It can become unstable if the gain of the system (“loop gain”) becomes greater than 1 ( Khoo et al., 1982). This negative feedback loop aims to maintain a constant partial pressure of arterial carbon dioxide and oxygen. The underlying mechanism of CSR is instability of the negative feedback loop controlling ventilation during sleep.
Naughton, in Encyclopedia of Respiratory Medicine(Second Edition), 2022 Pathogenesis Journal of Applied Physiology 5: 255–263. (B) Reproduced with permission from Lambertsen CJ, Kough RH, Cooper DY, Emmel GL, Loeschcke HH and Schmidt CF (1953) Comparison of relationship of respiratory minute volume to pCO 2 and pH or arterial blood and internal jugular blood in normal man during hyperventilation produced by low concentrations of CO 2 at 1 atmosphere and by O 2 at 3.0 atmospheres. The American Journal of Physiology 149:277–291. (1947) The effect of the inhalation of high and low oxygen concentrations on respiration, pulse rate, ballistocardiogram and arterial oxygen saturation (oximeter) of normal individuals. (A) Reproduced with permission from Dripps RD and Comroe JH, Jr. BTPS indicates at body temperature, atmospheric pressure and saturated with water. Minute ventilation, and PaCO 2 (femoral) in 8 healthy men ( Lambertsen et al., 1953) while inhaling 0–6% CO 2 in air at atmospheric pressure (mean slope is 2.5 L min − 1 mmHg − 1 artificial PaCO 2 rise). (B) Artificially raising PaCO 2 in humans stimulates chemoreceptors sufficiently to stimulate breathing. Equivalent SpO 2 points are derived from Ganong (1997). Equivalent PaO 2 points are aligned on the FiO 2 scale, with PaO 2 estimated before hyperventilation occurs using the alveolar gas equation (assuming 760 mmHg barometric pressure, RQ = 0.8, PaO 2 = PAO 2 and PaCO 2 = PACO 2) and the point afterwards is estimated based on dynamic forcing experiments in isocapnia (courtesy of Dr. N.B., Confusingly, Dripps and Comroe have unconventionally reversed the horizontal axis. Minute ventilation (± SE solid bars, ± SD open bars) in normal subjects ( Dripps and Comroe, 1947) as inspired oxygen is artificially lowered (strictly hypocapnic hypoxia exists once hyperventilation occurs). (A) Artificially lowering PaO 2 in humans stimulates chemoreceptors sufficiently to stimulate breathing. Nevertheless, other control systems can also be devised (see below) that do not involve chemoreceptors.įig. 1. The presumption has always been that chemoreceptors must form a major contribution to whatever measure metabolic rate. This is because CO 2 production rate can be partially dissociated from metabolic rate when metabolic substrates other than carbohydrate are used, or during respiratory compensation for metabolic acidosis. It is not quite accurate to derive metabolic rate from the rate of CO 2 production. This has (a)Ī sensor (an input = a chemoreceptor?) that continuously measures O 2 consumption somewhere, detecting O 2 levels falling as metabolic rate rises and generating a proportional signal, (b)Īn integrator (the brainstem) that converts this signal into a proportionate drive to (c)Īn effector (an output = breathing = respiratory muscles) to increase O 2 supply.īy definition, metabolic rate is the rate of O 2 consumption. An engineering control analogy similar to the classic negative feedback loop is useful.
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