Biomedical subjects
J R Rodarte
Publications and source records attributed to J R Rodarte.
Displacements and strains in the costal diaphragm of the dog.
Radiopaque markers were attached at 1- to 2-cm intervals along three nearby muscle bundles to cover rectangular regions of the mid-costal diaphragms of seven dogs. The markers were tracked by biplane video fluoroscopy during spontaneous breathing (SB), mechanical ventilation with the same tidal volume (MV), and at inflation to total lung capacity (TLC) in the prone and supine positions. The three-dimensional positions of the markers at functional residual capacity (FRC), at end inspiration during SB and MV, and at TLC were determined, and the strains in the plane of the diaphragm relative to FRC were calculated. The principal strains were found to lie nearly along the muscle bundle direction and perpendicular to it. The principal strains along the muscle bundles, which describe muscle shortening, were uniform among the three bundles and uniform along the bundle for MV. For SB, in the prone and supine positions, shortening was approximately 30% greater in the middle of the bundle than near the central tendon and chest wall. Although the tidal volumes were the same for SB and MV, the shortening was larger for SB. The strains perpendicular to the bundle direction were not significantly different from zero. It appears that, for the loads that occur during tidal breathing, the diaphragm is inextensible in the direction perpendicular to the muscle direction. There is a very small displacement of the costal diaphragm at its insertion on the chest wall. The displacement at the central tendon is primarily a result of muscle shortening and rotation of the arc of the muscle around its insertion on the chest wall.
Finite-element analysis of stress in the canine diaphragm.
Stress in the diaphragm, transdiaphragmatic pressure, and diaphragm shape are interrelated by a balance of forces. Using precise in vivo measurements of diaphragm shape and transdiaphragmatic pressure distribution in combination with finite-element analysis (ANSYS), we determined the direction and magnitude of stress in the passive diaphragm at relaxation volume. Lead spheres sutured along muscle bundles identified muscle bundle location and orientation in vivo. The x, y, and z coordinates of the lead spheres and entire surface of the diaphragm, excluding the zone of apposition, were determined to within 1.4 mm. Thin shell elements were used to construct a finite-element model of the diaphragm with a 2.1- to 4.2-mm internodal spacing. The diaphragm was assumed to have a uniform thickness of 2.5 mm, and magnitude and direction of the principal stresses were computed. The results show that 1) diaphragm stress is nonuniform and anisotropic (i.e., varies both with location on diaphragm surface and direction examined), 2) largest stress (sigma 1) is aligned with muscle bundles and is two to four times larger than sigma 2 (perpendicular to sigma 1 in diaphragm plane), and 3) stress along the muscle bundles is larger in vivo under conditions of biaxial stress than at same length in vitro under uniaxial stress. Although diaphragm stress and tension have often been assumed to be uniform, our finding that stress is oriented primarily along the muscle fibers should be considered in future models of the diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)
Inferences on passive diaphragm mechanics from gross anatomy.
The diaphragm is a relatively thin curved structure that is categorized in mechanics as a membrane. Tension in the membrane is given by the product of muscle thickness and stress parallel to the fiber bundles. If all muscle fibers were cylindrical and extended from origin to insertion, the ratio of thickness near the chest wall (CW) to thickness near the central tendon (CT) would vary inversely with the ratio of CW to CT perimeters. In freshly excised diaphragms of 36 mongrel dogs, the ratios of the perimeters (CT/CW) in the right and left costal diaphragm were 0.63 +/- 0.04 and 0.62 +/- 0.04, respectively. The means of the ratio of thickness near CW to that near CT in the right and left costal regions were 0.96 +/- 0.07 and 0.95 +/- 0.05, respectively, consistent with a nearly constant relationship between costal diaphragm membrane tension and muscle stress in the direction of the fibers. In the crural diaphragm, the average ratio of the perimeters of the insertions on CT to CW was 1.16 +/- 0.10. The average ratio of thickness of crural CW to CT was 1.25 +/- 0.11. The discrepancy between the perimeter ratio and thickness ratio in the costal diaphragm is incompatible with the muscle consisting of uniform fibers extending from CW to CT. Our data suggest that muscle fibers are either in series with a smaller number along the smaller perimeter or that they terminate by tapering within the muscle bundle. Both arrangements are consistent with previous anatomic studies (Gordon et al. J. Morphol. 201: 131-143, 1989). Having a nonuniform number of fibers mechanically in series is compatible with uniform stress in the fibers if the membrane is sufficiently curved as in a domed structure.
