Respiration: control of ventilation

Abstract

Ventilation of the lungs is tightly regulated to maintain a PaCO2 that supports optimal acid-base status and an adequate PaO2. Central and peripheral chemoreceptors feed into respiratory control centres in the brainstem. PaO2 exerts its influence mainly through peripheral chemoreceptors, whereas PaCO2 exerts its influence mainly through the central chemoreceptors and, to a much lesser extent, the peripheral chemoreceptors. The tightest physiologic control is over PaCO2. Indeed, a linear relationship exists between PaCO2 and alveolar ventilation through a broad range of PaCO2 values. In contrast, for PaO2, significant stimulation of respiration only occurs at low levels (approximately 8 kPa or less). The combination of hypoxaemia and hypercarbia exerts a synergistic effect on promoting ventilation. Acidosis, whether respiratory or metabolic, is also a potent stimulus for ventilation. Other influences on ventilatory control include airway reflexes to inhaled toxins. Various drugs used in anaesthesia and critical care medicine depress ventilation, most markedly opioids, while others notably caffeine are used to stimulate it. Evidence of disordered control of ventilation is seen in some disease states, the phenomenon of Cheyne-Stokes respiration being particularly well recognized. Measurement of respiratory drive is increasingly used in intensive care to individualize mechanical ventilation.