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Biomedical subjects

D F Rochester

Publications and source records attributed to D F Rochester.

At least 19 recordsLinked to original sources
PubMed1998

Respiratory ultrasonography of human parasternal intercostal muscle in vivo.

The parasternal intercostal muscle (PS) is phasically active during inspiration, but its mechanical function in humans is poorly understood. The aim of this study was to describe PS motion ultrasonographically during respiration. We used a 7.5-MHz curvilinear phased array transducer to obtain ultrasonograms of the second right and left interspace in the sagittal plane, 2-3 cm lateral to the sternum, in 4 seated subjects (3M, 1F), during tidal breathing and at residual volume (RV), functional residual capacity (FRC) and total lung capacity (TLC). Images were recorded on videotape and off-line, digitized, transferred to a workstation, and traced manually to outline the external and pleural borders of the PS muscle in relation to a rectangle bounded by the second and third ribs. To assess PS shape and motion, we measured inter-rib distance (Lics), PS thickness (Tps), and motion of the midpoint of the muscle relative to the midpoint of the reference rectangle (Mps). We also calculated the average radius of curvature of the external and pleural PS borders (Re, Rp) over the mid 50% of Lics, and 1/Re and 1/Rp. During tidal breathing, Mps moved ventrally by 0.42 +/- 0.06 mm (p = 0.001) against the pleural pressure gradient, and 1/Re and 1/Rp decreased by 1.1 x 10(-2) +/- 1.6 x 10(-3) mm-1 and 8.4 x 10(-3) +/- 1.4 x 10(-3) mm-1, respectively (p < 0.001). Lics and Tps did not change (p > 0.19). We conclude that, during inspiration, the PS moves ventrally and straightens, and lung volume, neural activation and pleural pressure influence PS shape and motion. The findings support an intercostal stabilizing function of the PS and suggest a novel mechanism by which the PS may contribute to the inspiratory fall in pleural pressure.

Adult↗
PubMed1996

Contractility of the ventilatory pump muscles.

The ventilatory muscles are striated skeletal muscles, and their in situ function is governed by the same relationships that determine the contractile force of muscles in vitro. The ventilatory muscles, however, are functionally distinct from limb skeletal muscles in several aspects, the most notable being that the ventilatory muscles are the only skeletal muscles upon which life depends. Among the muscles that participate in ventilation, the diaphragm is closest to its optimal resting length at functional residual capacity (FRC) and has the greatest capacity for shortening and volume displacement, making it the primary muscle of inspiration. All inspiratory muscles shorten when the lung is inflated above FRC, but interactions among the various inspiratory muscles make for a wider range of high force output than could be achieved by any one muscle group acting in isolation. The velocity of inspiratory muscle shortening, especially diaphragmatic shortening, causes maximal dynamic inspiratory pressures to be substantially lower than maximal static pressures. This effect is especially pronounced during maximal voluntary ventilation, maximal exercise, and maximal inspiratory flow, volume maneuvers over the full vital capacity. During quiet breathing, the ventilatory muscles operate well below the limits of their neural activation and contractile performance. During intense activity, however, the diaphragmatic excursion approaches its limits over the entire vital capacity, and respiratory pressures may near their dynamic maximum. Because the system may operate near its available capacities during increased ventilatory demands, multiple strategies are available to compensate for deficits. For example, if the diaphragm is acutely shortened, it can still generate the required respiratory pressure if it receives more neural drive. Alternatively, other muscles can be recruited to take over for an impaired diaphragm. Thus, the whole system is highly versatile.

Animals↗
PubMed1996

Chest wall and lung volume estimation by optical reflectance motion analysis.

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.

Humans↗
PubMed1994

Assessment of ventilatory function in patients with neuromuscular disease.

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)

Female↗
PubMed1994

Monitoring the respiratory system of the mechanically ventilated patient.

