Heart Failure and Copd

Chronic Obstructive Pulmonary Disease (COPD)

COPD constitutes a major source of mortality and morbidity across the globe, with a considerable economic effect. New GOLD (Global initiative for chronic Obstructive Lung Disease) guidance modifications refined patient classification for therapy by employing spirometry, exacerbation rate and symptom evaluation combined. Therapy attempts at decreasing both extant disease symptoms and vulnerability to adverse health conditions in the future. On account of their established effectiveness, the class of drugs known as bronchodilators, with their long-lasting effects are considered the backbone of COPD therapy (Tashkin & Ferguson, 2013).

The heterogeneous disease known as COPD may be grouped into a number of diverse "phenotypes". Practicing doctors have, for several years, observed two highly divergent COPD patient subcategories: emphysema patients and chronic bronchitis patients. COPD ought to be accorded orphan status because: 1) it is heterogeneous; 2) Its multiple phenotypes probably represent distinct, fairly uncommon conditions. Long-acting drugs belonging to the class of bronchodilators have been established as the best available medications for COPD thus far (Cazzola, 2015).

Discussion

COPD Pathophysiology

Comprehending COPD's primary pathophysiology will contribute significantly to disease diagnosis and treatment under circumstances wherein novel diagnostic examinations, mechanisms, and medications are rapidly developing. COPD pathophysiology is complex and remains mostly undiscovered. Its pathological effects stimulate a succession of physiological modifications that ultimately affect the patient's quality of life (QOL) and survival, when the disease advances naturally (Brashier & Kodgule, 2012).

Drug Classification and Medication

Drugs capable of increasing FEV1 (forced exhalation volume in one second) or bringing about improvements to other spirometric factors, often by changing the tone of the airways' smooth muscles, are called bronchodilators. Bronchodilator utilization is one among the major elements of COPD therapy. However, quite frequently, it reverses airflow blockage only to a limited extent. Clinicians commonly utilize the following three kinds of bronchodilators: (1) methylxantines, (2) adrenoceptor agonists and (3) anticholinergic medicines. Bronchodilators are prescribed or administered regularly or when required. It has been proven that continuous therapy using bronchodilators that have long-lasting action is easier and more effectual as compared to therapy using short-acting drugs. Bronchodilator combination with diverse pharmacological profiles can improve treatment efficacy (Antus, 2013).

Contraindications and Risk Factors Involved

COPD patients typically exhibit poly-pharmacy. However, there is a lack of information regarding drug-drug interaction (DDI) prevalence and import. Clinically, COPD doesn't contraindicate β-blocker usage. But researchers who gauged carevedilol tolerance in chronic HF (heart failure) and associated COPD patients revealed a 17% rise in peak exhalation flow prior to and a couple of hours following carvedilol administration, possibly because of decreased airflow blockage, filling pressure on better heart functioning and peribronchial fluid. Further, major differences exist between potential DDI rate among COPD and chronic HF patients, which might be mainly due to guidelines. While this potentially suggests improved clinical practice, increased risks of possibly significant DDI may be associated and must be appropriately dealt with. DDIs are more prevalent in comorbid COPD-HF patients, apparently because of the many drugs prescribed to them, of which some are avoidable. Renal function adjustments via eGFR may identify patients exhibiting hyperkalaemia and aggravated renal functioning risks (Roblek, Trobec, Mrhar, & Lainscak, 2014).

Protocol Design

When modelling COPD progression, prior models have grouped patients based on FEV% (a measure which reduces over time, causing patient shift from mild-severe condition) and evaluated disease severity. This model has 5 mutually exclusive COPD severity and mortality linked states. 'Death' implies a patient who reaches this state continues to be in it (ODPRN, 2014).

