Rib Cage Muscles Research Articles

Gas exchange during separate diaphragm and intercostal muscle breathing.

In patients with diaphragm paralysis, ventilation to the basal lung zones is reduced, whereas in patients with paralysis of the rib cage muscles, ventilation to the upper lung zones in reduced. Inspiration produced by either rib cage muscle or diaphragm contraction alone, therefore, may result in mismatching of ventilation and perfusion and in gas-exchange impairment. To test this hypothesis, we assessed gas exchange in 11 anesthetized dogs during ventilation produced by either diaphragm or intercostal muscle contraction alone. Diaphragm activation was achieved by phrenic nerve stimulation. Intercostal muscle activation was accomplished by electrical stimulation by using electrodes positioned epidurally at the T(2) spinal cord level. Stimulation parameters were adjusted to provide a constant tidal volume and inspiratory flow rate. During diaphragm (D) and intercostal muscle breathing (IC), mean arterial Po(2) was 97.1 +/- 2.1 and 88.1 +/- 2.7 Torr, respectively (P < 0.01). Arterial Pco(2) was lower during D than during IC (32.6 +/- 1.4 and 36.6 +/- 1.8 Torr, respectively; P < 0.05). During IC, oxygen consumption was also higher than that during D (0.13 +/- 0.01 and 0.09 +/- 0.01 l/min, respectively; P < 0.05). The alveolar-arterial oxygen difference was 11.3 +/- 1.9 and 7.7 +/- 1.0 Torr (P < 0.01) during IC and D, respectively. These results indicate that diaphragm breathing is significantly more efficient than intercostal muscle breathing. However, despite marked differences in the pattern of inspiratory muscle contraction, the distribution of ventilation remains well matched to pulmonary perfusion resulting in preservation of normal gas exchange.

Tests of Respiratory Muscle Strength In Neonates

After completing this article, readers should be able to: 1. Describe the underlying cause of respiratory failure in about 50% of preterm infants who require intubation and mechanical ventilation. 2. Compare compliance characteristics of the chest wall in infants, older children, and adults. 3. List some of the conditions seen in neonates that can adversely affect respiratory muscle function. 4. List noninvasive tests for assessing respiratory muscle strength in neonates. Chest wall mechanics of neonates and infants play an essential role in ventilation that frequently is underappreciated. Dysfunction of the respiratory muscles can cause both a disease process and an inability of the patient to compensate for it. As an example, respiratory muscle failure may be the underlying cause in about 50% of preterm infants who have ventilatory failure. (1) In this article, we detail the current understanding of the physiology of the respiratory muscles in neonates and discuss a number of tests designed to assess their function. Mechanically, the respiratory system can be thought of as being composed of two components. The first includes the respiratory muscles, the rib cage, and the anterior abdominal wall, which together make up the “pump,” whose function is to move air in and out of the lungs. The second includes the airways and lung parenchyma through which gas exchange occurs and can be referred to as the “load” on which the pump must act. For ventilation to occur, the respiratory pump must overcome both the frictional (eg, airway resistance) and tissue elastic forces (eg, lung and chest wall compliance) that create the load. The balance between the capabilities of the pump and the magnitude of the load can influence whether respiratory “success” or “failure” occurs. The chest wall, which contains muscles and skeletal structures, undergoes dramatic maturational changes over the first several years of life. In addition …

Airflow synchronous with oscillatory acceleration reflects involuntary respiratory muscle activity

To explore mechanisms causing involuntary airflow synchronous with oscillatory axial whole body acceleration (oscillatory axial acceleration, OAA) such as that during locomotion, we monitored airflow, acceleration, and electromyograms (EMGs) of the rib cage and abdominal muscles in standing subjects undergoing OAA at 3, 6, and 9 Hz at accelerations of 0.1-0.95 g. Subjects relaxed or performed static respiratory maneuvers at constant lung volume with glottis open. Oscillatory airflows (0.01-3.01 s(-1)) synchronous with OAA were not consistent with expectations for a passive respiratory system, and were larger during active respiratory efforts than during relaxation. Peak inspiratory airflow usually preceded peak upward acceleration by 90-180 degrees. In 80% of runs with respiratory muscles voluntarily activated or relaxed, EMGs showed activity synchronous with OAA. Changes in periodic muscle activity coincided with changes in oscillatory airflow. We conclude that periodic muscle activity, probably a reflex response to body wall deformation during OAA, strongly influences the involuntary airflow synchronous with OAA.

