Diaphragm Shortening Research Articles

Diaphragm interference pattern EMG and compound muscle action potentials: effects of chest wall configuration.

The effect of chest wall configuration on the diaphragm electromyogram (EMGdi) was evaluated in five healthy subjects with an esophageal electrode for both interference pattern EMGdi (voluntary contractions) and electrically evoked diaphragm compound muscle action potentials (CMAPs). Diaphragm CMAPs (both unilateral and bilateral) were evaluated for the baseline-to-peak amplitude (Ampl), the time from the onset of the CMAP to first peak (T1), root mean square (RMS), and center frequency (CF) values of the CMAP power spectrum. CF values from the interference pattern EMGdi power spectrum were also calculated. For CMAPs obtained at an electrode position least influenced by variations induced by electrode positioning, Ampl increased with diaphragm shortening from functional residual capacity (FRC) to total lung capacity (TLC) by 101 and 98% (unilateral and bilateral, respectively). Bilateral CMAP RMS values increased 116% from FRC to TLC. CMAP T1 values decreased with diaphragm shortening from FRC to TLC by 1.1 and 2.1 ms for the unilateral and bilateral stimulations, respectively, and CF increased for the bilateral diaphragm CMAPs with diaphragm shortening. CF values from the interference pattern EMGdi did not show any consistent change with chest wall configuration. Thus CF values of the interference pattern EMGdi obtained with an esophageal electrode can be considered reliable for physiological interpretation, at any diaphragm length (if electrode positioning and signal contamination are controlled for), contrary to the diaphragm CMAPs, which are sensitive to changes in chest wall configuration. It is speculated that the different results (over the effects of chest wall configuration on interference pattern EMGdi and diaphragm CMAPs) amy be because of summation properties of the signals and how these influence the EMG power spectrum.

Effects of diaphragm shortening on the mean action potential conduction velocity in canines.

1. The present study was designed to test if the mean muscle fibre action potential conduction velocity (VAPC) in the costal diaphragm changes with muscle length, in spontaneously breathing mongrel dogs. 2. VAPC was determined by the electromyogram (EMG) power spectrum 'dip' method, which is based on the bipolar electrode transfer function. A bipolar EMG electrode with a 20 mm fixed interelectrode distance was sutured to the costal diaphragm in the fibre direction, and in a region with a low density of motor endplates. Diaphragm length was measured with piezoelectric crystals positioned next to the EMG electrode. Seven dogs were vagotomized and spinally anaesthetized in order to increase diaphragmatic shortening, reduce velocity of shortening and abolish possible cross-talk signals from adjacent muscles. 3. Our results showed that VAPC in the canine costal diaphragm was 3.4 m s-1 and was not significantly related to diaphragmatic shortening.

Activity of costal and crural diaphragm during progressive hypoxia or hypercapnia.

Because costal and crural diaphragm segments have different functional characteristics, ventilatory stimulation with hypoxia or hypercapnia may elicit differential segmental function. We report measurements of diaphragm segmental length, shortening, and electromyogram (EMG) activity from 11 canines that were chronically implanted with sonomicrometry transducers and EMG electrodes and then studied a mean of 18 days postimplantation while awake and breathing spontaneously during CO2 rebreathing and progressive isocapnic hypoxia. Ventilatory responses to hypercapnia and progressive hypoxia were moderate at 1.13 +/- 0.31 (SD) 1. min-1. mm-1 arterial Pco2 and -0.98 +/- 0.51 l. min-1.%arterial O2 saturation-1. When tidal values for breathing pattern and segmental function were compared at matching tidal volumes that correspond to mean CO2 of 49.4 arterial Pco2 and 77% arterial O2 saturation, there was no significant difference in resting length, tidal shortening, or tidal EMG of costal or crural segments. Intrabreath profiles of flow, shortening, and EMG activity at matched tidal volumes showed that 1) inspiratory flow during hypoxia was significantly greater during early inspiration, 2) crural EMG activity preceded costal EMG activity in early inspiration during both hypercapnia and hypoxia, 3) both segments showed increased postinspiratory inspiratory activity with stimulated ventilation, and 4) postinspiratory shortening and EMG were greatest for the crural segment during hypoxia. These results suggest that costal and crural diaphragm segments exhibit differential function during chemical stimulation, especially during postinspiration.

Regional diaphragm shortening measured by sonomicrometry.

