Positive airway pressure (PAP) therapy is widely used to manage both acute and chronic respiratory failure and plays an increasingly important role in cardiology, particularly in treating patients with respiratory comorbidities. PAP, including continuous positive airway pressure and noninvasive ventilation, significantly impacts hemodynamics by altering intrathoracic pressure, affecting preload, afterload, and stroke volume. These changes are crucial in conditions such as acute cardiogenic pulmonary edema, where PAP can enhance gas exchange, reduce the work of breathing, and improve cardiac output. PAP reduces the left ventricular afterload, which in turn increases stroke volume and myocardial contractility in patients with left-sided heart failure. However, the role of PAP in right ventricular function and its effects on venous return and cardiac output are critical in the cardiac intensive care setting. While PAP provides respiratory benefits, it must be used cautiously in patients with right heart failure or preload-dependent conditions to avoid adverse outcomes. Additionally, in recent years, the use of PAP has expanded in the treatment of severe obstructive sleep apnea and obesity hypoventilation syndrome, both of which significantly influence cardiovascular events and heart failure. This review provides an in-depth analysis of the hemodynamic effects of PAP in cardiovascular disease, focusing on its impact on ventricular function in both acute and chronic conditions. Evaluating clinical studies, guidelines, and recent advancements offers practical insights into the physiological mechanisms and key clinical considerations. Furthermore, this review aims to serve as a helpful guide for clinicians, assisting in decision-making processes where PAP therapy is applied.

Introduction: Osimertinib is a third-generation tyrosine kinase inhibitor (TKI) of epidermal growth factor receptor (EGFR) used for the treatment of non-small cell lung cancer (NSCLC) presenting an EGFR mutation. Although Osimertinib has a better safety profile compared to older EGFR-TKIs and although adverse events (AEs) are described in literature, recently the relationship between Osimertinib therapy and cardiotoxicity is gaining attention. Case report: A 79-years old woman, with a history of lung adenocarcinoma on treatment with Osimertinib since 2019, was recovered in our department because of acute respiratory failure and acute heart failure with QT prolongation. The patient's history included hypertension, type 2 diabetes, breast carcinoma, Tuberculosis. Management and outcome: The patient discontinued Osimertinib therapy and we treated her with diuretics, ß-blocker, and oxygen. After an initial improvement, the heart failure worsened further, and the therapy had to be increased. We ruled out other respiratory causes of heart failure and cardiological causes of QT prolongation. After stable clinical improvement, the patient underwent coronary artery disease which was negative. Therefore, the most likely cause of acute heart disease was Osimertinib therapy. Discussion: This is a rare case of concomitant QT prolongation and congestive heart failure induced by Osimertinib therapy. The cause of cardiotoxicity probably depends on factors related to the action of the drug and patient specific factors. The cardiotoxic risk in these patients seems underestimated and cardiotoxicity induced by new anticancer treatments is increasing in importance. Cardiac monitoring is recommended in neoplastic patients receiving Osimertinib therapy with cardiological risk factors.

The role of indacaterol for chronic obstructive pulmonary disease (COPD)