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Biomedical subjects

R E Hyatt

Publications and source records attributed to R E Hyatt.

At least 55 records · Page 3Linked to original sources
PubMed1982

A computational model for expiratory flow.

A mathematical model of maximal expiratory flow was developed. Coupled equations describing the pressure losses in the flow and the pressure-area behavior of the airway were integrated along the airway from the periphery to the flow-limiting site. Equations describing pressure losses in the flow were adapted from studied of bronchial casts. The bronchial anatomy utilized was that described by Weibel. Bronchial mechanical properties were obtained from measurements in excised human lungs for the central airways and by extrapolations of these data for the peripheral airways. The maximal flow for air and helium predicted by the model agrees with that of five lungs from which mechanical properties were obtained. The model predictions agree with published values of density and viscosity dependence of maximal flow. At high and midlung volumes, maximal flow is determined primarily by the wave-speed mechanism. At low lung volumes, maximal flow is primarily determined by the coupling of viscous pressure losses and airway mechanical properties.

Biomechanical Phenomena↗
PubMed1981

Effect of length changes on bronchial diameters.

The effect of physiological changes in length on the pressure-diameter (PD) behavior of large, excised, intrapulmonary pig, dog, and human bronchi was studied. Length changes did not alter PD behavior of pig bronchi. Lengthening reduced the diameter of dog bronchi but did not alter the shape of the PD curve. In humans, lengthening reduced the diameter at high transmural pressures but not at zero transmural pressure. The wave-speed theory of flow limitation was used as a first approximation to estimate the effect of the length-induced changes on maximal expiratory flow (Vmax). Use of the usual in situ (parenchyma intact) PD curve would lead to a 16% overestimation of Vmax at 45% total lung capacity (TLC) in dog and to a 17% underestimation at 64% TLC in humans. The effect in humans was age dependent and was most pronounced in subjects more than 40 yr of age.

Aging↗
PubMed1981

Respiratory timing and depth of breathing in dogs anesthetized with halothane or enflurane.

Tidal volume (VT) and inspiratory (TI) and expiratory (TE) times were measured during enflurane and halothane anesthesia in 12 prone dogs before and after bilateral vagotomy. "Elastic" loading or airway occlusion was used to obtain a VT-to-TI relationship in each state and to examine the rate of change in airway pressure. VT, TI, and TE were significantly (P less than 0.05) larger during enflurane than during halothane anesthesia, both before and after bilateral vagotomy. Before vagotomy, the rate of change in airway pressure during airway occlusion was similar for the two agents, as was an index of impedance of the respiratory system (Z'rs). Thus the difference in maximal pressure generated and in VT was most likely due to the difference in TI. Before vagotomy, TI increased as VT decreased with loading during enflurane but not halothane anesthesia, demonstrating a different effect of the two agents on the phasic vagal inspiratory inhibitory mechanism. After bilateral vagotomy, TI was unaltered during elastic loading with both agents but was still significantly longer during enflurane than halothane anesthesia. Thus it was concluded that TI was longer in the enfluraneanesthetized dogs than in the halothane-anesthetized dogs because of a different effect of these two agents on the bulbopontine "pacemaker" mechanism and not because of different effects on the phasic vagal inspiratory inhibitory mechanism.

Anesthesia↗
PubMed1981

Pulmonary mechanics and gas exchange in seated normal men with chest restriction.

Lung volumes, static pressure-volume curves, maximal expiratory flow-volume curves, right-to-left intrapulmonary shunts (Qs/Qt), and distributions of ventilation and perfusion relative to the alveolar ventilation and perfusion ration (VA/Q) were determined in seated normal men before chest strapping while breathing air (Cair) and during chest strapping while breathing air (Sair) or 100% oxygen (So2). With Sair and So2, mean vital capacity was reduced by 44% from control. Elastic recoil pressure [Pst(L)] of the lung at 50% control total lung capacity (TLC) increased significantly (P less than 0.05) from 4.64 +/- 0.39 cmH2O (mean +/- SE) to 7.00 +/- 0.47 cmH2O with Sair and to 7.24 +/- 0.70 cmH2O with So2. Maximal expiratory flow at 50% of control TLC increased significantly (P less than 0.05) from 3.22 to 0.25 l/s (mean +/- SE) to 5.84 +/- 0.69 l/s with Sair and to 5.50 +/- 0.68 l/s with So2. With Sair, no significant increase in Qs/Qt from control was observed. With So2, mean Qs/Qt increased significantly (P less than 0.05) from 0 to 2.2 +/- 0.9% of the cardiac output. It is therefore unlikely that the development of atelectasis, as indicated by an increase in Qs/Qt, accounts for the increase in Pst (L) with Sair and So2. Current evidence suggests that either change in alveolar surface compliance or distortion of the lung or both are responsible for the increased recoil pressure but that neither mechanism alone appears to explain it totally.