Clinical Presentation

COPD is marked by continuous, increasing airflow restrictions linked to increased chronic inflammatory airway/lung response to harmful gases and particles. Smoking is its biggest risk factor. Smoking duration and quantity influences disease severity. Hence, the patient assessment and diagnosis stages must include determination of how many pack years have been smoked (cigarette packs smoked daily x smoking duration in years). Roughly 80% of American COPD patients were cigarette smokers. COPD's basic symptoms are dyspnea, sputum production, and chronic cough. Exertional dyspnea is its most widely reported initial-stage symptom. COPD patients commonly present in the following three ways (King Han, Dransfield, & Martinez, 2016):

1. Very sedentary lifestyle with not many complaints.

1. Respiratory symptoms typically including chronic cough and dyspnea (the latter might, at first, only surface with exertion).

1. Intermittent increased cough, dyspnea, fatigue, wheezing, and purulent sputum. Fever may or may not arise (Diagnosing these patients ispotentially problematic because a dyspnea-wheezing combination also suggests asthma).

Diagnosis

Protocol Design -- Treatment Algorithm (Stanford Hospitals & Clinics, 2015)

Findings

SHINE research results depict appreciably higher trough FEV1 improvements 26 weeks into treatment when indacaterom, tiotropium, and glycopyrronium are used combined than when employing mono-therapy. Dyspnea improvements were also evident (vs. Tiotropium and placebo), St. George's Respiratory Questionnaire (SGRQ) (vs. placebo), and decreased rescue drug utilization (vs. mono-therapies and placebo) (Tashkin & Ferguson, 2013).

Differential and Risk Factors

Differential diagnosis for middle age or old age patients presenting with cough, sputum production and dyspnea is broad (for instance, HF, COPD, thrombo-embolic disease or interstitial lung disease (ILD)). Consistent airflow restriction found by testing pulmonary functioning and a lack of radiographic ILG or HF features lead to a more limited COPD differential.

1. Chronic obstructive asthma -- In certain cases, one cannot easily distinguish between COPD and chronic asthma.

1. Central airway obstruction -- This may result from several malignant and benign processes, mimicking COPD with slow progressive dyspnea upon physical exertion and subsequent dyspnea even with very minimal activity at later stages.

1. Heart failure -- This commonly causes dyspnea in middle-old age patients; HF-linked fluid overload results in wheezing and chest tightness.

1. Bronchiectasis -- Abnormal bronchi widening linked to recurring or chronic infection. Airways get swollen and collapse easily, airflow gets blocked and its exacerbation leads to increased sputum production and dyspnea.

1. Tuberculosis -- A TB endemic locality showed overall airflow obstruction rate to be 31% in patients earlier diagnosed with TB and 14% in those who weren't.

1. Diffuse panbronchiolitis -- Mostly apparent among Asian male non-smokers. Nearly all suffer from chronic sinusitis.

1. Constrictive bronchiolitis -- Marked by peribronchiolar and submucosal fibrosis leading to concentric bronchiolar lumen narrowing.

1. Lymphangioleio myomatosis -- Chiefly exhibited by women in the childbearing age. Mild airflow blockage is seen; however, a mixed restrictive-obstructive pattern might be evident as well (Antus, 2013).

Treatment and follow-ups

A stepwise therapeutic approach ought to be adopted in case of COPD, based completely on spirometry-gauged disease severity. Stage I must involve actively reducing risks by additionally using bronchodilators with short-action when required. With disease advancement and decline of lung function (stages II through IV), maintenance therapy using at least one long-acting bronchodilator (e.g., long-acting anticholinergic, agonist or muscarinic antagonist) or ought to be administered separately or combined with inhaled corticosteroids (Antus, 2013). Follow-up appointments must involve patient evaluation for ascertaining medical regimen compliance, disease progression and therapy response. Exacerbation frequency and dyspnoea level with exercise and at rest must be ascertained (BMJ, 2016).

Alternate Approaches

The following emergent therapies may function as effective alternate treatments (Tashkin & Ferguson, 2013).

i. Triple Therapy

Inhaled corticosteroids, and long-acting muscarinic antagonists and beta-agonists have demonstrated benefits on lung functioning over mono-therapy. Further, a pilot research on advanced COPD patients reveals triple therapy and pulmonary rehabilitation in combination improves lung functioning.

ii. Dual Muscarinic Antagonist-B2-Agonists (MABAs)