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The case of a 57-year-old man who had previously undergone left lobectomy for echinococcal disease of the lung is described. Sixteen years later he presented with empyema and bronchopleural fistula, which were treated using a pedicled intercostal muscle bundle, an omental pedicle and partial thoracoplasty. The patient recovered and is well 6 years later.
In 5 healthy young men, the maximal voluntary breath holding--was studied under conditions of different initial values of PACO2--after oxygen inhalation at ordinary minute volume of respiration or at hyperventilation, or after breathing with oxygen mixtures with 2, 4, 6, 8 or 10% CO2. PACO2 was recorded at the moment of resuming of the intercostal muscles electric activity and at the point of breaking up the apnoea. A mathematical model was constructed. The hypothesis of participation of two independent factors (chemo- and mechanoreceptive) in genesis of the imperative stimulus for breathing was checked. The data obtained suggest that, in fact, the only factor restricting the duration of voluntary breath holding--is the summed up in time chemoreceptive stimulation. The involuntary contractions of respiratory muscles observed during apnoea are, apparently, a connecting link in formation of the imperative stimulus which breaks up the cessation of breathing.
The effects of aminophylline on diaphragmatic muscle contractility were studied in 8 dogs. The relationships of the electromyographic signal from the diaphragm and the pressures developed by this muscle were compared before and after the administration of aminophylline in doses of 6, 20, 40, 80, and 120 mg/kg. Measurements were made during occluded inspiratory efforts at functional residual capacity. In a second group of 4 dogs the relationships were compared while the rib cage expansion was limited by a plaster cast. Finally, in a third group of 4 dogs after the diaphragm had been paralyzed by phrenicotomy, the relationship of pleural pressure to the electromyographic signal of the intercostal muscles was assessed before and after administration of aminophylline. In all cases, aminophylline progressively shifted the electromyographic pressure relationship up and to the left. This effect became significant (p less than 0.01) at a dose of 20 mg/kg, reached a peak at 80 mg/kg, and then declined at a dose of 120 mg/kg. The amount producing blood concentrations closest to the human therapeutic blood concentration was 20 mg/kg. The peak increase in pressure compared with the control values were 58% in the first group, 27% in the second group, and 52% in the third group (p less than 0.01). We conclude that aminophylline increases respiratory muscle contractility in a dose-related manner. This may have important therapeutic and pathophysiologic implications.
The effects of en bloc autotransplantation of the heart and both lungs on the regulation of breathing were studied in four mongrel dogs. Tidal volume, respiratory rate, airflow, airway pressure and electromyograms from the intercostal muscles and diaphragm were recorded before and after the transplantation. The dogs breathed air or a mixture of 5% CO2 and air. Airway closure at functional residual capacity (FRC) level and after insufflation of 200 ml air was used as a mechanical stimulus. The following observations were made. 1) Stimulation by 5% CO2 after the transplantation increased the ventilatory minute volume by increasing the tidal volume while the respiratory rate remained unaltered. Before transplantation, both tidal volume and respiratory rate increased in response to CO2 stimulation. 2) After transplantation, stretching of the airways did not cause apnea (Hearing-Breuer reflex abolished) as it did preoperatively. 3) CO2 inhalation increased the efficiency of the respiratory muscles as expressed by the ratio of mechanical work (tidal volume or pressure impulse) to electrical activities of the respiratory muscles. This was most obvious in the dogs with transplant when the airways were closed at FRC level. Elimination of the afferent impulses due to en bloc transplantation of the heart and both lungs therefore modified the efferent impulses to the respiratory muscles. This effect was seen after both chemical and mechanical stimuli.
