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Author: Admin | 2025-04-28
And administered by continuous infusion. The initial dose for adults is 1 μg/min titrated to the desired hemodynamic response (2 to 10 μg/min).In Cardiac ArrestDuring cardiac arrest epinephrine may be administered by continuous infusion. The dose should be comparable to the standard IV dose of epinephrine (1 mg every 3 to 5 minutes). This is accomplished by adding 1 mg of epinephrine hydrochloride to 250 mL of normal saline or D5W to run at 1 μg/min and increased to 3 to 4 μg/min. Continuous infusions of epinephrine should be administered by central venous access to reduce the risk of extravasation and to ensure good bioavailability.VasopressinVasopressin is the naturally occurring antidiuretic hormone. In unnaturally high doses—much higher than those needed for antidiuretic hormone effects—vasopressin acts as a nonadrenergic peripheral vasoconstrictor. Vasopressin acts by direct stimulation of smooth muscle V1 receptors. This smooth muscle constriction produces a variety of effects, including pallor of the skin, nausea, intestinal cramps, desire to defecate, bronchial constriction, and in women, uterine contractions. Vasopressin, given intra-arterially, is an approved treatment for bleeding esophageal varices, because it causes vasoconstriction. Vasopressin also dispels bowel gas shadows during abdominal angiography by causing gastrointestinal smooth muscle constriction. It is usually not recommended for conscious patients with coronary artery disease because the increased peripheral vascular resistance may provoke angina pectoris. The half-life of vasopressin in animal models with an intact circulation is 10 to 20 minutes, which is longer than that of epinephrine during CPR.Endogenous vasopressin levels in patients undergoing CPR are significantly higher in patients who survive than in patients who do not have ROSC.36 37 This finding suggested that exogenous vasopressin might be beneficial during cardiac arrest. After a short duration of ventricular fibrillation, vasopressin during CPR increased coronary perfusion pressure,38 vital organ blood flow,39 ventricular fibrillation median frequency,40 and cerebral oxygen delivery.41 Similar results were found with prolonged cardiac arrest and pulseless electrical activity. Vasopressin did not result in bradycardia after ROSC.39Interaction of vasopressin with V1 receptors during CPR causes intense peripheral vasoconstriction of skin, skeletal muscle, intestine, and fat with relatively less constriction of coronary and renal vascular beds and vasodilatation of the cerebral vasculature.42 43 Vasopressin produces no skeletal muscle vasodilatation or increased myocardial oxygen consumption during CPR because it has no β-adrenergic activity. A combination of vasopressin and epinephrine versus vasopressin alone resulted only in comparable left ventricular myocardial blood flow but significantly decreased cerebral perfusion.44 Although vasopressin during CPR decreased catecholamine plasma levels in swine45 and humans,46 it remains to be determined whether it decreases myocardial oxygen consumption as well. Laboratory studies indicate that the same vasopressin dosage may be administered intravenously47 48 and intraosseously.49Repeated doses of vasopressin were more effective than epinephrine in maintaining coronary perfusion pressure above the critical threshold that correlates with successful ROSC.45 In the postresuscitation period, vasopressin produces no increased myocardial oxygen demand because baroreceptor-mediated bradycardia in response to transient hypertension remains intact. A reduction in cardiac index in the postresuscitation phase is transient and fully reversible without administration of
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