ch. 32: Inotropic drugs
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| this class of drugs combine with sodium potassium ATPase of cardiac cell membrane, inhibiting the Na/K pump. this prevents sodium from being pumped out. as such, sodium levels rise in cardiac cells. xs available Ca released from SR, increasing contractil | glycosides.
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| in the therapeutic index for cardiac glycosides high or low? | low, meanng there is a small difference between the therapeutic dose and the toxic dose. regular monitoring of serum drug levels is necessary.
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| uses of glycosdes? | severe left ventricular systolic dysfunction such as CHF
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| some side effects of glycosides? | change in vision (with objects appearing yellow), AV block, arrhythmias (due to decreased intracellulra potassium).
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| digoxin cannot be used in which patients? | those with liver problems as it relies on the liver for its metabolism.
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| these are beta agonists for the eta one receptor. | dobutamine, dopamine
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| MOA of beta agonsits/ | they bind to the receptor, activating adenyl cyclase, which is the enzyme that converts AMP to cAMP. by activating adenylyl cyclase, much AMP is converted to cAMP, which activates protein kinase.
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| MOA of PDe inhibitors? | PDE normally ocnverts cAMP to AMP. PDE inhibitors stop this conversion, resulting in an increase in intracellular calcium.
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| examples of PDE inhibitors? | inamrinone (amrinone), milrinone
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| all the inotropics have this same final mechanism of action | increase the amount of intracellular calcium so thta greater contractility can occur.
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| what enhances glycoside toxicity? | hypokalemia. a common mode of such hypokalemia is through concominant use of thiazide or loop diuretics.
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