Background: Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic, many individuals have reported persistent symptoms and/or complications lasting beyond 4 weeks, which is now called post-COVID-19 syndrome. SARS-CoV-2 is a respiratory coronavirus that causes COVID-19, and injury to the lungs is expected; however, there is often damage to numerous other cells and organs, leading to an array of symptoms. These long-term symptoms occur in patients with mild to severe COVID-19; currently, there is limited literature on the potential pathophysiological mechanisms of this syndrome.Objectives: The purpose of this integrative review is to summarize and evaluate post-COVID-19 syndrome from a biological perspective.Methods: An integrative review was conducted using Whittemore and Knafl's methodology for literature published through August 30, 2021. The PubMed, CINAHL, and Web of Science databases were searched for articles published as of August 30, 2021, using combinations of the following key words: post-COVID-19 syndrome, post-SARS-CoV-2, long COVID-19, long COVID-19 syndrome, and pathophysiology of post-COVID-19. Data were analyzed using the constant comparison method.Results: The search generated 27,929 articles. After removing duplicates and screening abstracts and full-text reviews, we retained 68 articles and examined 54 specific articles related to the pathophysiology of post-COVID-19 syndrome. The findings from our review indicated that there were four pathophysiological categories involved: virus-specific pathophysiological variations, oxidative stress, immunologic abnormalities, and inflammatory damage.Discussion: Although studies examining the pathophysiology of post-COVID-19 syndrome are still relatively few, there is growing evidence that this is a complex and multifactorial syndrome involving virus-specific pathophysiological variations that affect many mechanisms but specifically oxidative stress, immune function, and inflammation. Further research is needed to elucidate the pathophysiology, pathogenesis, and longer term consequences involved in post-COVID-19 syndrome.

Background: High-output heart failure (HF) is a type of HF characterized by signs and symptoms of HF and a cardiac output of 8 L/min or greater or a cardiac index greater than 3.9 L/min/m 2 . High-output HF occurs secondary to an underlying condition that requires high cardiac output due to an increase in oxygen consumption or decreased systemic vascular resistance. Obesity is a major cause of high-output HF, yet there is limited research on obesity-related high-output HF. Thus, the pathophysiologic mechanisms of this syndrome are not fully understood. Objective: The objectives of this integrative review were to describe the current state of the research regarding obesity-related highoutput HF and to recommend direction for future research. Methods: We conducted an integrative review focusing on the peer-reviewed literature on patients with obesity-related high-output HF using Whittemore and Knafl's methodology. MEDLINE, CINAHL, and EMBASE electronic databases were searched for all publications indexed in the databases as of March 9, 2022. A narrative synthesis of definitions and symptoms, obesity as an underlying condition, pathophysiology, and treatments of obesity-related high-output HF was completed. Results: A total of 6 articles were included in the integrative review, with 1 nonexperimental, retrospective study and 5 literature reviews. Understanding of obesity-related high-output HF is very limited because of scant empirical evidence in the existing literature. Possible pathophysiologic mechanisms include increased pressure in the upper airways, adipokine dysregulation, increased metabolic activity, and insulin resistance. Conclusion: Additional research is needed on the pathophysiologic mechanisms of obesity-related high-output HF to begin investigations on therapeutic interventions to improve health outcomes.