Determinants of diaphragm motion in unilateral diaphragmatic paralysis.

Cranial displacement of a hemidiaphragm during sniffs is a cardinal sign of unilateral diaphragmatic paralysis in clinical practice. However, we have recently observed that isolated stimulation of one phrenic nerve in dogs causes the contralateral (inactive) hemidiaphragm to move caudally. In the present study, therefore, we tested the idea that, in unilateral diaphragmatic paralysis, the pattern of inspiratory muscle contraction plays a major role in determining the motion of the inactive hemidiaphragm. We induced a hemidiaphragmatic paralysis in six anesthetized dogs and assessed the contour of the diaphragm during isolated unilateral phrenic nerve stimulation and during spontaneous inspiratory efforts. Whereas the inactive hemidiaphragm moved caudally in the first instance, it moved cranially in the second. The parasternal intercostal muscles were then severed to reduce the contribution of the rib cage muscles to inspiratory efforts and to enhance the force generated by the intact hemidiaphragm. Although the change in pleural pressure (DeltaPpl) was unaltered, the cranial displacement of the paralyzed hemidiaphragm was consistently reduced. A pneumothorax was finally induced to eliminate DeltaPpl during unilateral phrenic nerve stimulation, and this enhanced the caudal displacement of the inactive hemidiaphragm. These observations indicate that, in unilateral diaphragmatic paralysis, the motion of the inactive hemidiaphragm is largely determined by the balance between the force related to DeltaPpl and the force generated by the intact hemidiaphragm.

Task failure from inspiratory resistive loaded breathing: a role for inspiratory muscle fatigue?

The use of non-invasive resistive breathing to task failure to assess inspiratory muscle performance remains a matter of debate. CO2 retention rather than diaphragmatic fatigue was suggested to limit endurance during inspiratory resistive breathing. Cervical magnetic stimulation (CMS) allows discrimination between diaphragmatic and rib cage muscle fatigue. We tested a new protocol with respect to the extent and the partitioning of inspiratory muscle fatigue at task failure. Nine healthy subjects performed two runs of inspiratory resistive breathing at 67 (12)% of their maximal inspiratory mouth pressure, respiratory rate (fR), paced at 18 min(-1), with a 15-min pause between runs. Diaphragm and rib cage muscle contractility were assessed from CMS-induced esophageal (P(es,tw)), gastric (P(ga,tw)), and transdiaphragmatic (P(di,tw)) twitch pressures. Average endurance times of the first and second runs were similar [9.1 (6.7) and 8.4 (3.5) min]. P(di,tw) significantly decreased from 33.1 to 25.9 cmH2O in the first run, partially recovered (27.6 cmH2O), and decreased further in the second run (23.4 cmH2O). P(es,tw) also decreased significantly (-5.1 and -2.4 cmH2O), while P(ga,tw) did not change significantly (-2.0 and -1.9 cmH2O), indicating more pronounced rib cage rather than diaphragmatic fatigue. End-tidal partial pressure of CO2 ( PETCO2) rose from 37.2 to 44.0 and 45.3 mmHg, and arterial oxygen saturation (SaO2) decreased in both runs from 98% to 94%. Thus, task failure in mouth-pressure-targeted, inspiratory resistive breathing is associated with both diaphragmatic and rib cage muscle fatigue. Similar endurance times despite different degrees of muscle fatigue at the start of the runs indicate that other factors, e.g. increases in PETCO2, and/or decreases in SaO2, probably contributed to task-failure.

Synergism between the canine left and right hemidiaphragms.

