1. Epinephrine (sympathomimetic drug)
    1. MOA:
      1. Low doses: b-receptor agonist
      2. High doses: a-receptor agonist
    2. Indications: cardiac arrest associated with pulseless Vtach and Vfib, asystole, and pulseless electrical activity, severe anaphylactic reactions & anaphylactic shock.
  1. Norepinephrine:  preferentially an alpha agonist which promotes global vasoconstriction. It has fallen to 2nd line agent (compared to dopamine) for circulatory shock because of early reports of renal failure
    1. MOA: at therapeutic range (subtherapeutic ranges will increase CO via B-receptor mediated inotropy) NE stimulates alpha receptors via Gq coupled protein response to promote smooth muscle constriction
      1. OVERALL EFFECT: systemic vasoconstriction
  1. Indications: In cases of septic shock or critical hypotension when dopamine isn’t enough to reach the desired effect, NE can be added on as a second agent.
  2. Dosing: 1mg diluted in 250ml of normal saline with an initial infusion of 1ug/min titrating up to 2 to 4ug/min. NE dose can vary wildly and can range from 0.7 to 210ug/min.
  3. Adverse Effects
    1. Hypoperfusion
    2. Bradycardia
    3. Tremor, restlessness
    4. mental status changes
  1. Phenylephrine – selective sympathomimetic A1-receptor agonist for severe hypotension especially from septic shock, epidurals or subarachnoid anesthetics
    1. The vasoconstrictive effects of phenylephrine can lead to local infiltrative necrosis, thus a central line is preferred if administrating. Phentolamine (an alpha blocker) can be used to counteract these effects.
  1. Ephedrine – a sympathomimetic amine that increases the activity of Norepinephrine at the postsynaptic alpha and beta receptors.
    1. reinforces NE, similar effects and AE
  1. Metaraminol – potent sympathomimetic amine with mostly A1 adrenergic agonist effect with some B activity, used primarily in anesthesia related hypotension.
    1. similar type of drug to NE, similar effects and AE
  1. Dopamine
    1. MOA:
      1. Low Dose (< 3 mcg/kg/min):  Acts on dopamine receptors, dilates renal arteries; renal, mesenteric, and cerebral circulations and increases blood flow in these regions
      2. Intermediate Dose (3-10 mcg/kg/min): activates beta-1-adrenergic receptors in the heart and peripheral circulations, and this produces an increase heart rate and contractility → increase in cardiac output
      3. High Dose (10-20 mcg/kg/min): alpha-receptors in the systemic and pulmonary circulations. This results in increased systemic vascular resistance → progressive vasoconstriction
    2. Indications:
      1. Low dose dopamine preserves renal blood flow and to promote urine output in patients with oliguric acute renal failure
      2. Intermediate and high dose dopamine are good for systemic vasodilation and systemic shock because promote vasoconstriction & preserves cardiac stroke output.
      3. Moderate doses for heart failure (increase contractility; high dose increases afterload/workload ← do not use!)
      4. 2nd line after atropine for bradycardia
    3. Drug Administration:
      1. IV infusion 2-5 mcg/kg/min and titrate to BP, max 20 mcg/kg/min
    4. Adverse Effects:
      1. hypotension, hypertension, tachycardia
      2. chest pain, ectopic beats, vasoconstriction (cold extremities)
      3. nausea, vomiting, headache
      4. tissue necrosis and sloughing with extravasation → give phentolamine
    5. Drug Interactions:
      1. effects potentiated by MAO inhibitors (reduce dopamine dose by 90%)
      2. effects enhanced by tricyclic antidepressants
      3. increased risk of dysrhythmias with general anesthetics
      4. beta-adrenergic effects antagonized by beta blockers
      5. alpha-adrenergic effects antagonized by alpha blockers
    6. Notes
      1. correct hypovolemia before starting (use fluid resuscitation)
      2. monitor BP, pulse, and peripheral pulses every 15 mins
      3. monitor urine output every hour
      4. cardiac monitoring if infusion used
  1. Vasopressin: antidiuretic hormone, vasopressor
    1. MOA: vasoconstricts the smooth muscle in capillaries and small arterioles; reabsorbs water in the collecting ducts of the kidney (concentrates urine)
    2. Indications:
      1. asystole, vfib, pulseless vfib (alternative to 1st/2nd dose of epinephrine during cardiac arrest)
      2. given with norepinephrine in severe septic shock
      3. neurogenic/central diabetes insipidus (DI; treatment or diagnostic test; alternatively, desmopressin can be used, intranasal BID, with less vasopressor effect than vasopressin)
      4. GI hemorrhage from gastric ulcer or esophageal varices
    3. Drug Administration:
      1. cardiac arrest – IV bolus 40 units (can be given intraosseus or via endotracheal tube)
      2. GI bleed – load with 20 units slow IV bolus over 20 minutes → maintain with IV drip infusion 0.2-0.4 units/min, titrated up to 0.9 units/min
      3. DI – subcutaneous (SQ) or intramuscular (IM) 5-10 units, 3-4 times/day
      4. severe septic shock – IV drip infusion 0.03 units/min
    4. Adverse Effects:
      1. Life-threatening – hypertension, angina/MI, heart failure, dysrhythmias, bowel ischemia, TIA/CVA, anaphylaxis
      2. tissue necrosis if IV infiltration happens (catheter dislodged and fluid leaks into surrounding tissue) → give phentolamine
      3. tremor, circumoral and facial pallor, head pounding, water intoxication, sweating, angioneurotic edema
      4. eructations (belching), flatus, nausea, vomiting, heartburn, abdominal/uterine cramps
    5. Drug Interactions:
      1. decreased ADH effects with alcohol, demeclocycline, epinephrine, heparin, lithium, and phenytoin
      2. increased vasopressor effect with guanethidine and neostigmine
      3. increased ADH effects with chlorpropamide, clofibrate, carbamazepine, and thiazide diuretics
    6. Notes
      1. monitor vitals, especially BP, hourly during IV infusion
      2. monitor urine output and specific gravity
      3. look for signs of life-threatening conditions, i.e. MI/TIA
      4. can give IV nitroglycerin at the same time if angina/ischemia develop
      5. look for fluid volume changes, i.e. dehydration or water intoxication, especially in infants or elderly
      6. administer IV infusion through central venous line if possible


