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.
Respiratory
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
failure.

As V/Q mismatch worsens, (shunt or PE ) it will lead to respiratory failure with hypoxemia,
hypercarbia or both.
BPD
Respiratory Failure
Smoke Inhaltaion