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Phrenic nerve damage may occur as a complication of specific surgical procedures, prolonged mechanical ventilation, or physical trauma. The consequent diaphragmatic paralysis or dysfunction can lead to major complications. The purpose of this study was to elucidate the role of the nondiaphragmatic respiratory muscles during partial or complete diaphragm paralysis induced by unilateral and bilateral phrenic nerve damage at different levels of ventilatory pressure support in an animal model. Ten pigs were instrumented, the phrenic nerve was exposed from the neck, and spontaneous respiration was preserved at three levels of pressure support, namely, high, low, and null, at baseline condition, after left phrenic nerve damage, and after bilateral phrenic nerve damage. Breathing pattern, thoracoabdominal volumes and asynchrony, and pressures were measured at each condition. Physiological breathing was predominantly diaphragmatic and homogeneously distributed between right and left sides. After unilateral damage, the paralyzed hemidiaphragm was passively dragged by the ipsilateral rib cage muscles and the contralateral hemidiaphragm. After bilateral damage, the drive to and the work of breathing of rib cage and abdominal muscles increased, to compensate for diaphragmatic paralysis, ensuing paradoxical thoracoabdominal breathing. Increasing level of pressure support ventilation replaces this muscle group compensation. When the diaphragm is paralyzed (unilaterally and/or bilaterally), there is a coordinated reorganization of nondiaphragmatic respiratory muscles as compensation that might be obscured by high level of pressure support ventilation. Noninvasive thoracoabdominal volume and asynchrony assessment could be useful in phrenic nerve-injured patients to estimate the extent and type of inspiratory muscle dysfunction. [ABSTRACT FROM AUTHOR]

We hypothesized that walking at increased speed or increasing gradient might have different effects on chest wall kinematics and respiratory muscle power components, and contribute differently to respiratory effort sensation. We measured the volumes of chest wall compartments by optoelectronic plethysmography, esophageal, gastric and transdiaphragmatic (Pdi) pressures, and the sensation of the respiratory effort by a Borg scale in five normal subjects walking both at ascending gradient with constant speed (AG) and at ascending speed with constant gradient (AS). Chest wall kinematics, evaluated by displacement of chest wall compartments, did not show any significant difference between AS and AG. Muscle power, calculated as the product of mean flow and mean pressure, increased similarly, but its partitioning into pressure and velocity of shortening differed in the two modes. A greater increase in the pressure developed by the abdominal muscles (Pabm) (4.06-fold), and in the velocity of shortening of both rib cage inspiratory muscles (vrcm,i) (2.01-fold) and the diaphragm (vdi) (1.90-fold) was associated with a lower increase in the pressure developed by the rib cage inspiratory muscles (Prcm,i) (1.24-fold) and Pdi (0.99-fold) with AG. Instead, with AS, a lower increase in Pabm (2.12-fold), vrcm,i (1.66-fold) and vdi (1.54-fold) was associated with a greater increase in Prcm,i (1.56-fold) and Pdi (1.97-fold). A combination of Pabm and vdi during AG (Wald χ2=23.19, P<0.0000), with the addition of Prcm,i during AS (Wald χ2=29.46, P<0.0000), was the best predictor of Borg score. In conclusion, the general strategy adopted by respiratory centers during different walking modes does not differ in terms of ventilation, chest wall kinematics, and respiratory muscle power production, whereas it does in terms of partitioning of power into pressure and velocity of shortening, and respiratory muscle contribution to respiratory effort sensation. Combinations of different patterns of flow and pressure generation made the respiratory effort sensation similar during AS and AG modes. [ABSTRACT FROM AUTHOR]

Objective: We examined in rabbits the effects of more than 48 h of mechanical ventilation on the contractile properties and fiber type adaptations of the respiratory muscles.Design and Setting: Experimental prospective study in a university laboratory.Animals and Interventions: Nineteen rabbits were randomly allocated to two groups: control (n=10) or mechanically ventilated (MV; n=9) for 51+/-3 h.Measurements and Results: Respiratory muscles contractile properties were analyzed before and after a fatigue protocol using in vivo isometric 1-s tetanic contraction characteristics in both muscles: peak tetanic force, contraction time, relaxation time, and total contraction time. Both muscle fiber type proportions, diameter, and cross-sectional areas were measured using ATPase staining. The MV rabbits showed significant weight loss in both muscles, accompanied by a reduced peak tetanic force (9.96+/-3.2 vs. 7.44+/-2.2 N for diaphragm of control and MV animals respectively), fatigue resistance index, and increased relaxation time (57.5+/-8.7 vs. 85.8+/-9.4 ms for diaphragm of control and MV animals) and contraction time. These impairments in the MV group worsened after the fatigue runs. Both muscle showed a significant atrophy of type IIa and IIb fibers but a stability in type I fibers cross-sectional area.Conclusions: Mechanical ventilation in rabbits produces alterations in contractile properties of the diaphragm and 5th external intercostal muscle, increases both muscles fatigue, and promotes atrophy of type II fibers. [ABSTRACT FROM AUTHOR]

During acute asthma reversible increase in lung compliance and total lung capacity (TLC) have been observed. The magnitude of the increase in TLC, however, was found to be relatively small when TLC was measured radiographically. We wondered if structural distortion of the respiratory bellows develops during acute asthma attacks, accounting for the limited increase in TLC. We analyzed the chest wall dimensions using chest roentgenograms obtained in 32 patients who had previously participated in the study of radiographic evaluation of TLC. We found that the dimensional changes accompanying the small increase in TLC during acute asthma were nonuniform, consisting of mainly an increase in lung height (0.45 ± 0.15 cm) with limited coordinated expansion of other dimensions and a small but significant distortional contraction of lung width at the lowest portion of the rib cage (−0.25 ± 0.12 cm). These findings were interpreted to mean that in response to the decrease in elastic lung recoil (internal load) occurring during acute asthma, the diaphragm makes limited but effective further caudad descent without provoking serious structural distortion and that rib cage muscles, working at mechanical disadvantage at high lung volume, act largely as fixators. [ABSTRACT FROM AUTHOR]