Pharm Flashcards
Atropine Sulfate
Anticholinergic
Competes reversibly with acetylcholine at the site of muscarinic receipts affected, in order from the most sensitive to least sensitive, including salivary, bronchial, sweat glands, eyes, heart, and GI tract
Magnesium Sulfate
Electrolyte
Required for normal physiologic functioning. Mag is a cofactor in neurochemical transmission and muscular excitability. Mag sulfate controls seizures by blocking peripheral neuromuscular transmission. Mag is also a peripheral vasodilator and an inhibitor of platelet function
Amiodarone (Cardarone)
Antiarrhythmic, Class III
Acts directly on the myocardium to delay repolarization and increase the duration of the action potential
Nitroglycerin (NTG)
Anti Anginal Agent
Relaxes vascular smooth muscle, thereby dilating peripheral arteries and veins. This causes pooling of venous blood and decreases venous return to the heart, which decreases preload. NTG also reduces left vent systolic wall tension, which decreases afterload
Epinephrine
Adreneric Agent, Inotropic
Binds strongly with both alpha and beta receptors, producing increased BP, increased HR, and bronchodilation
Vasopressin
Nonadrenergic Vasoconstrictor
Vasopressin causes vasoconstriction independent of adrenergic receptors or neural innervation
Adenosine (Adenocard)
Antiarrhythmic
Slows the conduction of electrical impulses at the AV node
Aspirin (ASA)
Anti platelet, nonnarcotic analgesic, antipyretic
Prevents the formation of a known chemical known as thromboxan A2 which causes platelets to clump together, or aggregate, and form plugs that cause obstruction or constriction of small coronary arteries
Dopamine (Intropin)
Adrenergic Agonist, inotropic vasopressor
Stimulates alpha and beta adrenergic receptors. At moderate doses dopamine stimulates beta, receptors, resulting in inotropy and increased cardiac output while maintaining dopaminergic induced vasodilatory effects. At high doses alpha adrenergic agonism predominates and increase peripheral vascular resistance and vasoconstriction result
Morphine Sulfate
Opiate Agonist, Schedule C-II
Binds with opioid receptors. Morphine is capable of inducing hypotension by depression of the vasomotor centers of the brain, as well as release of the chemical histamine. In the management of angina, morphine reduces stimulation of the sympathetic nervous system caused by pain and anxiety. Reduction of sympathetic stimulation reduces heart rate, cardiac work, and myocardial O2 consumption
Diltiazem (Cardizem)
Calcium Channel Blocker, Class IV Antiarrhythmic
Blocks calcium from moving into the heart muscle cells, which prolongs the conduction of electrical impulses through the AV node
Verapamil (Isoptin)
Calcium Channel Blocker, Class IV AntiarrhythmicBlocks calcium from moving into the heart muscle cells, which prolongs the conduction of electrical impulses through the AV node
Lidocaine (Xylocaine)
Antiarrhythic, Class I-B
Blocks sodium channels, increasing the recovery period after repolarization; suppresses automaticity in the His-Purkinje systems and depolarization in the ventricles
Digoxin (Lanoxin)
Cardiac Glycoside
Inhibits sodium-potassium-adenosine triphosphate membrane pump. Resulting in an increase in calcium inside the heart muscle cell, which causes an increase in the force of contraction of the heart
Metoprolol (Lopressor)
Beta Adrenergic Antagonist, Anti Anginal, Anti Hypertensive, Class II Antiarrhythmic
Inhibits the strength of the hearts contractions, as well as heart rate. This results in a decrease in cardiac O2 consumption