Expansion of the lung during inspiration results from the coordinated contraction of the diaphragm and several groups of rib cage muscles, and we have previously shown that the changes in intrathoracic pressure generated by the latter are essentially additive. In the present studies, we have assessed the interaction between the right and left hemidiaphragms in anesthetized dogs by comparing the changes in airway opening pressure (DeltaPao) obtained during simultaneous stimulation of the two phrenic nerves (measured DeltaPao) to the sum of the DeltaPao values produced by their separate stimulation (predicted DeltaPao). The measured DeltaPao was invariably greater than the predicted DeltaPao, and the ratio between these two values increased gradually as the stimulation frequency was increased; the ratio was 1.10 +/- 0.01 (P < 0.05) for a frequency of 10 Hz, whereas for a frequency of 50 Hz it amounted to 1.49 +/- 0.05 (P < 0.001). This interaction remained unchanged after the rib cage was stiffened and its compliance was made linear, thus indicating that the load against which the diaphragm works is not a major determinant. However, radiographic measurements showed that stimulation of one phrenic nerve extends the inactive hemidiaphragm toward the sagittal midplane and reduces the caudal displacement of the central portion of the diaphragmatic dome. As a result, the volume swept by the contracting hemidiaphragm is smaller than the volume it displaces when the contralateral hemidiaphragm also contracts. These observations indicate that 1) the left and right hemidiaphragms have a synergistic, rather than additive, interaction on the lung; 2) this synergism operates already during quiet breathing and increases in magnitude when respiratory drive is greater; and 3) this synergism is primarily related to the configuration of the muscle.

Chest wall kinematics during chemically stimulated breathing in healthy man.

Chest wall compartment kinematics and respiratory muscle coordinate activity, during either hypercapnia or hypoxia, have not been comparatively assessed in healthy humans. We assessed the displacement volume of the chest wall (Vcw) in 5 normal subjects during hypoxic-normocapnic and hypercapnic-hyperoxic rebreathing by using linearized magnetometers. Vcw was divided into displacement volumes of the rib cage (Vrc) and the abdomen (Vab). Esophageal (Pes) and gastric (Pga) pressures were simultaneously recorded and transdiaphragmatic pressure (Pdi) was calculated by subtracting Pes from Pga. Pressure swings (sw) from end expiration (EE) to end inspiration (EI) were also calculated. During both hypoxia and hypercapnia, from quiet breathing to 40 L/min VE, Vrc,EI increased consistently but Vrc,EE, and Vab,EI did not. Moreover, Vab,EE decreased significantly during hypercapnia and remained unchanged during hypoxia. PesEI decreased (more negative values) and PesEE increased (less negative values) during either stimulus, while PgaEE increased with hypercapnia. Pdisw, calculated as the difference between PdiEE and PdiEI, increased significantly with both hypercapnia and hypoxia ( p = 0.002 for both). On the plot of Pes vs Pga, the slope of a line from end expiratory to end inspiratory lung volume between 20 and 40 L/min VE progressively increased during hypercapnia indicating increasing rib cage muscle (RCM) contribution to inspiratory pressure swings relative to the diaphragm. From these results we conclude that in healthy man: (i) with both chemical stimuli RCM contribution accounts for increase in Vrc displacement; (ii) with hypercapnia, the decrease in Vab,EE displacement indicates abdominal muscle (ABM) contribution to tidal volume; (iii) RCM and ABM assist the diaphragmatic function during hypercapnic stimulation.

Respiratory sensation and ventilatory mechanics during induced bronchoconstriction in spontaneously breathing low cervical quadriplegia.

