|Immediate effects of smoke inhalation on the lower airway include loss of ciliary action,|
|mucosal edema, bronchiolitis, alveolar epithelial damage, and impaired gas exchange, |
particularly oxygenation. Areas of atelectasis or air trapping, and loss of surfactant activity,
worsen ventilation–perfusion mismatch and hypoxemia.
|Hours later, sloughing of tracheobronchial mucosa and mucopurulent membrane formation|
|increases the degree of obstruction, poor gas exchange, and likelihood of infection.|
|Beyond the first 24 hours, looks like adult respiratory distress syndrome.|
|Indications for admission include respiratory distress, poor feeding, hypoxemia if not|
|previously receiving oxygen, increased oxygen requirement (increases of more than 0.5 |
L/min flow are significant), hypercarbia, apnea, RSV infection, or appearance of new
infiltrates on chest radiograph.
|Hypoxemic respiratory failure is defined by a PaO2 less than 60 mm Hg while on room air (at|
|sea level). A patient receiving supplemental oxygen can be in respiratory failure even with |
normal oxygen saturation.
|Hypercarbic respiratory failure is defined by a PaCO2 greater than 50 mm Hg.|
|Loss of diffusion capacity ( pneumonia, ARDS) primarily leads to hypoxemic respiratory|
|As V/Q mismatch worsens, (shunt or PE ) it will lead to respiratory failure with hypoxemia,|
|hypercarbia or both.|