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Pathophysiology of Deep Vein Thrombosis and Pulmonary Embolism: Beyond Virchow’s Triad

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Handbook for Venous Thromboembolism

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Abstract

Deep vein thrombosis (DVT) and pulmonary embolism (PE) result from a combination of pathophysiological states including endothelial injury, stasis, inflammation, and hypercoagulability. The extent of the PE, the patient’s underlying cardiopulmonary reserve, and compensatory neurohumoral adaptations determine the overall hemodynamic impact. The right ventricle (RV) plays a central role in PE pathophysiology. A sudden increase in RV afterload due to PE can lead to RV dilation and hypokinesis, RV ischemia, and ultimately acute RV failure.

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Authors and Affiliations

  1. Cardiovascular Division, Harvard Medical School Brigham and Women’s Hospital, Boston, Massachusetts, USA

    Gregory Piazza

  2. Department of Pharmacy Services, Brigham and Women’s Hospital, Boston, Massachusetts, USA

    Benjamin Hohlfelder

  3. Thrombosis Research Group, Harvard Medical School Brigham and Women’s Hospital, Boston, Massachusetts, USA

    Samuel Z. Goldhaber

Authors
  1. Gregory Piazza
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  2. Benjamin Hohlfelder
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  3. Samuel Z. Goldhaber
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© 2015 Springer International Publishing Switzerland

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Piazza, G., Hohlfelder, B., Goldhaber, S.Z. (2015). Pathophysiology of Deep Vein Thrombosis and Pulmonary Embolism: Beyond Virchow’s Triad. In: Handbook for Venous Thromboembolism. Springer, Cham. https://doi.org/10.1007/978-3-319-20843-5_3

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  • DOI: https://doi.org/10.1007/978-3-319-20843-5_3

  • Publisher Name: Springer, Cham

  • Print ISBN: 978-3-319-20842-8

  • Online ISBN: 978-3-319-20843-5

  • eBook Packages: MedicineMedicine (R0)

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