• G F Nieman, M Cigada, A M Paskanik, J Del Pozzo, W R Clark, E M Camporesi, and T S Hakim.
• Department of Surgery, SUNY Health Science Centre, Syracuse.
• Burns. 1994 Apr 1; 20 (2): 157-62.

AbstractThe pathophysiology of smoke inhalation includes surfactant inhibition and pulmonary vascular injury leading to a high permeability pulmonary oedema. It has been shown in surfactant deficient animal models that methods of ventilation (i.e. high-frequency ventilation - HFV) avoiding a large pressure excursion (i.e. pressure change from end expiration to peak inspiration) improves oxygenation and decreases hyaline membrane formation. Therefore, we compared HFV with conventional mechanical ventilation (CMV) on lung function in an acute animal model of smoke inhalation (SI). Mongrel dogs were anaesthetized, surgically prepared for haemodynamic and blood gas monitoring, and placed on either CMV (n = 6) or HFV (n = 7). Following baseline (BL) measurements both groups were ventilated with wood smoke for 10 min. Ventilator settings were not adjusted from baseline following smoke inhalation in either groups; positive and expiratory pressure (PEEP, approximately 6 mmHg) was added in both groups following smoke exposure. At the conclusion of the study (4 h postsmoke inhalation) lung samples were taken for surfactant function and lung water measurements. Smoke inhalation immediately increased the A-a gradient (CMV-BL = 6.9 +/- 2.4 to CMV-SI = 77.3 +/- 1.9; HFV-BL = 10.5 +/- 2.7; HFV-SI = 72.8 +/- 3.7 mmHg), venous admixture (CMV-BL = 6.9 +/- 2.8 to CMV-SI 69.8 +/- 6.6; HFV-BL = 7 +/- 1.7 to HFV-SI = 60.4 +/- 7.9 per cent) and decreased Pao2 (CMV-BL = 110 +/- 3.4 to CMV-SI = 28 +/- 3.5; HFV-BL = 103 +/- 3.6 to HFV-SI = 31 +/- 1.7 mmHg) to a similar level in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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