Bedside monitoring of respiratory status is designed to measure specific parameters and alert the clinician when these parameters exceed the limits of a desired range. Parameters should include measures of respiratory mechanics, oxygenation, and ventilation. Monitoring is the only form of communication between the physician and a patient receiving neuromuscular blocking agents. Airway pressure tracing alone, or in conjunction with concurrent flow, measures respiratory system mechanics, resistance, compliance, and the work of breathing. Pulse oximetry reflects oxygenation, while mixed venous oximetry indicates the balance between oxygen supply and demand. Capnography is a noninvasive way of assessing ventilation. Taken as a whole, noninvasive monitoring provides useful information, reflecting trends in oxygenation, ventilation, and mechanics. This article reviews the concepts of noninvasive monitoring of critically ill patients. Emphasis is given to the patient receiving neuromuscular blocking agents.

Airway Resistance↗
PubMed1993

Respiratory muscles and ventilatory failure: 1993 perspective.

Some conditions that predispose to ventilatory failure increase the work of breathing (chronic obstructive pulmonary disease [COPD], obesity, kyphoscoliosis), whereas others cause severe respiratory muscle weakness. Specific reasons for muscle weakness include critical illness (electrolyte imbalance, acidemia, shock, sepsis), chronic illness (poor nutrition, cachexia), and neuromuscular diseases. Inspiratory muscle weakness from mechanical disadvantage to the diaphragm is characteristic of asthma and COPD. The increased work of breathing combined with muscle weakness increases the pressure needed to inspire a breath and decreases maximal inspiratory pressure. When this pressure exceeds 0.4, dyspnea and inspiratory muscle fatigue ensue. One way to lower this pressure and avert fatigue is to lower the tidal volume. Ventilatory drive is high, not low, in ventilatory failure. Concomitant shortening of inspiration and breath duration cause the small tidal volume and increased respiratory rate. Gas exchange is compromised by ventilation/perfusion imbalance, and the ratio of dead space to tidal volume is also increased by rapid, shallow breathing. Reduction in tidal volume minimizes dyspnea, but the small tidal volume is inadequate for gas exchange. Acute treatment of respiratory muscle failure involves respiratory muscle rest through mechanical ventilation and removal of noxious influences (infection, metabolic disarray), whereas chronic treatment involves rebuilding the contractile apparatus by nutritional repletion and training.

Animals↗
PubMed1991

Relationships between abdominal and diaphragmatic volume displacements.

We investigated the relationship between the volumes displaced by the diaphragm and the abdominal wall during spontaneous breathing in supine anesthetized dogs. Diaphragmatic volume displacement (Vdi) was calculated from measurements taken from anteroposterior fluoroscopic images employing a previously described geometric model. The volume displacement of the abdominal wall (Vabd) was measured with a calibrated Respitrace. Shortening of single diaphragm muscle bundles in costal and crural regions was measured as the distance between radiopaque beads sutured to the peritoneal surface of the muscle. We found that Vdi always exceeded Vabd, but Vabd/Vdi was larger in animals in which the abdominal wall was more compliant. In this preparation, Vdi is better correlated with costal than with crural shortening. Vabd did not correlate with either costal or crural shortening. We infer that the difference between Vdi and Vabd reflects the volume displacement of the lower rib cage caused by diaphragm contraction. This volume difference was tightly correlated with costal shortening. We conclude from these data that coupling between Vdi and Vabd is influenced by the relative compliances of the chest wall and abdomen. Shortening of regions of the diaphragm may have variable relationships to the measured volume displacement, but costal shortening is intimately related to expansion of the lower rib cage.

Abdomen↗
PubMed1991

Evaluation of a new weaning index based on ventilatory endurance and the efficiency of gas exchange.