Diaphragmatic shortening measured by sonomicrometry has been compared in the two major anatomic segments, costal and crural. Data obtained by videofluoroscopy found a variation in subsegmental shortening within segments (Sprung et al. J. Appl. Physiol. 67: 655-662, 1989). No reproducible pattern of subsegmental shortening has emerged, and the mechanisms leading to this subsegmental variation in shortening are unknown. Therefore, we compared subsegmental shortening in both segments of the diaphragm in seven supine pentobarbital-anesthetized dogs. Seven pairs of sonomicrometer transducers were implanted in the two segments, and subsegmental shortening during spontaneous breathing was measured. To determine potential mechanisms contributing to the variation in shortening, measurements were made during stimulated breathing, after epiphrenic stimulation, and during occluded breaths. We found electrical stimulation at physiological frequencies of 10 and 20 Hz reduced the variation in subsegmental shortening, whereas stimulated breathing did not. Occluded breaths showed a consistent decrease in the amount of shortening, particularly in the dome of the costal diaphragm, compared with shortening in the area of apposition. Comparison of shortening between segments revealed greater crural than costal shortening. We conclude that subsegmental variation in activation can contribute to variation in subsegmental shortening and that the afterload can effect shortening during occluded breaths.

Tumor necrosis factor alpha decreases in vivo diaphragm contractility in dogs.

In this study, we hypothesized that tumor necrosis factor alpha (TNF alpha) is an important mediator of sepsis-related impairment in diaphragm contractility (1-2). In 12 anesthetized, ventilated dogs, bipolar stimulating electrodes were placed on the phrenic nerves and diaphragm electromyographic activity (EMG) and shortening were recorded with needle electrodes and piezoelectric crystals, respectively. Transdiaphragmatic pressure (Pdi) was also recorded using esophageal (Pes) and abdominal balloon catheters (Pdi = Pab-Pes). Dogs were randomized to receive saline injection (n = 6), or TNF alpha 60 micrograms/kg (n = 6). All parameters were recorded hourly for 6 h. Mean arterial blood pressure decreased 1 h after infusion in TNF alpha animals (p < 0.05) with no significant change thereafter. Cardiac output increased early after TNF alpha infusion (p < 0.05) and remained at greater than baseline values at study termination. Diaphragm pressure generation and costal shortening decreased progressively from 3 to 6 h post TNF alpha infusion (p < 0.05) with no significant change in control animals. Compound diaphragm action potential in response to supramaximal phrenic stimulation decreased in TNF alpha animals (p < 0.01) with no significant change in control animals 3 and 6 h postinfusion. We conclude that TNF alpha infusion was associated with significant declines in isotonic and quasi-isometric diaphragm contraction and that this could be explained, at least in part, by impaired neuromuscular transmission.

Three-dimensional reconstruction of the in vivo human diaphragm shape at different lung volumes

The ability of the diaphragm to generate pressures at different lung volumes (VLs) in humans may be determined by the following factors: 1) its in vivo three-dimensional shape, radius of curvature, and tension according to Laplace law; 2) the relative degree to which it is apposed to the rib cage (i.e., zone of apposition) and lungs (i.e., diaphragm dome); and 3) its length-force properties. To gain more insight into these factors we have reconstructed from nuclear magnetic images the three-dimensional shape of the diaphragm of four normal subjects under supine relaxed conditions at four different VLs: residual volume, functional residual capacity, functional residual capacity plus one-half of the inspiratory capacity, and total lung capacity. Under our experimental conditions the shape of the diaphragm changes substantially in the anteroposterior plane but not in the coronal one. Multivariate regression analysis indicates that the zone of apposition is dependent on both diaphragm shortening and lower rib cage widening with lung inflation, although much more on the first of these two factors. Because of the changes in anteroposterior shape and expansion of the insertional origin at the costal margin with lung inflation, the data therefore suggest that the diaphragm may be more accurately modeled by a "widening piston" (Petroll's model) than a simple "piston in a cylinder" model. A significant portion of the muscular surface is lung apposed, suggesting that diaphragmatic force has radial vectors in the dome and vectors along the body axis in the zone of apposition. The muscular surface area of the diaphragm decreased linearly by approximately 41% with VL from residual volume to total lung capacity. Diaphragmatic fibers may shorten under physiological conditions more than any other skeletal muscle. The large changes in fiber length combined with limited shape changes with lung inflation suggest that the length-twitch force properties of the diaphragm may be the most important factor for the pressure-generating function of this respiratory muscle in response to bilateral phrenic shocks at different VLs.

