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治疗 本病属危重急症,需紧急抢救。 体位:坐位,两腿下垂 吸氧:高流量或面罩吸氧,酒精除泡 镇静:吗啡5-10mg皮下或静脉注射 快速利尿:速尿20-40mg静脉注射 治 疗 血管扩张剂:硝普钠12.5-25μg/min或硝酸甘油;血压低者可与多巴胺或多巴酚丁胺合用 洋地黄:用快速洋地黄制剂,如1-2周内未用过洋地黄者,可静注西地兰0.4-0.8mg,2小时后可再给0.2-0.4 mg 其他:氨茶硷解除支气管痉挛;病因治疗;去除诱因 谢 谢 * Angiotensin II is the central molecule of the RAS, with a multitude of actions. Both the antihypertensive and the protective effects of RAS modulators are related to their influence on angiotensin II actions. ACE inhibitors block the conversion of angiotensin I to angiotensin II and also have other substrates including bradykinin, substance P, neurotensin, enkephalin, LHRH, N-acetyl-Ser-Asp-Lys-Pro. The effects on kinins is suggested to be responsible for the cough associated with ACE inhibitors. ACE inhibitors do not block the conversion of Ang I to Ang II by alternative enzymes prominent in heart tissue, such as chymase. Ang II receptor blockers such as valsartan block the action of Ang II directly at its receptor, regardless of synthesis pathway. * In heart failure, angiotensin II activity may play a pathological role. The deleterious effects of angiotensin II are mediated via the AT1 receptor subtype. There is also accumulating evidence that many of the more beneficial actions of angiotensin II are mediated via the AT2 receptor. Therefore selective blockade of the effect of angiotensin II at the AT1 receptor level (whilst leaving the AT2 receptor free for angiotensin II stimulation) may be expected to offer advantages over non specific blockade of the renin angiotensin system (e.g. by ACE inhibitors). * As can be seen, metoprolol and bisoprolol block only one of the damaging pathways, propranolol two of them, whereas carvedilol blocks all three pathways leading from sympathetic activation to cardiotoxicity. Comprehensive adrenergic blockade provided by carvedilol is likely to provide greater protection to the heart from the harmful consequences of sympathetic activation than selective, conventional, adrenergic blockade. * Patients
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