We hypothesized that the ventilatory capacity needed to wean from mechanical ventilation (mv) depends on two variables: ventilatory endurance and the efficiency of gas exchange. We also hypothesized that these variables could be assessed from data readily available at the bedside, including tidal volume (VT) on mv and during spontaneous breathing (sb), ventilator peak inspiratory pressure (Ppk), and patient negative inspiratory pressure (NIP). Ventilatory endurance was evaluated using a modified pressure-time index: PTI = TI/Ttot x Pbreath/NIP, where Pbreath = Ppk x VTsb/VTmv. Defining VE40 as the minute ventilation needed to bring PaCO2 to 40 mm Hg, the efficiency of gas exchange was evaluated by calculating VE40/VTsb = (VE x PaCO2)mv/VTsb x 40. Because high levels of inspiratory effort might cause patients to reduce VTsb and thereby compromise CO2 elimination, we devised a weaning index (WI) that combines ventilatory endurance and the efficiency of gas exchange: WI = PTI x (VE40/VTsb). The study population comprised 38 patients with chronic obstructive pulmonary disease, adult respiratory distress syndrome, pneumonia, neuromuscular disease, and miscellaneous other conditions. They had been mechanically ventilated more than 3 days and were considered by clinical criteria to be ready for weaning. Of 46 weaning trials, 19 were successful, 2 were partially successful, and 25 failed. PTI and VE40/VTsb were higher in patients who failed (p less than 0.05), but neither variable alone had sufficient sensitivity or specificity to predict the outcome of weaning trials accurately.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Human lower esophageal sphincter pressure response to increased intra-abdominal pressure.

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.

Abdomen↗
PubMed1990

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.

Adult↗
PubMed1990

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.

Animals↗
PubMed1990

A model approach to assess diaphragmatic volume displacement.

Diaphragmatic volume displacement (Vdi) is calculated from two models using measurements obtained from anteroposterior fluoroscopic images of supine anesthetized dogs. In model 1, diaphragmatic descent was treated as if it were a "piston in a cylinder." In contrast, model 2 incorporated thoracic configuration as well as inspiratory changes in rib cage diameter and diaphragm shape. In one dog, a computerized tomography reconstruction of Vdi was compared with Vdi calculated using the models. Vdi calculated from model 2 lay within 11% of the computerized tomographic value, whereas Vdi based on model 1 was 30% larger. In seven animals, radiopaque markers were sewn to the right costal diaphragm. Digitized fluoroscopic images were used to measure intermarker distance, an index of muscle shortening. For four tidal breaths per dog, in model 2 Vdi averaged 49 +/- 18% of tidal volume and was weakly correlated with costal diaphragm muscle shortening (R = 0.74). It is concluded that Vdi can be estimated from linear dimensions in the coronal plane, provided that inspiratory changes in rib cage diameter and diaphragmatic shape change are taken into account.

Animals↗
PubMed1989

Sphincteric action of the diaphragm during a relaxed lower esophageal sphincter in humans.

We studied the effects of involuntary and voluntary contraction of the diaphragm on esophagogastric junction (EGJ) pressure during esophageal distension in healthy human volunteers. The EGJ pressure was monitored using a Dent sleeve device. Along with the pressure we concurrently monitored diaphragm electromyogram (EMG) using intra-esophageal bipolar electrodes that were placed on the nonpressure sensing surface of the sleeve device. Graded esophageal distensions were performed by graded inflations of a 2-cm-diameter balloon that was positioned 7 cm above the EGJ. The graded esophageal distensions caused a graded increase in the amplitude of lower esophageal sphincter (LES) relaxation (end-expiratory EGJ pressure). In a majority of the subjects, esophageal distension had no effect on spontaneous inspiratory EGJ pressure increase and diaphragm EMG. During sustained LES relaxation of greater than 70% induced by sustained esophageal distention, graded voluntary contractions of the diaphragm induced proportional increases in the EGJ pressure and diaphragm EMG. The EGJ pressure and diaphragm EMG were similar during diaphragmatic contraction both before and during esophageal distension. During a maximal and sustained diaphragm contraction, esophageal distension had no effect on the EGJ pressure. We conclude that there are two distinct sphincteric mechanisms at the EGJ, the LES and crural diaphragm, and they respond differently to distension of the distal esophagus.

Adult↗