Adult↗
PubMed1981

Effects of rib cage or abdominal restriction on lung mechanics.

The effects on lung mechanics of equal (37%) reduction in total lung capacity (TLC) by rib cage or abdominal restriction were studied in 10 healthy males. Lung recoil pressure (Pst) was simultaneously measured from three sites in the esophagus. This also provided an estimate of the vertical pleural pressure gradient (PPG). Deformation of the right hemithorax was quantified by roentgenograms in three subjects. At the same lung volume, abdominal restriction decreased lung height and increased anteroposterior diameter compared with the control case, whereas rib cage restriction had opposite effects. Maximum expiratory flow increased equally with both types of restriction, and average Pst increased equally with both types of restriction. There was a significant correlation between degree of TLC reduction and increase in Pst that was similar for both types of restriction. This study indicates that changes in lung mechanics depend primarily on the amount of volume reduction and not on the type of deformation producing the volume decrease.

Abdomen↗
PubMed1980

Hypersensitivity pneumonitis induced by Penicillium species.

An entomologist developed an illness with typical features of hypersensitivity pneumonitis. On-site investigations indicated that on the days of his attacks he was exposed to dust laden with several species of mold, especially Penicillium spp., as well as to mists generated by reservoir-type humidifiers. Serologic tests to more than 40 antigens prepared from organisms and sources known to cause hypersensitivity pneumonitis showed strong reactions to Penicillium and to antigens prepared from the scum of a large industrial humidifier and from his laboratory humidifier. PFTs revealed a significant reduction in DLCO, Following a 4-mo period without laboratory exposure, he experienced no further episodes, a return to his previous exercise tolerance, and a normal DLCO, BP studies with extracts of Penicillium casei and humidifier water from his laboratory (H1) resulted in objective evidence, both clinically and by hematologic and pulmonary function testing, of hypersensitivity to Penicillium spp. and possibly also to the H1 preparation.

Adult↗
PubMed1980

Viscosity and density dependence during maximal flow in man.

Maximal expiratory flow curves were obtained from ten healthy subjects white breathing air and three other gas mixtures with different densities and viscosities. From these data, the magnitudes of the dependence of maximal flow on gas density and viscosity were obtained. The scaling laws of fluid mechanics, together with a model for the flow-limiting mechanism, were used to obtain a prediction of the relationship between the density dependence and the viscosity dependence of maximal flow. Although the data for individual subjects were too variable to allow a precise comparison with this prediction, the relationship between the mean density dependence and the mean viscosity dependence of all usbjects agreed with the theoretic prediction. This agreement supports the assumption, which is frequently made, that flow resistance rather than tissue visoelasticity is the dominant contributor to peripheral resistance. Information on the relationships between the pressure drop to the flow-limiting segment and flow, gas density and viscosity, and lung volume were also obtained.

Air↗
PubMed1980

Prediction of maximal expiratory flow in excised human lungs.

The predictions of the wave-speed theory of flow limitations were tested against measured values of maximal expiratory flow (Vmax) in nine normal excised human lungs. We obtained static pressure-volume curves and deflation pressure-area (PA) curves of the first three to four airway generations. The pressure drop from the alveolus to the flow-limitation site was assumed to consist of a peripheral frictional loss (estimated from a catheter upstream from the flow-limitation site) and a convective acceleration pressure drop. Predicted Vmax was determined graphically by finding the lowest flow for which the Bernoulli PA curve was tangent to one of the bronchial PA curves. At the point of tangency, local flow speed equals local wave speed. At low lung volumes a point of tangency with the PA curves of the first few generations did not exist, and the flow-limitation site was assumed to be the minimal bronchial area at zero transpulmonary pressure. There was good agreement between measured and predicted Vmax. Measured Vmax was not different from Vmax predicted from normal living man. The wave-speed theory predicted flow over much of the vital capacity, but other mechanisms may limit flow at low lung volumes.

Adolescent↗
PubMed1980

Chest wall motion and distribution of inspired gas in anesthetized supine dogs.

