These difficulties are reflected in the fact that patients with vasodilatory shock requiring high-dose vasopressors have a mortality rate approaching 50% at 1 month. However, these agents are not uniformly effective in reversing vasodilatory shock, and their use is associated with significant side effects including limb ischemia and cardiac arrhythmia. In addition to treating the underlying cause of vasodilatory shock, catecholamine (e.g., dopamine, norepinephrine, epinephrine) and non-catecholamine (e.g., vasopressin) vasopressors are agents that combat vasodilatory shock by inducing peripheral vasoconstriction. The most common form of shock is vasodilatory shock, commonly defined as shock in the setting of peripheral vasodilation and intact cardiac output. Shock is defined as any process resulting in insufficient blood pressure to provide adequate organ perfusion. In patients with severe vasodilatory shock (MAP 55-70 despite 0.2ug/kg/min norepinephrine or equivalent), administration of angiotensin II is associated with a 45% absolute increase in MAP response (defined as MAP increase ≥ 10mmHg or MAP > 75mmHg) when compared to placebo. In patients with severe vasodilatory shock requiring high-dose catecholamines, does angiotensin II result in improvement in mean arterial pressure (MAP) compared to placebo?
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