Tension Pneumothorax
A rapidly progressing life-threatening complication of pneumothorax, initiated by trapped air
within the pleural cavity causing increased intrathoracic pressure to occlude the venae cavae and
profoundly decrease venous return, leading to decreased cardiac output which is characterised
by decreasing conscious state, hypotension, tachycardia and cardiac arrest.
Acquired atelectasis describes the collapse of previously inflated lung parenchyma and is divided into 3 types
RESORPTIVE/OBSTRUCTIVE
ATELECTASIS
Occlusion in small bronchi
such as excessive secretions
in pneumonia or bronchitis
Decreased ventilation with
normal alveoli capillary
perfusion = V/Q mismatch
Mediastinum/tracheal deviation
shifts toward affected lung
Pulmonary barotrauma such
as rapid ascent during diving
Primary spontaneous
pneumothorax
Commonly tall, thin,
smoking males 20-40yo
Arise often in otherwise
healthy people without
precipitating event
Evidence of subpleural blebs
(congenital defect in connective
tissue of alveolar wall) & bullae
have been found in the lungs
in many patients post primary
spontaneous pneumothorax
COMPRESSION ATELECTASIS
CONTRACTION ATELECTASIS
Air/fluid/blood filling the pleural
due to local or generalised fibrosis
space (air=pneumothorax)
of the lung or pleura preventing
full expansion (eg tuberculosis)
Mediastinum/tracheal deviation
away from affected lung
Normally the visceral and parietal pleura surrounding the lungs are held
in balanced opposition by the natural expansion of the chest wall and
the natural inward recoil of the lungs, creating a vacuum-like negative
intrapleural pressure, and allowing air to flow from the atmosphere to the
lower pressure alveoli when the diaphragm flattens during inspiration
When a pneumothorax occurs, the transpulmonary pressure
and the negative vacuum is lost, and the lung collapses inward
under it’s now unimpeded natural elastic recoil
CAUSES OF PNEUMOTHORAX Iatrogenic causes such
as artificial or mechanical
ventilation, central line
misplacement, intercostal
Open/external chest wall trauma blocks, thoracocentesis,
lung biopsy, bronchoscopy
Common with fractured ribs or
penetrating chest wall injury
Secondary spontaneous
pneumothorax
If chest wound greater than
approximately 2/3 diameter of
the trachea, air will enter pleural Commonly due to underlying
space from atmosphere during lung disease in usually 60-70yo
inspiration preferentially over
the normal trachea route
Developed countries: Asthma
Loss of negative intrapleural & COPD, cancer, cystic fibrosis,
pressure = pneumothorax drug abuse, nitric oxide use
Use 3-sided dressing to cover Developing countries:
wound to allow air to move out during pneumonia, Tb, HIV with
expiration, avoiding air trapping and pneumocystis pneumonia
potential for tension pneumothorax. or other infection
(cont.)
Tension Pneumothorax CONT.

Shortness of breath (80% patients), unilateral chest pain Some patients asymptomatic and present to
(90% patients), deep inspiration, hyperventilation, cough medical care days after initial event

Air leak seals spontaneously Either disrupted visceral Active treatment to remove air from
in many cases or parietal pleura pleural space (eg thoracostomy)

Nil clinical deterioration Tension pneumothorax:

Spontaneous re-expansion of
pneumothorax over time without
active treatment intervention required
One-way valve formed where air
leaks continuously into pleural
space during inhalation and does
not escape on expiration

Air pressure increases in intrapleural

space on affected side

Subcutaneous emphysema forms Increased intrathoracic pressure Mediastinum pushed in

on chest, neck, face as air is opposite direction causing
forced into subcutaneous space ipsilateral tracheal deviation

Collapse of low pressure venae cavae

Increased pressure on opposite lung

Decreased ability of unaffected

lung to ventilate adequately

Decreased SPO2, increased

hypoxia, increased SOB

Further collapse of affected lung Rapid decrease in VR Increased JVP due to superior
vena cava occlusion

Decreased breath sounds Rapid decrease in CO

on affected side

Rapid decrease in conscious state

Dyspnoea, SOB, anxiety, & BP, increase in weak/rapid pulse
decreased SPO2

Cardiogenic shock and

Cerebral hypoxia leads to
cardiorespiratory arrest
combative behaviour