Breathing Retraining: From Sick/Victims to Superhumans

References: Kassabian et al, 1982

Kassabian J, Miller KD, Lavietes MH,

Respiratory center output and ventilatory timing in patients with acute airway (asthma) and alveolar (pneumonia) disease

Chest 1982 May; 81(5): p.536-543.

Pulmonary Division, Department of Medicine, College of Medicine and Dentistry of New Jersey, New Jersey Medical School, College Hospital, Newark, USA

To investigate the mechanism for hyperventilation in two common but dissimilar conditions, asthma (A) and lobar pneumonia (P), we examined the ventilatory pattern in 17 A and six P subjects. When acutely ill, hyperventilation (PaCO2) was similar in the two groups. Minute ventilation (VE) however, was slightly greater in group A than in P. In A patients, measurements of occlusion pressure (dP/dT) and inspiratory flow rate (VT/ti) during quiet breathing showed enhancement of respiratory center output. By contrast, in P patients, dP/dT and VT/ti were not elevated. Tidal volume (VT) was 0.59 +/- 0.19 L in A; 0.45 +/- 0.09 in P. Respiratory rate was increased in both groups. With supplementary oxygen therapy, neither VE nor PaCO2 changed in either group. The mechanism for the increased ventilatory drive in group A is unclear. Most likely, reflexes initiated by either bronchospasm or by the sudden increase of end-expiratory lung volume (EELV), not operative in P, account for the increased respiratory center output seen in A. To examine the latter possibility, we studied the ventilatory pattern at both normal and increased EELV in six nonasthmatic subjects. Both dP/dT and VT/ti were increased in all subjects after elevation of EELV. Thus, changes in EELV may be important for the regulation of ventilation during bronchospasm.

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