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Refractory Atrial Fibrillation With Conversion Pauses in Extensive-Stage Small Cell Lung Carcinoma Presenting With Hypoxic Respiratory Failure: A Case Report.

Source: PubMed, NCBI / U.S. National Library of Medicine

CureusAbdelwahed Ahmed R, Sharma Sandesh, Phillip MadonnaPublished 7/1/2026Last synced 8/6/2026Status: syncedPMID: 42553044DOI: 10.7759/cureus.112051

Small cell lung carcinoma (SCLC) is a high-grade pulmonary neuroendocrine carcinoma strongly associated with smoking and commonly presents with advanced intrathoracic disease. Atrial fibrillation (AF) is common in acutely ill patients and in patients with cancer; however, causal attribution in an individual patient is often difficult because multiple arrhythmogenic stressors coexist. A 72-year-old man with hypertension, morbid obesity, peripheral arterial disease, heavy prior tobacco exposure, and no known prior cardiac arrhythmia or structural heart disease presented with progressive dyspnea, cough, fatigue, weight loss, and hypoxemic respiratory failure. Thoracic imaging revealed bulky mediastinal and hilar lymphadenopathy, right bronchial obstruction with collapse and consolidation of much of the right lung, a large recurrent right pleural effusion, and an additional contralateral pulmonary lesion suspicious for malignancy. Integrated pleural cytology and tissue biopsy results supported the diagnosis of extensive-stage SCLC with malignant pleural involvement in this patient. The patient was treated empirically for post-obstructive pneumonia and required repeated pleural drainage procedures. During hospitalization, he developed recurrent AF with a rapid ventricular response and asymptomatic post-conversion pauses of up to six seconds, despite preserved left ventricular systolic function and no major structural hear

Abstract

Small cell lung carcinoma (SCLC) is a high-grade pulmonary neuroendocrine carcinoma strongly associated with smoking and commonly presents with advanced intrathoracic disease. Atrial fibrillation (AF) is common in acutely ill patients and in patients with cancer; however, causal attribution in an individual patient is often difficult because multiple arrhythmogenic stressors coexist. A 72-year-old man with hypertension, morbid obesity, peripheral arterial disease, heavy prior tobacco exposure, and no known prior cardiac arrhythmia or structural heart disease presented with progressive dyspnea, cough, fatigue, weight loss, and hypoxemic respiratory failure. Thoracic imaging revealed bulky mediastinal and hilar lymphadenopathy, right bronchial obstruction with collapse and consolidation of much of the right lung, a large recurrent right pleural effusion, and an additional contralateral pulmonary lesion suspicious for malignancy. Integrated pleural cytology and tissue biopsy results supported the diagnosis of extensive-stage SCLC with malignant pleural involvement in this patient. The patient was treated empirically for post-obstructive pneumonia and required repeated pleural drainage procedures. During hospitalization, he developed recurrent AF with a rapid ventricular response and asymptomatic post-conversion pauses of up to six seconds, despite preserved left ventricular systolic function and no major structural heart disease on echocardiography. Rate control with beta-blockade was limited by bradycardia and hypotension; flecainide incompletely suppressed recurrent episodes; amiodarone was later initiated because rhythm instability persisted, and alternatives were limited. Transesophageal echocardiography showed no intracardiac thrombus before the planned cardioversion, but the patient spontaneously converted to sinus rhythm before shock delivery and later reverted to AF after a coughing spell. This case highlights the complexity of managing AF in advanced thoracic malignancy complicated by hypoxemia, pleural disease, and suspected post-obstructive pneumonia.

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