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It is established that during tidal breathing the rib cage expands more than the abdomen in the upright posture, whereas the reverse is usually true in the supine posture. To explore the reasons for this, we studied nine normal subjects in the supine, standing, and sitting postures, measuring thoracoabdominal movement with magnetometers and respiratory muscle activity via integrated electromyograms. In eight of the subjects, gastric and esophageal pressures and diaphragmatic electromyograms via esophageal electrodes were also measured. In the upright postures, there was generally more phasic and tonic activity in the scalene, sternocleidomastoid, and parasternal intercostal muscles. The diaphragm showed more phasic (but not more tonic) activity in the upright postures, and the abdominal oblique muscle showed more tonic (but not phasic) activity in the standing posture. Relative to the esophageal pressure change with inspiration, the inspiratory gastric pressure change was greater in the upright than in the supine posture. We conclude that the increased rib cage motion characteristic of the upright posture owes to a combination of increased activation of rib cage inspiratory muscles plus greater activation of the diaphragm that, together with a stiffened abdomen, acts to move the rib cage more effectively.

Four patients with severe chronic obstructive lung disease and recent respiratory failure are described in whom two distinct simultaneous respiratory rhythms were identified, one at 8 to 13 breaths per minute and the other at 39 to 65 per minute. Magnetometer measurements of thoracoabdominal motion together with simultaneous electromyograms of multiple inspiratory muscles suggested that both rhythms were the result of coordinated action of several inspiratory muscles. We suggest that this phenomenon, which we have called dirhythmic breathing, results from the conflicting influence upon respiratory centers and motoneurons of two or more stimuli, some favoring rapid shallow breaths and others slow deep breaths.

Studies of thoracoabdominal motion using the respiratory magnetometer were performed in 30 patients with chronic obstructive pulmonary disease. Volume equivalency of thoracic and abdominal deflections was established by using the concepts and methods developed by Konno and Mead. Twenty patients were ambulatory, although disabled, and 10 were in acute respiratory failure and were studied in a respiratory intensive care unit. Five of 20 ambulatory patients and 8 of 10 patients in acute respiratory failure showed inward abdominal motion coincident with outward rib cage motion during inspiration, suggesting ineffective diaphragmatic function. This pattern of thoracoabdominal motion was identical to that seen in 2 high quadriplegics with diaphragmatic paralysis when they were breathing entirely with their neck muscles. Inspiratory ascent of the diaphragm was confirmed fluoroscopically in 3 of the 5 ambulatory patients. Patients showing this pattern were generally severely disabled and had the largest residual volumes. Two abnormal patterns of thoracoabdominal motion were observed during the performance of maximal voluntary ventilation in the ambulatory patients. The first, seen in 9 of 20 patients, was characterized by reciprocal or paradoxical motion of rib cage and abdomen, with increase in rib cage volume associated with decrease in abdominal volume during inspiration. The second pattern, seen in 5 of 20 patients, showed complete disorganization of rib cage and abdominal motion, with no consistent or reproducible pattern. Thus, a significant proportion of patients with disabling chronic obstructive pulmonary disease show abnormalities in thoracoabdominal motion that are observable with the respiratory magnetometer and ofter by simple inspection. Most of these abnormalities suggest malfunction of respiratory muscles, particularly the diaphragm.

Using a special gastroesophageal catheter, electromyographic measurements of the diaphragm (Edi) and transdiaphragmatic pressure (Pdi) were taken in the supine, standing, erect sitting, and leaning forward (sitting) positions in 8 normal subjects and 6 patients with severe chronic obstructive pulmonary disease (COPD) with marked hyperinflation and low fat diaphragms. Four patients had pronounced postural relief of their dyspnea from assuming the supine and/or leaning forward positions. All 8 normal subjects and 4 of the 6 patients with COPD showed substantial (2- to 5-fold) increases in delta Edi, the phasic inspiratory amplitude of Edi, on assuming the standing and erect sitting postures. In the normal subjects, delta Pdi, the phasic inspiratory increment in Pdi, was maintained in all 4 postures, whereas in all patients with COPD, it decreased significantly in the erect sitting and standing postures. In 2 of the 6 patients with COPD, the delta Edi did not increase in the erect postures. This suggested that in these patients a reflex, which normally compensates for reduced diaphragmatic efficiency because of shortened muscle fibers in the erect postures, was not operating. Although it is not clear what mechanism(s) might account for suppression of this compensatory reflex, such reflex suppression might be advantageous from the viewpoint of diaphragmatic muscle energetics. The diaphragm would be thus spared energetically wasteful attempts to accomplish a fatiguing mechanical task.

Seventeen patients with sleep apnea were studied with reference to the frequency and duration of apneic episodies, the mechanism of the apnea and the extent to which oxygen saturation was depressed by the apnea. In all patients, esophageal pressure was recorded simultaneously with respiratory magnetometer records of rib cage and abdominal motion. Thermistor records from the nose and mouth indicated the presence of apnea. Nine patients had purely obstructive apnea and eight a mixture of central and obstructive apnea. In all instances the magnetometer records alone permitted distinction between obstructive and central apnea. Inspiratory efforts against an occluded airway produced a very different pattern of motion when compared to unobstructed breathing or to central apnea. We propose that magnetometer monitoring of thoracoabdominal motion indicates upper airway obstruction reliably and provides a noninvasive and thus more acceptable alternative to esophageal pressure recording for detecting upper airway obstructive apnea.