Using the weighted spirometer technique we studied chest wall compliance (Cw) in 16 nonobese patients with chronic weakness of the respiratory muscles and 20 healthy control subjects. In order to evaluate the validity of the technique, while Cw was being measured, we monitored thoracoabdominal configuration with 2 pairs of linearized magnetometers and electrical activity of the external oblique with a concentric needle electrode in 3 healthy subjects and 4 patients; in addition, we recorded in 3 subjects the electrical activity from the intercostal muscles and diaphragm throughout the procedure. The method was reproducible within 5.8% and provided Cw values that compared well with those yielded by the relaxation technique. In each subject, the weight-induced shifts in end-expiratory lung volume showed a very good linear correlation with the changes in transrespiratory pressure at end-expiration (r greater than or equal to 0.91). In addition, in none of the subjects tested did the electromyograms reveal any intercostal, diaphragmatic, or abdominal muscle activity at end-expiration, nor did the end-expiratory level ever show a significant departure from the relaxed thoracoabdominal configuration, thus suggesting adequate respiratory muscle relaxation. The reduction in inspiratory muscle force in the patients ranged from 17 to 94% of predicted (mean +/- SE, 43 +/- 6). The decrease in vital capacity, total lung capacity, and functional residual capacity averaged 59, 34, and 15% of predicted, respectively. Both the patient and the control groups showed a large interindividual variability regarding Cw. It varied from 0.117 to 0.258 L/cm H2O (mean +/- SE, 0.162 +/- 0.012) in the patients and from 0.163 to 0.366 L/cm H2O (mean +/- SE, 0.248 +/- 0.013) in the healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Disinhibition or 'release' of expiratory muscle activity in response to focal cooling of various medullary structures was of two kinds: (1) release of rhythmic expiratory activity even when no such activity was recruited in the control situation and (2) release of tonic activity in the 'expiratory' muscles. Release of rhythmic expiratory activity was mainly elicited by focal cooling of structures in the intermediate part of the medulla and release of tonic activity was preferentially induced by cooling rostroventral structures, although a considerable overlap did occur. Release of rhythmic expiratory activity was not related to any changes in expiratory time (TE) or to any associated variations in the pattern of inspiratory activity. It showed a marked increase with increasing levels of PCO2. The release of tonic activity was not CO2-dependent. Both types of effects could be mimicked by focal microinjections of lignocaine and were reflected by corresponding changes in activity of a majority of the expiration-related neurons. These results suggest that complex and widespread neural substrates subserve the control of the intensity of rhythmic expiratory activity and of the tonic activity of the abdominal and intercostal muscles. These neural mechanisms can apparently operate independently from those controlling the inspiratory activity. The release of the tonic activity observed in the 'expiratory' muscles might reflect a disinhibition of mechanisms involved in non-respiratory functions of expiratory muscles.
Lung herniation is a rare event defined by protrusion of the lung through an abnormal weakness in the thoracic wall. We report a case of spontaneous intercostal pulmonary herniation, which occurred as a result of vigorous coughing. We repaired the herniation by approximating the ribs with heavy stitches. The mechanism of intercostal muscle disruption, and the etiology and treatment of lung herniations, are discussed.
Studies on respiratory muscle resting by negative pressure ventilation (NPV) in patients with stable COPD have given conflicting results. Probable explanations lie in criteria of patients' selection, method of NPV application, and lack of supervision of respiratory muscle rest. Thirteen hypercapnic patients with COPD were, therefore, randomly assigned to either a NPV group or a control group. The NPV was applied by an airtight jacket (pneumosuit), 5 h a day, 5 consecutive days a week for 4 weeks. Both NPV group and control group performed in-hospital pulmonary rehabilitation program for a 4-week period. Arterial blood gases, spirometry, maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP), breathing pattern, and electromyogram (EMG) of the diaphragm and parasternal intercostal muscles were measured on the preintervention day, and at the end of the second and fourth weeks of treatment (days 13 and 27, respectively). The short-term effect of NPV on EMG suppression was also checked throughout the ventilatory sessions in three different days (1, 12, and 26, respectively). A 6-min walking test (WT) and level of dyspnea by a modified Borg scale were evaluated on the preintervention and the last days. Negative pressure ventilation resulted in a significant reduction in EMG activity of both diaphragm and parasternal muscles, associated with significant increase in MIP, tidal volume, and ventilation, and increase in PaO2 and decrease in PaCO2. A significant relationship between change in MIP and change in PaCO2 was observed (r = 0.72, p < 0.01). Improve-ment in 6-min WT and dyspnea sensation was also observed, both being the sole changes in the control group. These data seem to indicate a beneficial role of respiratory muscle rest in improving respiratory function. Adequate supervision by personnel familiar with the equipment is likely to contribute to successful treatment.
