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109 Cards in this Set
- Front
- Back
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digitalis glycosides:
give class & drugs |
POSITIVE INOTROPIC AGENTS
Digitoxin digoxin |
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adrenergic receptor agonists:
give class & drugs |
POSITIVE IONOTROPIC AGENTS
dobutamine dopamine |
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phosphodiesterase inhibitors:
class & drugs |
POSITIVE IONOTROPIC AGENTS
amrinone jk milrinone |
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positive ionotropic agents common MOA
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increase cardiac contractility & stroke volume
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digitalis glycosides effects
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increase cardiac contractility
reduce preload may increase afterload + risk of arrhythmia increases PS tone decreases sympathetic tone **** note NO effect on HR |
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adrenergic receptor agonists effects
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significant increase in cardiac contractility
may increase HR may reduce preload may reduce afterload may have risk of arrhythmia |
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phosphodiesterase inhibitors effects
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may increase cardiac contractility
may increase HR reduces preload & afterload risk of arrhythmia |
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list thiazide diuretics
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HCTZ, Indapamide, Metolazone
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list loop diuretics
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Bumetanide, Ethacrynic acid, Furosemide, Torsemide
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list K-sparing diuretics
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Amiloride, Spironolactone, Triamterene
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list osmotic diuretics
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glycerol, mannitol
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list carbonic anhydrase inhibitors
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acetazolamide, dorzolamide
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Side effects of Quinidine
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TdP; TCP; diarrhea; conchism
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side effects of Procainamide
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SLE like reaction (reversible)
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side effects of Lidocaine
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decreased conduction, neurological defects (tremor, paresthesia)
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side effects of tocainide
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agranulocytosis
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side effects of fecainide & Propafenone
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increased risk of death when given to MI patient, ventricular arrhythmias, hem. Toxicities
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side effects of Ibutilide
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TdP
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side effects of Amiodarone
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hypotensiton, skin pigment changes (blue/green), corneal deposits, GI disturbances; be sure to check LFT, PFT, & TFT (liver, pulmonary, & thyroid fxn tests)
***note increased QT segment without TdP |
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Side effects of Bretylium
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transient HTN followed by prolonged hypotension
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side effects of Sotalol
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Bronchospasm, TdP
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Lidocaine metabolism
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hepatic
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Esmolol metabolism
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esterase (very rapid…must admin via IV)
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Esmolol uses & admin
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Supraventricular tachycardia during or after surgery; admin IV
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Quinidine uses
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SV/V arrhythmias
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Procainamide admin & uses
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SV arrhythmia=PO
V arrhythmia=IV/PO |
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Disopyramide admin & uses
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PO=V arrhythmias
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Lidocaine admin & Uses
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IV=V arrhythmia (including V tachy)
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Mexiletine admin & uses
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PO=V arrhythmias
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Tocainide admin & uses
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PO=V arrhythmias
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Flecainide admin & uses
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PO=SV arrhythmias & life threatening V arrhythmias
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Metaprolol uses
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SV/V arrhythmias; esp for MI patients (admin IV at first then maintenance via PO)
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Propranolol uses
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SV/V arrhythmias
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Ibutilide admin & uses
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IV=SV fib/flutter
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Amiodarone admin & uses
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PO=SV fib/flutter/tachy & life threateninng V tachy
IV=life threatening V fib & sustained V tachy |
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Amiodarone MOA
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K-channel blocker (increases AP duration); also blocks Na & Ca channels & inhibits Beta receptors
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Bretylium admin & uses
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IV=V fib
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Sotalol uses
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SV arrhythmia (including fib) & V arrhythmias
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meds for SV arrhythmias
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Quinidine, procainamide, Flecainide, class 2 drugs (Esmolol, Metaprolol, Propranolol), Class 3 (except Bret. ) (Ibutilide, Amiodarone, Sotalol)
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meds for SV tachycardia
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Esmolol, Amiodarone
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meds for SV fibrillation
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Ibutilide, Amiodarone, Sotalol
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meds for SV flutter
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Ibutilide, Amiodarone
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meds for V arrhythmias
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class IA (Quinidine, Procainamide, Disopyramide), Class IB (Lidocaine, Mexiletine, Tocainide), Flecainide, Metaprolol, Propranolol, Class 3 (except Ibut.)(Amiodarone, Bretylium, Sotalol)