Inotropic effects of aminophylline on canine diaphragm are enhanced by hyperinflation

During acute hyperinflation, patients with chronic obstructive pulmonary disease are likely to have foreshortened inspiratory muscles. Because the effects of aminophylline on contractile properties of the foreshortened diaphragm have never been studied in vivo, we compared these effects with those obtained at functional residual capacity (FRC). In 12 anesthetized dogs, bilateral phrenic nerve stimulation (1, 10, 20, and 100 Hz) was performed at FRC and near total lung capacity (TLC) before and 1 h after each injection of aminophylline, given in cumulative doses of 20, 40, and 80 mg/kg (serum levels of 18.7 +/- 6.3, 29.9 +/- 5.9, and 60.4 +/- 11.9 mg/l, respectively). Passive diaphragm shortening from FRC to TLC, measured in eight animals, averaged 30 +/- 12% of the resting length and increased to 35 +/- 12 and 34 +/- 13% after 40 and 80 mg/kg, respectively. After aminophylline, the increase in transdiaphragmatic pressure at FRC did not reach statistical significance, whereas near TLC transdiaphragmatic pressure significantly increased with 80 mg/kg at all stimulus frequencies (e.g., at 20 Hz from 4.4 +/- 2.9 to 6.7 +/- 2.9 cmH2O) and with 40 mg/kg at 10 and 20 Hz. Diaphragm length changes during stimulation were unchanged after aminophylline both at FRC and near TLC. We conclude that aminophylline has a pronounced inotropic effect on foreshortened canine diaphragm, even at concentrations close to the therapeutic range in humans.

Costal and crural diaphragm function during CO2 rebreathing in awake dogs

If costal and crural diaphragm segments can perform as separate muscles, then CO2-stimulated ventilation may elicit differential segmental function. We studied diaphragm segmental length, shortening, and electromyogram (EMG) activity in 10 awake dogs chronically implanted with sonomicrometer transducers and EMG electrodes. During CO2 rebreathing, segmental shortening and EMG activity per whole tidal breath progressively increased, but segmental responses could not be differentiated at any level of CO2. With increasing CO2, resting end-expiratory length of both diaphragm segments increased. During the complete intrabreath inspiratory-expiratory cycle, costal and crural diaphragm revealed distinctive segmental function. At rest, crural shortening exceeded costal shortening in earliest inspiration, costal and especially crural shortening persisted into early expiration, and EMG activity of the crural segment was greater than that of the costal segment in earliest inspiration and showed more end-inspiratory/early expiratory [post-inspiratory inspiratory activity (PIIA)] activity. During CO2-stimulated breathing, neither segment shortened during the inspiratory flow of earliest inspiration. During CO2 rebreathing, shortening of the crural segment exceeded that of the costal segment during early inspiration and outlasted costal shortening during expiration; for both segments, shortening persisted after termination of inspiratory airflow. With increased CO2, EMG activity of the crural segment preceded that of the costal segment in earliest inspiration and was dominant into expiration, whereas costal EMG activity terminated abruptly with inspiratory flow. Thus, costal EMG PIIA was not evident during hypercapnia, whereas crural EMG PIIA was significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in functional residual capacity and regional diaphragm lengths after upper abdominal surgery in anesthetized dogs.

The respiratory performance of the diaphragm may be altered by changes in mechanical or neural factors, or both, induced by upper abdominal surgery. We conducted this study to examine the effects of upper abdominal surgery on postoperative respiratory function. We studied resting lengths of four diaphragm regions, three in the costal and one in the crural diaphragm, with biplane video-roentgenography in six dogs immediately after upper abdominal surgery and up to 30 days postoperatively. Functional residual capacity was 16.7% smaller immediately after surgery compared with values obtained in the same animals after 30 days. Simultaneously measured resting lengths of each of the diaphragm regions immediately after surgery were longer, on average by 8.3%, than 30 days postoperatively. During the postoperative course, resting diaphragm lengths gradually and uniformly decreased as functional residual capacity increased. Phrenic nerve stimulation in four other dogs immediately after identical surgery resulted in large diaphragm shortening (from 42% to 55%), indicating that neither the diaphragm nor phrenic nerves were injured by the surgical manipulation. We hypothesize that respiratory dysfunction after upper abdominal surgery may be, at least in part, attributed to a decreased central drive for breathing caused by activation of the afferent limb of an inhibitory reflex owing to stretching of the diaphragm.

