Dopamine vs. Dobutamine

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  1. Both used to support hypotensive patients as positive inotropic agents
  2. Endogenous catecholamines and dobutamine have different effects on alpha, beta-1 and beta-2 receptors
    1. alpha-1 receptors are postsynaptic and located in the vascular smooth muscle causing vasoconstriction or in the myocardium causing weak positive inotropic and negative chronotropic responses
    2. alpha-2 receptors are presynatpic and generally decrease the sympathetic response by decreasing the amount of norepinephrine released by neuron stimulation
    3. beta-1 adrenergic receptors are located in the myocardium and are responsible for positive inotropic and chronotropic effects when stimulated
    4. beta-2 receptors are in the smooth muscle and facilitate vasodilation and are also found on the sinoatrial node causing increased chronotropic response
    5. dopamine receptors are in vascular smooth muscle and cause vasodilation when stimulated (greatest effect in renal, mesenteric, coronary, and cerebrovascular beds)
    6. dopamine-2 (D2) receptors cause inhibition of norepinephrine release and are found on postganglionic sympathetic nerve terminals but are not located on smooth muscle and therefore their effects seem to mostly be related to inhibition of sympathetic activity notably a decrease in heart rate and systemic vascular resistance
  3. dobutamine is mostly a beta-1 selective synthetic catecholamine with mild alpha-1 and beta-2 activity and therefore has mostly positive inotropic and chronotropic effects on the heart; dobutamine will often increase cardiac output with less tachycardia and arrhythmia than dopamine
  4. dopamine activates D1 receptors (1 microgram/kg up) leading to vasodilation; at higher doses dopamine also activates D2 receptors which inhibits the release of norepinepherine enhancing the dilation effect; dopamine also activates beta-1 receptors in the heart at doses of 2-10 micrograms/kg (not as much as dobutamine) and at higher doses (>10 micrograms/kg) activates alpha-1 receptors leading to vasoconstriction mimicking the action of catecholamines
  5. other inotropic drugs
  6. Dosage and administration
    1. Dobutamine-3 to 15 mcg/kg/min for cardiac output augmentation in normotensive patients, higher dose can be used ( up to 200 mcg/kg/min); not to be administrated with alcaline solutions
    2. Dopamine- 3 to 10 mcg/kg/min for cardiac output augmentation; > 10 mcg/kg/min for hypotension; not to be administrated with alcaline solutions

vasopressin= 0.01- 0.03 U /min- adjuvant to norepinephrine in septic shock

    1. amrinone – acts by inhibiting phosphodiesterase type III which results in increased cAMP in the myocardium and vascular smooth muscle; does not interact with alpha or beta receptors
    2. norepinephrine – catecholamine with large alpha-1 and mild beta-1 stimulation causing increase in heart rate and contractility and increases in smooth muscle and gland activity (similar to dobutamine)
    3. epinephrine – catecholamine with large alpha-1 and beta-1 stimulation (balanced alpha and beta activity) as well as some beta-2 stimulation
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