Intensity of dyspnea during induced bronchoconstriction in asthma is strongly related to the reduction in inspiratory capacity (IC) as a result of dynamic hyperinflation. To determine the role of rib cage and intercostal muscle afferents in symptom perception during bronchoconstriction, we measured the relationship between dyspnea intensity and IC during induced bronchoconstriction in six subjects with complete C4-C7 quadriplegia who did not require assisted ventilation. Spirometry, lung volumes, breathing pattern, esophageal pressure (Pes), and dyspnea intensity (Borg Scale) were measured during high-dose methacholine bronchoprovocation up to 256 mg/ml or a maximum change (Delta) in FEV(1) of 50%. Contemporaneous control data from subjects with asthma (n = 12) who had completed the same protocol were used for comparison. At maximum response in quadriplegia, FEV(1) decreased by 1.42 +/- 0.18 L (62 +/- 4%predicted) (mean +/- SEM), and IC decreased by 0.89 +/- 0.12 L (30 +/- 4%predicted). Dyspnea at maximum response was rated "moderate" to "severe": Borg 3.6 +/- 0.3. The predominant qualitative respiratory sensations were inspiratory difficulty and unsatisfied inspiration. The best correlate of dyspnea (Borg) was DeltaIC(%predicted) (p < 0.0005), whereas changes in FEV(1), Pes-derived measurements and breathing pattern did not contribute further to the strength of this relationship. Dyspnea intensity, quality, and changes in spirometry and lung volumes at maximum response were similar to those reported previously in asthma. The relationship between dyspnea intensity and DeltaIC(%predicted) was linear and consistent across groups. We conclude that the quality and intensity of dyspnea during methacholine-induced bronchoconstriction and dynamic hyperinflation was not altered by extensive chest wall deafferentation.

Proportional assist ventilation decreases thoracoabdominal asynchrony and chest wall distortion in preterm infants.

Thoracoabdominal asynchrony (TAA) and chest wall distortion (CWD) are commonly seen in preterm infants secondary to a highly compliant rib cage and poor compensation of distorting forces by inspiratory rib cage muscles. Continuous positive airway pressure (CPAP) reduces TAA and CWD by stenting the chest wall. We hypothesized that application of positive airway pressure only during inspiration and in proportion to an infant's inspiratory effort should have a similar but more pronounced effect than CPAP alone. A ventilator providing airway pressure changes in proportion to flow and volume generated by an infant (proportional assist ventilation) was used to unload the respiratory pump during inspiration. Ten preterm infants were studied [birth weight, 745 (635-1175) g; gestational age, 26.5 (24-31) wk; postnatal age 3 (1-7) d; medium (range)]. TAA and CWD were determined by respiratory inductive plethysmography. TAA was expressed as the phase angle between the rib cage and abdominal motion and CWD as the total compartmental displacement ratio. In addition, we measured tidal volume with a pneumotachograph and esophageal and airway pressure deflections with pressure transducers. Measurements were obtained during alternating periods of CPAP and two different degrees of support (Gain 1 = 1.09 +/- 0.68, Gain 2 = 1.84 +/- 0.84 cm H(2)O/mL) that were provided by a proportional assist ventilator. Phase angle and the total compartmental displacement ratio decreased with increasing gain compared with CPAP alone. Peak airway pressure increased from 0.6 to 3.8 to 7.6 cm H(2)O above positive end-expiratory pressure (PEEP) with CPAP, Gain 1, and Gain 2, respectively, as tidal volume increased from 2.8 to 4.1 to 4.7 mL/kg. Esophageal pressure changes decreased only little with increasing gain. Chest wall excursion increased and abdominal movement decreased, indicating a redistribution of tidal volume between chest and abdomen. We conclude that proportional assist ventilation reduces TAA and CWD by generating a small increase in airway pressure that occurs in synchrony and in proportion to each inspiratory effort.

Expiratory muscle pressure and breathing mechanics in chronic obstructive pulmonary disease.

