Term
| ACLS 2006 Mechanism of Action for Epinephrine |
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Definition
| Has a-adrenergic effects, i.e. vasoconstriction. Vasoconstriction increases cerebral and coronary blood flow during CPR as mean arterial pressure and aortic diastolic pressure are increased. |
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Term
| ACLS 2006 Mechanism of Action for Atropine |
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Definition
| Reverses cholinergic-mediated decreases in heart rate, systemic vascular resistance, and blood pressure. |
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Term
| ACLS 2006 Mechanism of Action for Lidocaine |
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Definition
| Ventricular excitability is depressed and the stimulation threshold of the ventricle is increased during diastole. The sinoatrial node is, however, unaffected. |
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Term
| ACLS 2006 Mechanism of Action for Procainamide |
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Definition
| Procainamide depresses the excitability of cardiac muscle to electrical stimulation, and slows conduction in the atrium, the bundle of His, and the ventricle. The refractory period of the atrium is considerably more prolonged than that of the ventricle. |
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Term
| ACLS 2006 Mechanism of Action for Vasopressin. |
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Definition
| Non-adrenergic peripheral vasoconstrictor that causes coronary and renal vasoconstriction. (pg 49) Overall vasopressin effects have not been shown to differ from epinephrine. |
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Term
| ACLS 2006 Mechanism of Action for Adenosine. |
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Definition
| Increases AV block and will terminate approximately 90% of reentry arrhythmias within 2 minutes. Adenosine will not terminate atrial flutter or atrial fibrillation but will slow AV conduction, allowing for identification of flutter or fibrillation waves. |
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Term
| ACLS 2006 Mechanism of Action for Magnesium. |
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Definition
| Magnesium (Mg++) is an important cofactor for enzymatic reactions and plays an important role in neurochemical transmission and muscular excitability. As a nutritional adjunct in hyperalimentation, the precise mechanism of action for magnesium is uncertain. |
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Term
| ACLS 2006 Mechanism of Action for Sodium Bicarbonate. |
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Definition
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Term
| ACLS 2006 Mechanism of Action for Morphine. |
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Definition
-Produces central nervous system analgesia, which reduces the adverse effects of neurohumoral activation, catecholamine release, and heightened myocardial oxygen demand.
-Produces venodilation, which reduces left ventricular (LV) preload and oxygen requirements.
-Decreases systemic vascular resistance, thereby reducing LV afterload.
-Helps redistribute blood volume in patients with acute pulmonary edema. |
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Term
| ACLS 2006 Mechanism of Action for Norepinephrine. |
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Definition
| Norepinephrine functions as a powerful peripheral vasoconstrictor (alpha-adrenergic action) and as a potent inotropic stimulator of the heart and dilator of coronary arteries (beta-adrenergic action). Both of these actions result in an increase in systemic blood pressure and coronary artery blood flow. Cardiac output will vary reflexly in response to systemic hypertension but is usually increased in hypotensive man when the blood pressure is raised to an optimal level. In myocardial infarction accompanied by hypotension. norepinephrine usually increases aortic blood pressure, coronary artery blood flow, and myocardial oxygenation, thereby helping to limit the area of myocardial ischemia and infarction. Venous return is increased and the heart tends to resume a more normal rate and rhythm than in the hypotensive state. |
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Term
| ACLS 2006 Mechanism of Action for Dopamine. |
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Definition
| Exerts an inotropic effect on the myocardium resulting in an increased cardiac output. Dopamine produces less increase in myocardial oxygen consumption than isoproterenol and its use is usually not associated with a tachyarrhythmia. Clinical studies indicate that dopamine at low and intermediate therapeutic doses usually increases systolic and pulse pressure with either no effect or a slight increase in diastolic pressure, and total peripheral resistance is usually unchanged. |
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Term
| ACLS 2006 Mechanism of Action for Dobutamine. |
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Definition
| Direct-acting inotropic agent whose primary activity results from stimulation of the b-receptors of the heart while producing less marked chronotropic, hypertensive, arrhythmogenic or vasodilatory effects. |
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Term
| ACLS 2006 Mechanism of Action for Isoproterenol. |
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Definition
| B-agonist activity, positive influence on contractility. |
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Term
| ACLS 2006 Mechanism of Action for Nitroglycerin. |
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Definition
| Produces generalized vasodilation, thereby decreasing venous return and workload on the heart. Both arterial and venous dilation occur, although venous effects predominate. Coronary vasodilation also occurs even in the presence of atherosclerosis. Relaxation of vascular smooth muscle is a result of stimulation of cyclic guanosine monophosphate (GMP) production as well as inhibition of thromboxane synthetase, permitting preferential formation of prostacyclin. Left ventricular end-diastolic pressure and volume are decreased, resulting in reduction of ventricular size and wall tension. Therapeutic doses reduce systolic, diastolic and mean arterial blood pressure; reflex tachycardia may occur, presumably in response to these effects. |
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Term
| ACLS 2006 Mechanism of Action for Furosemide. |
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Definition
| Inhibits sodium reabsorption in the ascending limb of Henle's loop as well as in both proximal and distal tubules. |
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Term
| ACLS 2006 Mechanism of Action for Tissue Plasminogen Activator. |
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Definition
| Alteplase is a serine protease which has the property of fibrin-enhanced conversion of plasminogen to plasmin. It produces minimal conversion of plasminogen in the absence of fibrin; and when introduced into the systemic circulation, alteplase binds to fibrin in a thrombus and converts the entrapped plasminogen to plasmin. This initiates local fibrinolysis with minimal systemic effects. |
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Term
| ACLS 2006 Mechanism of Action for Nitroprusside. |
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Definition
| The hypotensive effects of nitroprusside are caused by peripheral vasodilation as a result of a direct action on the blood vessels, independent of autonomic innervation. |
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