Archive for the ‘Lung Disease’ Category


The two patient populations best characterized for the purpose of comparing 24-hour arrhythmia prevalence are those patients postmyocardial infarction and patients with idiopathic dilated cardiomyopathy. In the postinfarction group, 15 to 25 percent have VPBs (^3/hour) and 10 to 15 percent have one or more runs of nonsustained ventricular tachycardia; whereas comparative prevalence rates in patients with symptomatic heart failure due to idiopathic dilated cardiomyopathy are higher (60 to 80 percent and 35 to 50 percent respectively). The prevalence of repetitive ventricular arrhythmias increases with more severe left ventricular dysfunction. In the present study, there was an analagous increase in repetitive VPBs in patients with edema, presumably those patients with more severe right ventricular dysfunction. (more…)

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  • Asymptomatic Ventricular Arrhythmias in Patients with Obstructive Lung DiseaseShould They Be IVeated?
    In this issue of Chest (see page 44) Shih and colleagues make important observations on the frequency and significance of cardiac arrhythmias during a 24-hour electrocardiographic (ECG) recording in a well-defined patient population with chronic obstructive lung disease. Previous studies have reported variable types, as well as a wide disparity of arrhythmia prevalence figures, in patients with obstructive lung disease. These discrepancies are partially explained by the differences in recording ECG duration, (12-lead ECG vs continuous ECG recording) severity of respiratory failure, (inpatient vs outpatient) and the frequency of concomitant organic heart disease (especially coronary artery disease). While previous observational studies have called attention to these arrhythmias, conclusions as to their importance are lacking due to the limitations described above. In contrast to the previous reports, the present study focused on a well-defined group of ambulatory patients selected from the Nocturnal Oxygen Therapy Trial Group, who were characterized by severe resting hypoxemia and hypercarbia, many of whom had right heart failure. This population would be a reasonable one in whom to consider prophylactic antiarrhythmia therapy if a clear indication (ie, increased mortality risk) could be demonstrated. http://www.combigan-eye-drops.com/ (more…)

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  • Our results confirm their hypothesis of an increased inspiratory drive, but seem to show that the P0A does not reflect the actual amount of neural output to the inspiratory muscles in patients with CILD (Fig 2). The factors underlying change in neuromuscular coupling are likely to be complex: (1) P0A represents the total output of the activated inspiratory muscles; although the diaphragm is the main contributor in generating P0>1, other inspiratory muscles, particularly the intercostal inspiratory muscles, assist the diaphragm function. Our data showing a progressive increase in EMGint activity indicate that there is no apparent reason to suspect in patients a low contribution of intercostal inspiratory muscles to aid the diaphragm to generate pleural pressure more efficiently. (2) It has been shown that poor nutrition impairs respiratory muscle function. Since our patients were not considered to be undernourished (Table 1), this factor is not thought to be involved in the low muscle output force they generated. (more…)

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  • Neural Respiratory Drive and Neuromuscular Coupling During C02 Rebreathing in Patients with Chronic Interstitial Lung Disease: OutcomeA second point deals with the method of assessing inspiratory neuromuscular coupling, ie, the P01/ EMGd relationship. Relating a parameter that evaluates total inspiratory muscle force (P01) with one that measures neural drive to only one inspiratory muscle, the diaphragm (EMGd), has previously been criticized. However, it has been pointed out that the diaphragm is the main contributor to the inspiratory muscle output, both during quiet breathing and at high levels of ventilatory effort. A further criticism deals with the possibility that in some instances the relaxation of the abdominal muscles may take place a few ms before inspiration starts, preventing the P01 from reflecting diaphragmatic EMG activity. (more…)

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  • On the other hand, with patients in a supine position, Martin and De Troyer noticed the absence of abdominal muscle action during loaded breathing. In this connection, abdominal muscles were suspected not to be involved in patients during the condition of the present study. (2) In filtering EMG, a low cutoff at 80 Hz was used. However, this may be a rather high frequency cutoff, since spectral analysis has shown diaphragm power to be down to 25 to 30 Hz, and thereby a part of the EMGd is probably being lost. Nevertheless, our preliminary measurements (see Material and Methods) showed that the integrated peak EMGd signal was not substantially altered by a low cutoff at 80 Hz, a datum consistent with a previous report. (3) The ECG represents an artifact on an EMG signal, and any increase in heart rate may cause an overestimation of both XP and XP/Ti. This seems not to be the case in the present study, where no substantial increase in heart rate during chemical stimulation occurred. In turn, all of these data corroborate the opinion that surface EMGd may represent a suitable tool in the assessment of inspiratory neural drive for clinical purposes. http://www.naturalbreastenhancementpill.com/ (more…)

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  • Neural Respiratory Drive and Neuromuscular Coupling During C02 Rebreathing in Patients with Chronic Interstitial Lung Disease: DiscussionOur data show a shallower and faster breathing in patients than in normal subjects. In fact, a lower Vt and Ti and a greater f were observed in patients during room air breathing and chemically stimulated breathing. These data are consistent with those of Di Marco et al and Savoy et al in patients with CILD. As in other studies, the Vt/Ii was greater in patients, and the value of this increase was slightly greater than that calculated by Di Marco et al and Renzi et al. The reasons for the abnormalities in time components of the breathing pattern in patients have previously been provided; basically, afferents arising from the lung and rib cage are expected to be involved in shortening Ti and increasing respiratory frequency. http://medicines-for-diabetes.com/ (more…)

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  • Matching the two groups for a given level of PetCQ2 (65 mm Hg) (Table 5) showed in patients a greater absolute value of both P01 (p<0.Ql) and diaphragmatic XP/Ti (p<0.01). The Vt (p<0.05) and Ti (p<0.01) were lower in patients, while Vr/Ti (p<0.05) and f (p<0.01) were greater than in the normal control group; in contrast, Ve and Tj/Ttot were similar in the two groups. To assess neuromuscular inspiratory coupling, both in individual normal subjects and in patients (Fig 2), the P01 response slope was plotted against EMGd response slope to PetC02. In the normal subjects but not in patients, this relationship was significant (Y = 0.065+ 0.25 PetC02, r = 0.862, and p<0.001). (more…)

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  • Neural Respiratory Drive and Neuromuscular Coupling During C02 Rebreathing in Patients with Chronic Interstitial Lung Disease: ResultsFunctional data of the 12 patients are shown in Table 2. All but two patients (3 and 12) exhibited a significant decrease in static pulmonary volumes (predicted — 1SD X 1.64): on average, the VC was 68.9 percent; RY 62.1 percent; FRC, 67.1 percent; and TLC, 67.3 percent of the predicted values; the FEV1 was significantly decreased in all patients but two (3 and 8) (mean = 66.2 percent of predicted), and the FEV^/VC ratio was normal in all patients but one (9) (mean = 82.85 percent). Diffusing lung capacity (Dsb) was significantly decreased in 11 of the 12 patients (mean = 62.7 percent of predicted). Mean Pa02 for the group, 68.6 mm Hg, was notably reduced in three patients (1, 4, and 11); in all but one (subject 5) the PaCO£ was <45 mm Hg. The MIP in percentage of the predicted value was significantly decreased in all patients but five (5 to 8 and 12); the mean value (69 percent ± 20.7) was significantly reduced compared with the mean value of the normal control group (103.9 ± 14.6, SD; p<0.001). Click Here (more…)

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