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meds for Ventricular tachycardia
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Lidocaine, Amiodarone
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meds for V fib
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Bretylium, Amiodarone
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meds for life-threatening V arrhythmias
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Flecainide, Amiodarone
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class IA antiarrhythmics: MOA & list
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Na channel blockers (high affinity for open state; slow recovery): Quinidine, Procainamide, Disopyramide
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class IB antiarrhythmics: MOA & list
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Na channel blockers (high affinity for inactivated, ischemic tissue; rapid recovery): Lidocaine, Mexiletine, Tocainide
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class IC antiarrhythmics: MOA & list
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Na channel blockers (open state, slowest recovery (most effect on ventricular conduction): Flecainide, Propafenone
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class II antiarrhythmics: MOA & list
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Beta-blockers: Esmolol (B1), Metoprolol (B1), Propranolol (B1/2)
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class III antiarrhythmics: MOA & list
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K-channel blocker: Amiodarone, Bretylium, Ibutilide, Sotalol
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class IV antiarrhythmics: MOA & List
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Ca channel blockrs: Verapamil, Diltiazem
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Manitol MOA
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proximal tubule: easily filtered poorly reabsorbed; increases urine osmolarity resulting in increased UO
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glycerine uses
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ophthalmic procedures (admin PO); osmotic diuretic for corneal edema (topical)
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Acetazolamide MOA
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Proximal tubule: inhibits carbonic anhydrase resulting in increased Urinary sodium bicarb; effective in 30 min; decr Cl excretion
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Furosemide MOA
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Thick ascending loop: inhibits Na/K/Cl symporter resulting in decreased urine osmolarity, increased urine Ca "loops lose Ca"; may also act as a carbonic anhydrase inhibitor
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Ethacrymic acid MOA
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Thick ascending loop: inhibits Na/K/Cl symporter resulting in decreased urine osmolarity, increased urine Ca "loops lose Ca"
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HCTZ MOA
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absorbed in early proximal tube (competes for same receptor as uric acid); acts in Distal tubule: inhibits NaCl reabsorption resulting in increased urinie osmolarity, decreased urinary Ca
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K-sparing diuretics "K-STAys" MOA
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Cortical collecting tubule
Spirolactone competitively inhibits Aldo in tubular cells=reduces Na reabsorption Triumterene inhibits Na channel in principle tubular cells Amiloride inhibits Na channel in principle tubular cells |
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Manitol uses
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glaucoma, cerebral edema, shock, drug OD; may help oliguria if secondary to decr GFR; prophylaxis for acute renal failure by maintaining steady, dilute urine flow
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Manitol side effects
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Pulmonary edema, dehydration
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mannitol contraindications
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anuria, CHF (b/c water is pulled out of cells & into BVs, worsening CHF)
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carbonic anhydrase uses
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rarely used as a diuretic; used for altitude sickness, epilepsy, metabolic alkalosis, acidic urine, glaucoma, gout, hypercystine
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carbonic anhydrase side effects & contraindications
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hyperCl acidosis, sulfa allergy, increased blood sugar & ammonia, hypokalemia, neuro (drowsy & paresthesias), kidney stones (alkaline urine decr solubility of Ca salts), may have exfoliative dermatitis or rash,
*****do not use with hepatic cirrhosis; hypoK |
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loop diuretics uses & contraindications
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edema (treat CHF by limiting acute pulmonary edema), HTN, hypercalcemia & halide poisoning; DOC for edema secondary to CHF or cirrhosis
****can be used in renal impaired patients |
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loop diuretics side effects
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"OH DANG" ototox (esp. ethacrymic acid), hypo(K, Ca, Mg, H, TN)/hyper(glycemia, uremia), dehydration, allergy to sulfa (except ethacrymic acid), nephritis (interstitual), gout
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loop diuretic drug interactions
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1) increase ototox, 2) reduce lithium clearance, 3) reduce salicylate excretion, 4) inhibits NM blocking effect of tubocurarine
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thiazides uses & contraindications
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HTN, edema (assoc. w/ CHF, cirrhosis, estrogen therapy, nephrotic syndrome), Diabetes Insipidus by increasing ADH, hypercalciuria (along with Ca related kidney stones)
***use cautiously w/ renal/hepatic diseases, diabetics |
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thiazides side effects
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"hyperGLUC"=hyper (glyc., lipids, uremia, Ca), hypoK, Na, Cl=metabolic alkalosis (leading to dizziness, confusion, irritability, weakness, arrhythmias) and decreased insulin, sulfa allergy, athrogenesis, pancreatitis
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K-sparing diuretics uses
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normally in combo w/ thiazide or loop diuretic; hyperaldosterone (adrenal hyperplasia & aldo producing adenoma), K-depletion, CHF; Amiloride & triamterene used for CHF, cirrhosis, & edema secondary to hyperaldo); Ami + HCTZ=for HTN;
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K-sparing diuretics side effects & contraindications
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glaucoma, cerebral edema, shock, drug OD; may help oliguria if secondary to decr GFR; prophylaxis for acute renal failure by maintaining steady, dilute urine flow
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K-sparing diuretics ADME
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PO=Spironolactone: absorbed by GI then metabolized by liver to diuretic Canrenone; several days to see effects; Triamterene & Amiloride: secreted into PT & effective after 2-4 hrs. (Triamterene is metabolized in the liver)
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drug combo to treat diuretic resistant patient
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Metolazone & loop diuretic
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Which diuretics are "high ceiling diuretics" & what does this mean?
