Chronic Obstructive Pulmonary Disease (COPD) Management

Chronic Obstructive Pulmonary Disease (COPD) attentionChronic obstructive pulmonary affection (COPD) is a multi-system disorder, resulting in manifold comorbidities and being the fourth common cause of mortality worldwide (1). cardiovascular disease (CVD) is one of the leading cause of morbidity and mortality in COPD, through manifestations such as ischemic heart disease, heart failure, arrhythmias, stroking and sudden cardiac death (2,3). Moreover, in the last years, a purpose to paradigm shift glide byed, the chronic respiratory disease itself being delimitate as a modifiable cardiovascular risk factor (4,5).This fundamental interaction between COPD and cardiovascular disease could be explained either by sh ard risk factors (aging, smoking, exposure to air pollution and passive smoke, underprescribing of key cardiovascular medication, such as -blockers) or mechanisms of increased risk that atomic number 18 incompletely understood, beyond the conventional risk factors (4,6) .There is increasing evidence that COPD negatively affect the cardiovascular and autonomic nervous system, leading to sympathovagal imbalance, with increased beneficent tone, loss of parasympathetic tone and altered baroreceptor sensitivity, which are essential dowers of cardiovascular risk (7-9). Recurrent episodes of hypoxemia and/or hypercapnea, intrathoracic pressure swings resulting from airway obstruction and hyperinflation, general inflammation, oxidative stress, increased respiratory effort and physical inactivity brush aside all be involved in autonomic dysfunction sight in COPD (8-10).Patients with COPD and functional alterations of cardiac autonomic modulation tend to acquit an elevated resting heart rate (11-13), reduced heart rate variant (HRV) (14), altered blood pressure variability (BPV) (15), an increase in muscle-builder sympathetic nerve activity (16), reduced baroreflex sensitivity (17) and increased plasm norepinephrine level (9). Other clincal findings related to sympathetic overdrive in COPD could be arterial stiffness, altered PWV and arterial compliance, as well as left ventricular hypertrophy and diastolic dysfunction which may occur through direct effect of tone, modulation of baroreceptor sensitivity or energizing of the renin-angiotensin system (4, 18-22).Hypoxemia, hypercapnia, pulmonary hyperinflation and activity avoidance are involved in developping cardiac autonomic dysfunction but on the other hand, these mechanisms are also responsible for exertional dyspnea and skeletal muscle deconditioning, including respiratory muscle dysfunction, in COPD patients (23,24). Thus develops a vicious spiral of physical deconditioning, stricken quality of life and early development of cardiovascular comorbidities, leading eventually to increased hospitalization and mortality (25).The golden standard in COPD steering is pulmonary rehabilitation, based on its main benefits, as resulted from clinical trials better exercise capacity and health-related quality of life, reduced symptoms and recovery after hospitalization, fall anxiety and depression, shortening the number of hospitalizations and days in the hospital (1, 26-28). The push of cardiovascular comorbidities on clinical outcomes of pulmonary rehabilitation and vice versa is unless(prenominal) partially investigated and understood. It seems that patients with metabolic and heart diseases might achieve lower degrees of good in exercise capacity or quality of life, but contradictory results from clinical trials have been published (29). Moreover, it is still unclear if pulmonary rehabilitation programs address cardiovascular risk factors in COPD patients, but there are encouraging results (30).Inspiratory muscle training (IMT) is a particular component of pulmonary rehabilitation, arising from the finding that inspiratory muscle dysfunction is an extrapulmonary manifestation of the disease which is often present in COPD patients. Inspiratory muscle wea kness is define as a maximal inspiratory mouth pressure (PI,max) of less than 60 cmH2O (31) and can be measured with handheld, electronic portable devices, providing automatically processed information on external inspiratory work, power and internal respiration pattern during loaded breathing tasks in patients with COPD. A new-fangled knowledge concluded that these information are valid estimation of physical units of energy during loaded breathing tasks, enabling healthcare providers to measure PI,max, peak inspiratory flow and quantify the load on inspiratory muscles in insouciant clinical practice (32). Also, it has been developed various pressure threshold fill medical devices, for standardized training, according to current recommendations although there is no formal guideline yet (33).The impact of IMT was extensively studied in recent years. Results from randomised controlled trials in patients with COPD show that IMT as a stand-alone therapy improves specialisatio n and endurance of inspiratory muscles, improves symptoms (dyspnea) and exercise capacity (31,34). In a meta-analysis including 32 randomised controlled trials (31), IMT and its effects in patients with COPD were analysed and improved inspiratory muscle potence (+ 13 cmH2O 95% CI 0.54-0.82 p