  1. Nitroglycerin
    1. MOA: binds to endothelial cells and becomes Nitric Oxide via two chemical reductions, which can cross to the smooth muscle layer promoting the formation of cGMP promoting muscle relaxation. Also inhibits platelet aggregation via g-coupled protein mediated receptor activities.
      1. OVERALL EFFECT: Promotes vasodilation in dose dependent fashion. Low dose = venous effect. Higher doses = arterial effect. As the dose increases the Cardiac output also begins to increase due to vasodilation.
    2. Indications:
      1. Low dose: decrease left ventricular filling
      2. Moderate dose: augment cardiac output
      3. High dose: lower blood pressure.
    3. Dosing: 400ug/ml infused at a rate of 5ug/min and increased at a rate of 5ug/ml every 5 minutes, not exceeding 400ug/min in new patients
    4. Adverse Effects:
      1. Flow related: Nitroglycerin is great at increasing flow to the lungs and brain
        1. Headaches, symptomatic intracranial htn,
        2. If augmented flow occurs at areas that are poorly ventilated = hypoxemia
      2. Methemoglobinemia
        1. metabolism of nitroglycerin can lead to the formation of inorganic nitrates which can lead to the oxidation of hemoglobin to methemoglobin which doesn’t carry oxygen as well.
          1. brown discoloration
          2. cyanosis
          3. mental status changes
          4. exercise intolerance
        2. fix with methylene blue and o2
      3. Solvent Tox: Nitroglycerin requires ethanol or propylene glycol to keep the drug in suspension
        1. mental status changes
        2. hypotension
      4. Nitrate Tolerance: unknown mechanism, but believed to be depletion of reducing agents in the endothelium which impairs conversion. Fix with cutting off nitroglycerin for at least 6 to 8 hours a day.
  1. Nitroprusside
    1. MOA: Same as nitroglycerin, the major difference being the dangers of using nitroprusside as it may be responsible for 1000 deaths yearly.
    2. Toxicology
      1. half of the Nitroprusside molecule is 5 molecules of cyanide. When the nitroprusside molecule is broken down, the only way to clear cyanide is to combine it with a sulfur group from thiosulfate (of which we have small stores) to form thiocyanate which is cleared by the kidneys. Problems therefore arise either when there is too much cyanide or when there are kidney problems leading to thiocyanate.
      2. Just like nitroglycerin, but the responses are rapid and short lived thus allowing for rapid dose titration. Vasodilation effects can be seen at levels as low as 0.5ug/kg/min
    3. Indications:
      1. severe hypertension with low cardiac output and because of the toxic potential of the drug only when there is NOTHING else to use
    4. Dosing
      1. Start low 0.2ug/kg/min titrating up at 5 minute increments to no greater than 10ug/kg/min over a 10 minute period.
      2. Nitroprusside should be coadministered with Sodium Thiosulfate (500mg of Sod. Thiosulfate for every 50mg of Nitroprusside)
    5. Contraindications: like Nitroglycerin, because of it’s effects on flow, Nitroprusside should not be used for intracranial hypertension intracranial encephalopathy.
  1. Morphine sulfate
    1. MOA: opioid analgesic (dilates veins, moderately dilates arteries, analgesic effect through mu receptors)
    2. Indications:
      1. chest pain in acute coronary syndrome
      2. acute pulmonary edema with cardiac origin
    3. Drug Administration:
      1. slow IV push – 2-4 mg, repeated at 5-15 minute intervals (cardiac); or 2-10 mg q4h prn
      2. PO – 10-30 mg q4h in adults
      3. IM – 5-20 mg q4h prn (noncardiac)
    4. Adverse Effects:
      1. drowsiness (fall risk), mental clouding, anxiety reduction, euphoria, disorientation
      2. orthostatic hypotension
      3. respiratory depression
      4. constipation
      5. urinary retention (sphincter is constricted)
      6. cough suppression
      7. biliary colic (Sphincter of Oddi is constricted)
      8. nausea, emesis
      9. miosis (pupils are constricted)
    5. Drug Interactions:
