Clinical Medicine Insights-Circulatory Respiratory and Pulmonary Medicine最新文献

Introduction: Obesity is associated with increased risk of hypercapnic respiratory failure, prolonged duration on mechanical ventilation, and extended weaning periods.

Objective: Pilot study to determine whether morbidly obese adult tracheotomized subjects (body mass index [BMI] ⩾ 40) can be more efficiently weaned from the ventilator by optimizing their positive end-expiratory pressure (PEEP) using either an esophageal balloon or the best achieved static effective compliance.

Methods: We randomly assigned 25 morbidly obese adult tracheotomized subjects (median [interquartile range] BMI 53.4 [26.4]; range 40.4-113.8) to 1 of 2 methods of setting PEEP; using either titration guided by esophageal balloon to overcome negative transpulmonary pressure (Ptp) (goal Ptp 0-5 cmH₂O) (ESO group) or titration to maximize static effective lung compliance (Cstat group). Our outcomes of interest were number of subjects weaned by day 30 and time to wean.

Results: At day 30, there was no significant difference in percentage of subjects weaned. 8/13 subjects (62%) in the ESO Group were weaned vs. 9/12(75%) in the Cstat Group (P = 0.67). Among the 17 subjects who weaned, median time to ventilator liberation was significantly shorter in the ESO group: 3.5 days vs Cstat group 14 days (P = .01). Optimal PEEP in the ESO and Cstat groups was similar (ESO mean ± SD = 26.5 ± 5.7 cmH₂O and Cstat 24.2 ± 7 cmH₂O (P = .38).

Conclusions: Optimization of PEEP using esophageal balloon to achieve positive transpulmonary pressure did not change the proportion of patients weaned. Among patients who weaned, use of the esophageal balloon resulted in faster liberation from mechanical ventilation. There were no adverse consequences of the high PEEP (mean 25.4; range 13-37 cmH₂O) used in our study. The study was approved by the Institutional Review Board at our institution (UMCIRB#10-0343) and registered with clinicaltrials.gov (NCT02323009).

Background: Anemia is reported in one-third of the patients with chronic obstructive pulmonary disease (COPD). Anemia, by decreasing oxygen content, can be a contributing factor for hypoxemia. We determined to find whether anemia causes more prominent hypoxia by decreasing the total oxygen content after exercise in anemic patients with COPD.

Methods: Stable moderate-to-severe COPD patients with and without anemia were recruited. Arterial blood gas analyses were performed on room air before and after a 6-minute walking test (6MWT). Walking distance, oxygen saturation, and heart rate were recorded in each case before and after the 6MWT. Pulmonary function test measurements and other data were obtained from the chart. The mean and standard deviations were calculated for continuous variables. The independent t-test and Kruskal-Wallis test were performed for numerical covariate and univariate analyses. The paired t-test was used for the analyses of data before and after exercise.

Results: A total of 24 male patients were included in the study; 12 of which were anemic. The oxygen content was decreased in the anemic group (15.22 ± 1.28 vs 15.07 ± 1.22) after exercise, but it was not significant. In the non-anemic group, no oxygen content decrease was observed after exercise (18.83 ± 1.41 vs 18.9 ± 1.37). Interestingly, the Spo₂, but not Sao₂, was significantly lower after exercise in anemic patients with COPD (93.46% ± 5.06% vs 88.20% ± 6.35% before and after exercise, respectively).

Conclusions: Anemia does not cause more prominent hypoxemia after exercise in patients with COPD. However, the recorded Spo₂ levels were significantly lower after exercise in the anemic patients with COPD.

Background and objective: Over 2000 genotypes in the cystic fibrosis (CF) gene have been described. These genotypic differences result in variable clinical manifestations of CF, with severity of disease dependent on CF transmembrane conductance (CFTR) protein function. CFTR is widely distributed in nucleated cells, including cardiac myocytes, but the effect of genotype on cardiac function is not known.

Methods: This retrospective review of echocardiographic data is from a single adult CF centre between 2000 and 2015. Patients were cohorted based on the functional classification of genotype. 'Severe' patients had both CF genes from functional classification groups 1-3; 'mild' patients had one or no gene from these groups, or in the event of the second gene being unknown were pancreatic sufficient.

