Estimation of chest wall motion by surface measurements only allows one-dimensional measurements of the chest wall. We have assessed on optical reflectance system (OR), which tracks reflective markers in three dimensions (3-D) for respiratory use. We used 86 (6-mm-diameter) hemispherical reflective markers arranged circumferentially on the chest wall in seven rows between the sternal notch and the anterior superior iliac crest in two normal standing subjects. We calculated the volume of the entire chest wall and compared inspired and expired volumes with volumes obtained by spirometry. Marker positions were recorded by four TV cameras; two were 4 m in front of and two were 4 m behind the subject. The TV signals were sampled at 100 Hz and combined with grid calibration parameters on a personal computer to obtain the 3-D coordinates of the markers. Chest wall surfaces were reconstructed by triangulation through the point data, and chest wall volume was calculated. During tidal breathing and vital capacity maneuvers and during CO2-stimulated hyperpnea, there was a very close correlation of the lung volumes (VL) estimated by spirometry [VL(SP)] and OR [VL(OR)]. Regression equations of VL(OR) (y) vs. VL(SP) (x, BTPS in liters) for the two subjects were given by y = 1.01x-0.01 (r = 0.996) and y = 0.96x + 0.03 (r = 0.997), and by y = 1.04x + 0.25 (r = 0.97) and y = 0.98x + 0.14 (r = 0.95) for the two maneuvers, respectively. We conclude spirometric volumes can be estimated very accurately and directly from chest wall surface markers, and we speculate that OR may be usefully applied to calculations of chest wall shape, regional volumes, and motion analysis.

We studied 53 patients with proximal myopathy to determine at what level of muscle weakness hypercapnic respiratory failure is likely, and which tests of pulmonary function or respiratory muscle strength would best suggest this development. Respiratory muscle strength was determined from maximal static efforts and in half the patients, both inspiratory and expiratory muscle strengths were less than 50% of normal. In the 37 patients without lung disease respiratory muscle weakness was accompanied by significant decreases in vital capacity, total lung capacity, and maximum voluntary ventilation; by significant increases in residual volume and arterial carbon dioxide tension (Paco2); and greater likelihood of dependence on ventilators, atelectasis, and pneumonia. Hypercapnia was particularly likely when respiratory muscle strength was less than 30% of normal in uncomplicated myopathy, and when vital capacity was less than 55% of the predicted value in any patient.Myopathies which affect proximal limb muscles may also affect respiratory muscles;'-' but the relationships between the extent to which respiratory muscles are affected, abnormality of pulmonary function, and the onset of respiratory failure have not been defined. We addressed these questions in a group of 53 patients with various proximal myopathies. MethodsThe patients studied were adults with myopathy from the neurology and medicine services of Harlem Hospital Center and Columbia Presbyterian Medical Center in New York and the University of Virginia Hospital in Charlottesville. They were referred for evaluation of pulmonary or respiratory muscle function or both. They represent about one-third of all patients with a diagnosis of myopathy at these hospitals during the period of the study.Myopathy was diagnosed by conventional criteria

To assess the consequences to the human diaphragm of alterations in body weight and muscularity, we measured the mass, thickness, area, and length of diaphragm muscle at necropsy. Of 33 subjects who were clinically well until sudden death, 27 had sedentary occupations and normal weight (group N), while 6 were nonobese laborers whose average weight was 40% greater than normal (group M). Among 37 patients dying of more prolonged illness, 23 were of normal weight (group W), while 14 weighed 71% of normal (group U). Subjects with obesity, chronic pulmonary disease, or edema were excluded. Disease per se did not significantly affect diaphragm dimensions. However, in group M diaphragm muscle mass, thickness, area, and length were 165, 129, 125, and 117% of normal (P less than 0.005), whereas in group U the corresponding values were 57, 73, 77, and 83% (P less than 0.001). Thus alterations in body weight and muscularity profoundly affect diaphragm muscle mass, causing a nearly threefold variation between muscular normal subjects and underweight patients.

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To determine the effect of contraction of the diaphragm on the lower esophageal sphincter (LES) pressure, we studied eight healthy volunteers during spontaneous breathing, maximal inspiration, and graded inspiratory efforts against a closed airway (Muller's maneuver). Electrical activity of the crural diaphragm (DEMG) was recorded from bipolar esophageal electrodes, transdiaphragmatic pressure (Pdi) than Pdi and correlated with it in a linear fashion (P < 0.001). We conclude that the contraction of the diaphragm exerts a sphincteric action at the LES, and that this effect is an important component of the antireflux barrier.

To characterize the in vivo force-length relation of the human diaphragm, we related pressures during static inspiratory efforts (Pmus and Pdi, respiratory muscle and transdiaphragmatic pressures, respectively) to diaphragm lengths measured on chest X rays from 22 normal subjects. At total lung capacity, the intersection of diaphragm and chest wall contours corresponds to the anatomic junction of diaphragm and chest wall. This point is located by skeletal landmarks to reveal the entire diaphragm contour on films taken at lower lung volumes. To validate the X-ray measurements, corresponding diameters were measured on 32 normal diaphragms at necropsy. After correction for height and diaphragm position, in vivo and necropsy length estimates along the coronal section agreed within 9%. The diaphragm length-lung volume relation is curvilinear, with length increasing primarily in the portion of the diaphragm apposed to the chest wall. As length increases, Pmus and Pdi rise sharply then plateau, generally conforming to force-length behavior of isolated muscle. However, absence of a Pdi peak at presumed diaphragm resting length suggests that Pdi is submaximal during voluntary inspiratory effort.

We studied the effects of increased intra-abdominal pressure on the lower esophageal sphincter (LES) pressure in 15 healthy subjects. The role of the diaphragm in the genesis of LES pressure during increased intra-abdominal pressure was determined by measuring diaphragm electromyogram (EMG). The latter was recorded using bipolar intraesophageal platinum electrodes that were placed on the nonpressure sensing surface of the sleeve device. We also measured the LES pressure response to increased intra-abdominal pressure during inhibition of the smooth muscles of the LES by intravenous atropine (12 micrograms/kg). Straight-leg raising and abdominal compression were used to increase intra-abdominal pressure. Our results show that the increase in LES pressure during straight-leg raising is greater than the increase in gastric pressure. During abdominal compression, the rate of LES pressure increase is faster than that of the gastric pressure, suggesting an active contraction at the esophagogastric junction. The increase in LES pressure during periods of increased intra-abdominal pressure is associated with a tonic contraction of the crural diaphragm as demonstrated by EMG recording. Atropine inhibited the resting LES pressure by 50-70% in each subject but had no effect either on the peak LES pressure attained during increased intra-abdominal pressure or tonic crural diaphragm EMG. We conclude that 1) there is an active contraction at the esophagogastric junction during periods of increased intra-abdominal pressure and 2) tonic contraction of the crural diaphragm is a mechanism for this LES pressure response.