The natriuretic peptides, specifically brain natriuretic peptide (BNP), are the most specific and applicable laboratory tests available to establish fluid overload associated with HF.9 BNP is secreted by cardiac cells in the ventricles in response to stretch-receptor stimuli. When fluid volumes increase, the ventricles stretch and, in turn, secrete BNP. The BNP then provides feedback to the renin-aldosterone system in an attempt to regulate this fluid imbalance.

The use of BNP in determining fluid overload in patients with dyspnea has become well established over the past several years. Citing several studies that supported the use of BNP in patients with dyspnea and with comorbid heart and lung disease, Le Jemtel et al. suggested that BNP >500 pg/mL is indicative of overt congestive HF in a patient with established COPD.10

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Likewise, a BNP <100 pg/mL provided evidence against HF as a contributing cause of dyspnea in patients with COPD.10 A BNP level should be drawn in any patient with progressive dyspnea who has established comorbid heart and lung diseases. This provides useful information regarding fluid status and can greatly assist the PCP in delineating cardiac causes of dyspnea.

Imaging studies of the dyspneic patient

The importance of chest radiographs in the diagnosis of a dyspneic individual cannot be overstated. These x-rays provide a great deal of information that assists the PCP in sorting out the origin of a dyspneic episode.

The presence of lobar infiltrates, hyperinflation, decreased pulmonary vasculature, bullae, thickened bronchial markings and an enlarged right heart are indicative of pulmonary abnormalities that may be contributing to a patient’s dyspnea (Figure 1).

In contrast, increased pulmonary vasculature, interstitial infiltrates confirmed by Kerley B lines, and pleural effusions indicate a cardiac cause of dyspnea (Figure 2). Of these findings, the presence of interstitial infiltrates is the most suggestive of HF. The presence of interstitial infiltrates also helps to rule out pulmonary causes of dyspnea.7

ECG will determine the presence of dysrhythmia, conduction abnormalities, ischemia, or infarct. Although ECG cannot indicate the mechanical status of the heart, it can alert the practitioner to any new abnormalities, especially when compared with past ECGs.

In the primary-care setting, echocardiograms are referred out. Echocardiograms help establish a baseline EF, determine chamber size, distinguish the type of HF, and point to disease progression, but their utility in determining acute exacerbations is limited.7

PFTs are similar to echocardiograms in that they can be used to establish a baseline and determine disease progression. For more acute exacerbations, however, their use is limited. PFTs also require referral and are not necessary on a routine basis.

Coronary CT angiograms, nuclear stress tests, cardiac catherizations, and V/Q scans can be used in the initial workup of a patient who is suspected of having comorbid COPD and HF. However, these tests are not recommended in acute exacerbations of dyspnea in patients well-known to a primary-care practice.

Table 2 summarizes the most common signs and symptoms of dsypnea.

COPD treatment guidelines

According to the Global Initiative for Chronic Obstructive Lung Disease (GOLD), the goals of treatment for COPD are relief of symptoms, prevention of disease progression, improvement of exercise tolerance, prevention and treatment of complications and exacerbations, and reduction of mortality.1 To date, no pharmacologic therapies have been shown to slow the progression of COPD symptoms. Aggressive patient education and nonpharmacologic support is the cornerstone of treatment.1

The pharmacologic management of COPD is determined by the GOLD classifications, which are based on PFT parameters; medication recommendations are made within each classification. Five stages of COPD are recognized:1

Stage 0 (at risk). Characterized by the presence of cough, sputum, and breathlessness without airflow obstruction.

Stage I (mild). Characterized by mild airflow limitation (FEV1/FVC <0.70; FEV1 ≥80% predicted).

Stage II (moderate). Characterized by worsening airflow limitation (FEV1/FVC <0.70; FEV1 50% to 80% predicted).

Stage III (severe). Characterized by further worsening of airflow limitation (FEV1/FVC <0.70; FEV1 30% to 50% predicted).

Stage IV (very severe). Characterized by severe airflow limitation (FEV1/FVC <0.70; FEV1 <30% predicted or <50% predicted plus the presence of chronic respiratory failure).

Patient assessment is driven by symptom severity — especially breathlessness and reduced exercise capacity — as well as by the development of complications. Management decisions are often based on symptomatic response (bronchodilator treatment) rather than changes in spirometry, which is a poor predictor. Nevertheless, spirometry is a necessary requirement for the diagnosis of COPD and is a useful indicator of disease progression.11

Bronchodilators with beta2-agonists, anticholonergics, and methylxanthines are central to the management of COPD and are used singly or in combination. Regular treatment with long-acting bronchodilators has proven to be more effective and convenient than that with short-acting bronchodilators.

The addition of inhaled glucocorticosteroids is appropriate for symptomatic COPD with FEV1 <50% and repeated exacerbations. However, chronic treatment with glucocorticosteroids should be avoided due to an unfavorable benefit-to-risk ratio.1