Costal diaphragm curvature in the dog.
The curvature of the midcostal region of the diaphragm in seven dogs was determined at functional residual capacity (FRC) and end inspiration during spontaneous breathing and mechanical ventilation and at total lung capacity in the prone and supine positions. Metallic markers were attached to muscle fibers on the abdominal surface of the diaphragm, and the dog was allowed to recover from surgery. The three-dimensional positions of the markers were determined by biplane videofluoroscopy. A quadratic surface was fit to the bead positions. The principal axes of the quadratic surface lie nearly along and perpendicular to the muscle fibers. In both the supine and prone positions, the values of the principal curvatures were similar at FRC and end inspiration during spontaneous breathing, when muscle tension and transdiaphragmatic pressure both increase with increasing lung volume, and during mechanical ventilation and passive inflation to total lung capacity, when both decrease relative to their magnitude at FRC. No abrupt change of curvature, which might be expected at the edge of the zone of apposition, was apparent. The curvature along the muscle fiber was 0.35 +/- 0.07 cm-1; the curvature perpendicular to the muscle fiber was much smaller, 0.06 +/- 0.01 cm-1. The costal region of the diaphragm displaces and shortens as lung volume increases, but its shape, as described by its curvatures, does not change substantially.
Expiratory airflow limitation and hyperinflation during methacholine-induced bronchoconstriction.
To investigate the role of airflow limitation on the increase of end-expiratory lung volume (EELV) during bronchoconstriction, nine stable asthmatic subjects and seven healthy subjects were challenged with inhaled methacholine (MCh). Changes in airway caliber were assessed by using forced expiratory volume in 1 s, partial forced expiratory flow at 50% of control forced vital capacity, and specific airway conductance. To detect airflow limitation, tidal flow-volume curves were superimposed on partial forced flow-volume curves at absolute lung volume. The electromyogram of the diaphragm was recorded by surface electrodes in four asthmatic and four healthy subjects, and the electrical diaphragmatic activity (DIA) during expiration was expressed as a percentage of the duration of expiratory time. In 10 subjects (9 asthmatic and 1 healthy) the partial forced expiratory flow recorded after some MCh dose impinged on tidal expiratory flow recorded before MCh. When this occurred it was associated with an increase in EELV by 0.54 +/- 0.07 (SE) liter (P < 0.001), which was larger than that occurring when lower MCh doses (0.11 +/- 0.04 liter, P < 0.05) were used, and with a moderate increase in DIA of 15 +/- 2.5% (P < 0.01). Six healthy subjects did not increase EELV after MCh despite a significant degree of bronchoconstriction; in these subjects tidal expiratory flow never impinged on forced expiratory flow, and DIA never increased. These results suggest that hyperinflation during MCh-induced bronchoconstriction is triggered by dynamic compression of the airways and is associated with moderate increase of DIA during expiration.
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.
Exercise capacity and breathing mechanics in patients with airflow limitation.
