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Systemic blood pressure is determined by systemic vascular resistance (SVR) and cardiac output. Inotropes increase cardiac contractility and cardiac output via stimulation of beta1-receptors in the heart. 
Catecholamines mediate their cardiovascular actions predominately through 3 types of receptors: 1) alpha-adrenergic, 2) beta-adrenergic, and 3) dopaminergic. Dopamine displays dose-related receptor activity, targeting dopaminergic receptors at low doses, dopaminergic and beta-receptors at mid-range doses, and shifting to beta- and (preferentially) alpha-receptor stimulation at high doses. Dobutamine is a synthetic catecholamine with a strong affinity for both beta1- and beta2-receptors. Epinephrine is a potent nonselective alpha- and beta-agonist. Its beta effects predominate at lower doses, while alpha1-mediated vasoconstriction predominates at high doses. Isoproterenol is a potent nonselective beta-agonist with a very low affinity for alpha-receptors.  
Milrinone is a phosphodiesterase inhibitor (PDI) distinct from other inotropes. PDIs increase cyclic adenosine monophosphate (cAMP) by inhibiting breakdown within cardiac and vascular muscle cells, which leads to an increase in myocardial contractility. 
Receptor Pharmacology of Catecholamines    
0.5 to 5
5 to 10
10 to 20
0.01 to 0.1
0.1 to 0.2
*Dose listed for dose-related receptor activity only
Locations and Responses of Select Receptors   
vascular smooth muscle
positive inotropy and chronotropy
vascular and bronchial smooth muscle
renovascular smooth muscle
Inotropes may decrease blood pressure and induce hypotension; vasodilatory effects are most common with milrinone and less likely with dobutamine and low-dose dopamine.  Similar to vasoconstrictors, inotropic agents can induce arrhythmias and myocardial ischemia by increasing myocardial oxygen consumption. Beta-agonists and phosphodiesterase inhibitors (PDIs) increase myocardial oxygen consumption by increasing heart rate and contractility. Risk of tachycardia and tachyarrhythmias is generally highest with dopamine and lowest with milrinone, although milrinone can cause reflex tachycardia. 
Catecholamines may have potentially harmful effects on pituitary hormone secretion and immune function; these effects appear to be greatest with dopamine.     
Epinephrine can increase blood glucose and lactate concentrations via stimulation of beta-receptors.  Beta2-agonists such as isoproterenol and dobutamine can decrease serum potassium concentrations.
In general, antihypertensives decrease the response to sympathomimetics. The cardiac effects of dopamine are antagonized by beta-blockers. However, beta-blockers may potentiate the pressor and arrhythmogenic effects of epinephrine. 
Halogenated anesthetics increase cardiac autonomic irritability and may sensitize the myocardium to the action of intravenous catecholamines resulting in ventricular arrhythmias.   
Use sympathomimetic amines with caution in patients taking monoamine oxidase inhibitors (MAOIs), including linezolid, due to the risk of severe, prolonged hypertension; reduce the initial inotropic dose and carefully titrate. In general, do not use sympathomimetic agents concurrently or within 14 days of an MAOI due to an increased risk of hypertensive crisis.    
Use sympathomimetic amines with caution in patients taking tricyclic antidepressants due to the risk of severe, prolonged hypertension.
Correct hypovolemia by restoring blood volume with a suitable plasma expander or whole blood before inotrope administration; inotropes will worsen tachyarrhythmias and induce ischemia if preload is inadequate. 
Milrinone has the potential to cause hypotension based on its mechanism of action; avoid loading doses, and decrease the initial maintenance dose in patients with hypotension, if necessary. Vasodilatory effects are most common with milrinone and less likely with dobutamine and low-dose dopamine and more likely in patients with hypovolemia or low systemic vascular resistance (SVR).
Milrinone is primarily eliminated by the kidneys and requires dosage adjustment in those with renal insufficiency. 
Use phosphodiesterase inhibitors and sympathomimetic amines with beta effects with caution in patients with severe aortic or pulmonary valve stenosis; severe myocardial ischemia may occur.
Patients with a pheochromocytoma may experience a greater sensitivity to the adverse effects of catecholamines.
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