checking patency, depth, site and the opposite chest.
06
Allowing POCUS to prolong a CPR pause or delay bilateral decompression in traumatic arrest.