tailieunhanh - Báo cáo y học: " Dear vasopressin, where is your place in septic shock"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care cung cấp cho các bạn kiến thức về ngành y đề tài: Dear vasopressin, where is your place in septic shock? | Critical Care April 2005 Vol 9 No 2 Duenser and Hasibeder Commentary Dear vasopressin where is your place in septic shock Martin W Duenser1 and Walter R Hasibeder2 1 Resident Division of General and Surgical Intensive Care Medicine Department of Anesthesiology and Critical Care Medicine The Medical University of Innsbruck Austria 2Head Department of Anesthesiology and Critical Care Medicine Krankenhaus der Barmherzigen Schwestern Ried im Innkreis Austria Corresponding author Martin W Duenser csab3987@ Published online 15 November 2004 This article is online at http content 9 2 134 2004 BioMed Central Ltd See review page 212 http content 9 2 212 Critical Care 2005 9 134-135 DOI cc2996 Abstract Cardiovascular failure is one of the central therapeutic problems in patients with severe infection. Although norepinephrine is a potent and in most cases highly effective vasopressor agent very high dosages leading to significant side effects can be necessary to stabilize advanced shock. As a supplementary vasopressor arginine vasopressin can reverse hemodynamic failure and significantly decrease norepinephrine dosages. Whether the promising possibility of bridging advanced septic shock when the benefit risk ratio of catecholamine therapy leaves a clinically tolerable range may improve quantitative and qualitative patient outcome can only be determined by a large prospective randomized study. Cardiovascular failure is one of the central therapeutic problems in patients with severe infection. Current recommendations for the treatment of septic shock include volume therapy and the use of dobutamine and dopamine or norepinephrine 1 . Although particularly norepinephrine is a potent and in most cases highly effective vasopressor agent it cannot stabilize cardiovascular function in some patients with severe hemodynamic failure and sepsis-mediated vascular hyposensitivity to endogenous and exogenous catecholamines 2 . By further increasing