Impact of carbon monoxide on cardiopulmonary dysfunction after smoke inhalation injury

K. Sugi, J. L. Theissen, L. D. Traber, David Herndon, D. L. Traber

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

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 ml/breath) of cotton smoke, and five sheep (control group) were insufflated with air using a modified bee smoker (smoke group: COHb, 90 ± 6%; control group: COHb, 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.

Original languageEnglish (US)
Pages (from-to)69-75
Number of pages7
JournalCirculation Research
Volume66
Issue number1
StatePublished - 1990

Fingerprint

Smoke Inhalation Injury
Carbon Monoxide
Smoke
Sheep
Inhalation
Heart Ventricles
Carbon Monoxide Poisoning
Lymph
Air
Pressure Transducers
Lung
Insufflation
Control Groups
Bees
Lymph Nodes
Blood Pressure

Keywords

  • acute lung injury
  • acute respiratory distress syndrome
  • carbon monoxide
  • cardiac function
  • inhalation injury
  • lung lymph fistula
  • myocardial depression
  • sheep

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Sugi, K., Theissen, J. L., Traber, L. D., Herndon, D., & Traber, D. L. (1990). Impact of carbon monoxide on cardiopulmonary dysfunction after smoke inhalation injury. Circulation Research, 66(1), 69-75.

Impact of carbon monoxide on cardiopulmonary dysfunction after smoke inhalation injury. / Sugi, K.; Theissen, J. L.; Traber, L. D.; Herndon, David; Traber, D. L.

In: Circulation Research, Vol. 66, No. 1, 1990, p. 69-75.

Research output: Contribution to journalArticle

Sugi, K, Theissen, JL, Traber, LD, Herndon, D & Traber, DL 1990, 'Impact of carbon monoxide on cardiopulmonary dysfunction after smoke inhalation injury', Circulation Research, vol. 66, no. 1, pp. 69-75.
Sugi K, Theissen JL, Traber LD, Herndon D, Traber DL. Impact of carbon monoxide on cardiopulmonary dysfunction after smoke inhalation injury. Circulation Research. 1990;66(1):69-75.
Sugi, K. ; Theissen, J. L. ; Traber, L. D. ; Herndon, David ; Traber, D. L. / Impact of carbon monoxide on cardiopulmonary dysfunction after smoke inhalation injury. In: Circulation Research. 1990 ; Vol. 66, No. 1. pp. 69-75.
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