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We studied the influence of diaphragmatic fatigue on the control of ventilation and respiratory muscle contribution to pressure swings in six normal seated subjects. CO2 was rebreathed before and after diaphragmatic fatigue induced by breathing against an inspiratory resistance requiring 60% maximal transdiaphragmatic pressure with each breath until exhaustion. After diaphragmatic fatigue for a given level of end-tidal PCO2, we found that tidal volume, breathing frequency, minute ventilation, duty cycle, and mean inspiratory flow did not change; esophageal pressure swings were the same, but gastric and transdiaphragmatic pressure swings were decreased; and the slope of the transpulmonary pressure-gastric pressure relationship determined at zero flow points at end expiration and end inspiration was increased. End-expiratory transpulmonary pressure progressively decreased and end-expiratory gastric pressure progressively increased with increasing end-tidal PCO2 by the same magnitude before and after diaphragmatic fatigue. We conclude that diaphragmatic fatigue induces proportionately greater contributions of inspiratory rib cage muscles than of the diaphragm, which results in the preservation of ventilatory response to CO2 despite impaired diaphragmatic contractility.
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PMID:Effect of diaphragmatic fatigue on control of respiratory muscles and ventilation during CO2 rebreathing. 822 52

We evaluated the effect of global inspiratory muscle fatigue on ventilation and respiratory muscle control during CO2 rebreathing in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. CO2 response curves were measured before and after fatigue. During CO2 rebreathing, global fatigue caused a decreased tidal volume (VT) and an increased breathing frequency but did not change minute ventilation, duty cycle, or mean inspiratory flow. Both esophageal and transdiaphragmatic pressure swings were significantly reduced after global fatigue, suggesting decreased contribution of both rib cage muscles and diaphragm to breathing. End-expiratory transpulmonary pressure for a given CO2 was lower after fatigue, indicating an additional decrease in end-expiratory lung volume due to expiratory muscle recruitment, which leads to a greater initial portion of inspiration being passive. This, combined with the reduction in VT, decreased the fraction of VT attributable to inspiratory muscle contribution; therefore the inspiratory muscle elastic work and power per breath were significantly reduced. We conclude that respiratory control mechanisms are plastic and that the respiratory centers alter their output in a manner appropriate to the contractile state of the respiratory muscles to conserve the ventilatory response to CO2.
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PMID:Effect of global inspiratory muscle fatigue on ventilatory and respiratory muscle responses to CO2. 822 53

Patients with neuromuscular disease can display paradoxic motion of the rib cage (RC) and abdomen (AB), which increases the work of breathing and predisposes to respiratory muscle fatigue. Long-term mechanical ventilation can reverse chronic hypercapnea and decrease the work of breathing in these patients. Changes in chest wall motion (CWM) that occur during mechanical ventilation have not been studied. We have assessed CWM using a calibrated respiratory inductive plethysmograph before and during mechanical ventilation in 5 children and young adults with neuromuscular disease and paradoxic breathing at rest. Asynchrony of CWM was quantitated by measuring the phase shift, theta, between RC and AB motion (0 degree = synchronous motion, 180 degrees = paradoxic motion). The volume contribution of the paradoxing compartment to tidal volume (PC/VT) was calculated. Before mechanical ventilation, mean +/- SEM VT was 122 +/- 17 mL, theta was 131 +/- 15 degrees C, and PC/VT was -27 +/- 6%. During mechanical ventilation, VT increased to 274 +/- 47 mL (P < 0.05), theta decreased to 41 +/- 14 degrees (P < 0.05), and PC/VT increased to +39 +/- 9% (P < 0.02). We conclude that mechanical ventilation improves RC/AB asynchrony and reverses the negative contribution to tidal volume of the paradoxing compartment in children and young adults with neuromuscular disease. This implies that mechanical ventilation assumes most or all the role of the respiratory pump in these patients, which provides a rationale for the use of chronic or nighttime ventilation in the treatment of respiratory muscle fatigue. Assessment of CWM may be useful in the determination of optimal ventilator settings in this population.
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PMID:Chest wall motion before and during mechanical ventilation in children with neuromuscular disease. 836 22

