Articles: intubation.
-
Critical care medicine · Oct 1983
Noncardiac pulmonary edema precipitated by tracheal intubation in patients with inhalation injury.
Ten patients with body surface burn and clinical evidence of inhalation injury developed transient, reversible pulmonary edema within 5 min after endotracheal intubation. Hemodynamic studies within 1 hr after intubation revealed normal cardiac output and pulmonary artery wedge pressure (WP). ⋯ It is postulated that glottic generated expiratory retard may increase alveolar pressure, thus preventing pulmonary edema. Bypass of glottis by tracheal intubation may render alveolar pressure atmospheric and facilitate edema formation.
-
There is an increase in endotracheal tube-cuff volume and pressure due to nitrous oxide diffusion into the cuff during anaesthesia. A rise of the cuff pressure up to 100 mm Hg (high volume-low pressure cuffs!) within only two hours is nothing out of the ordinary. The inspiratory nitrous oxide concentration influences the cuff pressure rises. ⋯ In endotracheal tubes with a Rediffusion System, cuff pressure never exceeds capillary perfusion pressure of the tracheal mucosa. In our in vitro-experiments we found an increase of cuff pressure from 14.2 +/- 0.5 mm Hg to only 27.3 +/- 1.9 mm Hg within six hours (FIN2O = 0.66). Within 150 minutes of endotracheal anaesthesia (FIN2O = 0.66) cuff pressure rose from 14.6 +/- 0.5 mm Hg to only 21.5 +/- 3.6 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)