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      Increased parasympathetic cardiac modulation in patients with acute exacerbation of COPD: how should we interpret it?

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          Cardiac autonomic modulation (CAM) is impaired in patients with stable COPD. Exacerbation aggravates the patients’ health status and functional capacity. While the clinical and functional effects of exacerbation are known, no studies investigated CAM during exacerbation and whether there is a relationship between CAM and functional capacity and dyspnea.


          Thirty-two patients with moderate to severe COPD were enrolled into two groups: stable COPD (GSta, n=16) and acute exacerbation of COPD (GAE, n=16). The GAE patients were evaluated 24–48 hours after starting standard therapy for COPD exacerbation during hospitalization; the GSta patients were evaluated in an outpatient clinic and included in the study if no decompensation episodes had occurred during the previous month. The heart rate (HR) and R-wave peak detection intervals in ms (RRi) were registered using a heart rate monitor (Polar ® system) at rest in seated position during 10 minutes. CAM was assessed by heart rate variability (HRV) linear and non-linear analysis. Functional capacity was evaluated by handgrip strength test, performed by Jamar ® dynamometer, and dyspnea was scored using the modified scale of the Medical Research Council.


          GAE presented higher parasympathetic CAM values compared with GSta for square root of the mean squared differences of successive RRi (RMSSD; 17.8±5.6 ms vs 11.7±9.5 ms); high frequency (HF; 111.3±74.9 ms 2 vs 45.6±80.7 ms 2) and standard deviation measuring the dispersion of points in the plot perpendicular to the line of identity (SD1; 12.7±3.9 ms vs 8.3±6.7 ms) and higher CAM values for standard deviation of the mean of all of RRi (STD RRi; 19.3±6.5 ms vs 14.3±12.5 ms); RRi tri (5.2±1.7 ms vs 4.0±3.0 ms); triangular interpolation of NN interval histogram (TINN; 88.7±26.9 ms vs 70.6±62.2 ms); low frequency (LF; 203±210.7 ms 2 vs 101.8±169.7 ms 2) and standard deviation measuring the dispersion of points along the line of identity (SD2; 30.4±14.8 ms vs 16.2±12.54 ms). Lower values were observed for the complexity indices: approximate entropy (ApEn; 0.9±0.07 vs 1.06±0.06) and sample entropy (SampEn; 1.4±0.3 vs 1.7±0.3). Significant and moderate associations were observed between HF (nu) and handgrip strength ( r=−0.58; P=0.01) and between LF (ms 2) and subjective perception of dyspnea ( r=−0.53; P=0.03).


          COPD exacerbated patients have higher parasympathetic CAM than stable patients. This should be interpreted with caution since vagal influence on the airways determines a narrowing and not a better clinical condition. Additionally, functional capacity was negatively associated with parasympathetic CAM in COPD exacerbation.

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          Important influence of respiration on human R-R interval power spectra is largely ignored.

          Frequency-domain analyses of R-R intervals are used widely to estimate levels of autonomic neural traffic to the human heart. Because respiration modulates autonomic activity, we determined for nine healthy subjects the influence of breathing frequency and tidal volume on R-R interval power spectra (fast-Fourier transform method). We also surveyed published literature to determine current practices in this burgeoning field of scientific inquiry. Supine subjects breathed at rates of 6, 7.5, 10, 15, 17.1, 20, and 24 breaths/min and with nominal tidal volumes of 1,000 and 1,500 ml. R-R interval power at respiratory and low (0.06-0.14 Hz) frequencies declined significantly as breathing frequency increased. R-R interval power at respiratory frequencies was significantly greater at a tidal volume of 1,500 than 1,000 ml. Neither breathing frequency nor tidal volume influenced average R-R intervals significantly. Our review of studies reporting human R-R interval power spectra showed that 51% of the studies controlled respiratory rate, 11% controlled tidal volume, and 11% controlled both respiratory rate and tidal volume. The major implications of our analyses are that breathing parameters strongly influence low-frequency as well as respiratory frequency R-R interval power spectra and that this influence is largely ignored in published research.
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            Reference values for lung function tests. II. Maximal respiratory pressures and voluntary ventilation.

            The strength of the respiratory muscles can be evaluated from static measurements (maximal inspiratory and expiratory pressures, MIP and MEP) or inferred from dynamic maneuvers (maximal voluntary ventilation, MVV). Although these data could be suitable for a number of clinical and research applications, no previous studies have provided reference values for such tests using a healthy, randomly selected sample of the adult Brazilian population. With this main purpose, we prospectively evaluated 100 non-smoking subjects (50 males and 50 females), 20 to 80 years old, selected from more than 8,000 individuals. Gender-specific linear prediction equations for MIP, MEP and MVV were developed by multiple regression analysis: age and, secondarily, anthropometric measurements explained up to 56% of the variability of the dependent variables. The most cited previous studies using either Caucasian or non-Caucasian samples systematically underestimated the observed values of MIP (P < 0.05). Interestingly, the self-reported level of regular physical activity and maximum aerobic power correlates strongly with both respiratory and peripheral muscular strength (knee extensor peak torque) (P < 0.01). Our results, therefore, provide a new frame of reference to evaluate the normalcy of some useful indexes of respiratory muscle strength in Brazilian males and females aged 20 to 80.
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              Time course of recovery of health status following an infective exacerbation of chronic bronchitis.

              The magnitude and time course of effect of an acute exacerbation of chronic bronchitis (AECB) on health status are not known. Data from the GLOBE study, a randomised double blind trial of antibiotic therapy, were used to investigate these effects. 438 patients with AECB received either gemifloxacin 320 mg once daily for 5 days (214 patients) or clarithromycin 500 mg twice daily for 7 days (224 patients) and were followed up for 26 weeks. St George's Respiratory Questionnaire (SGRQ) scores were obtained at baseline and after 4, 12, and 26 weeks. At presentation during an exacerbation SGRQ scores were worse (Total score difference 5.4 units, 95% CI 1.9 to 8.8, p=0.002) in patients who had a subsequent exacerbation during follow up. The greatest improvement in SGRQ score occurred within the first 4 weeks (mean 8.9 units, 95% CI 6.5 to 11.5, p<0.0001). Subsequently, scores improved more rapidly in patients with no further exacerbations. At 26 weeks the difference between the two groups was 9.6 units (95% CI 5.7 to 13.4, p<0.0001). In patients with no further exacerbations the SGRQ score improved between 4 and 12 weeks by a further 4.1 units (95% CI 2.2 to 5.9, p<0.0001). A single infective AECB has a sustained effect on health status. The recovery period is long even in patients who have no further exacerbations. A second episode within 6 months limits recovery markedly. Treatments that reduce exacerbation frequency could have a significant impact on health status.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                28 July 2017
                : 12
                : 2221-2230
                Department of Physical Therapy, Cardiopulmonary Physiotherapy Laboratory, Federal University of Sao Carlos, Sao Carlos, Sao Paulo, Brazil
                Author notes
                Correspondence: Renata Gonçalves Mendes, Department of Physical Therapy, Cardiopulmonary Physiotherapy Laboratory, Federal University of Sao Carlos, Rodovia Washington Luís, Km 235, Jardim Guanabara, 13565-905 Sao Carlos, Sao Paulo, Brazil, Tel +55 16 3306 6704, Fax +55 16 3361 2081, Email renatamendes@ 123456ufscar
                © 2017 Kabbach et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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