Effect of lung inflation and upright posture on diaphragmatic shortening in dogs

In an earlier study (Road and Leevers (1988), J. Appl. Physiol. 65: 2283–2389), the application of continuous positive airway pressure (CPAP) produced a marked reduction in diaphragm initial length (L FRC) and tidal diaphragmatic shortening (%L FRC), tidal volume (V t) and transdiaphragmatic pressure swings (ΔPdi) in supine dogs after vagotomy. We postulated that the reduced diaphragmatic shortening was mainly a result of the decrease in diaphragm L FRC but an increase in afterload could not be excluded. In this study, we attempted to define the role of these two mechanisms during postural change. Eight, pentobarbital-anaesthetized, vagotomized dogs were studied in the supine position during CPAP and during postural change (tilting towards upright). As before, CPAP produced a prompt reduction in diaphragm L FRC and tidal %L FRC, V t and ΔPdi. Tilting produced similar decreases in crural diaphragm L FRC (23% from control values) as the weight of the abdominal contents was removed, but less decrease in costal L FRC (17% during CPAP compared to 10% during tilting). A given reduction in crural diaphragm initial length (15%) resulted in less tidal shortening during tilting compared to CPAP, whereas costal diaphragm shortening was similar at a given reduction in initial length (10%). Both CPAP and tilting reduced tidal volumes ( 47.8 ± 5.1 and 56.5 3.1% of control), however, ΔPdi decreased less during (20%) than CPAP (47%). There was no significant change in the level of diaphragmatic EMG with either CPAP or tilting. These results suggest that decreased initial length is the major factor limiting costa %L FRC during postural change to the upright position, whereas crural %L FRC is limited by the afterload, as well as initial length.

Videofluoroscopic assessment of muscle fiber shortening in the in situ canine diaphragm

We tested the hypothesis that dynamic shortening of the costal diaphragm can be accurately estimated from measurements of the radiographic width of the zone of apposition (WZapp) by studying seven supine anesthetized dogs. Both muscle fiber length, represented by the distance between implanted radiopaque markers, and WZapp were measured from digitized recordings of fluoroscopic images utilizing interactive computer software. The WZapp was highly correlated with the length of costal fibers during active respiration in all animals (mean R2 = 0.94). The accuracy in the prediction of fiber length and shortening during breathing is enhanced by inclusion of additional variables describing the displacement of the abdominal wall and the resting geometric orientation of the fibers. We conclude that dynamic fluoroscopic measurement of WZapp is a valuable technique for estimating dynamic diaphragm fiber length and shortening. Depending on the experimental circumstances, WZapp may be a more easily acquired indicator of diaphragm shortening than other variables that have been previously utilized. As such, it may provide a suitable approach to assess active shortening of the diaphragm in humans.

Effect of lower rib cage expansion and diaphragm shortening on the zone of apposition

The relationship among diaphragm length (LD), the width of the zone of apposition (WZapp), and transverse chest diameter (Drc) was developed from model equations and statistical analysis. We present a theoretical model of diaphragm motion that predicts that the decrease in WZapp during inspiration is the result not only of shortening of the diaphragm muscle but also of expansion of the lower rib cage. To test our model, static lengths of costal LD, WZapp, and Drc were measured in 15 normal volunteers using posteroanterior chest X-ray films taken at four or five lung volumes spanning the vital capacity. We found a strong correlation between WZapp and LD: WZapp = 0.95 LD - 15.2 (R2 = 0.81). Expressing WZapp as a combined function of LD and Drc significantly reduced the unexplained variance in WZapp: WZapp = 0.96 LD - 0.47 Drc - 2.18 (R2 = 0.95). The coefficients for LD and Drc derived statistically are close to those predicted from our theoretical model. Repeating the analysis with LD as the dependent variable, we obtained similar results: LD = 0.85 WZapp + 17.1 (R2 = 0.81) and LD = 0.98 WZapp + 0.46 Drc + 3.48 (R2 = 0.94). We conclude that shortening of WZapp is dependent on both diaphragm shortening and rib cage expansion and that roentgenographic measurements of Drc and WZapp can be used to predict diaphragm length and length change.

Effects of acute hyperinflation on chest wall mechanics in dogs.