Changes in the anterior-posterior (AP) and lateral diameters of the rib cage and abdomen were assessed by magnetometry in seven anesthetized supine dogs during spontaneous respiration (SR) and mechanical ventilation after muscle paralysis (MV). Regional distribution of inspired gas was measured for both modes of ventilation by determining regional 133Xe clearances. Marked differences in chest wall motion were observed between SR and MV: during MV, the changes in lateral rib cage diameter from FRC to end inspiration were larger, and the changes in both abdominal diameters smaller than during SR. AP rib cage diameter changes were similar for both modes of ventilation. Inward motion of the lateral rib cage during initial inspiration was observed in four dogs during SR; it disappeared consistently with MV. Regional 133Xe clearances were not significantly different: there was no cephalocaudal gradient, and the vertical gradient in regional ventilation was similar with MV and SR. We conclude that significant changes in chest wall motion and shape are not necessarily associated with detectable differences in the distribution of regional ventilation.

Animals↗
PubMed1980

Halothane anesthesia and respiratory mechanics in dogs lying supine.

Functional residual capacity (FRC) and quasi-static deflation pressure-volume (PV) curves of the total respiratory system, lung, and chest wall were measured in eight trained dogs lying supine, first awake and then anesthetized with halothane. Two of the eight dogs were repetitively examined 10 times during a 15-mo period. FRC decreased with anesthesia in six of the eight dogs and incresed with anesthesia in the remaining two dogs. There was a significant mean anesthesia-induced reduction in FRC of 16.9% (P < 0.05). FRC change with anesthesia varied between studies in one of the two dogs repetitively examined. Mean PV curves of the total system, lung, and chest wall of the six dogs whose FRC decreased with anesthesia were shifted to the right by anesthesia. PV curves from the two dogs whose FRC increased with anesthesia were shifted to the left. Anesthesia produced a significant reduction (P < 0.05) in mean lung compliance and significant increases (P < 0.05) in mean chest wall and total system compliances.

Anesthesia, Inhalation↗
PubMed1980

Determinants of maximal expiratory flow and density dependence in normal humans.

There is a large variability in maximal expiratory flow (V) and density dependence (DD) in normal humans. Lung mechanics and flow-volume curves were obtained in 40 normal males while they breathed air or helium-oxygen (80%-20%). Static lung recoil (Pst) at 50% vital capacity, total lung capacity, and pulmonary resistance each correlated (P < 0.05) with airflow at 50% vital capacity. The relationship of V and Pst was described by Pst = 1/2 p V2/A2 + RV, where p is gas density, A is the critical area at the flow-limiting site, and R is peripheral resistance. At constant Pst and R, this simplified equation predicts an inverse relation between DD and airflow, which was found at recoil pressures of 8 and 7 cmH2O (P < 0.05). If peripheral losses are small, subjects with smaller flow-limiting airways would have lower airflows but higher DD than subjects with larger airways. Our findings are consistent with concept of dysanaptic growth and suggest that the central airways play a significant role in determining V and DD in normal humans.

Adult↗
PubMed1980

Density dependence of maximal expiratory flow in chronic obstructive pulmonary disease.

Pulmonary mechanics were studied in 22 patients with chronic obstructive pulmonary disease (COPD) who had no evidence of asthma. Eleven of the 22 patients had a density dependence of maximal expiratory flow within the reported normal range. Patients with normal density dependence (responders) were not different from those with decreased density dependence (nonresponders) in mean age, smoking history, symptoms of cough or dyspnea, maximal expiratory flow at 75, 50, and 25% of the vital capacity during air breathing, total lung capacity, or static elastic lung recoil at 50% of the vital capacity. The nonresponders had smaller vital capacity values, larger ratios of residual volume to total lung capacity, higher resistance, and lower static recoil at total lung capacity. There was a correlation between diffusing capacity for CO and density dependence. There was an inverse relationship between the change in density dependence after inhalation of isoproterenol and initial density dependence. Dysanaptic lung growth and increased compliance of the central airways are potential mechanisms for normal density dependence in these patients. The prevalence of normal density dependence in these patients with established COPD raises serious questions concerning the usefulness of density dependence in the early detection of COPD. The differences in density dependence may indicate differences in pathogenesis of the airflow obstruction and hence may be of prognostic significance.

Airway Resistance↗
PubMed1979

Respiratory mechanics in recumbent dogs anesthetized with thiopental sodium.

Pressure-volume (PV) and conductance-volume (GV) curves were obtained in trained dogs awake and then anesthetized with thiopental sodium, in the prone left lateral decubitus, and supine positions. By paired analyses, induction of anesthesia had no significant effect on lung volumes, static PV curves of the lung or chest wall, or static compliance of the lung or chest wall. In addition, change of posture had little effect on these variables in either the awake or the anesthetized state. Frequently, however, individual dogs showed changes in lung PV curves after induction of anesthesia or change of posture. These PV curve shifts were not accompanied by predictable changes in GV relations. Therefore, we concluded that such changes in the lung PV curve reflect either local artifacts or local deformation of the respiratory system.

Anesthesia↗