An integrated model of the human ventilatory control system: the response to hypoxia.
The mathematical model of the respiratory control system described in a previous companion paper is used to analyse the ventilatory response to hypoxic stimuli. Simulation of long-lasting isocapnic hypoxia at normal alveolar PCO2 (40 mmHg=5.33 kPa) shows the occurrence of a biphasic response, characterized by an initial peak and a subsequent hypoxic ventilatory decline (HVD). The latter is about as great as 2/3 of the initial peak and can be mainly ascribed to prolonged neural hypoxia. If isocapnic hypoxia is performed during hypercapnia (PACO2=48 mmHg =6.4 kPa), the ventilatory response is stronger and HVD is minimal (about 1/10-1/5 of the initial peak). During poikilocapnic hypoxia, ventilation exhibits smaller changes compared with the isocapnic case, with a rapid return toward baseline within a few minutes. Moreover, a significant undershoot occurs at the termination of the hypoxic period. This undershoot may lead to apnea and to a transient destabilization of the control system if the peripheral chemoreflex gain and time delay are twofold greater than basal.
Ursino
M
M
Department of Electronics, Computer Science and Systems, University of Bologna, Bologna, Italy.
Magosso
E
E
Avanzolini
G
G
D001049:Apnea / Q000503:physiopathology; D002245:Carbon Dioxide / Q000097:blood; D002628:Chemoreceptor Cells / Q000502:physiology*; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D008962:Models, Theoretical; D012143:Respiratory Physiological Phenomena
D002245:Carbon Dioxide