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A white man aged 55 years presents to a primary-care clinic complaining of increased dyspnea on exertion over the past three months. Before the onset of dyspnea, he was able to walk 50 yards before having to rest and catch his breath. He currently cannot walk more than 50 feet without resting.

The man is a frequent patient with a history of chronic obstructive pulmonary disease (COPD) — most likely attributable to a 72-pack-year history of cigarette use — and heart failure (HF) secondary to prolonged undiagnosed hypertension.

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According to the Global Initiative for Chronic Obstructive Pulmonary Diseases guidelines, the patient has stage II (moderate) COPD.1 This man also has stage III HF, based on the New York Heart Association (NYHA) functional classification system (Table 1).2

He is compliant with his medications, which include a cardioselective beta blocker, an ACE inhibitor, a diuretic for HF, and a combination short-acting beta-agonist and anticholinergic/long-acting beta-agonist for COPD. The patient’s last pulmonary nction test (PFT) was three years ago and showed a forced expiratory volume in one second (FEV1) of 45% of normal and a ratio of FEV1 to forced vital capacity (FVC) of 51%.

His most recent ejection fraction (EF), obtained one year ago and measured by means of coronary CT angiography, was 21%. All acute pulmonary and cardiac differential diagnoses, including MI and pulmonary embolism, have been ruled out based on history of present illness or physical-exam findings.

The overlapping signs and symptoms of comorbid heart and lung diseases make it difficult to determine the cause of dyspnea in this patient and present a number challenges for the primary-care practitioner (PCP).

Although not every patient who presents with dyspnea will have coexisting heart and lung diseases, it is estimated that between 20% and 30% of patients who have HF have comorbid COPD.3 While there are long-established guidelines for the management of COPD1 and HF4 as separate conditions, there are no guidelines and few clinical recommendations for the management of these disease processes when they appear concurrently.

This article outlines the principles and considerations of managing progressive dyspnea in an adult with coexisting COPD and HF from a primary-care perspective.

Delineating dyspnea

Because multiple pathologic processes likely contribute to progressive dyspnea in patients with coexisting heart and lung diseases, it is unlikely that a single causative agent can be established. The challenge becomes determining the extent to which the patient’s existing pathologic processes are contributing to his or her progressive dyspnea once obvious differential diagnoses have been ruled out.

Establishing the likely causes of a patient’s dyspnea is crucial to effective management because the interventions used to treat HF have little positive effect — and potential adverse effects — on the pulmonary system. The converse is also true with interventions used to treat pulmonary causes of dyspnea. An example of this is the use of beta blockers for HF and beta-agonists for COPD.

The mechanism of dyspnea in HF

The isolated cardiac differential diagnoses, including HF, are all disease processes that lead to the heart failing as a pump.5 In such cases, the dyspnea is not caused by inadequate oxygenation but by inadequate distribution.

This inadequate distribution can manifest itself as pulmonary edema (as seen in left-sided HF) or peripheral edema, ascites, and jugular venous distension (as seen in right-sided HF). Similarly, a weakened pump compromises systemic perfusion, and although the blood may be adequately oxygenated, there is inadequate circulation to meet the body’s metabolic needs.

The mechanism of dyspnea in COPD

The isolated pulmonary disorders, which include COPD, are similar to the cardiac disorders in that they all share a common mechanism. With the isolated pulmonary disorders, ventilation deficit is the common cause of dyspnea.

Patients who have COPD are usually classified as having either emphysema or chronic bronchitis. This is somewhat misleading because most patients have both conditions, one of which is predominant.5 In COPD, emphysema is caused by inadequate ventilation attributable to poor lung compliance, whereas chronic bronchitis is caused by obstruction due to secretions.

Objective physical findings consistent with HF

The underlying pathology of HF contributes to inadequate fluid distribution and subsequent fluid overload. Patients experiencing fluid overload often present with increased BP, pulmonary rales, an S3 gallop, ascites, and lower-extremity edema.

The PCP may be able to elicit jugular venous distension (JVD) and hepatojugular reflex (HJR).6 Of these physical findings, the presence of an S3 gallop had the highest suggestive value for affirming HF. The presence of pulmonary rales, any cardiac murmur, JVD, HJR, and lower-extremity edema were also highly suggestive of HF.7

Objective physical findings consistent with COPD

The physical-exam findings in COPD reflect mechanical processes that impair gas exchange. Wheezes and rhonchi are often present on auscultation, and percussion tends to reveal hyperresonance. The presence of wheezes helps rule in pulmonary causes and rule out cardiac causes of dyspnea.7

Because of physical changes in the patient’s thorax, inadequate chest excursion and barrel-chest deformity are commonly found. In patients with acute exacerbations following physical exertion, tripod positioning and pursed-lip breathing are frequently seen in an attempt to provide the best position for full lung expansion and to keep terminal airways open.

Individuals who are chronic-bronchitis-dominant will often have a cough that produces copious amounts of sputum. Patients who are emphysema-dominant will have a dry cough and a flushed appearance related to polycythemia.5

Subjective findings consistent with HF

Individuals who experience dyspnea related to HF will often get some relief in an upright position. In the supine position, there is an increase in venous return from the lower extremities. This increased volume cannot to be managed effectively by the failing pump, leading to pulmonary congestion.3

Patients often complain of having to sleep on multiple pillows due to orthopnea and report difficulty breathing at night (paroxysmal nocturnal dyspnea). Those with dyspnea caused by HF will describe their breathing difficulty as “air hunger” or “suffocation.”8 This response is likely related to inadequate perfusion and distribution caused by pump failure.8

Subjective findings consistent with COPD

Positioning for COPD patients is relevant but for different reasons than those of HF patients. Individuals with COPD prefer to sit upright because of the mechanics of breathing. These patients will assume positions that allow for maximal lung expansion and create positive end-expiratory pressure (PEEP) through pursed-lip breathing.

When asked to describe their dyspnea, COPD patients use such phrases as, “I can’t take a deep enough breath,” or “It takes more effort to breathe.”8 This may be related to the structural pathology of COPD and the fact that increasing the work of breathing often helps to reduce signs and symptoms by aiding in the expansion of the thoracic cavity, which allows for greater filling of the lungs; providing a greater PEEP, which resists full collapse of the alveoli; and raising the respiratory, which provides more oxygenated air available for gas exchange.

The absence of orthopnea strongly suggests a pulmonary cause of dyspnea in patients with coexisting COPD and HF.7

Laboratory tests used to determe the cause of dyspnea

To rule out acute coronary syndrome as a causative agent in HF, testing for such cardiac biomarkers as troponin and creatinine kinase is advised in patients complaining of dyspnea. Similarly, a complete blood count (CBC) helps rule out anemic causes of dyspnea. A renal panel will determine whether the kidneys are contributing to the patient’s fluid overload.

If malnutrition and cachexia are suspected — as is often the case in advanced COPD — liver function tests (LFTs), including serum albumin, are advisable. Serum electrolytes, including magnesium, calcium and D-dimer, are helpful in discerning noncardiac causes of dyspnea. Arterial blood gases are not widely used in the primary-care setting and have been omitted from this discussion.