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Biomedical subjects

K C Beck

Publications and source records attributed to K C Beck.

At least 37 records · Page 2Linked to original sources

Access to medical care and health-related quality of life for low-income persons with symptomatic human immunodeficiency virus.

Despite growing interest in the accessibility of medical care and health-related quality of life for persons infected with human immunodeficiency virus, an association between these variables has not been documented. The authors conducted a cross-sectional study of access to care and its association with health-related quality of life among 205 persons of low income infected with the human immunodeficiency virus with constitutional symptoms and/or diarrhea at one public and one Veterans Administration hospital, using a 9-item measure of perceived access and a 55-item health-related quality of life instrument. Problems with access were widespread: 55% traveled for longer than 30 minutes to their usual source of care (compared with 9% to 12% of general populations in national surveys), 49% had problems meeting costs of care, and 48% had problems with clinic hours (compared with 23% in national surveys). In multivariate analyses, uninsured patients reported worse access than patients with Medicaid or Veterans Administration insurance, particularly for meeting the cost of care (P < 0.01). Adjusted health-related quality of life scores in this sample were far lower (by about 1 SD) than those of subjects in a large national acquired immune deficiency syndrome clinical trial. For 8 of 11 health-related quality of life subscales, worse perceived access was significantly (P < 0.05) associated with poorer health-related quality of life, even after controlling for T-4 lymphocyte count, symptoms and other factors. Access and health-related quality of life measures similar to those used in this study may prove useful in future evaluations of medical care systems serving poor, clinically ill populations infected with human immunodeficiency virus.

Acquired Immunodeficiency Syndrome↗

Regulation of ventilatory capacity during exercise in asthmatics.

In asthmatic and control subjects, we examined the changes in ventilatory capacity (VECap), end-expiratory lung volume (EELV), and degree of flow limitation during three types of exercise: 1) incremental, 2) constant load (50% of maximal exercise capacity; 36 min), and 3) interval (alternating between 60 and 40% of maximal exercise capacity; 6-min workloads for 36 min). The VECap and degree of flow limitation at rest and during the various stages of exercise were estimated by aligning the tidal breathing flow-volume (F-V) loops within the maximal expiratory F-V (MEFV) envelope using the measured EELV. In contrast to more usual estimates of VECap (i.e., maximal voluntary ventilation and forced expiratory volume in 1 s x 40), the calculated VECap depended on the existing bronchomotor tone, the lung volume at which the subjects breathed (i.e., EELV), and the tidal volume. During interval and constant-load exercise, asthmatic subjects experienced reduced ventilatory reserve, higher degrees of flow limitation, and had higher EELVs compared with nonasthmatic subjects. During interval exercise, the VECap of the asthmatic subjects increased and decreased with variations in minute ventilation, due in part to alterations in their MEFV curve as exercise intensity varied between 60 and 49% of maximal capacity. In conclusion, asthmatic subjects have a more variable VECap and reduced ventilatory reserve during exercise compared with nonasthmatic subjects. The variations in VECap are due in part to a more labile MEFV curve secondary to changes in bronchomotor tone. Asthmatics defend VECap and minimize flow limitation by increasing EELV.

Adult↗

Experimental emphysema.

This animal model of emphysema exhibits the same abnormalities in respiratory mechanics as those seen in human emphysema. The histologic and radiographic findings also closely resemble changes of panacinar disease. Moreover, the progressive hypoxemia preceding hypercarbia also parallels the clinical course seen in human disease. Drawbacks of this model include the long time period required to develop significant changes and the cost of maintaining the animals for such a time period. Large cystic areas were not noted in our animals and one would have to turn to another model to address the problem of giant bullous emphysema. There is no ideal animal model of pulmonary emphysema, and the usefulness of an experimental model should be judged on how well it answers the specific questions. Significant information has been obtained using various animal models of emphysema in lung transplantation, diaphragmatic function, pulmonary hemodynamics, and in several other areas. The dog appears to be a suitable model for thoracic surgical research on emphysema.

Animals↗

Bronchoconstriction occurring during exercise in asthmatic subjects.

