Current indications for long-term oxygen therapy (LTOT) primarily are based on thresholds of arterial oxygen saturation (Sao2) or Pao2 that ignore fundamental mechanisms of adaptation and intolerance to hypoxia. In individuals exposed to chronic hypoxic conditions, the accumulation of hypoxia-inducible factors in the cell nucleus upregulates target genes that favor tolerance to hypoxia. Adaptations include hyperventilation, systemic vascular bed development, increased erythropoiesis, and cellular metabolic adjustments. Excessive responses to hypoxia also may develop, leading to pulmonary vasculature remodeling and other end-organ dysfunctions. Biomarkers of hypoxia may complement the measurement of Sao2 or Pao2 in personalizing oxygen prescription before end-organ dysfunction becomes clinically apparent.

The precise impact of cardiovascular risk factors (CVRFs) on the right ventricle-pulmonary circulation unit remains unclear.

With the sudden onset of the COVID-19 pandemic, countries rushed to implement guidelines for triage. Some were unprepared. In Germany, academic discourse had focused on criteria for triage, while often neglecting their translation into clinically applicable protocols in ICUs.

Pulmonary arteriovenous malformations (PAVMs) require therapeutic embolization and careful surveillance to prevent serious complications, including stroke, brain abscess, and hemoptysis. Although initial treatment guidelines are well established, posttreatment surveillance practices remain heterogeneous, with no standardized approach for monitoring treated lesions or detecting PAVM persistence. This variability in follow-up care may affect patient outcomes, particularly in high-risk populations such as those with hereditary hemorrhagic telangiectasia (HHT).

Pulmonary hypertension (PH) is a complex, life-threatening condition requiring noninvasive, accessible, and accurate diagnostic tools, particularly in resource-limited settings. Early and precise identification of PH and its subtypes is critical for effective management and timely intervention.

Increasing evidence supports lung cancer screening with low-dose CT (LDCT) imaging. However, the benefits of LDCT screening for lung cancer may not be immediate, making it unlikely to benefit patients with limited life expectancy.

Establishing the cause of a pleural effusion can be challenging. Analysis of pleural fluid (PF) is a powerful tool to determine the cause of a pleural effusion. Surprisingly, despite the diagnostic power of PF analysis (PFA), it is often underused. This review provides a practical framework to maximize the diagnostic potential of the PFA. We describe the role of a PFA in establishing the cause of a pleural effusion. We also discuss challenges and limitations of PFA.

A 54-year-old woman with a history of recurrent exertional dyspnea for 5 years was admitted for evaluation. Six months prior, she noted a worsening of her symptoms, with progressive physical activity limitation caused by exertional fatigue and dyspnea (climbing 2 to 3 flights of stairs). She also experienced palpitations, with an estimated heart rate that ranged from 120 to 150 beats per minute. The patient denied chest pain, hemoptysis, or other notable symptoms. Notably, the patient underwent surgical repair of an atrial septal defect more than 20 years earlier, with a good postoperative recovery. Regular postoperative echocardiograms revealed no residual shunt, no valvular abnormalities, and no pulmonary hypertension. The patient had no history of smoking, drug abuse, or alcohol consumption.

A 94-year-old man presented with a 1-day history of dyspnea and no infective symptoms. There was no associated chest pain, cough, or fever. Systemic review was negative for loss of appetite or weight. He had a medical history of ischemic heart disease with an ejection fraction of 45%, hypertension, hyperlipidemia, and Alzheimer dementia.

A 47-year-old woman initially presented with recurrent coughing caused by the ingestion of gritty foods such as nuts over 20 years ago. Subsequently, she experienced frequent postprandial episodes of white sputum containing food particles and suffered from acid reflux and heartburn, which were originally overlooked.

Pulmonary alveolar proteinosis (PAP) is a rare lung condition characterized by the accumulation of proteinaceous material within the alveoli. The acquired form is often autoimmune, driven by autoantibodies against granulocyte-macrophage colony-stimulating factor. Presentation of autoimmune PAP may range from incidental detection in asymptomatic patients to advanced respiratory failure. Treatment typically involves whole lung lavage or granulocyte-macrophage colony-stimulating factor therapy in symptomatic patients; spontaneous resolution is rare in severe cases. Here, we report 3 cases of autoimmune PAP who presented with resting hypoxia and exhibited spontaneous resolution without significant treatment. All 3 cases had a history of occupational inhalational exposure to noxious gases, and they improved following sustained cessation of exposure. We hypothesize that occupational or environmental noxious inhalation exposure may have a role in disease expression in some cases of autoimmune PAP, and such cases may show spontaneous resolution following cessation of the offending exposure.