To investigate the impact of expiratory airflow limitation on ventilation during exercise, we studied six control subjects with normal lung function (FEV1/FVC = 79 +/- 6%) and eight patients with borderline-to-mild airflow limitation (FEV1/FVC = 68 +/- 4%) during cycle ergometry. VO2, HR, and VE/MVV were not different between the control subjects or patients during maximal or submaximal exercise. In contrast, five of the eight patients achieved maximal expiratory flow over a large portion (37%) of their tidal volume (VT) during submaximal exercise, whereas none of the control subjects achieved maximal expiratory flow. To estimate the fraction of expiratory capacity used by the control subjects and the patients, we calculated a mechanical ventilatory maximum (VEmaxCal) for each level of exercise using the individual's VT, end-expiratory lung volume (EELV), and maximal expiratory flow-volume curve. The patients used a greater fraction of their VEmaxCal at each level of submaximal exercise (P less than 0.03). Despite the flow limitation during submaximal exercise, EELV was similar between the control subjects and patients. In conclusion, even patients with borderline-to-mild airflow limitation achieve maximal expiratory flow during submaximal exercise and these restrictions are not reflected by VE/MVV nor by EELV.
More about the mechanisms of diaphragm displacement during spontaneous breathing.
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Effect of mild-to-moderate airflow limitation on exercise capacity.
To determine the effect of mild-to-moderate airflow limitation on exercise tolerance and end-expiratory lung volume (EELV), we studied 9 control subjects with normal pulmonary function [forced expired volume in 1 s (FEV1) 105% pred; % of forced vital capacity expired in 1 s (FEV1/FVC%) 81] and 12 patients with mild-to-moderate airflow limitation (FEV1 72% pred; FEV1/FVC % 58) during progressive cycle ergometry. Maximal exercise capacity was reduced in patients [69% of pred maximal O2 uptake (VO2max)] compared with controls (104% pred VO2max, P less than 0.01); however, maximal expired minute ventilation-to-maximum voluntary ventilation ratio and maximal heart rate were not significantly different between controls and patients. Overall, there was a close relationship between VO2max and FEV1 (r2 = 0.62). Resting EELV was similar between controls and patients [53% of total lung capacity (TLC)], but at maximal exercise the controls decreased EELV to 45% of TLC (P less than 0.01), whereas the patients increased EELV to 58% of TLC (P less than 0.05). Overall, EELV was significantly correlated to both VO2max (r = -0.71, P less than 0.001) and FEV1 (r = -0.68, P less than 0.001). This relationship suggests a ventilatory influence on exercise capacity; however, the increased EELV and associated pleural pressures could influence cardiovascular function during exercise. We suggest that the increase in EELV should be considered a response reflective of the effect of airflow limitation on the ventilatory response to exercise.
Lung volumes during low-intensity steady-state cycling.
The use of inspiratory capacity (IC) to estimate end-expiratory lung volume (EELV) during exercise has been questioned because of the assumption of constant total lung capacity (TLC). To investigate lung volumes during low-intensity steady-state cycling, we measured EELV by the open-circuit N2 washout method (MR-1, currently Sensormedics 2100) in eight healthy men while at rest and during unloaded and 60-W cycling. TLC was calculated by adding EELV and IC. Measurement variation of TLC was 142 ml at rest, 121 ml during unloaded cycling, and 158 ml during 60-W cycling. TLC did not differ significantly among the three conditions studied. EELV decreased during unloaded (P less than 0.002) and 60-W cycling (P less than 0.001) compared with rest. End-inspiratory lung volume increased only during 60-W cycling (P = 0.03). The decrease in EELV accounted for 100% of the increase in tidal volume during unloaded cycling. Although minute ventilation was similar in the subjects during unloaded cycling, we noted that breathing patterns varied among the subjects. The increase in respiratory frequency was negatively correlated to the change in tidal volume (R2 = 0.54, P = 0.038) and to the change in end-inspiratory lung volume (R2 = 0.68, P = 0.012). We conclude that TLC does not differ significantly during low-intensity steady-state cycling and that use of IC to estimate changes in EELV is appropriate.
Pleural pressure distribution and its relationship to lung volume and interstitial pressure.
