Major Effects Flashcards
Adenocard (adenosine)
slows conduction time through AV. Interrupts re-entry pathways through AV
ACE Inhibitors
block conversion of Angiotensin I into Angiotensin II, promoting vascular relaxation, a drop in systemic vascular resistance, and eventual diminishment of myocardial workload due to drop in left ventricular afterload. The improved function enhances cardiac output, limits infarction size, slows progression of heart failure, and decreases sudden death and recurrence of infarctions
Adrenalin (epinephrine)
stimulates both alpha and beta receptors of the autonomic nervous system. B1 causes increased HR (chronotropy), contractility (inotropy), conduction (dromotropy). B2 causes bronchodilation. Alpha stimulation causes increased peripheral vasoconstriction, increasing BP
Amiodarone (cordarone)
decreases number of VT/VF events by increasing threshold. Prolongs duration of action potentials in cardiac fibers
Aspirin (Acetylsalicylic acid)
reduces risk of occlusive vascular events by inhibiting platelet aggregation, thus preventing blood clots
Atropine Sulfate
blocks acetylcholine receptors (muscarinic receptors, thereby inhibiting the effect of the neurotransmitter, and diminishing or preventing the influence of vagal tone on the heart). It increases HR by blocking vagal tone
Beta Blockers
inhibits strength of heart contractions and HR, resulting in decrease of cardiac oxygen consumption
Calan, Isotopin (Verapamil)
blocks calcium from moving into the heart muscle cell, which prolongs the conduction of electrical impulses through the AV node, dilates arteries
calcium chloride 10% (CaCl)
calcium has an influence on cardiac muscle contraction by increasing force of contraction when it enters the portion of the cell where actin and myosin filaments interact. the ion also aids in peripheral vasoconstriction
calcium channel blockers (-dipine)
inhibits the influx of calcium ions through slow channels during membrane depolarization of cardiac and vascular smooth muscle. effective in SVTs because it slows conduction through AV node and reduces ventricular rate, thus reducing HR
Clopidrogel (Plavix)
blocks platelet aggregation by antagonizing GP IIb/IIIa receptors
Diltiazem (Cardiazem)
inhibits the influx of calcium ions through slow channels during membrane depolarization of cardiac and vascular smooth muscle. effective in SVTs because it slows conduction through the AV node and reduces ventricular rate, thus reducing HR
Dopamine (intropin)
stimulates alpha and beta receptors. At moderate doses it stimulates B1, resulting in increased cardiac output. At high doses it stimulates alpha receptors, causing vasoconstriction
fentanyl citrate (Sublimaze)
binds to opiate receptors, producing analgesia and euphoria
Fibrinolytic therapy
quickly dissolve an occluding blood clot and reopen a pathway through which the myocardium can receive oxygenated blood, limiting overall size of infarction
Lanoxin (digoxin)
inhibits sodium-potassium pump, resulting in an increase in calcium inside heart muscle cell, causing an increase in the force of contraction
Lasix (furosemide)
acts on proximal and distal ends of the tubules and ascending limb of Loop of Henle to excrete water, sodium, chlorides and potassium. blocks reabsorption of sodium in tubules of kidneys. very potent. rapid onset
Lidocaine HCl (Xylocaine)
depresses conduction velocity through ischemic ventricular tissue and depresses its increased automaticity. Raises ventricular fibrillation threshold. Shortens refractory period and action potential duration. Decreases cell permeability and prevents loss of sodium and potassium ions
magnesium sulfate
counteracts uterine tetany and the effects of oxytocin. produces anticonvulsant effect. CNS depressant. blocks neuromuscular electrical transmissions for seizures. Bronchial dilator for asthma. Decreases SA node firing. prolongs conduction time
Nipride (sodium nitroprusside)
relaxes both arteriolar and venous smooth muscle
Nitrostat (nitroglycerin)
lowers BP by relaxing vascular smooth muscle, dilating vasculature and reducing preload and afterload. Dilates coronary arteries and promotes collateral circulation to ischemic regions
Quinidine
Decreases conduction velocity. strong vagal blocking properties. decreases automaticity in His Purkinje system prolonging refractory period and action potential duration in His-Purkinje system
Sodium Bicarbonate (NaHCO3)
alkalinizing which helps maintain osmotic pressure and ion balance. Buffer agent in blood
Vasopressin
direct stimulation of smooth muscle receptors which promote vasoconstriction during periods of cardiac arrest
