Pathophysiology of COPD.

This article provides an overview of the pathophysiology of chronic obstructive pulmonary disease including the physiological mechanisms that are known precursors. The roles of environmental and genetic causes are considered. α1-Antitrypsin deficiency is also discussed as it relates to the development of airflow obstruction.

Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide and results in an economic and social burden that is both substantial and increasing. The natural history of COPD is punctuated by exacerbations, which have major short- and long-term implications on the patient and health care system. Evidence-based guidelines stipulate that early detection and prompt treatment of exacerbations are essential to ensure optimal outcomes and to reduce the burden of COPD. In this review, we provide a concise overview of COPD exacerbations and their risk factors and etiology (infection vs noninfectious), outlining the initial evaluation, triaging, and current management including invasive and noninvasive ventilation, in addition to the prognosis and the preventive strategies.

COVID-19: Epidemiology, Pathophysiology, Transmission, Symptoms.

COVID-19 is caused by the coronavirus known as SARS-CoV2. This virus may lead to asymptomatic cases, mild illness, or acute respiratory distress syndrome. Here we describe the epidemiology, pathophysiology, transmission, and symptoms of the virus.

Paralytics, Sedation, and Steroids in Acute Respiratory Distress Syndrome.

In this article, we discuss the literature behind the use of paralytics, sedation, and steroids in acute respiratory distress syndrome. We explore the controversies and discuss the recommendations for the use of these agents.

Acute Respiratory Distress Syndrome Definition, Causes, and Pathophysiology.

First successfully described in 1967, acute respiratory distress syndrome has since garnered much interest and debate. Extensive studies and clinical trials have been carried out in efforts to address the associated high mortality; however, it remains a significant burden on health care. Despite the heterogeneous etiologies that lead to the development of acute respiratory distress syndrome, this rapidly progressing form of respiratory failure, characterized by severe hypoxemia and nonhydrostatic pulmonary edema, has a recognizable pattern of lung injury. In this chapter, we will review the clinical manifestations, definitions, causes, and a brief overview of the pathophysiology of this complex syndrome.

Diagnostic Considerations of Venous Thromboembolic Disease.

Venous thromboembolism (VTE) includes deep venous thrombosis (DVT) and pulmonary embolism (PE). The clinical presentation of VTE is nonspecific and requires confirmatory testing. The most common diagnostic tool for DVT is duplex ultrasonography since it is a noninvasive test with high accuracy. Contrast venography is considered the gold standard modality to diagnose DVT, but it is an invasive test. Magnetic resonance venography and computed tomography venography are alternative diagnostic methods for DVT, which can be helpful in certain circumstances. Pulmonary embolism is commonly diagnosed by computed tomography pulmonary angiography. Ventilation perfusion scanning is an alternative imaging to diagnose PE in patients who cannot receive intravenous contrast. Pulmonary angiography is still the gold standard in the diagnosis of PE and is usually needed in specific conditions. D-dimer assay can be utilized in ruling VTE out in low-risk patients. Estimating the pretest clinical probability for having VTE is the key step in guiding the clinicians and nurses to the appropriate diagnostic method for patients with suspected DVT or PE.

Management of Respiratory Failure.

The management of acute respiratory failure varies according to the etiology. A clear understanding of physiology of respiration and pathophysiological mechanisms of respiratory failure is mandatory for managing these patients. The extent of abnormality in arterial blood gas values is a result of the balance between the severity of disease and the degree of compensation by cardiopulmonary system. Normal blood gases do not mean that there is an absence of disease because the homeostatic system can compensate. However, an abnormal arterial blood gas value reflects uncompensated disease that might be life threatening.

Topological variations of the PDP ligand and its prospects in molybdenum(0) dearomatization agents.

The compounds fac-(κ(3)-PDP)Mo(CO)(3) {1; PDP = 2-[[2-(1-(pyridin-2-ylmethyl)pyrrolidin-2-yl)pyrrolidin-1-yl]methyl]pyridine}, [(cis-ß-PDP)Mo(NO)(CO)]PF(6) ([cis-ß-3]PF(6)), [(cis-α-PDP)Mo(NO)(CO)]PF(6) ([cis-α-3]PF(6)), [(cis-α-PDP)Mo(NO)Br]PF(6) ([4]PF(6)), [(trans-PDP)Cu](BF(4))(2)·CH(3)CN ([5](BF(4))(2)·CH(3)CN), and [(trans-PDP)Cu](OSO(2)CF(3))(2) ([5](OSO(2)CF(3))(2)) have been synthesized and structurally characterized by single-crystal X-ray diffraction. These are the first reported complexes of PDP on metal centers other than iron(II). The observed configurations indicate a broader range of accessible PDP topologies than has been reported. The {(cis-α-PDP)Mo(NO)}(+) fragment is found to be less π-basic than the dearomatizing {Tp(MeIm)Mo(NO)} fragment [Tp = hydridotris(1-pyrazolyl)borato; MeIm = 1-methylimidazole].