To demonstrate physiologic changes associated with asthma symptoms that many patients with asthma develop during exercise, we used sustained constant-load and interval exercise protocols with subjects breathing dry room temperature air. In constant-load exercise, subjects pedaled a stationary bicycle at 50% of their maximal power capacity for 36 min. In interval protocols, subjects pedaled at 60% of maximal capacity for 6 min and then 40% of maximal for 6 min; the 12-min cycle was repeated three times for a total exercise time of 36 min. Maximal expiratory flow versus volume maneuvers (MEFV) were obtained before, at 6-min intervals during, and at 5-min intervals after exercise. Changes in peak expiratory flow (PEF), forced expiratory volume in 1 s (FEV1), and forced expiratory flow at 50% of pre-exercise vital capacity (FEF50) were compared with pre-exercise values. Within 15 min after a maximal 1-min incremental exercise protocol, mean flows decreased compared with pre-exercise (PEF, mean -22%, range -46 to 5%; FEV1, mean -21%, range -42 to -3%; FEF50, mean -41%, range -80 to 3%; all p < 0.05). There were no significant changes in MEFV flows until 18 min of constant-load exercise, when FEV1 and FEF50 fell (FEV1, mean -6%, range -15 to 2%; FEF50, mean -14%, range -32 to 6%; both p < 0.05), although changes in PEF were minimal and were not significantly different compared with pre-exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Comparison of four methods for calculating diffusing capacity by the single breath method.

In 283 patients referred for testing in an outpatient pulmonary function laboratory, we studied the single-breath diffusing capacity of the lungs for carbon monoxide (Dco) using the Ogilvie (Og), Jones-Meade (JM), Epidemiological Standardization Project (ESP), and three-phase iterative methods (3PIT, similar to the three equation method). The Dco maneuvers were performed using automated equipment and American Thoracic Society (ATS) recommended procedures. There were small but significant differences in mean Dco, the ESP method yielding the largest, followed in order by JM, 3PIT, and Og methods. The 3PIT and JM Dcos were in close agreement in all degrees and patterns of pulmonary function abnormality. The Og Dco method was 6 percent less than JM in patients with normal pulmonary function, although the difference was less in patients with expiratory flow limitation, restriction, or reduced Dco. There were no differences in the reproducibility of Dco measurements among the methods. Based on these results and a review of the literature, we conclude the following: (1) when measuring single-breath Dco using automated equipment that follows ATS recommended procedures for collecting a single expired gas sample of 500-ml volume, calculated Dco is largest using ESP method, following by JM, 3PIT, and Og methods; (2) in patients with reduced Dco associated with obstructive or restrictive abnormalities, the Og, 3PIT, and JM timing methods are nearly equivalent; and (3) reproducibility of Dco is the same by all methods.

Airway Obstruction↗

Exercise limitation and pulmonary rehabilitation in chronic obstructive pulmonary disease.

Impairment of exercise tolerance is a common problem in patients with severe chronic obstructive pulmonary disease. The cause of exercise intolerance in patients with severe chronic obstructive pulmonary disease is multifactorial and includes impaired lung mechanics, fatigue of inspiratory muscles, impaired gas exchange, right ventricular dysfunction, malnutrition, occult cardiac disease, deconditioning, and psychologic problems; however, impaired lung mechanics and gas exchange abnormalities seem to be the major limiting factors. Recently, the approach to management of pulmonary rehabilitation in patients with chronic obstructive pulmonary disease has changed because improvement in exercise tolerance has been demonstrated after pulmonary rehabilitation. Other adjunctive measures that have been shown to contribute to the observed improvement in exercise tolerance include administration of oxygen, nutritional support, cessation of smoking, and psychosocial support. The roles of ventilatory muscle endurance training, respiratory muscle rest therapy, nasally administered continuous positive airway pressure, and training of the muscles of the upper extremities are less clearly defined.

Dyspnea↗

Gas exchange in dogs in the prone and supine positions.

To determine the cause of the difference in gas exchange between the prone and supine postures in dogs, gas exchange was assessed by the multiple inert gas elimination technique (MIGET) and distribution of pulmonary blood flow was determined using radioactively labeled microspheres in seven anesthetized paralyzed dogs. Each animal was studied in the prone and supine positions in random order while tidal volume and respiratory frequency were kept constant with mechanical ventilation. Mean arterial PO2 was significantly lower (P less than 0.01) in the supine [96 +/- 10 (SD) Torr] than in the prone (107 +/- 6 Torr) position, whereas arterial PCO2 was constant (38 Torr). The distribution of blood flow (Q) vs. ventilation-to-perfusion ratio obtained from MIGET was significantly wider (P less than 0.01) in the supine [ln SD(Q) = 0.75 +/- 0.26] than in the prone position [ln SD (Q) = 0.34 +/- 0.05]. Right-to-left pulmonary shunting was not significantly altered. The distribution of microspheres was more heterogeneous in the supine than in the prone position. The larger heterogeneity was due in part to dorsal-to-ventral gradients in Q in the supine position that were not present in the prone position (P less than 0.01). The decreased efficiency of oxygenation in the supine posture is caused by an increased ventilation-to-perfusion mismatch that accompanies an increase in the heterogeneity of Q distribution.