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Loop diuretics=dose dependent response throughout dosage range
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What side effect makes one vulnerable to digitalis-induced cardiac arrhythmias
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hypoK
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Which diuretics have a side effect of hyperglycemia
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Loop & Thiazides
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digitalis glycosides
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digitoxin, digoxin
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adrenergic receptor agonists
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dobutamine, dopamine
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phosphodiesterase inhibitors
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amrinone, milrinone
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digitalis glycosides MOA
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inhibits Na/K/ATPase-->decreased fxn of Na/Ca antiport-->incr intracellular Ca
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Digitalis glycosides effects
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positive inotropic (increased force of contraction, increases intracellular Ca by inhibitina Na/K/ATPase -->incr contraction; incr SV & CO at any preload), negative chronotropic (decrease in HR), negative dromotropic (decrease in conduction velocity); indirectly increase parasympathetic tone while reducing sympathetic tone (& VC); increases AV refractory period;
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digitalis glycosides side effects
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anorexia, nausea, vomiting, arrhythmias (incr afterdepolarization--> extrasystoles & tachy; AV block), neuro (blurred vision & chromatopsia (objects appear unnaturally colored), estrogenic activity (gynecomastia), antidote=digoxin immune Fab
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digoxin ADME
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T1/2=35 hrs; renal excretoin
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digitoxin ADME
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T1/2=1 wk with extensive metabolism
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digitalis EKG effects
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decreases QT interval, increases PR interval, ST segment depression; T-wave inversion
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digitalis uses
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heart failure (does not prolong survival but does reduce symptoms); atrial fib (drug slows ventricular rate)
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adrenergic receptor agonists admin & uses
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IV=short term management of acute heart failure & cardiogenic shock
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adrenergic receptor agonists effect
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stimulate cardiac contractility-->less tachy than other B-adrenergic agonists; Dobutamine=mild VD; Dopamine=renal & splanchnic VD
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phosphodiesterase inhibitors uses
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short term management of acute heart failure or acute exacerbations of chronic heart failure
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phosphodiesterase inhibitors side effects
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thrombocytopenia & ventricular arrhythmias
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phosphodiesterase inhibitors MOA
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inhibits type 3 phosphodiesterase & increases cAMP-->incr cardiac contractility & VD
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adenosine use
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DOC for diagnosing/abolishing AV nodal arrhythmia
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potassium uses
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depresses ectopic pacemakers, especially in digoxin toxicity
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Magnesium uses
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effective in TdP & digoxin toxicity
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Ca channel blockers: Verapamil & Diltiazem MOA
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primarily affects AV nodal cells; decreases conduction velocity, increases ERP, increases PR interval
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Ca channel blockers: Verapamil & Diltiazem uses
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prevention of nodal arrhythmias (SVT)
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Ca channel blockers: Verapamil & Diltiazem side effects
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constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
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list antiarrhythmics that decrease HR
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class 2, class 3 (exc Bret.), class 4, digoxin *note class1A +/-
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list antiarrhythmics that increase PR interval
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class IC, class 2, class 3 (except Bret.), class 4, digoxin, adenosine *note class 1A +/-
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list antiarrhythmics that increase QRS duration
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class 1A & C, Amiodarone
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list antiarrhythmics that increase QT interval
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class 1A & C, class 3 (exc.Bret.), *****Amiodarone is greatest prolongation
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list antiarrhythmics that decrease QT interval
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class 1B, digoxin
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list antiarrhythmics that increase HR
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adenosine
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list antiarrhythmics with increased ectopic automaticity
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Bretylium & digoxin
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list antiarrhythmics with no change to AV conduction velocity
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Class IB, Bret., MgSO4
**note all other drugs in this chapter decrease AV conduction velocity & Increased AV refractory period |
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list antiarrhythmics with decreased His conduction velocity
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Class I, Amiodarone; ***note all others in this chapter have no change (exc Bret may increase His conduction velocity)
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list antiarrhythmics with increased His refractory period
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Class I, class 3 **note IB may decrease
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list antiarrhythmics with decreased His refractory period
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digoxin, (& maybe class IB)
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antiarrhythmics associated with torsade de pointes (TdP)
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Quinidine, Ibutilide, Sotalol
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