Vasopressors and Inotropes

alpha receptors

• location: systemic vasculature

• action: vasoconstriction

• effect: increases SVR

beta 1 receptors

• location: myocardium

• action: increases HR and contractility

• effect: increases CO

beta 2 receptors

• location: systemic vasculature

• action: vasodilation

• effect: decreases SVR

norepinephrine (levophed) action

• potent alpha effects with moderate beta effects

• primary action is vasoconstriction → increases SVR

• secondary action is increased cardiac contractility and HR → increases CO

norepinephrine (levophed) doses

• 2-30 mcg/min

• 0.05-0.5 mcg/kg/min

norepinephrine (levophed) uses

• clear drug of choice for septic shock

  • mortality benefit demonstrated over dopamine

• suggested drug of choice for undifferentiated and cardiogenic shock

note: potential rate limiting tachycardia/tachyarrythmias

phenylephrine (neosynephrine) action

• pure alpha agonist

• causes vasoconstriction → increased SVR

• unopposed alpha effects can lead to significant ischemia

phenylephrine (neosynephrine) dose

• 20-200 mcg/min

• bolus dose: 100-200 mcg q3-5 min

phenylephrine (neosynephrine) uses

• septic shock in pt who do not tolerate norepi

• anesthetic induced hypotension

• shock in pt with aortic/mitral stenosis

note: least arrythmogenic and risk for reflex bradycardia

vasopressin (vasostrict) action

• V1 receptor → vasoconstrictors vascular smooth muscles → increases SVR

• V2 receptor → reabsorbs water from renal collecting duct → decreases UOP

phenylephrine (neosynephrine) dose

0.03 u/min

phenylephrine (neosynephrine) uses

• adjuct to norepi in refractory shock

• does not provide morbidity/mortality benefit

• reduces norepi requirement

• best for patients with aortic/mitral stenosis, pulmonary HTN, GI hemorrhage

notes: preserved effect in severe acidosis, not arrythmogenic

epinephrine (adrenalin) action

• potent alpha and beta activity

• vasoconstriction → increases SVR

• increased contractility and HR → increased CO

epinephrine (adrenalin) dose

• 1-20 mcg/min

• .01-0.5 mcg/kg/min

epinephrine (adrenalin) uses

• refractory shock, adjunct 2nd or 3rd line agent

• consider in pt with cardiogenic shock component

• drug of choice in anaphylaxis

• also used in cardiac arrest

note: increased arrythmogenicity, can cause hyperglycemia and lactatemia d/t inhibition of insulin secretion and promotion of glycogenolysis and inhibition of glycogen production

epinephrine (adrenalin) dose for anaphylaxis

0.3 mg IM - use 1 mg/1 mL vial or EpiPen

epinephrine (adrenalin) dose for cardiac arrest

1 mg IV - use 1 mg/10 mL emergency syringe

dobutamine (dobutrex) action

• potent beta 1 and beta 2 with minimal alpha activity

• increased contractility and HR → increased CO

• systemic vasodilation → decreases SVR

dobutamine (dobutrex) doses

• 2.5-20 mcg/kg/min

• usual inotropic range: 5-10 mcg/kg/min

dobutamine (dobutrex) use

• shock with decreased CO

• patients with decompensated HF

notes: can cause hypotension so best to start with low doses and titrate up and if patient is hypotensive, if patient is hypotensive consider starting vasopressor (norepi) first, high arrythmogenicity with highest doses >10 mcg/kg/min, increases myocardial O2 demand

milrinone (primcor) use

• phosphodiesterase-3 inhibitor

• increases intracellular cAMP → activation of calcium channels

• increased contractility and HR → increased CO

• systemic vasodilation → decreased SVR

milrinone (primcor) dose

• loading dose: 50 mcg/kg over 10 min

• 0.125-0.75 mcg/kg/min

milrinone (primcor) uses

• shock with decreased CO

• pt with decompensated HF

note: renal elimination and half life of 2-3 hours, hard to titrate for acutely unstable patients, high arrythmogenicity, increases myocardial O2 demand

administration of vasopressors

• PIV not recommended d/t risk of infiltration and extravasation injury

• if no central access available, appropriate to start vasopressors peripherally

• short term PIV use has been found to be minimal risk

• use largest PIV site

• use least concentrated formulation of whichever agent is most appropriate based on patient scenario

• once pt stabilized, work on obtaining central access, ideally within 6-12 hours of starting vasopressors

management of extravasation

• extravasation of vasopressors can result in severe ishemia injury and tissue necrosis

• antidotes: phentolamine, nitroglycerin ointment

phentolamine

• alpha blocker

• antidote for extravasation

• drug of choice

• 5-10 mg diluted in 10 mL flush

• inject locally in affected area

nitroglycerin ointment

• antidote for extravasation

• described for mild extravasation injuries

• apply to affected area

key points

• ongoing assessment of fluid status and maintaining euvolemia is critical

• hypoxia and acidemia may blunt effects of catecholamine vasopressors and inotropes

• vasopressins effects are preserved

• hypocalcemia may lead to inadequate response

• replete patients with hypocalceia

• consider empiric calcium in patients receiving multiple blood transfusions