Citations

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.

We compared pulmonary mechanics measured during long-term exercise (LTX = 20 min) with long-term isocapnic hyperventilation (LTIH = 20 min) in the same asthmatic individuals ( n = 6). Peak expiratory flow (PEF) and forced expiratory volume in 1 s (FEV1) decreased during LTX (−19.7 and −22.0%, respectively) and during LTIH (−6.66 and 10.9%, respectively). In contrast, inspiratory pulmonary resistance (Rl I) was elevated during LTX (57.6%) but not during LTIH (9.62%). As expected, airway function deteriorated post-LTX and post-LTIH (FEV1 = −30.2 and −21.2%; Rl I = 111.8 and 86.5%, respectively). We conclude that the degree of airway obstruction observed during LTX is of a greater magnitude than that observed during LTIH. Both modes of hyperpnea induced similar levels of airway obstruction in the posthyperpnea period. However, the greater airway obstruction during LTX suggests that a different process may be responsible for the changes in airway function during and after the two modes of hyperpnea. This finding raises questions about the equivalency of LTIH and LTX in the study of airway function during exercise-induced asthma.

Proctor, David N., and Kenneth C. Beck. Delay time adjustments to minimize errors in breath-by-breath measurement ofV˙o2during exercise. J. Appl. Physiol. 81(6): 2495–2499, 1996.—If the delay time between gas concentration and flow signals is not adequately corrected during breath-by-breath analysis of expired gas, an error in calculation of oxygen consumption (V˙o2) will result. To examine the frequency and delay time dependences of errors inV˙o2measurement, six healthy men exercised at 100, 200, and 250 W on a cycle ergometer while breath-by-breath assessment ofV˙o2was made simultaneously with collection of expired air. Subjects breathed first at normal rates (15–30 breaths/min) and then at 70 breaths/min. Each subject performed each level of exercise twice by using erroneous values for the delay time between gas concentration and flow signals. At normal breathing frequencies, errors inV˙o2measurement were ±10% over the full range of delay times used, and the errors were not tightly correlated with variations in delay times from optimum. However, at 70 breaths/min, errors approached ±30% as the variations in delay times deviated ±0.1 s from the optimal, and the errors were highly correlated with the variations in delay times. We conclude that there is greater potential for errors inV˙o2measurement with incorrect delay time at higher breathing frequencies. These findings suggest that the optimal delay time for breath-by-breath systems should be adjusted by using high breathing frequencies.

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.

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.

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.

ObjectiveTo compare patients with large‐vessel giant cell arteritis (LV‐GCA) characterized by wall thickening, stenosis, and/or occlusion of subclavian arteries to those with subclavian dilatation.MethodsFor the purposes of the present retrospective study, 2 different subsets of LV‐GCA were identified and compared from an established cohort of patients with radiographic evidence of subclavian artery vasculitis secondary to GCA: LV‐GCA with wall thickening, stenosis, and/or occlusion of subclavian arteries (Group 1), and LV‐GCA with dilatation of subclavian arteries without wall thickening or stenotic changes (Group 2).ResultsThe study included 109 patients in Group 1 and 11 in Group 2. Large‐vessel involvement secondary to GCA was diagnosed significantly later in patients from Group 2 compared to those from Group 1 (median 15.3 versus 0.0 months; P = 0.010). Compared to patients from Group 1, those from Group 2 were more frequently male (17% versus 45%; P = 0.027), ever smokers (42% versus 73%; P = 0.048), and more frequently had a history of coronary artery disease (11% versus 36%; P = 0.018). At LV‐GCA diagnosis, 10 of the 11 patients (91%) from Group 2 had aortic dilatation compared to 13 of 109 patients (12%) from Group 1 (P < 0.001). During the followup period, the prevalence of aortic aneurysm was significantly higher in patients from Group 2 compared with those from Group 1 (64% versus 7% at 5 years; P < 0.001).ConclusionTwo different subsets of LV‐GCA were identified. Given the strong association between subclavian artery dilatation and aortic aneurysm, such patients should be evaluated and monitored carefully for aortic dilatation.

Abstract Background and study aims Little is known about the learning curve for image interpretation in volumetric laser endomicroscopy (VLE) in Barrett’s esophagus (BE). The goal of this study was to calculate the learning curve, competence of image interpretation, sensitivity, specificity, and accuracy of VLE among novice users. Methods 31 novice users viewed 96 VLE images electronically at three academic institutions after a brief training session. There were 24 images of each histologic type: normal gastric cardia, normal esophageal squamous epithelium, non-neoplastic BE, and neoplastic BE. The users were asked to identify the correct tissue type and level of confidence. The cumulative summation (CUSUM) technique was used to construct a learning curve. Results 22 (71 %) of the physicians achieved VLE interpretation competency during their 96-slide review. Half of the physicians achieved competency at 65 images (95 % confidence interval [CI] 45 – 85). There was a statistically significant association between confidence in diagnosis and selecting the correct histologic tissue type (P < 0.001). The median accuracy for esophageal squamous epithelium, normal gastric cardia, non-neoplastic BE, and neoplastic BE was 96 % (95 %CI 95 % – 96 %), 95 % (95 %CI 94 % – 96 %), 90 % (95 %CI 88 % – 91 %), 96 % (95 %CI 95 % – 96 %). The overall accuracy was 95 % (95 %CI 93 % – 95 %). Conclusion The majority of novice users achieved competence in image interpretation of VLE for BE, using a pre-selected image set, with a favorable learning curve after a brief training session. An electronic review of VLE images, prior to real-time use of VLE, is encouraged.

Abstract The University at Buffalo's neuroendovascular fellowship is one of the longest running fellowship programs in North America. The burgeoning neurointerventional workforce and the rapid growth in the neurointerventional space on the heels of groundbreaking clinical trials prompted us to assess the fellowship's academic impact and its graduates’ perceptions and productivity. An anonymized web-based survey was sent to all former neuroendovascular fellows with specific questions pertaining to current practice, research and funding, and perceptions about the fellowship's impact on their skills, competitiveness, and compensation. Additionally, the h -index was calculated to assess the academic productivity of each graduated fellow. Among 50 former fellows, 42 (84%) completed the survey. The fellows came from various countries, ethnic backgrounds, and specialties including neurosurgery (n = 39, 93%), neurology (n = 2, 5%), and neuroradiology (n = 1, 2%). Twenty (48%) respondents were currently chairs or directors of their practice. Most (n = 30, 71%) spent at least 10% of their time on research activities, with 27 (64%) receiving research funding. The median h -index of all 50 former fellows was 14. The biggest gains from the fellowship were reported to be improvement in endovascular skills (median = 10 on a scale of 0-10 [highest]) and increase in competitiveness for jobs in vascular neurosurgery (median = 10), followed by increase in academic productivity (median = 8), and knowledge of vascular disease (median = 8). In an era with open calls for moratoriums on endovascular fellowships, concerns over market saturation, and pleas to improve training, fellowship programs perhaps merit a more objective assessment. The effectiveness of a fellowship program may best be measured by the academic impact and leadership roles of former fellows.