An 87-year-old woman with a medical history of stroke, paroxysmal atrial fibrillation, type 2 diabetes mellitus, diastolic heart failure, and chronic bilateral lymphedema presents with 1 week of shortness of breath. The patient had a 20-pack-year smoking history and at baseline was able to ambulate freely without assistance. Her symptoms of dyspnea were mostly exertional and progressively worsening for 1 week before admission, despite compliance with her home furosemide. On admission, her temperature was 36.3 °C, BP was 101/59 mm Hg, heart rate was 82 beats/min, respirations were 18 breaths/min, and oxygen saturation was 91% on room air. On physical examination, the patient was tachypneic at rest, and auscultation of the lungs revealed minimal breath sounds on the left side. Admission laboratory test results were notable for leukocyte count of 11.67 × 109/L (82.2% neutrophils, 8.3% monocytes, 6.4% lymphocytes, and 2.1% eosinophils). Results of HIV screening tests were negative.

A 34-year-old man presented to our institution with lightheadedness and dyspnea on exertion. His medical history included chronic pancreatitis, juvenile rheumatoid arthritis (JRA), gastroesophageal reflux disease, hypertension, lumbar degenerative disc disease, seizure disorder, anterior uveitis, and multiple vertebral fractures. In addition, he was a cigarette smoker with a 10-pack-year smoking history.

A 26-year-old woman with no significant past medical history sought treatment for worsening dyspnea and hypoxia. The exertional dyspnea began 2 years prior and was associated with substernal chest discomfort. She did not report myalgia, edema, or worsening of dyspnea on supine or upright position. The patient reported no personal history of tobacco or illicit drug use. Family history was unremarkable. She was started on supplemental oxygen at 3 L/min. Initial workup included CT scan angiography of the chest, which showed no pulmonary embolism and normal lung parenchyma. Transthoracic echocardiography showed unremarkable results. She was not given a clear diagnosis for hypoxia and was treated empirically with antibiotics and bronchodilators without improvement. Over the course of 2 years, her condition progressed to requiring 6 L/min nasal canula at rest and associated dyspnea with minimal exertion and a 30-pound unintentional weight loss. During this time, pulmonary function tests noted normal spirometry results and lung volumes, but a decreased diffusing capacity for carbon monoxide of 33%. She also was discovered incidentally to be leukopenic and thrombocytopenic, with subsequent bone marrow biopsy revealing hypocellularity of 30% to 40%. The patient concurrently demonstrated bilateral visual impairment secondary to retinal telangiectasias with increased severity of deficit in the right eye. She subsequently was referred to our institution for further evaluation.

A 30-year-old man presents with dry cough and dyspnea on exertion (modified Medical Research Council dyspnea scale of 3), with progressive worsening over several months. He denies other respiratory or cardiac symptoms such as wheezing, hemoptysis, thoracalgia, palpitations, or leg swelling. He also denies constitutional symptoms, namely fever, sweating, anorexia, or weight loss. The patient is a current smoker (five cigarettes per day), with no other significant exposures, diseases, or medications. He had no personal history of respiratory diseases or TB. Relevant family history included an aunt with nonspecified interstitial lung disease and lung transplant.

A 79-year-old woman was admitted to the hospital for progressive dyspnea and severe hypoxemia, requiring oxygen supplementation. The dyspnea started approximately 3 to 4 weeks before presentation and was slowly progressive throughout the following weeks. Her medical history mentioned an adenocarcinoma with an epidermal growth factor receptor (EGFR) exon 19 deletion of the lung with metastases to the bones and brain for which treatment with osimertinib was started 14 months earlier. Furthermore, she was treated with rivaroxaban for a first episode of a pulmonary embolism. In the months leading up to her current presentation there were no changes in medication and no use of antibiotics. She had no known exposure to toxic fumes or substances, she was a nonsmoker, and her family history was unremarkable for autoimmune disorders or interstitial lung disease (ILD).

A 49-year-old woman sought treatment at the hospital for evaluation of an enlarging cavitary mass of the right lung associated with worsening ipsilateral pleuritic chest pain and cough. She had recent hospitalizations for complications relating to recurrent lung abscesses, including one in which she underwent wedge resection of the right lung. She had been treated with several courses of antibiotics, which only temporarily relieved her symptoms. She did not report any fevers, chills, skin changes, diarrhea, or changes to her bowel habits. Her long-term medications included albuterol, dapsone, and prednisone 15 mg or 20 mg doses alternating daily. Her only past medical history was asthma and primary cutaneous pyoderma gangrenosum. The patient never smoked and did not report any recent sick contacts.

A 44-year-old man with a history of asthma presented with intermittent convulsion of the right limb, fever in the late afternoon, and decreased exercise tolerance over 2 months. Occasional productive cough, no hemoptysis, and weight loss of nearly 6 kg were observed during this period. Neither chemotherapy nor oral immunosuppressive drugs had been administered, and no exposure to toxic substances was known. He was a cook and had smoked approximately one pack of cigarettes per day for the past 20 years. The living environment was relatively humid. The patient presented to a local hospital, where the workup was notable for low-density shadows in the left parieto-occipital lobe and a cavity in the right upper lobe of the lung with bilateral diffuse interlobular septal thickening and multiple patchy ground-glass opacities. The brain and lung lesions were 18F-fluorodeoxyglucose avid on PET/CT scan. Bronchoscopy with BAL and transbronchial biopsy were nondiagnostic. While preparing for another diagnostic procedure, the patient gradually developed increasing dyspnea and more frequent convulsions with the progression of lesions on the follow-up chest CT scan. The patient was transferred to our hospital.

In critically ill patients receiving mechanical ventilation, expiratory muscles are recruited with high respiratory loading and/or low inspiratory muscle capacity. In this case report, we describe a previously unrecognized patient-ventilator dyssynchrony characterized by ventilator triggering by expiratory muscle relaxation, an observation that we termed expiratory muscle relaxation-induced ventilator triggering (ERIT). ERIT can be recognized with in-depth respiratory muscle monitoring as (1) an increase in gastric pressure (Pga) during expiration, resulting from expiratory muscle recruitment; (2) a drop in Pga (and hence, esophageal pressure) at the time of ventilator triggering; and (3) diaphragm electrical activity onset occurring after ventilator triggering. Future studies should focus on the incidence of ERIT and the impact in the patient receiving mechanical ventilation.