The mechanics of the pleural space has long been controversial. We summarize recent research pertaining to pleural mechanics within the following conceptual framework, which is still not universally accepted. Pleural pressure, the force acting to inflate the lung within the thorax, is generated by the opposing elastic recoils of the lung and chest wall and the forces generated by respiratory muscles. The spatial variation of pleural pressure is a result of complex force interactions among the lung and other structures that make up the thorax. Gravity contributes one of the forces that act on these structures, and regional lung expansion and pleural pressure distribution change with changes in body orientation. Forces are transmitted directly between the chest wall and the lung through a very thin but continuous pleural liquid space. The pressure in pleural liquid equals the pressure acting to expand the lung. Pleural liquid is not in hydrostatic equilibrium, and viscous flow of pleural liquid is driven by the combined effect of the gravitational force acting on the liquid and the pressure distribution imposed by the surrounding structures. The dynamics of pleural liquid are considered an integral part of a continual microvascular filtration into the pleural space. Similar concepts apply to the pulmonary interstitium. Regional differences in lung volume expansion also result in regional differences in interstitial pressure within the lung parenchyma and thus affect regional lung fluid filtration.
Mechanisms of blood flow during cardiopulmonary resuscitation.
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Shape of the chest wall in the prone and supine anesthetized dog.
The shape of the passive chest wall of six anesthetized dogs was determined at total lung capacity (TLC) and functional residual capacity (FRC) in the prone and supine body positions by use of volumetric-computed tomographic images. The transverse cross-sectional areas of the rib cage, mediastinum, and diaphragm were calculated every 1.6 mm along the length of the thorax. The changes in the volume and the axial distribution of transverse area of the three chest wall components with lung volume and body position were evaluated. The decrease of the transverse area within the rib cage between TLC and FRC, as a fraction of the area at TLC, was uniform from the apex of the thorax to the base. The volume of the mediastinum increased slightly between TLC and FRC (14% of its TLC volume supine and 20% prone), squeezing the lung between it and the rib cage. In the transverse plane, the heart was positioned in the midthorax and moved little between TLC and FRC. The shape, position, and displacement of the diaphragm were described by contour plots. In both postures, the diaphragm was flatter at FRC than at TLC, because of larger displacements in the dorsal than in the ventral region of the diaphragm. Rotation from the prone to supine body position produced a lever motion of the diaphragm, displacing the dorsal portion of the diaphragm cephalad and the ventral portion caudad. In five of the six dogs, bilateral isovolume pneumothorax was induced in the supine body position while intrathoracic gas volume was held constant.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of body position and lung volume on in situ operating length of canine diaphragm.
The performance of the diaphragm is influenced by its in situ length relative to its optimal force-generating length (Lo). Lead markers were sutured to the abdominal surface of the diaphragm along bundles of the left ventral, middle, and dorsal regions of the costal diaphragm and the left crural diaphragm of six beagle dogs. After 2-3 wk postoperative recovery, the dogs were anesthetized, paralyzed, and scanned prone and supine in the Dynamic Spatial Reconstructor (DSR) at a total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV). The location of each marker was digitized from the reconstructed DSR images, and in situ lengths were determined. After an overdose of anesthetic had been administered to the dogs, each marked diaphragm bundle was removed, mounted in a 37 degrees C in vitro chamber, and adjusted to Lo (maximum tetanic force). The operating length of the diaphragm, or in situ length expressed as percent Lo, varied from region to region at the lung volumes studied; variability was least at RV and increased with increasing lung volume. At FRC, all regions of the diaphragm was shorter in the prone posture compared with the supine, but there was no clear gravity-dependent vertical gradient of in situ length in either posture. Because in vitro length-tension characteristics were similar for all diaphragm regions, regional in vivo length differences indicate that the diaphragm's potential to generate maximal force is nonuniform.
Effect of body position on regional diaphragm function in dogs.