Animals↗

Contributions of ventilation and perfusion inhomogeneities to the VA/Q distribution.

The anatomic distributions of ventilation (VA) and perfusion (Q) in prone and supine dogs have been described in the literature. These data also provide frequency distributions, i.e., the distribution of lung units as a function of VA or Q. A comprehensive distribution that encompasses these two distributions is described, and the properties of the comprehensive distribution that determine the width of the VA/Q distribution are identified. Using data on the VA and Q distributions taken from various sources in the literature, we estimated the widths of the VA/Q distributions. The widths estimated from the independent data on the VA and Q distributions agree well with the widths obtained from gas exchange data. The analysis provides information about the relative contributions of the VA and Q distributions to the width of the VA/Q distribution. In the prone dog, the VA and Q distributions, as described by the available data, have different length scales, and we argue that these distributions are therefore not highly correlated. As a result, the variance of the VA/Q distributions is approximately the sum of the variances of the VA and Q distributions. Two-thirds of the variance in VA/Q is a result of nonuniform Q, and one-third is a result of nonuniform VA. In the supine dog, the variance of VA is larger than in the prone dog because of a vertical gradient and the variance of Q is larger, in part, because of a vertical gradient. Because the magnitudes of the vertical gradients of VA and Q are about equal, the vertical gradient of VA/Q is small, and these components of the VA and Q inhomogeneities contribute little to the width of the VA/Q distribution. The other components of Q inhomogeneity cause the additional variance of VA/Q in the supine dog.

Analysis of Variance↗

Body plethysmography in the evaluation of intrathoracic airway abnormalities.

A patient with a previously unsuspected intrathoracic tracheal malignancy presented with symptoms suggestive of asthma and an unusual pattern seen by conventional PFTs. Reduced expiratory flows with a large difference between FVC and SVC, normal inspiratory flows and high MVV/FEV1 were found. Body plethysmography using normal and panting efforts with increasing tidal volume and flow helped define the lesion as a variable intrathoracic obstruction and document its regression after palliative therapy.

Adult↗

Influence of vascular distending pressure on regional flows in isolated perfused dog lungs.

To confirm the regional differences in vascular pressure vs. flow properties of lung regions that have been documented in zone 2 conditions [pulmonary venous pressure (Ppv) less than alveolar pressure], regional distending pressure vs. flow curves in zone 3 were generated by use of isolated blood-perfused dog lungs (3 right and 5 left lungs). Each lung was kept inflated at constant inflation pressure (approximately 50% of full inflation volume) while radioactively labeled microspheres were injected at different settings of Ppv. To achieve maximal vascular distension, Ppv was increased to approximately 30 cmH2O above alveolar pressure for the first injection. Subsequent injections were made at successively lower Ppv's. The difference between pulmonary arterial pressure and Ppv was kept constant for all injections. As was found in zone 2 conditions, there were differences in the regional distending pressure vs. flow curves among lung regions. To document the regional variability in the curves, the distribution of flow at a regional Ppv of 30 cmH2O above alveolar pressure was analyzed. There was a statistically significant linear gradient in this flow distribution from dorsal to ventral regions of the lungs but no consistent gradient in the caudad to cephalad direction. These results indicate that, even in near-maximally distended vessels, the dorsal regions of isolated perfused dog lungs have lower intrinsic vascular resistance compared with ventral regions.

Animals↗

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.

Adult↗

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.

Airway Resistance↗

Actions of enflurane, isoflurane, vecuronium, atracurium, and pancuronium on pulmonary resistance in dogs.

The effects of enflurane, isoflurane, vecuronium, atracurium, and pancuronium on pulmonary resistance and heart rate were studied in 30 vagotomized dogs lying supine and anesthetized with chloralose-urethane. None of the five drugs affected pulmonary resistance when the airway was unstimulated. Enflurane and isoflurane significantly attenuated the increase in pulmonary resistance induced by electrical stimulation of the vagus nerves. This effect was dose-dependent and similar for both anesthetics at equivalent multiples of their minimum alveolar concentration. Atracurium significantly (P less than 0.05) enhanced the increase in pulmonary resistance induced by vagus nerve stimulation; vecuronium had no significant effect. Pancuronium, up to a cumulative dose of 0.14 mg/kg, also significantly (P less than 0.05) enhanced the increase in pulmonary resistance induced by vagus nerve stimulation; but this effect was reversed by further increasing the dose. Pancuronium also attenuated the cardiodecelerator response to vagus nerve stimulation in a dose-dependent fashion. The underlying mechanisms for the attenuation of responses to vagus nerve stimulation by enflurane or isoflurane or for the increase in response with atracurium are unknown. Pancuronium at lower doses increases the response most likely by blocking prejunctional muscarinic receptors (M2) that physiologically inhibit vagally mediated increases in pulmonary resistance.