Expiratory muscle recruitment is common in stable chronic obstructive pulmonary disease (COPD) patients. Due to airway obstruction, there is little reason to believe that active expiration in COPD would be mechanically effective in lowering operating lung volume. The physiological significance of expiratory muscle recruitment in COPD, therefore, remains unknown. The purpose of this study was to assess, in COPD patients breathing at rest, the effect of expiratory muscle contraction on force generating ability of the diaphragm. The force generating ability of the diaphragm was evaluated from its pressure swing (Pdi) for a given diaphragm electrical activity (Edi), where Edi was normalized as % of its maximal value (Pdi/Edi/Edi,max). Phasic expiratory muscle contraction was measured as the total expiratory rise in gastric pressure (Pga,exp.rise). Nineteen seated patients with moderate to severe COPD, participated in the study and 10 exhibited phasic rise in Pga during expiration with a mean Pga,exp.rise of 1.91+/-0.89 cmH2O. The patients were thus divided into passive expiration (PE) and active expiration (AE) groups. There was no significant difference in various lung function and breathing pattern parameters between the two groups. Pdi/Edi/Edi,max was 0.63+/-0.07 and 0.54+/-0.07 cmH2O/% in PE and AE groups, respectively, and was not significantly different between each other. Compared with PE group, AE group not only recruited expiratory muscles, but also preferentially recruited inspiratory rib cage muscles and derecruited the diaphragm. The results do not support a significant improvement of the force-generating ability of the diaphragm by phasic contraction of expiratory muscles at rest in chronic obstructive pulmonary disease patients.

Response of respiratory muscles to intravenous nicotine challenge in anaesthetized cats

The effects of an intravenous nicotine challenge on the ventilation and activity of rib cage muscles were studied in 33 pentobarbitone-chloralose anaesthetized cats. Bolus injection of nicotine (200 μg) into the right femoral vein evoked in 19 of the intact animals prompt, short-lived apnoea, or prolongation of the first expiration after the drug, the occurrence of which was significantly reduced by midcervical vagotomy ( P<0.001). In breaths that followed the apnoea, peak activity of the parasternal intercostal muscles increased from a baseline of 3.1±0.8 to 9.2±1.8 arbitrary units ( P<0.001). Nicotine produced a similar increase in peak phrenic ENG (7.0±0.5 to 14.5±1.2 arbitrary units; P<0.001). Peak triangularis sterni muscle EMG was reduced from 8.9±1.2 to 6±1.7 arbitrary units ( P<0.05) and the onset of response was delayed to 30 s after the challenge. The changes of respiratory effectors induced by nicotine were independent of vagal integrity. The results show that post-nicotine apnoea is to large extent vagally dependent though the response of the respiratory muscles is mediated by non-vagal influences.

THE EFFECT OF OXYGEN ON PULMONARY MUSCLE FUNCTION IN PATIENTS WITH SPINAL CORD INJURY

S421 INTRODUCTION: Pulmonary muscle dysfunction is common in Spinal Cord injury (SCI) patients [1] Depending on the level and degree of SCI, respiration may be impaired by paralysis of intercostal, accessory and abdominal muscles. Oxygen therapy has been shown to improve pulmonary function in normal volunteers [2]. The purpose of this study was to see if oxygen therapy might improve the pulmonary function of SCI patients. METHODS: This study was approved by Human Subjects Committee. SCI patients were eligible for study entry. Three groups of patients were studied. Group I - included quadriplegic patients with level of injury C1-C7, Group II - included paraplegic patients with level of injury T1-T7 and Group III - included paraplegic patients with level of injury T8-T12. We measured tidal volume (TV), respiratory rate (RR), labored breathing index (LBI) and oxygen saturation (SaO2) before and after oxygen administration (4L/min) in each patient. Tidal volume was measured using a spirometric flowmeter (Ohmeda 5410). Labored breathing index (LBI), an index of rib cage and abdominal respiratory muscle synchrony, was measured with a Respitrace (non-invasive monitoring system; NIMS; Miami Beach, Fl). The Respitrace uses a respiratory impedance plethysmographic method with two elastic bands, one band is placed around the rib cage (at the nipple line) and the other band is around the abdomen (at the umbilicus). Oxygen saturation was measured with a pulse oximeter (Ohmeda 3700). We evaluated the effect of oxygen on pulmonary function using 2-way ANOVA with post - hoc testing as appropriate. A p < 0.05 was considered statistically significant. RESULTS: Five patients were studied in each group Table 1Table 1A normal LBI is 1.0.; an LBI > 1.3 indicates dys-coordination between abdominal and rib cage respiratory muscles. DISCUSSION: Oxygen therapy significantly improved LBI. Cervical SCI patients had significantly higher LBI than thoracic SCI as measured by LBI and TV. The degree of pulmonary muscle dysfunction in SCI patients varies with the level of injury; the higher the level of injury, the greater the dysfunction. Cervical SCI patients had the worst breathing pattern and smallest TV.

