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SUMMARY1. The pattern of breathing during the approach to the steady state following step changes of end-tidal Pco, and PO, has been determined in normal conscious human subjects. Three types of step were studied: (a) steps of PA, co, against a constant background of hyperoxia (PA 0, 200) A single exponential fitted the ventilation response up to about 4 min (mean half time 83 see for the 'up' and 69 see for the 'down' transients). During the transient the pattern of change of tidal volume (VT) and expiratory time (TE) was the same as in the steady state. Inspiratory time (TI), however, in the early part of the transient, changed in the opposite direction to TE, returning to its steady value only after 1 1-3 min. This effect occurred in both 'up' and 'down' transients and resulted in a smaller change of respiratory frequency than would have been predicted from the steady-state response.3. Hypoxic steps produced the fastest approach to the steady state with mean half-times for ventilation of 10 9 see for the 'up' transients and 6 6 sec for the 'down'. T1 followed the same pattern during the transient as in the steady state, whereas TE, following the step out of hypoxia, lengthened to far beyond its final steady value within five breaths of the step, only returning to its steady-state value 3-4 min after the step. This resulted in an exaggerated change of frequency during the early part of the transient. 4. Steps of CO2 in hypoxia, a mixed peripheral and central chemoreceptor stimulus, showed a ventilation response which was best fitted by two exponential, the halftimes of which were consistent with those obtained for the separate responses. The patterning was also consistent with a mixed response, more so for T1 than for TE.5. The steady-state pattern derived from the pre-switch means was consistent with the pattern previously described.6. Possible mechanisms are discussed. It is suggested that these results could

SUMMARY1. The effects of section of the brain stem caudally (through the upper pons or mid-collicular) or rostrally (through the caudal hypothalamus or anterior commissuresuprachiasmatic nucleus) were studied in fetal lambs from 118 days gestation, after recovery in utero.2. In lambs sectioned caudally, breathing movements and electrocortical activity were dissociated. After some days recovery breathing tended to become continuous, with an abnormal prolongation of inspiratory time. Isocapnic hypoxia caused an increase in the rate and amplitude of breathing. After carotid denervation hypoxia still caused an increase in the amplitude of breathing. 3. In lambs sectioned rostrally, there was also dissociation between breathing movements and electrocortical activity. Breathing remained episodic, with an incidence similar to that of intact fetal lambs. In two lambs after 10 days of recovery the breathing and electrocortical rhythms returned, from time to time, to their normal phasic relationship. Isocapnic hypoxia caused a diminution or arrest of breathing, as in intact lambs.4. The cardiovascular effects of transaction were examined. Baroreflex sensitivity was normal in those lambs sectioned caudally and enhanced in those sectioned rostrally.5. It is concluded first that as a result of rostral section, independent episodic rhythms of fetal breathing and electrocortical activity can be dissociated. Secondly, moderate isocapnic hypoxia causes arrest of fetal breathing indirectly, requiring the integrity of a suprapontine mechanism. And thirdly, after caudal section of the brain stem, hypoxia causes enhancement of fetal breathing efforts, independently of the carotid chemoreceptors. Possible mechanisms are discussed.

TI, and (c)

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Many physicians believe that the hyperventilation syndrome is invariably associated with anxiety or undiagnosed organic disease such as asthma and pulmonary embolus, or both. Twenty one patients referred by specialist physicians with unexplained somatic symptoms and unequivocal chronic hypocapnia (resting end tidal Pco2. < 4 kPa (30 mm Hg) on repeated occasions during prolonged measurement) were investigated. All but one complained of inability to take a satisfying breath. Standard lung function test results and chest radiographs were normal in all patients, but histamine challenge showed bronchial hyper-reactivity in two of 20 patients tested, and skin tests to common allergens were positive in three of 18. Ventilation-perfusion scanning was abnormal in a further three of 15 patients studied, with unmatched perfusion defects in two and isolated ventilation defects in one. None of the 21 had thyrotoxicosis, severe coronary heart disease, or other relevant cardiovascular abnormalities. Ten of the 21 patients were neurotic and suffered from chronic psychiatric disturbance characterised by anxiety, panic, and phobic symptoms. The remainder had no detectable psychiatric disorders but reported proportionately more somatic than anxiety symptoms.Severe hyperventilation can occur in the absence of formal psychiatric or detectable respiratory or other organic abnormalities. Asthma and pulmonary embolus must be specifically excluded.

Background-We have consistently argued that mild asthma is an important underlying aetiological factor in patients with severe symptomatic hyperventilation. While hyperventilation has been demonstrated in acute asthma, there have been few studies in mild chronic asthma, and mechanisms are uncertain. Methods-Twenty Conclusion-Mild asymptomatic asthmais not associated with clinically significant hyperventilation but is associated with a significant reduction in both arterial and end tidal PCO 2 which relates to airway hyperresponsiveness rather than to the degree of airway obstruction or mucosal inflammation. Anxiety and depression appear not to be implicated.

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