Airway Resistance↗

Quantification of thoracic volumes by three-dimensional imaging.

End-expiratory thoracic cavity volume (Vthx) was measured in eight volunteers lying supine by three-dimensional X-ray computed tomography using the Dynamic Spatial Reconstructor. Untrapped end-expiratory pulmonary gas volume at functional residual capacity (FRC) was determined by nitrogen clearance. Both measurements were done before and after induction of anesthesia-paralysis. After induction of anesthesia-paralysis, Vthx and FRC were consistently and significantly (P less than 0.01) reduced by 0.28 +/- 0.22 (SD) and 0.59 +/- 0.24 liter, respectively. The reduction of FRC was larger than the reduction of Vthx (delta Vthx) in six of the eight subjects, a finding suggesting that intrathoracic fluid (blood) plus trapped gas volume (Vtt) increased. Changes in Vthx were partitioned into volume changes from the thoracic rib cage (delta Vrc) and from shape and/or position changes of the diaphragm (delta Vdi). delta Vrc contributed significantly (0.17 +/- 0.15 liter, P less than 0.02) to delta Vthx, whereas delta Vdi contributed only in four of the eight subjects. We conclude that delta Vrc, delta Vdi, and delta Vtt contribute to the reduction of FRC after induction of anesthesia-paralysis in humans; the relative contribution of them varies among subjects.

Adult↗

Regional trapping of microspheres in the lung compares well with regional blood flow.

Microspheres (MS) are often used to measure the distribution of pulmonary blood flow in the assumption that the number of MS trapped in a region is proportional to blood flow. However, regional distribution of trapped MS has not been directly compared with regional blood flow in the lung. Regional trapping of MS was compared with regional flow of erythrocytes (RBC's) in isolated, perfused left lungs of dogs. Radioactivity from labeled MS and RBC's was measured by external detection using a gamma camera. We defined six regions of interest in the image of the left lateral surface of the lung: a dorsocaudal, a caudal, two ventral, an apical, and a central region. In each lung, regional trapping of MS was measured from the image of radioactivity obtained after slow injection of a suspension of MS into the arterial perfusion tubing. A radioactive bolus of labeled RBC's was injected during rapid imaging of the lung to obtain radioactivity vs. time curves from each region. The peaks of the regional radioactivity vs. time curves were used to estimate regional flows, though compensation had to be made for overlap of the washout and washin phases of the bolus of labeled RBC's. The results indicated that there were no differences in the regional distribution of MS compared with the regional distribution of RBC flow in isolated, perfused dog lungs.

Animals↗

Muscarinic M1 receptors mediate the increase in pulmonary resistance during vagus nerve stimulation in dogs.

The physiologic roles of the 2 muscarinic receptors (M1 and M2) in the vagal control of pulmonary resistance were studied by comparing the effects of pirenzepine (PZ, M1-blocker), gallamine (GAL, M2-blocker), and atropine (AT, M1- and M2-blocker) on the increase in pulmonary resistance (RL) and on the reduction in heart rate (HR) during bilateral cervical vagus nerve stimulation in 18 anesthetized (chloralose and urethane) and paralyzed (vecuronium) dogs. PZ, AT, and GAL all inhibited the reduction in HR during vagus nerve stimulation, although the inhibition required relatively high doses of PZ and GAL. AT and PZ inhibited the increase in RL during vagus nerve stimulation. The ratio of the dose needed to inhibit by 50% the HR response to the dose needed to inhibit by 50% the RL response was approximately 45:1 for PZ, 12:1 for AT, and less than 0.4:1 for GAL. Thus, compared with AT, PZ is a more selective blocker of vagally induced increases in RL, indicating that M1 receptors are present in the airway smooth muscle of intact anesthetized dogs. In the same dose range as that which caused the inhibition of the HR response, GAL had no consistent effect on the increase in RL during vagus nerve stimulation, indicating that M2 receptors do not mediate the increase in RL in intact anesthetized dogs.

Airway Resistance↗