Rib cage muscle interaction in airway pressure generation.

We have previously demonstrated in dogs that the change in airway opening pressure (DeltaPao) produced by isolated maximum activation of the parasternal intercostal or triangularis sterni muscle in a single interspace, the sternomastoids, and the scalenes is proportional to the product of muscle mass and the fractional change in muscle length per unit volume increase of the relaxed chest wall. In the present study, we have assessed the interactions between these muscles by comparing the DeltaPao obtained during simultaneous activation of a pair of muscles (measured DeltaPao) to the sum of the DeltaPao values obtained during their separate activation (predicted DeltaPao). Measured and predicted DeltaPao values were compared for the following pairs of muscles: the parasternal intercostals in two interspaces, the parasternal intercostals in one interspace and either the sternomastoids or the scalenes, two segments of the triangularis sterni, and the interosseous intercostals in two contiguous interspaces. For all these pairs, the measured DeltaPao was within approximately 10% of the predicted value. We therefore conclude that 1) the pressure changes generated by the rib cage muscles are essentially additive; and 2) measurements of the mass of a particular muscle and of its fractional change in length during passive inflation can be used to estimate the potential pressure-generating ability of the muscle during coordinated activity as well as during isolated activation.

Cervical magnetic stimulation as a method to discriminate between diaphragm and rib cage muscle fatigue.

Inspiratory muscle fatigue can probably determine hypercapnic respiratory failure. Diaphragm fatigue is detected by electrical phrenic stimulation (ELS), but there is no simple tool to assess rib cage muscle (RCM) fatigue. Cervical magnetic stimulation (CMS) costimulates the phrenic nerves and RCM. We reasoned that changes in transdiaphragmatic pressure twitch (Pdi,tw) with CMS and ELS should be different after selective diaphragm vs. RCM fatigue. Five volunteers performed inspiratory resistive tasks while voluntarily uncoupling diaphragm and RCM. Baseline Pdi,twELS and Pdi,twCMS were 28.57 +/- 1.68 and 32.83 +/- 2.92 cmH2O. After selective diaphragm loading, Pdi,twELS and Pdi,twCMS were reduced by 39 and 26%, with comparable decreases in gastric pressure twitch (Pga,tw). Esophageal pressure twitch (Pes,tw) was better preserved with CMS. Therefore Pes,tw/Pga,tw was lower with ELS than CMS (-1.24 +/- 0.16 vs. -1.73 +/- 0.11, P = 0.05). After selective RCM loading, there was no diaphragm fatigue, but Pes,twCMS was significantly reduced (-30%). These findings support the role of rib cage stiffening by CMS-related RCM contraction in the ELS-CMS differences and suggest that CMS can be used to assess RCM fatigue.

Inspiratory maneuver effects on peak expiratory flow. Role of lung elastic recoil and expiratory pressure.

We investigated the effects of two different inspiratory maneuvers (fast or slow) on the ability of normal subjects to generate peak expiratory flows (PEF) and maximal dynamic expiratory pressures (Pexp) during the performance of a forced vital capacity maneuver. During the fast maneuver (F), the subject inspired rapidly to total lung capacity (TLC) and immediately performed a maximal expiration, whereas in the slow maneuver (S) the subject inspired slowly to TLC, paused for 4-5 s at TLC and then performed a maximal expiration. Ten normal subjects performed a series of such maneuvers. In addition to PEF and Pexp, we measured EMG activity of abdominal (EMGabd) and rib cage muscles, and lung elastic recoil pressure (PesL). Overall, F yielded higher PEF values than S (by approximately 7%); in addition, PesL, Pexp, rate of rise of Pexp (dPexp/dt), and EMGabd were similarly higher with F than with S (p < 0.05 for all). Analysis of individual data showed that the intermaneuver differences in PEF were largely explained by differences in PesL, Pexp or dPexp/dt. Our data suggest that, in comparison with the slow maneuver, the fast maneuver induces a greater change in both the lung elastic recoil and expiratory muscle activation which account for differences in PEF between the two maneuvers. The enhanced expiratory muscle activation with the fast maneuver suggests a specific inspiratory-expiratory muscle interaction analogous to agonist-antagonist interactions described for skeletal muscles.

