Minelle L. Hulsebus

Influence of bronchial blood flow and conductance on pulmonary function in stable systolic heart failure

BACKGROUND The aim of this study was to determine the relationship between airway blood flow (Q(aw)), airway conductance (G(f-aw)) and pulmonary function in patients with stable HF. METHODS 12 controls (CTRL: age=63±9 years, FVC=98±15%pred, LVEF=61±6%) (all data presented as mean±SD), 16 patients with mild HF (HF-A, NYHA I-II: age=64±9 years, FVC=90±17%pred, LVEF=28±6%), and 14 patients with moderate/severe HF (HF-B, NYHA III-IV: age=65±6 years, FVC=84±12%pred, LVEF=26±6%) were studied. Q(aw) was assessed using soluble gas measurements; perfusion pressure across airway bed (ΔP(aw)) was estimated from systemic and pulmonary pressure measurements; G(f-aw) was calculated as Q(aw)/ΔP(aw); PF was assessed by spirometry. RESULTS While Q˙(aw) was not significantly different between CTRL (61.3±17.9 μL min(-1)mL(-1)), HF-A (70.1±26.9 μL min(-1)mL(-1)) and HF-B (56.2±14.9 μL min(-1)mL(-1)) groups, G(f-aw), was elevated in HF-A (1.1±0.4 μL min(-1)mL(-1)mm Hg(-1), p<0.03) and tended to be elevated in HF-B (1.2±0.6 μL min(-1)mL(-1)mm Hg(-1), p=0.07) when compared to CTRL (0.8±0.3 μL min(-1)mL(-1)mm Hg(-1)). Significant positive correlations were found between G(f-aw) and RV/TLC for HF-A (r=0.63, p<0.02) and HF-B (r=0.58, p<0.05). CONCLUSIONS These results support the hypothesis that increased bronchial conductance and bronchial congestion may be related to greater small airway obstruction and as such may play a role in the PF abnormalities and symptoms of congestion commonly observed in HF patients.

Validation of a Simplified, Portable Cardiopulmonary Gas Exchange System for Submaximal Exercise Testing~!2009-10-25~!2010-01-09~!2010-03-17~!

Shape Medical Systems, Inc. has developed a new miniaturized, simplified system for non-invasive cardiopulmonary gas exchange quantification and has targeted their system for submaximal clinical exercise testing in order to abbreviate testing in an expanding clinical market during a climate of escalating health care costs. The focus of the present study was to compare this new device to a validated, standardized system for measures of cardiopulmonary gas exchange. Eighteen healthy adults (10 male/8 female, age 29±7 yr, BMI 23.8±2.4 kg/m 2 ) were brought to the laboratory and instrumented with both measurement systems via in-series pneumotachs. Additionally, the Shape system included a pulse oximeter for heart rate (HR) and oxygen saturation (SaO2), while the standard system included separate 12-lead ECG and oximetry devices. The protocol included 2-min resting breathing, followed by 3-min at each of 3 workloads (50, 70, 125 watts) on a cycle ergometer. Data were collected breath-by-breath and averaged the last 30-sec of each workload. After a 15-min rest period, the pneumotach order was reversed and the study repeated. Since gas exchange data were similar (p>0.05) within a given metabolic testing system between sessions the data were pooled for comparing the Shape and Standard systems. There were no differences (p>0.05) between the systems for oxygen consumption-VO2, carbon dioxide production-VCO2, ventilation-VE, end tidal CO2-PetCO2, tidal volume-VT, respiratory rate-fb, and HR at rest or any work load. SaO2 was slightly, but significantly lower using the Shape embedded oximeter (p 0.05). These data suggest that the new, simplified metabolic system developed by Shape Medical Systems, Inc. accurately quantifies key cardiopulmonary variables over a range of workloads, has a coefficient of variation similar to a well validated system and can be used with mouthpiece or mask.

Hypoxia induced changes in lung fluid balance in humans is associated with beta-2 adrenergic receptor density on lymphocytes.

BACKGROUND Previous studies have demonstrated an important role for beta-2 adrenergic receptors (β(2)AR) in lung fluid clearance. The purpose of this investigation was to examine the relationship between β(2)AR density on lymphocytes and indices of lung water in healthy humans exposed to ≈ 17 h of hypoxia (FIO2 = 12.5% in a hypoxia tent). METHODS Thirteen adults (mean ± SEM; age=31 ± 3 years, BMI=24 ± 1 kg/m(2), VO2 Peak = 40 ± 2 ml/kg/min ) participated. Pulmonary function, CT derived lung tissue volume (V(tis)-tissue, blood and water), lung diffusing capacity for carbon monoxide (D(CO)) and nitric oxide (D(NO)), alveolar-capillary conductance (D(M)), pulmonary capillary blood volume (V(c)) and lung water (CT V(tis)-V(c)) were assessed before and after ≈ 17 h normobaric hypoxia (FIO2 = 12.5%). β(2)AR density on lymphocytes was measured via radioligand binding. Arterial oxygen saturation (SaO2), cardiac output (Q), right ventricular systolic pressure (RVSP) and blood pressure (BP) were also assessed. RESULTS After 17 h hypoxia, SaO2 decreased from 97 ± 1 (normoxia) to 82 ± 4% and RVSP increased from 14 ± 3 (normoxia) to 29 ± 2 mmHg (p<0.05) with little change in Q or BP. V(c) and D(M) both increased with hypoxia with a small increase in D(M)/V(c) ratio (p>0.05). CT V(tis) decreased and lung water was estimated to decline 7 ± 13%, respectively. β(2)AR density averaged 1497 ± 187 receptors/lymphocyte and increased 21 ± 34% with hypoxia (range -31 to +86%). The post-hypoxia increase in β(2)AR density was significantly related to the reduction in lung water (r=-0.64, p<0.05), with the subjects with the greatest increase in density demonstrating the largest decline in lung water. CONCLUSIONS Lung water decreases with 17 h normobaric hypoxia are associated with changes in beta adrenergic receptor density on lymphocytes in healthy adults.