In order to test the hypothesis whether the breathing pattern is helpful in predicting weaning outcome in patients being weaned from mechanical ventilation, 38 patients who underwent operation for esophageal cancer were evaluated at weaning from mechanical ventilation (19 unsuccessful weanings, group U, and 19 successful weanings in age-matched patients, group S). Since all patients initially fulfilled our weaning criteria, ventilatory parameters such as tidal volume, respiratory frequency, minute ventilation, and arterial blood gas analysis showed no significant differences between the groups. The breathing pattern was registered quantitatively by means of respiratory inductive plethysmography at 3 cmH2O (0.3 kPa) of CPAP prior to weaning. The contribution of rib cage movement to tidal volume (%RC) was significantly greater in group U than in group S (P < 0.05). Indeed, 84% of the patients in group S showed %RC less than 50%, compared to only 16% of the patients in group U (P < 0.05). The results suggest that the breathing pattern is one important factor in predicting the outcome of weaning in patients after thoraco-abdominal surgery. Diaphragmatic fatigue is suspected to be the mechanism for the increase in the RC component in patients with unsuccessful weaning outcome.
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PMID:Contribution of rib cage and abdominal movement to ventilation for successful weaning from mechanical ventilation. 844 3

Breathing against inspiratory loads can be accomplished with different degrees of coupling between the diaphragm and the other muscles attached to the rib cage (RCM). Thus, the electromyographic signs of fatigue develop separately in each muscle group. While breathing with diaphragm emphasis, the occurrence of diaphragmatic fatigue was found to be related to the tension-time index TTdi (= Pdi/Pdimax x Ti/Ttot). Above the critical range of 0.15 to 0.18, the endurance of the diaphragm is less than 1 h and it is inversely related to the TTdi value. However, in most loaded breathing conditions, the spontaneous pattern of breathing is characterized by predominant activation of RCM. The tension-time conditions at which fatigue develops during breathing with RCM emphasis are not known. We assessed the critical tension-time value in four normal subjects breathing with RCM emphasis against inspiratory threshold loads. RCM predominance was achieved by developing negative abdominal pressure swings during inspiration, and it was characterized by the tension-time index TTrc (Ppl/Pplmax x Tl/Ttot), where Ppl is pleural pressure developed under this condition. Above a critical TTrc value of 0.30, endurance time was inversely related to TTrc, and it resulted from failure of the RCM rather than of the diaphragm. We conclude that the critical threshold, as assessed by TTrc, is higher for breathing patterns with RCM emphasis than previously described by TTdi for diaphragm emphasis. However, when predominantly recruited, as in breathing patterns commonly adopted in loaded conditions, the RCM fatigue earlier than the diaphragm.
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PMID:Effect of pressure and timing of contraction on human rib cage muscle fatigue. 846 20

Unlike the standard electrical approach, cervical magnetic stimulation of the phrenic nerves is less painful and achieves a constant degree of diaphragmatic recruitment, features that should enhance its applicability in a clinical setting. An unexplained phenomenon is the greater transdiaphragmatic twitch pressure (Pditw) with magnetic vs. electrical stimulation. We hypothesized that this greater Pditw is due to coactivation of extradiaphragmatic muscles. Because impedance to rib cage expansion is increased at high lung volumes and efficiency of extradiaphragmatic muscles is less than that of the diaphragm, we reasoned that the difference between electrical Pditw and magnetic Pditw would be less evident at high volumes than at end-expiratory lung volume. In human volunteers, magnetic Pditw and electrical Pditw were 37.7 +/- 1.9 (SE) and 32.3 +/- 2.2 cmH2O, respectively, at end-expiratory lung volume (P < 0.005) and 24.0 +/- 2.9 and 27.2 +/- 2.8 cmH2O, respectively, at one-half inspiratory capacity (not significant); at total lung capacity, magnetic Pditw was less than electrical Pditw (10.6 +/- 0.8 and 16.2 +/- 2.9 cmH2O, respectively; P < 0.05). Magnetic stimulation caused significant extradiaphragmatic muscle depolarization and rib cage expansion, whereas electrical stimulation caused virtually no extradiaphragmatic muscle depolarization and rib cage deflation. Despite these differences, the induction of respiratory muscle fatigue produced reductions in both electrical and magnetic Pditw values (P < 0.01), which were of similar magnitude and closely correlated (r = 0.96). In conclusion, magnetic stimulation recruits both extradiaphragmatic and diaphragmatic muscles, and it is equally as effective as electrical stimulation in detecting diaphragmatic fatigue.
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PMID:Comparison of magnetic and electrical phrenic nerve stimulation in assessment of diaphragmatic contractility. 872 61