The contribution of the diaphragm and that of the other inspiratory muscles (scaleni and all the other extradiaphragmatic muscles) at different levels of tidal volume (VT) and during static inspiratory efforts of various strengths has been studied in supine anaesthetized rabbits by blocking phrenic conduction with an electrotonic current. Rabbits spinalized at T1 were used to measure the separate contribution of the scaleni. When the vagi are left intact there is an hyperactivity of the extradiaphragmatic muscles during the phrenic block which has been ascribed to Hering-Breuer reflexes. The relative contribution of the diaphragm to tidal volume, during quiet breathing, appears to approach 9O percent and is reduced to 75 percent during the maximum tidal volume attained. The scaleni appear to account for about 1/3 of the tidal volume contributed by all the other inspiratory extradiaphragmatic muscles during quiet breathing and their share goes up to 1/2 at the highest ventilation. The contribution of the scaleni starts at the same level of inspiratory output found for all extradiaphragmatic muscles and therefore these muscles should not be considered "accessory" Within the range of VT considered the sternomastoids did not appear to contribute, as shown by the fact that their disinsertion did not change the results obtained in spinalized rabbits. Immediately after block of the phrenic nerves there is a marked decrease of VT which then increases within 10-15 breaths to a steady value, three to four times that of the first breath after the paralysis, which is maintained thereafter. The respiratory frequency decreases immediately to a slightly lower value after phrenic block In control animals and does not change when the vagi are cut. In any case a fairly steady value is maintained thereafter even when various types of stimulation are applied. Only changes in body temperature could change respiratory frequency. Chronically phrenicectomized rabbits show some compensatory phenomena either functionally or morphologically. They become able to change their ventilation when chemical drive is increased. In the external intercostal muscles the myoglobin concentration increases and ultrastructural modifications become apparent.
Although blunt chest injuries frequently lead to respiratory failure, the effects of flail chest on the mechanics of breathing have not been evaluated. In the present studies, we have measured the respiratory displacements of the ribs and sternum and the electromyograms (EMG) of the parasternal and external intercostal muscles in eight supine, anesthetized, spontaneously breathing dogs before and after the third to sixth ribs on the right side of the chest were fractured both dorsally and ventrally. After flail, the fractured ribs moved inward, rather than outward, during inspiration, but their inspiratory cranial displacement remained unchanged. The inspiratory outward and caudal displacement of the sternum, the inspiratory EMG activity of the parasternal intercostals, the pattern of breathing, and the arterial blood gases were also unaltered. However, the inspiratory EMG activity recorded from the external intercostals increased consistently to 327 +/- 101% of control (p < 0.05). These observations indicate that with flail chest, the disconnected segment of the rib cage shows paradoxical motion exclusively along the lateral axis; the increased external intercostal activation may account, at least in part, for the persistent inspiratory cranial motion of the ribs. These observations also suggest that the harmful effects of blunt chest injuries are related to pulmonary contusion and pain, rather than to flail chest per se.
The actions of the canine external and internal interosseous intercostal muscles on the lung were assessed by applying the Maxwell reciprocity theorem. The external intercostals in the dorsal part of the cranial interspaces were found to have a large inspiratory effect. However, this effect decreases continuously in the caudal and the ventral direction, such that the muscles in the ventral part of the caudal interspaces have an expiratory effect. The internal intercostals also show marked gradients, such that the muscles in the dorsal part of the caudal interspaces have a large expiratory effect and those in the ventral part of the most cranial interspaces have a small inspiratory effect. During breathing, however, inspiratory activity is found only in the external intercostals with an inspiratory effect, and expiratory activity is confined to the internal intercostals with an expiratory effect. The spatial distribution of inspiratory activity among the canine external intercostals closely mirrors the distribution of inspiratory effect, and the distribution of expiratory activity among the internal intercostals closely mirrors the distribution of expiratory effect. Therefore, the external intercostals have a clear-cut inspiratory action on the lung during breathing, whereas the internal intercostals have a definite expiratory action. The distribution of neural drive among these muscles appears to be equally well matched to the distribution of respiratory effect in humans.
A single fiber EMG (SFEMG) study was performed in 51 patients with idiopathic juvenile scoliosis of moderate degree (mean 23.8 degrees of Cobb), aged 7-18 years (mean 13.2 years). The findings in the extensor digitorum communis muscle (EDC) include a moderate but significant increase in fiber density (mean 2.02, +/- 0.21, P less than 0.001), a mild but significant (P less than 0.001) neuromuscular transmission abnormality (7.6% of fibers showed increased jitter and 4.5% intermittent blocking), and a moderately prolonged mean interspike interval (mean 0.98 msec, +/- 0.20, P less than 0.005) in EDC. Five of the patients had normal fiber density, 9 had a normal jitter study, and further 7 had a normal mean interspike interval. However only one had all the parameters normal. The paraspinal and intercostal muscles at the apex of the scoliotic curvature examined in some of the patients showed similar abnormalities. The study thus suggests the existence of a subclinical systemic neuromuscular disorder in nearly all of our patients with idiopathic scoliosis, which might have a pathogenetic significance.
