A43-26 Inflammation Meets Ischemia: A Deadly Synergy

Introduction Interstitial lung disease (ILD) is a heterogenous group of disorders involving lung parenchyma. An acute exacerbation consists of respiratory distress, often requiring ICU care, as well as a new widespread alveolar abnormality on imaging. Hypoxic respiratory failure limits oxygen supply to the myocardium, leading to a supply-demand mismatch causing myocardial injury; this is referred to as demand ischemia. In demand ischemia, troponin elevations are lesser than in an acute coronary event. In critically ill patients, cardiac ischemia may be underrecognized because cardiac biomarker elevations are frequently attributed to demand ischemia in the setting of sepsis or respiratory failure. This case highlights the diagnostic challenges of patients presenting with sepsis or ILD exacerbation and concomitant acute myocardial infarction. Case Presentation We present a case of a 75-year-old male who presented with progressive dyspnea. His medical comorbidities were significant for ILD in the usual interstitial pneumonia (UIP) pattern. He was febrile, hypoxic, and hypertensive. Troponins were elevated to 602.0 then 816.7. CTA chest showed extensive worsening of his ILD with extensive bilateral airspace opacities. He was admitted to cardiology and was not initially heparinized due to suspicion of demand ischemia in the setting of ILD flare. An echocardiogram revealed a newly reduced ejection fraction of 39% with anterior wall hypokinesis. Left heart catheterization revealed 90% stenosis of the left main artery and of the right coronary artery. He was transferred to a tertiary hospital for complex coronary evaluation, but his hospitalization was further complicated by multi-organ failure. He developed hypotension, requiring vasopressor support. His hypoxia worsened, requiring intubation. He also developed an oliguric kidney injury, requiring continuous renal replacement therapy. He was deemed too unstable to undergo any cardiac intervention, goals of care conversation were held, and family opted for hospice care. Discussion This case highlights the complexity of acute hypoxemic respiratory failure in fibrotic ILD who developed new peribronchovascular consolidations and rising troponins. The presentation was concerning for an acute exacerbation of ILD (AE-ILD), though concurrent ischemic cardiomyopathy and systemic inflammation likely contributed to his deterioration. Despite broad-spectrum antibiotics and pulse-dose corticosteroids, his respiratory failure and shock progressed, reflecting the limited efficacy of current therapies for AE-ILD, especially when complicated by cardiac dysfunction. This case underscores the challenge of distinguishing AE-ILD from infection or cardiac causes of decompensation and highlights the importance of early multidisciplinary and goals-of-care discussions in patients with advanced fibrotic lung disease facing critical illness. This abstract is funded by: None