Vasopressors discontinuation

Inspect die needle site and surrounding tissues at frequent intervals for leakage (extravasation, infiltration) of die solution into die subcutaneous tissues surrounding die needle site If eitiier situation occurs, establish anotiier IV line immediately, discontinue the IV containing the vasopressor, and... 

Vasopressin levels are increased during hypotension to maintain blood pressure by vasoconstriction. However, there is a vasopressin deficiency in septic shock. Low doses of vasopressin increase MAP, leading to the discontinuation of vasopressors. However, routine use of vasopressin is not recommended because of lack of evidence of efficacy. Vasopressin is a direct vasoconstrictor without inotropic or chronotropic effects and may result in decreased cardiac output and hepatosplanchnic flow. Vasopressin use may be considered in patients with refractory shock despite adequate fluid resuscitation and high-dose vasopressors.24,27-28... 

Discontinue antihypertensive medications IV fluids to maintain systolic blood pressure greater than 80-90 mm Hg or vasopressor support with an a-agonist such as phenylephrine as indicated. 

Plasma volume depletion Prolonged use of vasopressors may result in plasma volume depletion correct this by appropriate fluid and electrolyte replacement therapy. If plasma volumes are not corrected, hypotension may recur when these drugs are discontinued. 

Discontinue these drugs if possible Intravascular volume expansion and/or vasopressors... 

Therapy with vasopressors and inotropes is continued until the myocardial depression and vascular hyporesponsive-ness of septic shock improve, usually measured in hours to days. Discontinuation of vasopressor or inotropic therapy should be executed slowly therapy should be "weaned" to avoid a precipitous worsening in regional and systemic hemodynamics. 

I. Pharmacology. Norepinephrine is an endogenous catecholamine that stimulates mainly alpha-adrenergic receptors. It is used primarily as a vasopressor to increase systemic vascular resistance and venous return to the heart. Norepinephrine is also a weak beta-1-adrenergic receptor agonist, and it may increase heart rate and cardiac contractility in patients with shock. Norepinephrine is not effective orally and is erratically absoihed after subcutaneous injection. After intravenous administration, the onset of action is nearly immediate, and the duration of effect is 1-2 minutes after the infusion is discontinued. 

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