A 44-Year-Old Man With Suspected Exacerbation of COPD and Atrial Fibrillation^* FREE TO VIEW

A 44-year-old man with a long smoking history, COPD, and hypertension presented to the emergency department with 5 days of fever, productive cough, and shortness of breath. He had a 2-year history of dyspnea after walking one city block. Spirometry performed several months earlier showed a FVC ratio (FEV₁/FVC) of 62% of predicted. He worked in a factory with extensive exposure to sawdust. His medications included diltiazem, albuterol, and salmeterol inhalers. He denied any allergies, and his family history was noncontributory.

Vital signs revealed a BP of 107/73 mm Hg, heart rate of 120 to 140 beats/min, respiratory rate of 30 to 40 breaths/min, temperature of 36.3°C, and oxygen saturation of 94% on 3 L/min of oxygen by nasal cannula. He appeared thin with moderate respiratory distress and audible wheezing. On cardiovascular examination, his rate and rhythm were tachycardic and irregularly irregular with a 2/6 systolic murmur heard loudest at the apex. Lung examination revealed bilateral prominent wheezes and crackles. The remainder of his examination was normal.

The WBC count was 10,100/μL with 74% neutrophils, and the hemoglobin was 12.0 g/dL. The hematocrit was 35.3%, and the mean corpuscular volume was 81.4 femtoliters. The chemistries revealed a sodium concentration of 131 mmol/L; creatinine, 1.8 mg/dL; serum aspartate aminotransferase, 86 U/L; and serum alanine aminotransferase, 123 U/L. The total bilirubin was 3.0 mg/dL with normal cardiac enzymes. An arterial blood gas analysis done on 3 L/min of oxygen by nasal cannula revealed a pH 7.56; Pco₂, 24 mm Hg; Po₂, 83 mm Hg; and bicarbonate, 21 mmol/L. An ECG revealed atrial fibrillation with right-axis deviation and occasional premature ventricular complexes. A chest radiograph, shown in Figure 1 , was obtained on hospital admission. A chest radiograph from 2 years earlier is shown in Figure 2 .

The patient was treated for a COPD exacerbation and community-acquired pneumonia. He was administered inhaled bronchodilators, IV corticosteroids, and gatifloxacin. Atrial fibrillation was managed with a diltiazem drip and a loading dose of digoxin.

By the third hospital day, he remained tachypneic, diaphoretic, and anxious with diffuse wheezing. Repeat examination revealed jugular venous distension (measured at 16 cm) and + 1 lower-extremity edema bilaterally. He remained in atrial fibrillation with a heart rate of 115. The patient was placed on bilevel positive airway pressure (BiPAP; Respironics; Murrysville, PA) and administered IV furosemide. Despite diuretics and bilevel pressure ventilation support, he continued to deteriorate and was intubated on the fifth hospital day.

The most common cause of mitral stenosis remains rheumatic fever. The association between sore throat and rheumatic fever was first described > 100 years ago. A subset of patients with rheumatic fever acquire an inflammatory process affecting the valvular endocardium that can progress to fibrosis and deformity of the mitral valve with eventual impairment of valvular function. Although the acute symptoms of rheumatic fever usually subside in weeks or months, manifestations of valvular dysfunction generally do not appear for 10 to 30 years. Rheumatic fever and rheumatic heart disease are more prevalent in developing countries than the United States. Some resurgence of acute rheumatic fever, however, was observed in Utah, Pennsylvania, and Ohio during the 1980s, which may increase the prevalence of rheumatic heart disease in these regions in coming decades. The prevalence of mitral stenosis in adults is estimated to be < 1 in 100,000 in the United States. Only 50% of patients with mitral stenosis who have had rheumatic fever will be aware of their cardiac disease.

The pulmonary manifestations of mitral stenosis develop as a consequence of pulmonary vascular engorgement. Typical radiographic findings include enlargement of the left atrium and atrial appendage with prominence of the pulmonary trunk, which causes straightening of the left heart border, pulmonary vascular cephalization, and interstitial edema. Other findings may include alveolar edema and pulmonary ossification. The latter is a rare, late-sequela pathognomonic for mitral stenosis and manifests radiographically as densely calcified, 1- to 5-mm nodules mainly in the middle and lower lung fields.

Pulmonary function can be impaired in mitral stenosis due to the elevated pulmonary arterial and venous pressures. These impairments include reduced static and dynamic lung compliance, abnormal ventilation-perfusion ratios, peripheral airway obstruction, and decreased pulmonary diffusing capacity. Correction of mitral stenosis usually improves pulmonary function. The obstructive ventilatory pattern demonstrates reversibility with bronchodilators. Hyperreactivity may result from pulmonary congestion that activates sensory nerve endings in the lower airways and increases vagal tone.

Therapy for mitral stenosis depends on the severity of the symptoms, the degree of stenosis, and the nature of valvular calcification. Balloon valvotomy is widely used, with long-lasting results for patients with sufficient mitral valve mobility and a limited degree of subvalvular and valvular thickening and calcification. Patients with severely calcified valves require mitral valve replacement to improve survival.

What is the role of brain natriuretic peptide in the setting of congestive heart failure caused by mitral stenosis? Brain natriuretic peptide, which is released by the ventricles in response to myocyte stretch, is a sensitive indicator of ventricular dysfunction and volume overload. It can be elevated in the setting of mitral stenosis when there is right ventricular dysfunction and normal left ventricular function. However, brain natriuretic peptide levels may also be elevated in the setting of atrial fibrillation without overt heart failure, due to increased production in the atrium. Thus its value in indicating right ventricular dysfunction in mitral stenosis is reduced if there is atrial fibrillation.

In the setting of worsening dyspnea in a patient with COPD, the presence of an acute arrhythmia should widen the differential diagnosis beyond an acute exacerbation of COPD. One study retrospectively reviewed 86 patients hospitalized for acute COPD exacerbations. Only 10 patients had arrhythmias on presentation, of whom 6 had atrial fibrillation. Most of the patients had coexisting cardiac disease. Thus, while COPD is associated with atrial arrhythmias, new-onset atrial fibrillation should not be simply attributed to a COPD exacerbation.

The present patient presented with progressive dyspnea suggestive of an acute COPD exacerbation. His chest radiograph, however, demonstrated typical findings of mitral stenosis with straightening of the left border of the heart. New-onset atrial fibrillation further suggested a cardiac etiology for his clinical presentation. The obstructive findings on his previous pulmonary function tests most likely developed from his smoking history or, perhaps, his mitral stenosis.

His pulmonary function tests from several months prior to hospital admission are consistent with an obstructive defect. The relatively acute onset of dyspnea was due to the sudden development of atrial fibrillation, resulting in the patient’s presentation to the hospital. When questioned about rheumatic fever, he denied any history to the best of his knowledge.

He underwent evaluation by transesophageal echocardiography, which demonstrated enlargement of the left atrium with minimal opening of a markedly fibrosed and thickened mitral valve (Fig 3 ). The valve was calcified to the point of immobility with a small valve area. The extremely depressed blood flow across the valve explained why no opening snap or diastolic murmur were audible. A small thrombus was visible in the left atrial appendage. He underwent cardiac catheterization that showed normal coronary arteries and an estimated mitral valve area of 0.7 cm². He underwent mitral valve replacement with resolution of his congestive heart failure. After initiation of amiodarone, the cardiac rhythm converted to normal sinus rhythm. A follow-up chest radiograph several days after surgery showed improvement of the interstitial edema with decreased prominence of the left heart border (Fig 4 ).