Results: Genotype and echocardiography were recorded during the inclusion period in 100 patients, 79 of whom were classified as having severe genotypes. Although the severe group were younger they had a lower fractional shortening (33.66 ± 6.6 vs 36.9 ± 6.3, P < .05), left atrial area (14.9 ± 3.6 versus 18.0 ± 4.2 cm²; P < .01) and volume (39.9 ± 18.7 versus 51.0 ± 18.7 mL; P < .05) and showed a trend to lower left ventricular ejection fraction.

Conclusions: This study is the first to show that in CF, severity of genotype (functional classification) is associated with cardiac impairment. Patients with severe CF genotype and cardiac dysfunction should be identified to evaluate cardiac response to gene-modifying treatments prior to consideration for lung transplantation.

We hypothesized that the slope of relation ventilation to carbon dioxide output (V'E/V'CO2-slope) could be predictive already during the very first days after submassive pulmonary embolism (PE) to right ventricular systolic pressure (RV_sys by echocardiography) after 6 months. We evaluated 21 hemodynamically stable patients at admittance, at days 3, 7, 90, and 180 by cardiopulmonary exercise testing and echocardiography. V'E/V'CO2-slope (48.4 ± 10.8) decreased within the first week (43.0 ± 9.8 at day 7) and normalized until follow-up at 6 months (35.0 ± 11.3; P < 10^-4), p(a-ET)CO₂ remained abnormal between days 1 and 3 (5.0 ± 3.9 to 6.7 ± 5.3 mmHg). RV_sys declined from 41.7 ± 14.3 to 26.3±13.1 mmHg (P < 10^-4) at 6 months. V'E/V'CO2-slope (r²= 0.27; P < .02) and RV_sys (r² = 0.28; P = .03) at day 7 correlated with RV_sys at 6 months. p_(a-ET)CO₂, p_(a-ET)O₂, V'D/V'T were not related to RV_sys after 6 months. RV_sys 6 months after acute PE is positively correlated with the V'E/V'CO2-slope at day 7.

Cardiac hemodynamic assessment during cardiopulmonary exercise testing (CPET) is proposed to play an important role in the clinical evaluation of individuals with cystic fibrosis (CF). Cardiac catheterization is not practical for routine clinical CPET. Use of oxygen pulse (O₂pulse) as a noninvasive estimate of stroke volume (SV) has not been validated in CF. This study tested the hypothesis that peak exercise O₂pulse is a valid estimate of SV in CF. Measurements of SV via the acetylene rebreathe technique were acquired at baseline and peak exercise in 17 mild-to-moderate severity adult CF and 25 age-matched healthy adults. We calculated $O_{2}pulse=\stackrel{.}{V}{O}_{2}HR$ . Baseline relationships between SV and O₂pulse were significant in CF (r = .80) and controls (r = .40), persisting to peak exercise in CF (r = .63) and controls (r = .73). The standard error of estimate for O₂pulse-predicted SV with respect to measured SV was similar at baseline (14.1 vs 20.1 mL) and peak exercise (18.2 vs 13.9 mL) for CF and controls, respectively. These data suggest that peak exercise O₂pulse is a valid estimate of SV in CF. The ability to noninvasively estimate SV via O₂pulse during routine clinical CPET can be used to improve test interpretation and advance our understanding of the impact cardiac dysfunction has on exercise intolerance in CF.

Inhaled corticosteroids are widely used in the treatment of chronic obstructive pulmonary disease (COPD). However, their use has been questioned for appropriate dose and a possible increased risk of pneumonia. Here, we reviewed patients with COPD who had received fluticasone-salmeterol combination treatment using data from a linked electronic medical record database. A total of 180 patients received salmeterol with 250 µg fluticasone propionate twice daily and 78 received salmeterol and 100 µg fluticasone propionate twice daily. In both groups, there was no difference in the improved forced expiratory volume in 1 second and COPD assessment test score and the proportion of patients with exacerbations. Although the incidence of common toxicity was approximately equal, that of pneumonia was much higher in the 250 µg group (8.9% vs 1.3%, P=.01). The beneficial effects of inhaled corticosteroids might be obtained at lower doses.

Background: Pulmonary hypertension (PH) is an underdiagnosed cause for chest pain in patients without significant coronary artery disease (CAD). Studies showed that enlarged pulmonary arterial (PA) and right ventricular chamber sizes correlate with the severity of PH. Therefore, we studied the association between chest pain, right ventricular dimensions (RVDs), and PA size on coronary coronary tomographic angiography (CCTA).

