Effect of volume expansion on systemic hemodynamics and central and arterial blood volume in cirrhosis☆
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2017, Digestive and Liver DiseaseCitation Excerpt :From a pathophysiological viewpoint, portal hypertension and arteriolar vasodilatation are the key factors, leading to the hyperdynamic circulation [1]. Total blood volume (TBV) and plasma volume (PV) are increased, whereas the central and arterial blood volume (CBV) is decreased, causing an activation of the renin–angiotensin–aldosterone system (RAAS) and the sympathetic nervous system (SNS) [2,3]. The abnormal distribution of blood volume is further characterized by severe splanchnic congestion with a marked increase in splanchnic blood volume [4].
Comparison Between 2 Strategies of Fluid Management on Blood Loss and Transfusion Requirements During Liver Transplantation
2017, Journal of Cardiothoracic and Vascular AnesthesiaThe Hemostatic and Hematopoietic System in Liver Disease
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2016, Critical Care ClinicsClinical implications of the hyperdynamic syndrome in cirrhosis
2014, European Journal of Internal MedicineCitation Excerpt :The splanchnic vasodilation in cirrhosis precedes the increase in cardiac output and heart rate [18]. However, when the splanchnic vasodilatation becomes more pronounced, the hyperdynamic circulation may no longer be sufficient for correcting hypovolemia [12,17] (Fig. 2). Central arterial blood volume (heart, lungs, and central arterial tree blood volume) is more often decreased, while the non-central blood volume (splanchnic) is usually increased in cirrhotics.
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Supported by The John and Birthe Meyer Foundation and The Danish Hospital Foundation for Medical Research, Region of Copenhagen, The Faroe Islands, and Greenland. Søren Møller holds a research fellowship at the University of Copenhagen, Copenhagen, Denmark.