Effect of metabolic rate on the occurrence of periodic breathing.
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Biomedical subjects
Publications and source records attributed to G S Longobardo.
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Periodic breathing (recurrent central apneas) occurs frequently during sleep. Periodic breathing can arise as a result of unstable behavior of the respiratory control system. A mathematical model of the respiratory control system was used to investigate, systematically, the effect of severity of disturbances to respiration and certain system parameters on periodic breathing occurring during sleep. The model consisted of multi-compartment representation of O2 and CO2 stores, a peripheral controller sensitive to O2 and CO2, and a central controller sensitive to CO2. The effects of hypoxia and hypercapnia on the upper airway muscles were not considered in the model. Episodes of hyperventilation or asphyxia were used to disturb the control system and explore the boundaries of stable breathing. Circulation time and metabolic rate were also varied. Simulations with the model produced the following findings: The number of central apneas associated with periodic breathing were greater as circulation time increased; controller gain increases also made the number of apneas greater, although periodic breathing occurs with lower controller gains as circulation time increases. At each level of circulation time there was a range of controller gain changes which caused little change in the number of apneas. There were more apneas with hypoxia; also the number of apneas increased with sleep-associated reductions in metabolic rate. The more rapidly resting PCO2 rose at sleep onset, the greater the likelihood of recurrent apneas. Finally, the more intense the disturbance, the more apneas there were.
The effect on CO2 storage and elimination of variations in the slope and intercept of the ventilatory response to CO2 curve was examined. Theoretical and experimental results show that although CO2 elimination rate following a transient ventilatory disturbance is decreased at low ventilatory response slopes, this decrease can be compensated by elevated PCO2 intercepts, or thresholds. Conversely, high CO2 elimination rate following a ventilatory disturbance due to a high ventilatory response slope can be off-set by a depressed PCO2 threshold. The results suggest that elevated thresholds which often accompany depressed ventilatory response slopes may be part of a compensatory mechanism for minimizing transient hypercapnia and acidosis.
It has been shown that gas exchange between the alveolar space and pulmonary capillary blood is affected by the pattern of airflow at the mouth in the non-homogeneous lung. The present theoretical study shows that even in the homogeneous lung, the pattern of airflow can affect gas exchange. When tidal volume, inspiratory and expiratory times remain constant, variations in the pattern of airflow result in significantly different values of steady state arterial PO2 and PCO2. This difference in steady state blood gases is exaggerated by low levels of minute ventilation and by long inspiratory times, but is unaffected by changes in the diffusion coefficient of the alveolar-capillary membrane.
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