Abstract
Early detection of tissue hypoxia in the intensive care unit is essential for effective treatment. Reduced nicotinamide adenine dinucleotide (NADH) has been suggested to be the most sensitive indicator of tissue oxygenation at the mitochondrial level. However, no experimental evidence comparing the kinetics of changes in NADH and other physiological parameters has been provided. The aim of this study is to obtain the missing data in a systematic and reliable manner. We constructed four acute hypoxia models, including hypoxic hypoxia, hypemic hypoxia, circulatory hypoxia, and histogenous hypoxia, and measured NADH fluorescence, tissue reflectance, cerebral blood flow, respiration, and electrocardiography simultaneously from the induction of hypoxia until death. We found that NADH was not always the first onset parameter responding to hypoxia. The order of responses was mainly affected by the cause of hypoxia. However, NADH reached its alarm level earlier than the other monitored parameters, ranging from several seconds to >10 min. As such, we suggest that the NADH can be used as a hypoxia indicator, although the exact level that should be used must be further investigated. When the NADH alarm is detected, the body still has a chance to recover if appropriate and timely treatment is provided.
Highlights
Most deaths in the intensive care unit (ICU) arise from multiple organ dysfunction syndrome, which is widely recognized to be a result of tissue hypoxia[1] and is associated with many life-threatening conditions
The integrated system of the direct current (DC) fluorometer/reflectometer and the laser Doppler perfusion monitor was developed by Mayevsky and Chance and has been utilized for over 20 years in studies on the combination of NADH and cerebral blood flow (CBF), as well as other parameters, such as electrocorticography, DC potential, extracellular ions, and oxyhemoglobin in the cerebral cortex under hypoxic hypoxia, hypemic hypoxia, and circulatory hypoxia
The changes in the patterns of NADH and CBF exposed to hypoxic hypoxia were similar to those that have been previously reported.[12]
Summary
Most deaths in the intensive care unit (ICU) arise from multiple organ dysfunction syndrome, which is widely recognized to be a result of tissue hypoxia[1] and is associated with many life-threatening conditions. Current intensive care monitoring includes the use of electrocardiography (ECG), blood pressure monitoring, central venous catheters, pulmonary artery catheterization, cardiac output, pulse oximetry, airway CO2 monitoring, transcutaneous blood gases, respiratory mechanics, respired gas analysis, etc.[2] respired gas analysis determines the oxygen uptake from inspiration and pulse oximetry provides an estimate of oxygen saturation in arteries. Central venous catheters and pulmonary artery catheterization provide information regarding the oxygen saturation in veins, and transcutaneous blood gases reflect the partial pressure of oxygen at the tissue level.[2] Oxygen is transported in the body as a result of differences in partial pressure at different locations. The partial pressure of oxygen varies from 104 mm Hg in alveoli to 40 mm Hg in veins, 23 mm Hg in tissue cells, and is
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