ARDS and Pneumothorax

ARDS

Type II pneumocytes: (1) surfactant -- prevents atelectasis; (2) repair

There are more Type II pneumocytes than Type I pneumocytes

Type II pneumocytes proliferate in repair phase post-ARDS

The three main causes of acute respiratory distress syndrome: (1) gram negative sepsis; (2) gastric aspiration; (3) severe trauma

Findings in ARDS: (1) Severe hypoxemia (PaO2 less than 50) not relieved by 100 percent oxygen; (2) Pulmonary wedge pressure less than 18, ruling out cardiogenic pulmonary edema

What causes hypoxemia in ARDS? (1) Shunting (perfusion but no ventilation due to atelectasis caused by injury to Type II pneumocytes); (2) Diffusion defect (hyaline membrane formation due to alveolar capillary and Type I pneumocyte damage)

Late complications of ARDS: chronic interstitial fibrosis --> restrictive lung disease

Pneumothorax

The critical distinction is between spontaneous pneumothorax and a tension pneumothorax. A spontaneous pneumothorax is caused most commonly by bursting of a subpleural bleb (underlying condition may be emphysema), causes a minimal or ipsilateral mediastinal shift, and is benign since the air in the pleural space will slowly be reabsorbed (atmospheric pressure > arterial pressure). Treat by observation if mild (less than 15%)

OTOH, a tension pneumothorax is usually due to penetrating wound (knife, shrapnel) and involves a check valve, where can get into the pleural space with inspiration but not out with expiration; this causes GREATER THAN ATMOSPHERIC pressure in the pleural space. Hence there is contralateral mediastinal shift and since pressure buildup can cause compression atelectasis in the contralateral and only remaining lung, this is a medical emergency. Treat by inserting a needle at the 2nd intercostal space on the midclavicular line

Common findings in both types of pneumothorax is pleuritic chest pain, tympanitic percussion and absent breath sounds.