A total of 65 acute experiments on rats anesthetized with urethane were made to study bioelectrical activity of the external intercostal muscles on the right and left sides of the chest and neuronal activity of both halves of the respiratory center during electrical stimulation (4--15 v, 60 Hz) of the right or left anterior gyrus cinguli. The data obtained showed varied asymmetrical and asynchronous changes in the electromyogram of the respiratory muscles and disclosed some features of the effect of the left and right anterior gyrus cinguli on the electromyogram of the respiratory muscles and diverse reactions of respiratory center neurons to unilateral stimulation of the gyrus cinguli. The presence of functional asymmetry of the right and left anterior gyrus cinguli and their effect on the respiratory center are suggested.
To determine whether the isometric force of concentration of the inspiratory muscles could be used to assess respiratory efferent neural activity, the tracheal pressure generated by the inspiratory muscles during airway occlusion (occluded tracheal pressure) was measured during progressive hypercapnia in anesthetized dogs breathing normally and breathing against added flow-resistive loads. Hypercapnia increased the peak end-inspiratory tracheal pressure and the occluded tracheal pressures generated 100, 200, and 300 ms after the onset of inspiration. The duration of the occluded inspiratory effort generally remained unchanged and the configuration of the pressure tracing was not affected. During normal breathing occluded tracheal pressures increased linearly with tidal volume and with the electrical activity of the diaphragm and the external intercostal muscles both before and after vagotomy. Inspiratory flow-resistive loading reduced the ventilatory response to CO2 but did not affect occluded tracheal pressures at any given PCO2 or the change in pressures with hypercapnia both before and after vagotomy. Similarly, expiratory flow-resistive loading failed to affect occluded tracheal pressures. These results suggest that occluded tracheal pressures measure respiratory efferent neural activity and can be used as indices of CO2 responsivity even during mechanical loading in anesthetized animals.
We report a case of a 46-year-old man who presented with a chest wall tumor in the right hemithorax. He underwent thoracotomy to remove the mass, which was found to be an arteriovenous hemangioma arising from the intercostal muscle. Arteriovenous hemangioma is a rare tumor and chest wall is an extremely rare site for this tumor. This tumor should be considered in the differential diagnosis of the chest wall tumors. Complete surgical excision offers the best treatment.
We used 15-microns radiolabeled microspheres to study the regional distribution of blood flow (Q) among parasternal (PS), transversus thoracis, and external (EI) and internal intercostal muscles (II) in nine anesthetized supine mongrel dogs. We measured Q (ml.min-1.100 g-1) in each intercostal space (ICS) during spontaneous breathing, inspiratory resistive loading, and mechanical ventilation following paralysis. At necropsy the EI, II, and PS were excised and sampled separately for each ICS. During paralysis there was no consistent gradient in Q among the PS, II, and EI muscles. During spontaneous breathing, Q to PS increased linearly by 125% between the first and fourth to sixth ICS, Q to EI decreased progressively from the first/second ICS to the fifth/sixth ICS, whereas Q to the II was uniform. During inspiratory resistive loading, in which mouth pressures of -16 +/- 4 cmH2O were generated, the PS gradient was similar to that during spontaneous breathing. Also, Q to the EI increased in the cranial interspaces (P less than 0.02), whereas Q to the II of the seventh/eighth ICS was greater than that of the first/second ICS (P less than 0.001). Furthermore, with loading, ventrodorsal gradients in Q appeared within both EI and II interspaces. There was no consistent gradient in Q within the transversus thoracis muscle during any of the interventions. Our results demonstrate nonuniform Q within PS, EI, and II during both spontaneous and inspiratory resistive loaded breathing. On the assumption that changes in Q reflect changes in activation, our results suggest systematic topographical patterns of recruitment of rib cage respiratory muscles.
To study the detailed normal ultrasonic anatomy of the pleura and chest wall, high resolution (7.5 MHz) ultrasonograms were obtained from cadaver chest wall specimens and compared with thin section computed tomograms and anatomical specimens. Ultrasonograms show three layers of the intercostal muscles (internal, external and innermost), covered by the "echogenic pleural line." The "echogenic pleural line" is caused by composite echoes from the inner parietal pleura, and the outer endothoracic fascia, with the fatty tissue covering both sides of the fascia, which are located deep to the chest wall muscles. On ultrasonograms, the subpleural fat tissue, when abundant, appeared as an apron-like structure hanging down from the inner surface of the rib (subpleural fat pad), or diffuse fat accumulation mimicking the pleural thickening.
Composite intercostal muscle flaps were experimentally used to repair major intrathoracic tracheal defects in the mongrel dog. These composite flaps provided an adequate tracheal lumen with both sufficient mobility and structural stability. Stenosis of the reconstructed trachea was an uncommon finding, but the incidence of early postoperative mortality was high.