ArticlePhysiological reports2020
Non-invasive hemodynamic profile of early COVID-19 infection.
Article in Physiological reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Echocardiographic assessment of the right ventricle in COVID-19: a systematic review.The international journal of cardiovascular imaging · 2021Pooled it
- COVID-19. Biology, pathophysiology, and immunology: a pathologist view.Pathologica · 2023Review
- Echocardiography in COVID-19 Pandemic: Clinical Findings and the Importance of Emerging Technology.Cardiac electrophysiology clinics · 2022Review
- Cardiac involvement in hospitalized patients with COVID-19 and its incremental value in outcomes prediction.Scientific reports · 2021Article
- The pathogenic role of epithelial and endothelial cells in early-phase COVID-19 pneumonia: victims and partners in crime.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Review
- Non-invasive hemodynamic profile of early COVID-19 infection.Physiological reports · 2020Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionLittle is known about the systemic and pulmonary macrohemodynamics in early COVID-19 infection. Echocardiography may provide useful insights into COVID-19 physiopathology.
methodsTwenty-three COVID-19 patients were enrolled in a medical ward. Gas exchange, transthoracic echocardiographic, and hemodynamic variables were collected.
resultsMean age was 57 ± 17 years. The patients were hypoxemic (PaO
conclusionsIn the early stages of COVID-19 infection the hemodynamic profile is characterized by a hyperdynamic circulatory state with high CI and low SVRI, while the right heart is functionally unaffected. Our findings suggest that hypoxemia, viral sepsis or peripheral shunting are possible mechanisms for the vasodilation that dominates at this stage of the disease and may itself worsen the gas exchange.
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