In this paper, I would like to discuss 1. some measurement methods of pulmonary extravascular water volume related to lung edema and 2. abnormal respiration during sleeping from the viewpoint of acute and chronic respiratory failures, respectively.
1. Measurement methods of pulmonary extravascular water volume.
At present, chest X-ray photograph is regarded as the best clinical measurement method of pulmonary extravascular water volume. But, as this method has some undeniable disadvantages, establishment of other measurement methods desired. This is the reason why we tested some other methods experimentally.
1) Static lung compliance and closing volume.
Closing volume is far more sensitive than static lung compliance as the index of pulmonary extravascular water volume, and clinical application is possible. But, closing volume has its own disadvantage, because it does not express water volume quantitatively.
2) Impedance plethysmography.
Although impedance plethysmography has the disadvantage that it does not distinguish between intrapleural effusion and intrapulmonary water, and does not detect slight increase of pulmonary extravascular water volume, this method has a merit of facilitating continuous monitering.
3) Double indicator dilution method.
Double indicator dilution method is the most excellent method theoretically, but indicator has some problems to be solved. So, we investigated the heat-indocyanine green method, heat-heat method, heat-conductivity method, and came to the conclusion that heat-conductivity method was the best when instream catheter of our invention was used.
2. Abnormal respiration during sleeping.
1) We investigated apnea and hypopnea types of abnormal respiration during sleeping in patients with chronic respiratory failure, and confirmed the serious decrease of SaO
2 during REM sleeping in both types.
2) Usually, in normal cases, abdominal movement is greater than ribcage movement related to respiration during REM sleeping; but in cases of chronic respiratory failure caused by ribcage abnormality, abdominal movement did not become greater in REM sleeping, in spite of smaller ribcage movement. This phenomenon seems to be one of the causes of severe decrease of SaO
2 during REM sleeping.
3) In cases of chronic respiratory failure, maximal Ptc CO
2 during nocturnal oxygen inhalation did not show significant difference from that during room air inhalation in non-REM sleep stage, but showed significant difference in REM sleep stage. This phenomenon shows the possibility that increased PaCO
2 during REM sleep stage does not decrease during non-REM stage or while awake.
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