We evaluated the effect of global inspiratory muscle fatigue (GF) on respiratory muscle control during exercise at 30, 60, and 90% of maximal power output in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. Esophageal and gastric pressures, anteroposterior displacement of the rib cage and abdomen, breathing pattern, and perceived breathlessness were measured. Induction of GF had no effect on the ventilatory parameters during mild and moderate exercise. It altered, however, ventilatory response to heavy exercise by increasing breathing frequency and minute ventilation, with minor changes in tidal volume. This was accompanied by an increase in perceived breathlessness. GF significantly increased both the tonic and phasic activities of abdominal muscles that allowed 1) the diaphragm to maintain its function while developing less pressure, 2) the same tidal volume with lesser shortening of the rib cage inspiratory muscles, and 3) relaxation of the abdominal muscles to contribute to lung inflation. The increased work performed by the abdominal muscles may, however, lead to a reduction in their strength. GF may impair exercise performance in some healthy subjects that is probably not related to excessive breathlessness or other ventilatory factors. We conclude that the respiratory system is remarkably adaptable in maintaining ventilation during exercise even with impaired inspiratory muscle contractility.
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PMID:Influence of global inspiratory muscle fatigue on breathing during exercise. 892 56

We evaluated the effect of global inspiratory muscle fatigue (GF) on respiratory muscle control during exercise at 30%, 60%, and 90% of maximal power output in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. Respiratory pressures, breathing pattern, and perceived breathlessness were measured. Induction of GF had no effect on the ventilatory parameters during mild and moderate exercise. It altered, however, ventilatory response to heavy exercise by increasing breathing frequency and minute ventilation, with minor changes in tidal volume. This was accompanied by an increase in perceived breathlessness. GF significantly increased both the tonic and phasic activities of abdominal muscles that allowed 1) the diaphragm to maintain its function while developing less pressure, 2) the same tidal volume with lesser shortening of the rib cage inspiratory muscles, and 3) relaxation of the abdominal muscles to contribute to lung inflation. The increased work performed by the abdominal muscles may, however, lead to a reduction in their strength. GF may impair exercise performance in some healthy subjects that is probably not related to excessive breathlessness or other ventilatory factors. The respiratory system is remarkably adaptable in maintaining ventilation during exercise even with impaired inspiratory muscle contractility.
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PMID:[Effect of respiratory muscle fatigue on their function during exercise]. 899 54

Patients with severe chronic obstructive pulmonary disease (COPD) have a greater neural drive to the parasternal intercostal and scalene muscles and greater inspiratory expansion of the rib cage than do healthy individuals. However, such patients also have a reduced outward displacement or a paradoxical inward displacement of the ventral abdominal wall during inspiration. This has led to the suggestion that they may have less use of the diaphragm, possibly secondary to chronic muscle fatigue. To assess the effect of COPD on the neural drive to the diaphragm, we inserted needle electrodes into the costal part of the right hemidiaphragm in eight patients with severe disease (mean [+/- SD] FEV1: 0.82 [+/- 0.27] L) and six control subjects of similar age, and measured the discharge frequencies of single motor units during resting breathing. A total of 115 diaphragmatic motor units were recorded in the control subjects and 122 in the patients. All motor units discharged rhythmically in phase with inspiration. However, whereas 95% of the units in the control subjects had a peak discharge frequency between 7 and 14 Hz, 79% of the units in the COPD patients had a peak discharge frequency greater than 15 Hz. As a result, the discharge frequency of all units averaged 10.5 [+/- 2.4] Hz in the control subjects, but 17.9 [+/- 4.3] Hz in the patients (p < 0.001). These observations indicate that patients with severe COPD have an increased neural drive not only to the rib cage inspiratory muscles, but also to the diaphragm. Consequently, the reduced inspiratory expansion of the abdomen in severe COPD results from mechanical factors alone.
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PMID:Neural drive to the diaphragm in patients with severe COPD. 910 76

Diaphragmatic phonomyogram (PMG) evoked by maximal bilateral phrenic nerve stimulation has previously been described as a good index of contractility of fresh and fatigued diaphragm. In the present study we hypothesized that diaphragmatic contractility changes could be even more simply evaluated by recording the relationship between the PMG and the compound motor action potential (CMAP) amplitudes during graded submaximal unilateral phrenic nerve stimulation at various intensities. Relationships between CMAPs and PMGs from left and right hemidiaphragms were recorded by means of surface electrodes and miniature microphones placed over the lower rib cage (eighth intercostal space) in five healthy subjects before and after a diaphragmatic fatigue task. These relationships in each subject were linear. The slope of these relationships decreased by 61.1 +/- 20.7% and by 70.4 +/- 14.6% on the right and left side respectively, but the intercepts did not change significantly. By comparison, transdiaphragmatic twitch pressure during maximal bilateral stimulation (PdiT) declined by 49.4 +/- 15%. We conclude that PMG during submaximal unilateral phrenic nerve stimulation is a reliable index of diaphragm contractility changes caused by fatigue. Using this method we have shown that all diaphragmatic motor units can be affected by fatigue.
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PMID:Diaphragmatic fatigue investigated by phonomyography. 911 4


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