Impact of Carbon Monoxide on Cardiopulmonary Dysfunction After Smoke Inhalation Injury

• Published in: Circulation research 1990-01, Vol.66 (1), p.69-75
• Main Authors: Sugi, Kazuro, Theissen, Josef L, Traber, Lillian D, Herndon, David N, Traber, Daniel L
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood Proteins - analysis; Carbon Monoxide Poisoning - physiopathology; Carboxyhemoglobin - analysis; Cardiac Volume; Heart - physiopathology; Heart Rate; Hemodynamics; Lung - physiopathology; Lymph - physiology; Medical sciences; Sheep; Smoke Inhalation Injury - physiopathology; Stroke Volume; Time Factors; Tobacco, tobacco smoking; Toxicology
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.RES.66.1.69

With the inhalation of smoke, there are both cardiopulmonary changes and elevated levels of carbon monoxide (CO). We hypothesize that these changes in cardiopulmonary function are the result of a histotoxic hypoxia associated with CO poisoning. This hypothesis was tested in chronically instrumented sheep (n=19). Piezoelectric crystals were attached to the left ventricle for the measurement of its external minor and major diameters in addition to wall thickness. A pressure transducer was placed in the left ventricle via the apex. The caudal-mediastinal lymph node was also cannulated. After a five-day recovery period, six sheep (smoke group) were insufflated with four series of 16 breaths (700 mllbreath) of cotton smoke, and five sheep (control group) were insufflated with air using a modified bee smoker (smoke groupCOHb, 90±6%; control groupCOHb, 6±1%). Eight sheep (CO group) were ventilated with 2% CO in air to reach a COHb of 90% (COHb, 92±1%). In the smoke group, lung lymph flow reached 42±10 ml/hr at 24 hours after smoke insufflation (baseline, 6±1 ml/hr). The maximum elastance of the left ventricle (end-systolic pressure-volume ratio), a sensitive index of myocardial contractility, was significantly decreased from a baseline of 6.5±0.9 to 3.3±0.7 mm Hg/ml. In the control and CO group, neither lung lymph flow nor maximum elastance varied from the baseline value. We conclude that the cardiopulmonary dysfunction after smoke inhalation does not occur after a similar exposure to CO. Initial CO poisoning alone is not a causative factor of cardiopulmonary dysfunction after smoke inhalation.