The in situ lengths of muscle bundles of the crural and three regions of the costal diaphragm between origin and insertion were determined with a video roentgenographic technique in dogs. At total lung capacity (TLC) in both the prone and supine positions, the length of the diaphragm is not significantly different from the unstressed excised length, suggesting that the diaphragm is not under tension at TLC and that there is a hydrostatic gradient of pleural pressure on the diaphragmatic surface. Except for the ventral region of the costal diaphragm, which does not change length at lung volumes greater than 70% TLC, all other regions are stretched during passive deflations from TLC. Therefore below TLC the diaphragm is under passive tension and supports a transdiaphragmatic pressure (Pdi). The length of the diaphragm relative to its unstressed length is not uniform at functional residual capacity (FRC) and does not follow a strict vertical gradient that reverses when the animal is changed from the supine to the prone position. By inference, the length of muscle bundles is determined by factors other than the vertical gradient of Pdi. During mechanical ventilation, regional shortening is identical to the passive deflation length-volume relationship near FRC. Prone and supine FRC is the same, but the diaphragm is slightly shorter in the prone position. In both positions, during spontaneous ventilation there are no consistent differences in regional fractional shortening, despite regional differences in initial length relative to unstressed length.
Carbon monoxide diffusing capacity of the lungs determined by single-breath and steady-state exercise methods.
We measured carbon monoxide diffusing capacity of the lungs (DL,CO) by both the resting single-breath (SB) and steady-state (SS) exercise methods in 95 patients referred for pulmonary function testing. A 10-second breath-holding method was used for the SB test. DL,CO (SS) was measured during the last minute of a 3-minute exercise test on a 9-inch step. Results of the two methods showed good agreement, the SB-SS difference averaging -0.70 (SD, 3.39) ml/min per mm Hg. The difference between the two methods was not correlated with other measurements of pulmonary function except minute ventilation during the exercise performed in the DL,CO (SS) procedure. In a separate study of laboratory personnel, the day-to-day variabilities of the two tests were similar (SD, 1.4 ml/min per mm Hg). Alveolar volume obtained by helium dilution during the SB test was comparable to total lung capacity (TLC) estimated by multiple-breath nitrogen washout in patients without severe airway obstruction. In severe airway obstruction, the mean SB alveolar volume was 13.8% less than the TLC by nitrogen washout, a difference that may be useful as an indicator of inefficiency of gas mixing in the lungs. We conclude that the SB and SS exercise methods provide similar estimates of DL,CO in patients referred to a pulmonary function laboratory.
Partitioning of pulmonary resistance in dogs: effect of tidal volume and frequency.
To determine the sensitivity of pulmonary resistance (RL) to changes in breathing frequency and tidal volume, we measured RL in intact anesthetized dogs over a range of breathing frequencies and tidal volumes centering around those encountered during quiet breathing. To investigate mechanisms responsible for changes in RL, the relative contribution of airway resistance (Raw) and tissue resistance (Rti) to RL at similar breathing frequencies and tidal volumes was studied in six excised, exsanguinated canine left lungs. Lung volume was sinusoidally varied, with tidal volumes of 10, 20, and 40% of vital capacity. Pressures were measured at three alveolar sites (PA) with alveolar capsules and at the airway opening (Pao). Measurements were made during oscillation at five frequencies between 5 and 45 min-1 at each tidal volume. Resistances were calculated by assuming a linear equation of motion and submitting lung volume, flow, Pao, and PA to a multiple linear regression. RL decreased with increasing frequency and decreased with increasing tidal volume in both isolated and intact lungs. In isolated lungs, Rti decreased with increasing frequency but was independent of tidal volume. Raw was independent of frequency but decreased with tidal volume. The contribution of Rti to RL ranged from 93 +/- 4% (SD) with low frequency and large tidal volume to 41 +/- 24% at high frequency and small tidal volume. We conclude that the RL is highly dependent on breathing frequency and less dependent on tidal volume during conditions similar to quiet breathing and that these findings are explained by changes in the relative contributions of Raw and Rti to RL.