Inspiratory muscle mechanics of patients with chronic obstructive pulmonary disease during incremental exercise.

Inspiratory muscles are weak and contribute to exercise limitation in chronic obstructive pulmonary disease (COPD). Differential inspiratory pressure contributions from the diaphragm and inspiratory rib cage muscles (RCMs) during exercise in patients with COPD patients are insufficiently described. We measured, in 16 patients with COPD, the global inspiratory muscle pressure (delta Pmus) and transdiaphragmatic pressure (delta Pdi) during an incremental bicycle exercise to exhaustion. The pressures needed to overcome the elastic load were further partitioned into portions for overcoming the PEEPi-imposed inspiratory threshold load (before the beginning of inspiratory flow) and for inflating the respiratory system (between the beginning and end of inspiratory flow). The delta Pdi/delta Pmus ratio was used to quantify the pressure contribution from RCMs relative to that from the diaphragm for a given inspiratory effort. We observed that in patients with COPD during exercise (1) there is a progressive increase in total inspiratory pressure contribution from RCMs relative to that of the diaphragm, and the magnitude of this increase appears to depend on the RCMs reserves during resting breathing; (2) most of the diaphragmatic pressure contribution occurs before the beginning of inspiratory flow, to overcome the PEEPi-imposed inspiratory threshold load; (3) RCMs pressure contribution predominates during the period of inspiratory flow once PEEPi is neutralized, not only for overcoming the elastic load caused by increased tidal volume, but also for compensating for the diaphragmatic pressure contribution during this interval that was gradually lost with increasing exercise work load.

Differential inspiratory muscle pressure contributions to breathing during dynamic hyperinflation.

During dynamic hyperinflation, the ventilatory pump is facing increased demand because it must overcome the intrinsic positive end-expiratory pressure (PEEPi) and decreased capacity since it must operate at a dynamically increased end-expiratory lung volume (EELV). The aim of this study was to evaluate the relative pressure contribution by the diaphragm and inspiratory rib cage muscles (RCMs) during dynamic hyperinflation. In six healthy subjects, dynamic hyperinflation was induced by limiting expiratory flow. The global inspiratory muscle pressure (delta Pmus,i) and transdiaphragmatic pressure (delta Pdi) were partitioned into the portion used to overcome PEEPi and the portion used to inflate the respiratory system. The delta Pdi/delta Pmus,i ratio was used to estimate the pressure contribution of RCMs relative to that of the diaphragm. Our results suggest that (1) with increasing severity of dynamic hyperinflation, there is a significant increase in the inspiratory pressure contribution of RCMs relative to that of the diaphragm for inflating the respiratory system; (2) during dynamic hyperinflation, especially at high EELV, the major pressure contribution of the diaphragm is to overcome the PEEPi-imposed inspiratory threshold load, whereas the inspiratory pressure needed for the subsequent task of inflating the respiratory system is largely contributed by RCMs. This arrangement is consistent with the change in mechanical advantages of RCMs and the diaphragm during the development of dynamic hyperinflation.

Cervical magnetic stimulation of the phrenic nerves in bilateral diaphragm paralysis.