      1. CNS depression can be potentiated with other narcotics, alcohol, barbiturates, and benzodiazepines
      2. anticholinergic effects (i.e. constipation, urinary retention) can be potentiated with antihistamines, tricyclic antidepressants, and atropine
      3. hypotension if combined with other anti-hypertensive drugs or vasodilators
    6. Notes:
      1. monitor the blood pressure before giving the drug; do not give if systolic BP < 100 mmHg or 30 mmHg below baseline
      2. monitor the respiratory rate before giving the drug
      3. reassess pain after giving the drug
      4. monitor for respiratory depression and hypotension often up to 24 hours later
      5. overdose treatment – ventilatory support and opiate antagonist, i.e. naloxone
      6. tolerance and physical dependence may develop
  1. Amrinone: is a phosphodiesterase inhibitor that has is both a vasodilator and a positive inotropic agent. It has not been shown to be a superior single-action cardiotonic agent like dobutamine.
    1. MOA:
      1. increase in cardiac stroke output, w/o increase in cardiac stroke work
      2. effect on cardiac performance similar to dobutamine
      3. can be used to add to the effects of dobutamine
    2. Indications
      1. management of low output states caused by systolic heart failure
      2. most often used as second agent added to case refractory heart failure
    3. administration
      1. should not be used with dextrose-containing fluids; will be degraded
      2. should be protected from light
      3. loading dose 0.75-1.5mg/Kg, followed by continuous infusion of 5-10ug/kg/min
    4. adverse effects
      1. thrombocytopenia
      2. hypotension due to vasodilation
    5. contraindications
      1. patients with hypertrophic cardiomyopathy
      2. thrombocytopenia
  1. Dobutamine
    1. MOA: primarily a beta-1-adrenergic receptor agonist (cardiac stimulation), but it also has mild b-2 effects (vasodilation).
      1. low dose: positive inotropic effect (increased force of contraction)
      2. high dose: stronger B1 effect leading to positive inotropy but also includes a stronger B2 effect leading to vasodilation.
    2. Indications: Acute management of low output states secondary to systolic heart failure like cardiogenic shock. Doesn’t raise MAP, so not used as monotherapy for heart failure
    3. Administration: IV infusion: 2 – 20 mcg/kg/min continuous infusion by pump
    4. Adverse Effects: headaches, tremors, paresthesias, cramps, increased BP. Signs of Toxicity include; fatigue, angina, tachycardia.
  1. Labetalol
    1. MOA: beta blocker (blocks B1 receptor activity in the heart–negative inotropic, negative chronotropic–that also blocks A1 receptor activity → resulting in smooth muscle relaxation.)
      1. OVERALL EFFECT: dose related decrease in blood pressure without reflex tachycardia or increase in cardiac output
    2. Indications:
      1. severe hypertension without increase in cardiac output
      2. hypertension caused by excessive catecholamines, like would be the case in post-operative patients
      3. aortic dissection because it’s an antihypertensive that doesn’t increase cardiac output
    3. Drug Administration: 5mg/ml
      1. Bolus Therapy: supine position, initial dose of 20mg with repeat doses of 40mg every 10 minutes. Manufacturer recommends no more than 300mg but it has been used to greater than that without ill effect.
      2. Continuous Injection: initial dose of 20mg because of the longer halflife requires more half lives 5 to 6 to reach steady state concentration
    4. Adverse Effects:
      1. orthostatic Hypotension because of a-blockade
      2. myocardial depression because of b1-blockade
      3. bronchospasm because of b2-blockade
      4. avoid in heart failure or asthma


Kee, V.R. (2003, August). Hemodynamic pharmacology of intravenous vasopressors. Critical Care Nurse. Retrieved from

(2009, April 5). Hemodynamic drugs. Intensive Care Unit: Emergency Diagnosis and Treatment. Retrieved from

Hemodynamic medications. Truman State University. Retrieved from

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