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Articles in PresS, published online ahead of print March 29, 2002
J Appl Physiol, 10.1152/jap.00911.2001
Submitted on September 4, 2001
Accepted on March 27, 2002
1 Shriners Burn InstituteHospital, Boston, MA, USA; Pediatrics-Pulmonary Division, Massachusetts General Hospital, Boston, MA, USA; Center for Engineering in Medicine, Massachusetts General Hospital, Boston, MA, USA
2 Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA
3 Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA, USA
4 Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; Shriners Burn InstituteHospital, Boston, MA, USA
5 Radiology, Massachuets General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; Shriners Burn InstituteHospital, Boston, MA, USA
6 Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA, USA; Center for Engineering in Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: jvenegas{at}vqpet.mgh.harvard.edu.
Regional changes in ventilation and perfusion occurring in the early hours following smoke inhalation injury were evaluated through the use of Positron Emission Tomography. Five lambs were imaged before and 1, 2 and 4 hours after receiving 100 breaths of cotton smoke. Utilizing a recently developed model of Nitrongen-13 (13N) tracer kinetics [26], changes in ventilation, perfusion, shunt and regional gas content were evaluated in non-dependent, middle, and dependent lung zones. The data demonstrated a progressive development of regional shunt in dependent (dorsal) regions where perfusion remained the highest throughout the study. These findings together with decreasing regional ventilation and fractional gas content in the dependent regions correlated with decreasing PaO2 values over the course of the study. A negative correlation between regional shunt fraction and regional gas content in dependent and middle regions suggests that shunt was caused by progressive alveolar derecruitment or flooding.
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