Methods: The CCTA of 87 patients presenting with chest pain without evidence of obstructive CAD was examined. The PA diameter (PAD), right atrial dimension (RAD), and RVD were measured. A comparative control cohort included 31 patients who presented without cardiopulmonary complaints and underwent thoracic CT. The risk for obstructive sleep apnea (OSA) was assessed using STOP-BANG questionnaires.

Results: Patients with chest pain without obstructive CAD showed markedly dilated right atrial and ventricular chambers compared with standard parameters (right atrium: 48 ± 6.4 mm; right ventricle long axis: 61 ± 9.5 mm). When comparing chest pain vs non-chest pain group, respectively, the mean PAD measured 25.92 ± 0.43 mm vs 22.89 ± 0.38 mm (P < .001), RAD2 measured 40.1423 ± 0.7108 mm vs 34.8800 ± 1.0245 mm (P = .0048), and RVD2 measured 31.7729 ± 0.7299 mm vs 27.6379 ± 1.6178 mm (P = .034). Chest pain was associated with higher PAD (odds ratio [OR]: 11.11, P < .05) after adjusting for age, sex, body mass index, history of hypertension, hyperlipidemia, congestive heart failure, chronic obstructive pulmonary disease, OSA, and smoking. The chest pain group had a mean STOP-BANG score of 3.9 ± 1.8 in all patients, and 3.62 ± 0.20 in patients without known history of OSA, representing an elevated risk index for the disease.

Conclusions: In patients presenting with chest pain without obstructive CAD on CCTA, there is a strong association between the presence of chest pain and enlarged PAD. They also represent a high-risk group for OSA.

We describe the first isolation of Mycobacterium hassiacum, a rapid-growing, partial acid-resistant mycobacterium, in a respiratory specimen from a patient with exacerbated chronic obstructive pulmonary disease. To provide therapeutic recommendation for future cases, antibiotic susceptibility testing of 3 clinical isolates was performed by broth microdilution. All strains tested showed susceptibility to clarithromycin, imipenem, ciprofloxacin, and doxycycline. The role of M hassiacum as a respiratory pathogen remains unclear and needs to be evaluated by future reports.

We developed a simplified automated algorithm to interpret noninvasive gas exchange in healthy subjects and patients with heart failure (HF, n = 12), pulmonary arterial hypertension (PAH, n = 11), chronic obstructive lung disease (OLD, n = 16), and restrictive lung disease (RLD, n = 12). They underwent spirometry and thereafter an incremental 3-minute step test where heart rate and SpO₂ respiratory gas exchange were obtained. A custom-developed algorithm for each disease pathology was used to interpret outcomes. Each algorithm for HF, PAH, OLD, and RLD was capable of differentiating disease groups (P < .05) as well as healthy cohorts (n = 19, P < .05). In addition, this algorithm identified referral pathology and coexisting disease. Our primary finding was that the ranking algorithm worked well to identify the primary referral pathology; however, coexisting disease in many of these pathologies in some cases equally contributed to the cardiorespiratory abnormalities. Automated algorithms will help guide decision making and simplify a traditionally complex and often time-consuming process.

Background: In 2015, New York City experienced the worst outbreak of Legionnaires' disease in the history of the city. We compare patients seen during the 2015 outbreak with sporadic cases of Legionella during the past 5 years.

Methods: We conducted a retrospective chart review of 90 patients with Legionnaires' disease, including sporadic cases of Legionella infection admitted from 2010 to 2015 (n = 55) and cases admitted during the 2015 outbreak (n = 35).

Results: We saw no significant differences between the 2 groups regarding demographics, smoking habits, alcohol intake, underlying medical disease, or residence type. Univariate and multivariate analyses showed that patients with sporadic case of Legionella had a longer stay in the hospital and intensive care unit as well as an increased stay in mechanical ventilation. Short-term mortality, discharge disposition, and most clinical parameters did not differ significantly between the 2 groups.

Conclusions: We found no specific clinicoradiological characteristics that could differentiate sporadic from epidemic cases of Legionella. Early recognition and high suspicion for Legionnaires' disease are critical to provide appropriate treatment. Cluster of cases should increase suspicion for an outbreak.