Mechanism underlying accelerated arterial oxygen desaturation during recurrent apnea
| Autor: | Malcolm R. Davidson, Malcolm Howard Wilkinson, Vanessa J. Kelly, Bradley A. Edwards, Scott A. Sands, Elizabeth M. Skuza, Philip J. Berger |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
Pulmonary and Respiratory Medicine
Cardiac output Resuscitation Apnea Critical Care and Intensive Care Medicine Models Biological Hypoxemia Recurrence Intensive care medicine Animals Humans Hypoxia Sheep business.industry Pulmonary Gas Exchange Infant Newborn Intermittent hypoxia Venous blood Hypoxia (medical) Pulmonary Alveoli Animals Newborn Anesthesia Oxyhemoglobins Linear Models medicine.symptom business Infant Premature |
| Zdroj: | American journal of respiratory and critical care medicine. 182(7) |
| ISSN: | 1535-4970 |
| Popis: | Rationale: Brief recurrent apneas in preterm infants and adults can precipitate rapid and severe arterial O2 desaturation for reasons that remain unclear. Objectives: We tested a mathematically derived hypothesis that when breathing terminates apnea, mixed–venous hypoxemia continues into the subsequent apnea; as a result, there is a surge in pulmonary O2 uptake that rapidly depletes the finite alveolar O2 store, thereby accelerating arterial O2 desaturation. Methods: Recurrent apneas were simulated in an experimental lamb model. Pulmonary O2 uptake was calculated from continuously measured arterial and mixed–venous O2 saturation and cardiac output. Measurements and Main Results: Direct measurements revealed that asynchrony in the desaturation and resaturation of arterial and venous blood gave rise to dips and surges in O2 uptake. After desaturation to 50%, a typical nadir in preterm infants, O2 uptake surged to a peak of 176.9 6 7.8% of metabolic rate. During subsequent apneas, desaturation rate was increased two- to threefold greater than during isolated apneas, in direct proportion to the magnitude of the surge in O2 uptake (P , 0.001; R2 5 0.897). Application of our mathematical model to a published recording of cyclic apneas in a preterm infant precisely reproduced the accelerated desaturation rates of up to 15% � s21 observed clinically. Conclusions: Rapid depletion of alveolar O2 stores by surges in O2 uptake almost completely explains the acceleration of desaturation that occurs during recurrent apnea. This powerful mechanism is likely to explain the severity of intermittent hypoxemia that is associated with neurocognitive and cardiovascular morbidities in preterm infants and adults. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|