By use of the method of Konno and Mead and the respiratory magnetometer, the partition of respired gas volumes into rib cage and diaphragm-abdomen components was accomplished in 81 normal subjects including 32 young and middle-aged men, 29 young and middle-aged women, and 20 elderly men. Studied were isovolume maneuvers and the relaxation configuration over the inspiratory capacity range, quiet tidal breathing, increased amplitudes of slow breathing, rapid inspirations and expirations, and both quiet and forceful phonation. No major differences were noted between men and women or between the young and the elderly during any respiratory acts. During quiet breathing most normal subjects are abdominal breathers when supine and thoracic breathers when upright. Rapid respiratory maneuvers were accomplished mostly through rib cage displacement suggesting that rib cage muscles are capable of more rapid action than diaphragm and abdominal muscles. Data from deep breathing and rapid maneuvers supported the view that abdominal and rib cage muscles often act to optimize the mechanical (length-tension) advantage of the diaphragm.

Inspiratory muscle function is impaired in many patients with severe COPD. This functional impairment often leads to hypercapnic respiratory failure via inspiratory muscle fatigue. Factors responsible for this functional impairment are: (1) an excessive mechanical load (high resistance and low compliance) for the inspiratory muscles to overcome; (2) the low, flat configuration of the diaphragm owing to lung hyperinflation; (3) reduced inspiratory muscle blood flow relative to the increased respiratory work requirement; and (4) tachypnea which increases the duty cycle (TI/Ttot) for inspiratory muscles, increases hyperinflation, wastes ventilation, and otherwise causes deterioration of gas exchange. Therapy is directed toward improving inspiratory muscle function and has three strategic goals: (1) to reduce the load imposed on the inspiratory muscles and reduce their mechanical disadvantage; (2) to improve the contractile characteristics of the inspiratory muscles; and (3) if goals 1 and 2 cannot be attained otherwise, to rest the inspiratory muscles using mechanical ventilation. Inspiratory muscle training offers promise as a means of preventing hypercapnic respiratory failure. Available data suggest that some COPD patients benefit from it. To be determined are which patients will benefit from it and which will not, as well as which training regimens are most effective.

The respiratory magnetometer method of Konno and Mead was used to measure separately the rib cage and the diaphragm-abdomen components of the total respiratory system compliance in 11 subjects with normal respiratory systems. Measurements made in the awake, relaxed state by the method of Heaf and Prime were compared with similar measurements made in the anesthetized, paralyzed state by the supersyringe method. The rib cage component was greater in the paralyzed than the relaxed state in 9 of 11 subjects, but the diaphragm-abdomen component was greater in the relaxed than the paralyzed state in 8 of 11 subjects. We believe that these differences can be explained by respiratory muscle activity in the presumed relaxed state. The fraction of the tidal volume attributable to rib cage displacement compared to abdominal displacement was greater during mechanical ventilation in the paralyzed state than during awake, spontaneous breathing. This can be explained by the different distribution of inflating forces produced by diaphragmatic contraction compared to positive airway and alveolar pressure, in particular by the very different patterns of diaphragmatic displacement in the 2 states.

Tilt-table polygraphic study in four patients with Shy-Drager syndrome demonstrated periodic apnoea in the erect posture. In one patient reduced hypercapneic ventilatory response and necropsy findings of neuronal loss and astrocytosis in the pontine tegmentum suggested dysfunctional respiratory neurones in the brainstem. One patient had Cheyne-Stokes respiration during the late stage of the illness.

This study sought answers to 2 questions: (1) Is severe dyspnea to the point of exhaustion regularly accompanied by diaphragmatic fatigue in patients with moderately severe chronic obstructive pulmonary disease (COPD)? (2) When diaphragmatic fatigue occurs in such patients, does theophylline prevent or delay its onset? Eight eucapnic patients with moderately severe COPD were subjected to 2 different stresses to the point of severe dyspnea requiring cessation of the stress. The stresses were cycle exercise and inspiratory resistive breathing, the latter requiring a tidal Pdi equal to 60% of Pdimax. Despite incapacitating dyspnea, objective evidence of diaphragmatic fatigue was not encountered during cycle exercise. During inspiratory resistive breathing, diaphragmatic fatigue was encountered in all patients as defined by consistent inability to attain a target Pdi during final moments of the resistance run. Patients were uniformly extremely dyspneic at this point. In neither stressful maneuver did oral sustained-release theophylline show a convincing or significant advantage over placebo when administered in a randomized double-blind crossover protocol. These results suggest that the diaphragmatic fatigue encountered in this sort of COPD patient may be of predominantly central rather than peripheral (myogenic) origin and that theophylline may not be effective in this type of fatigue.