Determining the cause of a pleural effusion remains clinically challenging. Pleural fluid analysis (PFA) is an essential component of the diagnostic approach that we have reviewed in detail in a companion paper. However, despite the importance of PFA in establishing the cause of a pleural effusion, pathognomonic pleural fluid findings are rare. The true diagnostic value of PFA lies in its integration with the broader clinical picture. This diagnostic approach requires a systematic evaluation combining PFA with medical history, physical examination, laboratory data, and radiographic studies. In this manuscript, we review clinical features beyond PFA that are important in determining the cause of a pleural effusion. A detailed medical history may reveal important comorbidities, exposures, and previous surgical procedures that have diagnostic relevance. Radiographic findings, including the anatomic locations of pleural fluid, radiographic features, and the chronicity of the effusion, also may be diagnostically important. Blood tests may supply additional diagnostic information. Underpinning this diagnostic approach is that the clinician requires a deep understanding of the breadth of pleural diseases and their associated clinical presentations.

Targeting hypercapnia during invasive mechanical ventilation with subsequent respiratory acidosis may impair right ventricular (RV) function and cause RV failure. RV dysfunction is common after cardiac arrest and may be associated with poor outcomes.

Mitral valve disease has a significant impact on the respiratory system. Present-day pulmonologists must be aware of its myriad presentations and evolving treatment landscape.

Interstitial lung diseases (ILDs) are a heterogeneous group of entities characterized by similar clinical, pathologic, and radiologic features. High-resolution CT scan is the first-line imaging modality; however, the use of ionizing radiation in patients requiring several follow-ups, the limitation in distinguishing active inflammation from fibrosis, as well as its poor tissular characterization properties have opened a scenario in which MRI may have a role in patients with ILD. The high prevalence of lung cancer in ILD and the frequently unrecognized ILD-related pulmonary hypertension (PH) have raised interest in the potential application of MRI in these patients.

Follow-up of incidental lung nodules in real-world clinical practice is often inconsistent and suboptimal. Improving these follow-up processes presents a complex challenge, particularly for institutions without existing infrastructure. Although advanced tools such as natural language processing and artificial intelligence hold promise, many successful programs have relied on low-cost, manual approaches tailored to local workflows and resource availability. This article outlines a practical, experience-based framework for enhancing incidental lung nodule follow-up across diverse health care settings-including those with limited resources-by proposing scalable, feasible strategies that help bridge the gap between evidence-based guidelines and routine clinical practice.

The 2009 Family Smoking Prevention and Tobacco Control Act granted the US Food and Drug Administration regulatory authority over tobacco products, extended to include electronic cigarettes (ECs) in 2016. Regulatory science informs potential market restrictions based on the population health standard. The CHEST Tobacco and Vaping Workgroup is charged with prioritizing tobacco-related advocacy. To identify critical gaps in the science guiding EC regulation, wean exploration of existing evidence to develop future research recommendations.

Pulmonary exacerbations (PExs) are associated with lung function decline and poor quality of life in people with cystic fibrosis (CF). Standard clinical measurements are limited in predicting future PEx events; pulmonary MRI scan has been shown to be a sensitive measure of CF lung disease, but its ability to predict PExs is currently unknown.

The standard of care for management of asthma attacks has remained unchanged for 70 years, relying on a symptom-based, severity-stratified approach. Severe asthma attacks are defined by a worsening of asthma requiring oral corticosteroid (OCS) treatment for unresolved symptoms for at least 48 hours, decreased lung function, or both. The 1-size-fits-all strategy with OCS treatment overlooks the biological mechanisms driving attacks and may lead to suboptimal outcomes. Importantly, OCS-related toxicities lead to significant morbidity, and cumulative OCS use has been associated with increased mortality. Antibiotics, often used indiscriminately, also increase adverse events and antimicrobial resistance.

Chronic thromboembolic pulmonary disease corresponds to exercise impairment after a pulmonary embolism due to persistent chronic thrombi and exercise pulmonary hypertension (PH). Diagnosis requires exercise right heart catheterization (RHC), whereas data on noninvasive diagnosis are scarce.

A 17-year-old previously elite-level tennis player was referred with dyspnea, fatigue, and excessive sleepiness during prolonged matches. He would become somnolent between tennis sets to the point where he had several episodes of near collapse during play. He was not excessively sleepy during the day (Epworth Sleepiness Scale score 6) and did not report any non-exertional episodes of collapse or cataplexy. His medical history was notable for a significant road traffic accident at age 10, requiring endotracheal intubation and prolonged ventilation for 14 days. His recovery was complicated by subglottic stenosis that was later repaired with laryngotracheal reconstruction. At age 13, he underwent subglottic balloon dilatation as well as a left arytenoidectomy and division or interarytenoid scar band. The patient was referred to a specialized dyspnea service for further evaluation.

A 65-year-old man with a history of paroxysmal atrial fibrillation, hypertension, and OSA was admitted to the hospital with worsening dyspnea on exertion and generalized edema. He had no history of malignancy, immunosuppression, surgery, radiation, or autoimmune conditions. He was born in the United States with no recent travel, substance use, or homelessness. He did not report any fevers, night sweats, joint pain or swelling, phalangeal discoloration, nail or skin lesions, or ocular concerns. Transthoracic echocardiography demonstrated preserved systolic function. The patient was discharged with a presumed diagnosis of heart failure with preserved ejection fraction (HFpEF) after demonstrating clinical improvement with diuresis. He was readmitted after several weeks with worsening ascites, functional decline, and transaminitis. Paracentesis demonstrated an elevated ascitic total protein with a borderline serum ascitic albumin gradient slightly < 1.1 g/dL. The patient was discharged with gastroenterology follow-up to evaluate for malignancy. Several weeks later, he was readmitted to cardiology for worsening hypervolemia and suspected HFpEF exacerbation, despite adherence to outpatient diuretics.

A 28-year-old man with an unremarkable medical history, no regular medication regimen, and no recent travel history or animal exposure was admitted to the emergency department with new onset of disorientation, slurred speech, and hearing loss. One day prior, the patient had consulted his general practitioner for fever, recurrent vomiting, and myalgia. According to his family, the patient smoked cigarettes and daily ingested γ-hydroxybutyrate. Because of the patient's limited ability to communicate, recent ingestion of other substances could not be ruled out. The patient was admitted to the ICU because of severe metabolic acidosis, electrolyte imbalances, and acute renal failure of indeterminate origin. Hemodialysis was started right after admission.