Modeling the nuclear magnetic resonance behavior of lung: from electrical engineering to critical care medicine.
The present article reviews the basic principles of a new approach to the characterization of pulmonary disease. This approach is based on the unique nuclear magnetic resonance (NMR) properties of the lung and combines experimental measurements (using specially developed NMR techniques) with theoretical simulations. The NMR signal from inflated lungs decays very rapidly compared with the signal from completely collapsed (airless) lungs. This phenomenon is due to the presence of internal magnetic field inhomogeneity produced by the alveolar air-tissue interface (because air and water have different magnetic susceptibilities). The air-tissue interface effects can be detected and quantified by magnetic resonance imaging (MRI) techniques using temporally symmetric and asymmetric spin-echo sequences. Theoretical models developed to explain the internal (tissue-induced) magnetic field inhomogeneity in aerated lungs predict the NMR lung behavior as a function of various technical and physiological factors (e.g., the level of lung inflation) and simulate the effects of various lung disorders (in particular, pulmonary edema) on this behavior. Good agreement has been observed between the predictions obtained from the mathematical models and the results of experimental NMR measurements in normal and diseased lungs. Our theoretical and experimental data have important pathophysiological and clinical implications, especially with respect to the characterization of acute lung disease (e.g., pulmonary edema) and the management of critically ill patients.
Cutillo
A G
AG
Department of Internal Medicine, School of Medicine, University of Utah, Salt Lake City, USA. acutillo@hsc.utah.edu
Ailion
D C
DC
D015824:Blood-Air Barrier / Q000502:physiology; D003422:Critical Care; D004738:Engineering; D005544:Forecasting; D006801:Humans; D008168:Lung / Q000033:anatomy & histology / Q000502:physiology*; D008171:Lung Diseases / Q000473:pathology / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008280:Magnetics; D008954:Models, Biological; D011650:Pulmonary Alveoli / Q000473:pathology / Q000503:physiopathology; D001261:Pulmonary Atelectasis / Q000473:pathology / Q000503:physiopathology; D011654:Pulmonary Edema / Q000473:pathology / Q000503:physiopathology