Used to produce vasoconstriction and cardiac stimulation as an adjunct to correct hemodynamic imbalances in the treatment of shock that persists after adequate fluid volume replacement. (See Hypovolemia under Cautions.)
If severe peripheral vasoconstriction exists, norepinephrine may be ineffective and may have a deleterious effect by causing further reductions in plasma volume and blood flow to vital organs.
Value of pressor therapy in shock, especially when due to septicemia, burns, trauma, or drug overdosage, is questionable, either because the effectiveness has not been proved or because vasoconstriction caused by the drug may adversely affect the patient.
May be indicated if patient fails to respond to administration of fluids, a change in position, or other measures directed to the specific cause of shock such as anti-infectives in septicemia, epinephrine in anaphylactic shock, or specific antidotes and/or removal of the drug in cases of drug overdosage.
Pressor therapy in overdosage of barbiturates or other sedatives is especially controversial; some clinicians have stated that the incidence of mortality may actually be increased when a pressor is given.
May be useful to control shock following pheochromocytomectomy, but shock generally can be prevented by maintenance of adequate blood volume and/or preoperative administration of an α-adrenergic blocking agent.
May be used as an adjunct in the management of shock resulting from sympathectomy or poliomyelitis.
Epinephrine is the drug of choice in the emergency treatment of severe acute anaphylactic reactions, including anaphylactic shock.
Once adequate ventilation is assured, maintenance of blood pressure in patients with anaphylactic shock may be achieved with other pressor agents, such as norepinephrine.
In hypotension associated with MI, cautious administration of norepinephrine may be of value and some clinicians consider it to be the pressor drug of choice.
This type of shock generally has a poor prognosis even when pressor agents are used, and norepinephrine-induced increases in myocardial oxygen demand and the work of the heart may outweigh the beneficial effects of the drug.
Cardiac arrhythmias due to norepinephrine are more likely to occur in patients with MI.
May be used for ACLS as an adjunct to maintain adequate BP when severe hypotension (e.g., SBP <70 mm Hg) and low total peripheral resistance persist and renal and cerebral perfusion remain inadequate after an effective heartbeat, palpable pulse, and ventilation have been established by other means.
Exhibits both positive inotropic and vasoconstrictive activity; therefore, may be particularly useful in elevating systolic arterial pressures to 70–100 mm Hg. Once such elevations are achieved, dopamine therapy can be initiated.
Relatively contraindicated in patients with hypovolemia.
Use cautiously in patients with ischemic heart disease because it may increase myocardial oxygen requirements.
May be used to treat hypotension occurring during spinal anesthesia, but other vasopressors having a longer duration of action and which can be administered IM such as metaraminol, methoxamine, or phenylephrine are more commonly used.
May be used to treat hypotension occurring during general anesthesia; however, the possibility of cardiac arrhythmias should be considered. (See Anesthetics, general under Interactions.)
If a vasopressor is required, norepinephrine should not be used in obstetric patients (see Pregnancy under Cautions); ephedrine usually is preferred.
May be added to solutions of some local anesthetics to decrease the rate of vascular absorption of the anesthetic, thereby localizing anesthesia and prolonging the duration of anesthesia.
Decreases risk of systemic toxicity due to the local anesthetic.
Not as potent as epinephrine and must be used in higher concentrations to prolong local anesthetic effects; epinephrine is more commonly used for this purpose.
Has been used with some success intraperitoneally† or via a nasogastric tube† as a hemostatic agent for severe upper GI bleeding†.
Has been used to increase cardiac output by increasing ventricular emptying and temporarily increasing cardiac filling pressure in pericardial tamponade†.
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