Abstract
Pulmonary hypertension (PH) is the consequence of either acute or chronic diseases resulting in the loss of the low pressure-high flow characteristics of pulmonary circulation. In 1977, Zapol and Snider demonstrated that PH is a physiological hallmark of ARDS as shown by the occurrence of a mean pulmonary arterial pressure (mPAP) > 25 mmHg in 58% of patients with severe ARF in the early phase [1]. In over 100 patients with ARDS, studied from 1–30 days after onset of symptoms, Zapol et al. observed mPAP to be around 22–28 mmHg in absence of severe hypoxemia, and in the range of 28–35 mmHg or more in presence of severe hypoxemia [2].
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Brienza, A., Brienza, N. (2000). Pulmonary Hypertension in ARDS: Management Strategies. In: Gullo, A. (eds) Anesthesia, Pain, Intensive Care and Emergency Medicine — A.P.I.C.E.. Springer, Milano. https://doi.org/10.1007/978-88-470-2286-7_5
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DOI: https://doi.org/10.1007/978-88-470-2286-7_5
Publisher Name: Springer, Milano
Print ISBN: 978-88-470-0095-7
Online ISBN: 978-88-470-2286-7
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