We studied chest wall mechanics at functional residual capacity (FRC) and near total lung capacity (TLC) in 14 supine anesthetized and vagotomized dogs. During breathing near TLC compared with FRC, tidal volume decreased (674 +/- 542 vs. 68 +/- 83 ml; P less than 0.025). Both inspiratory changes in gastric pressure (4.5 +/- 2.5 vs. -0.2 +/- 2.0 cmH2O; P less than 0.005) and changes in abdominal cross-sectional area (25 +/- 17 vs. -1.0 +/- 4.2%; P less than 0.001) markedly decreased; they were both often negative during inspiration near TLC. Parasternal intercostal shortening decreased (-3.0 +/- 3.7 vs. -2.0 +/- 2.7%), whereas diaphragmatic shortening decreased slightly more in both costal and crural parts (costal -8.4 +/- 2.9 vs. -4.3 +/- 4.1%, crural -22.8 +/- 13.2 vs. -10.0 +/- 7.5%; P less than 0.05). As a result, the ratio of parasternal to diaphragm shortening increased near TLC (0.176 +/- 0.135 vs. 0.396 +/- 0.340; P less than 0.05). Electromyographic (EMG) activity in the parasternals slightly decreased near TLC, whereas the EMG activity in the costal and crural parts of the diaphragm slightly increased. We conclude that 1) the mechanical outcome of diaphragmatic contraction near TLC is markedly reduced, and 2) the mechanical outcome of parasternal intercostal contraction near TLC is clearly less affected.

Respiratory changes in thoracic muscle length during bronchoconstriction.

The purpose of the present study was to assess the effects of bronchoconstriction on respiratory changes in length of the costal diaphragm and the parasternal intercostal muscles. Ten dogs were anesthetized with pentobarbital sodium and tracheostomized. Respiratory changes in muscle length were measured using sonomicrometry, and electromyograms were recorded with bipolar fine-wire electrodes. Administration of histamine aerosols increased pulmonary resistance from 6.4 to 14.5 cmH2O X l-1 X s, caused reductions in inspiratory and expiratory times, and decreased tidal volume. The peak and rate of rise of respiratory muscle electromyogram (EMG) activity increased significantly after histamine administration. Despite these increases, bronchoconstriction reduced diaphragm inspiratory shortening in 9 of 10 dogs and reduced intercostal muscle inspiratory shortening in 7 of 10 animals. The decreases in respiratory muscle tidal shortening were less than the reductions in tidal volume. The mean velocity of diaphragm and intercostal muscle inspiratory shortening increased after histamine administration but to a smaller extent than the rate of rise of EMG activity. This resulted in significant reductions in the ratio of respiratory muscle velocity of shortening to the rate of rise of EMG activity after bronchoconstriction for both the costal diaphragm and the parasternal intercostal muscles. Bronchoconstriction changed muscle end-expiratory length in most animals, but for the group of animals this was statistically significant only for the diaphragm. These results suggest that impairments of diaphragm and parasternal intercostal inspiratory shortening occur after bronchoconstriction; the mechanisms involved include an increased load, a shortening of inspiratory time, and for the diaphragm possibly a reduction in resting length.

Analysis of volume displacement and length changes of the diaphragm during breathing

Diaphragmatic volume displacements cause equal displacements of abdominal contents. Since the rib cage forms a variable part of the abdominal container (the variable part being its area of apposition with the diaphragm) the rib cage and ventral abdominal wall share in abdominal displacements. The fraction of total rib cage volume displacement (delta Vrc) contributing to abdominal displacement is predicted from anatomic considerations and measurements. During quiet inspirations it is estimated that more than half of delta Vrc goes into abdominal expansion. This displacement plus the outward displacement of the anterolateral abdominal wall constitute the diaphragmatic displacement. In a typical inspiration in which delta Vrc accounts for 3/4 of the lung volume change, the diaphragm displaces nearly the same volume. Associated changes in diaphragm length are estimated with a model. Diaphragm shortening during an inspiration in which only the rib cage expands is estimated to be only 11% less than during a normal inspiration. We conclude that the direct rib cage contribution to lung volume change is much less, and that diaphragmatic contribution is much more than was previously thought.

Mechanics of the human diaphragm during voluntary contraction: statics

We related diaphragm electromyographic activity (Edi) to transdiaphragmatic pressure (Pdi) in man during graded inspiratory efforts. Estimates of rib cage and abdominal volume displacements were based on their anteroposterior (AP) diameter changes. The diaphragm was assumed to contract isometrically when subjects performed inspiratory efforts against a closed airway at specified abdominothoracic configurations, increasing Edi and Pdi while holding lung volume and rib case and abdominal AP diameters constant. The relationship between Pdi and Edi depends primarily on abdominothoracic configuration rather than lung volume. For equal increments in lung volume, the Pdi developed at constant Edi is four to eight times more sensitive to changes in abdominal than in rib cage AP diameter. We demonstrate an isofunctional state of the diaphragm at different lung volumes, when increases in lung volume and rib cage AP diameter are compensated for by slight decreases in abdominal AP diameter, resulting in a constant relationship between Edi and Pdi. We conclude that diaphragm shortening is reflected more directly in abdominal displacement than in lung volume change.