Cervical magnetic stimulation (CMS) produces a greater twitch transdiaphragmatic pressure (TwPdi) than electrical stimulation. This may be because CMS produces rib cage muscle activation, thus producing an inspiratory action independent of the diaphragm. Alternatively, CMS could merely stiffen the rib cage, allowing the diaphragm to act efficiently, by contracting against a stable rib cage. To examine these two hypotheses we studied five patients with isolated bilateral diaphragm paralysis using CMS and bilateral electrical phrenic stimulation (BES). TwPdi, twitch esophageal pressure (TwPes), and twitch gastric pressure (TwPgas) were measured. We also assessed maximal sniff esophageal and transdiaphragmatic pressures (SnPes) (SnPdi), maximal inspiratory and expiratory mouth pressures (MIP) (MEP), and fall in VC on moving from an upright to a supine position. Respiratory muscle strength tests were consistent with bilateral diaphragm paralysis, and the MEPs confirmed normal expiratory muscle function. The patients were able to generate a mean SnPes of -30 cm H2O, mainly because of inspiratory activity of rib cage and neck muscles. However, TwPdi and TwPes during both CMS and BES were close to zero. We conclude that in our patients with diaphragm paralysis caused by neuralgic amyotrophy, CMS stiffens the rib cage but does not have an inspiratory action independent of the diaphragm.

Hyperinflation and respiratory muscle interaction

Hyperinflation clearly affects respiratory muscle interaction. It commonly increases the rib cage contribution to chest wall motion, whilst it reduces the abdominal contribution. This change is thought to result from the fact that hyperinflation severely reduces the mechanical advantage of the diaphragm, whilst it affects the mechanical advantage of the neck and rib cage muscles to a lesser extent. The mechanical disadvantage in the diaphragm induced by hyperinflation is presumably primarily the result of the length changes undergone by the diaphragm in acute hyperinflation. Changes in diaphragmatic geometry are generally considered to be less important in the reduction of the diaphragm's force-generating capacity. Further factors contributing to the mechanical disadvantage in the diaphragm include a reduction in the appositional component of diaphragmatic action (through reduction in the zone of apposition), and a reduction in the insertional component (through a shift in the alignment of the diaphragmatic fibres from axial to radial). In chronic hyperinflation, the diaphragm adapts to the chronically hyperinflated state. This adaptation to chronic foreshortening is similar to the adaptation occurring in the skeletal muscle. It is caused by a dropout of sarcomeres in series along the muscle fibres. It restores the force-generating capacity of the muscle, in part, but it reduces the capacity of the muscle to undergo length changes. The mechanical advantage of the parasternal intercostals and the scalenes is possibly less affected, because the length changes undergone by these muscles during hyperinflation are smaller. The factors determining the mechanical advantage of the parasternal intercostals are complex. Variables related to the mechanical advantage of the parasternal intercostals include: length changes; changes in angle between the parasternal intercostals and the sternum and between rib and sternum; and changes in mechanical arrangement among different parasternals. At present, it is difficult to develop an integrated view of these factors and of their change with hyperinflation. Finally, hyperinflation commonly results in recruitment of expiratory muscles. The functional significance of this expiratory muscle recruitment in patients is still debated.

The role of pulmonary stretch receptor activation during cough in dogs.

The role of pulmonary stretch receptors in the modulation of expiratory muscle activity during cough is controversial. To evaluate their potential influence on expiratory effort during cough, we compared expiratory muscle activity during unobstructed cough to that during obstructed cough in which the trachea was occluded at the end-inspiration and maintained throughout the subsequent expiration. Cough was evoked by mechanical stimulation of the intrathoracic trachea in 9 anesthetized, tracheotomized dogs. Peak triangularis sterni (TS), internal intercostal (IIC) and transversus abdominis (TA) muscle EMG were monitored to assess both rib cage and abdominal muscle activation during expiration. During cough, expiratory activity increased and peak activity shifted from Stage II to Stage I expiration. Peak expiratory muscle activation during unobstructed and occluded coughs were not significantly different: during unobstructed coughs, peak EMG's (mean +/- SE as percent of resting breathing) were TS, 212 +/- 18; IIC, 425 +/- 72; TA, 406 +/- 66; and during obstructed cough: TS, 188 +/- 24; IIC, 365 +/- 44; TA, 387 +/- 77 (n = 9). These data indicate that enhanced vagal stimulation resulting from airway occlusion does not affect expiratory activity during cough. We suggest that during cough, the expiratory muscles are activated in a stereotypical pattern by the neural network generating the cough and this pattern of activation is not affected by phasic vagal input.