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109 Cards in this Set

  • Front
  • Back
digitalis glycosides:
give class & drugs
adrenergic receptor agonists:
give class & drugs
phosphodiesterase inhibitors:
class & drugs
amrinone jk milrinone
positive ionotropic agents common MOA
increase cardiac contractility & stroke volume
digitalis glycosides effects
increase cardiac contractility
reduce preload
may increase afterload
+ risk of arrhythmia
increases PS tone
decreases sympathetic tone
**** note NO effect on HR
adrenergic receptor agonists effects
significant increase in cardiac contractility
may increase HR
may reduce preload
may reduce afterload
may have risk of arrhythmia
phosphodiesterase inhibitors effects
may increase cardiac contractility
may increase HR
reduces preload & afterload
risk of arrhythmia
list thiazide diuretics
HCTZ, Indapamide, Metolazone
list loop diuretics
Bumetanide, Ethacrynic acid, Furosemide, Torsemide
list K-sparing diuretics
Amiloride, Spironolactone, Triamterene
list osmotic diuretics
glycerol, mannitol
list carbonic anhydrase inhibitors
acetazolamide, dorzolamide
Side effects of Quinidine
TdP; TCP; diarrhea; conchism
side effects of Procainamide
SLE like reaction (reversible)
side effects of Lidocaine
decreased conduction, neurological defects (tremor, paresthesia)
side effects of tocainide
side effects of fecainide & Propafenone
increased risk of death when given to MI patient, ventricular arrhythmias, hem. Toxicities
side effects of Ibutilide
side effects of Amiodarone
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
Side effects of Bretylium
transient HTN followed by prolonged hypotension
side effects of Sotalol
Bronchospasm, TdP
Lidocaine metabolism
Esmolol metabolism
esterase (very rapid…must admin via IV)
Esmolol uses & admin
Supraventricular tachycardia during or after surgery; admin IV
Quinidine uses
SV/V arrhythmias
Procainamide admin & uses
SV arrhythmia=PO
V arrhythmia=IV/PO
Disopyramide admin & uses
PO=V arrhythmias
Lidocaine admin & Uses
IV=V arrhythmia (including V tachy)
Mexiletine admin & uses
PO=V arrhythmias
Tocainide admin & uses
PO=V arrhythmias
Flecainide admin & uses
PO=SV arrhythmias & life threatening V arrhythmias
Metaprolol uses
SV/V arrhythmias; esp for MI patients (admin IV at first then maintenance via PO)
Propranolol uses
SV/V arrhythmias
Ibutilide admin & uses
IV=SV fib/flutter
Amiodarone admin & uses
PO=SV fib/flutter/tachy & life threateninng V tachy
IV=life threatening V fib & sustained V tachy
Amiodarone MOA
K-channel blocker (increases AP duration); also blocks Na & Ca channels & inhibits Beta receptors
Bretylium admin & uses
IV=V fib
Sotalol uses
SV arrhythmia (including fib) & V arrhythmias
meds for SV arrhythmias
Quinidine, procainamide, Flecainide, class 2 drugs (Esmolol, Metaprolol, Propranolol), Class 3 (except Bret. ) (Ibutilide, Amiodarone, Sotalol)
meds for SV tachycardia
Esmolol, Amiodarone
meds for SV fibrillation
Ibutilide, Amiodarone, Sotalol
meds for SV flutter
Ibutilide, Amiodarone
meds for V arrhythmias
class IA (Quinidine, Procainamide, Disopyramide), Class IB (Lidocaine, Mexiletine, Tocainide), Flecainide, Metaprolol, Propranolol, Class 3 (except Ibut.)(Amiodarone, Bretylium, Sotalol)
meds for Ventricular tachycardia
Lidocaine, Amiodarone
meds for V fib
Bretylium, Amiodarone
meds for life-threatening V arrhythmias
Flecainide, Amiodarone
class IA antiarrhythmics: MOA & list
Na channel blockers (high affinity for open state; slow recovery): Quinidine, Procainamide, Disopyramide
class IB antiarrhythmics: MOA & list
Na channel blockers (high affinity for inactivated, ischemic tissue; rapid recovery): Lidocaine, Mexiletine, Tocainide
class IC antiarrhythmics: MOA & list
Na channel blockers (open state, slowest recovery (most effect on ventricular conduction): Flecainide, Propafenone
class II antiarrhythmics: MOA & list
Beta-blockers: Esmolol (B1), Metoprolol (B1), Propranolol (B1/2)
class III antiarrhythmics: MOA & list
K-channel blocker: Amiodarone, Bretylium, Ibutilide, Sotalol
class IV antiarrhythmics: MOA & List
Ca channel blockrs: Verapamil, Diltiazem
Manitol MOA
proximal tubule: easily filtered poorly reabsorbed; increases urine osmolarity resulting in increased UO
glycerine uses
ophthalmic procedures (admin PO); osmotic diuretic for corneal edema (topical)
Acetazolamide MOA
Proximal tubule: inhibits carbonic anhydrase resulting in increased Urinary sodium bicarb; effective in 30 min; decr Cl excretion
Furosemide MOA
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
Ethacrymic acid MOA
Thick ascending loop: inhibits Na/K/Cl symporter resulting in decreased urine osmolarity, increased urine Ca "loops lose Ca"
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
K-sparing diuretics "K-STAys" MOA
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
Manitol uses
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
Manitol side effects
Pulmonary edema, dehydration
mannitol contraindications
anuria, CHF (b/c water is pulled out of cells & into BVs, worsening CHF)
carbonic anhydrase uses
rarely used as a diuretic; used for altitude sickness, epilepsy, metabolic alkalosis, acidic urine, glaucoma, gout, hypercystine
carbonic anhydrase side effects & contraindications
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
loop diuretics uses & contraindications
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
loop diuretics side effects
"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
loop diuretic drug interactions
1) increase ototox, 2) reduce lithium clearance, 3) reduce salicylate excretion, 4) inhibits NM blocking effect of tubocurarine
thiazides uses & contraindications
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
thiazides side effects
"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
K-sparing diuretics uses
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;
K-sparing diuretics side effects & contraindications
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
K-sparing diuretics ADME
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)
drug combo to treat diuretic resistant patient
Metolazone & loop diuretic
Which diuretics are "high ceiling diuretics" & what does this mean?
Loop diuretics=dose dependent response throughout dosage range
What side effect makes one vulnerable to digitalis-induced cardiac arrhythmias
Which diuretics have a side effect of hyperglycemia
Loop & Thiazides
digitalis glycosides
digitoxin, digoxin
adrenergic receptor agonists
dobutamine, dopamine
phosphodiesterase inhibitors
amrinone, milrinone
digitalis glycosides MOA
inhibits Na/K/ATPase-->decreased fxn of Na/Ca antiport-->incr intracellular Ca
Digitalis glycosides effects
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;
digitalis glycosides side effects
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
digoxin ADME
T1/2=35 hrs; renal excretoin
digitoxin ADME
T1/2=1 wk with extensive metabolism
digitalis EKG effects
decreases QT interval, increases PR interval, ST segment depression; T-wave inversion
digitalis uses
heart failure (does not prolong survival but does reduce symptoms); atrial fib (drug slows ventricular rate)
adrenergic receptor agonists admin & uses
IV=short term management of acute heart failure & cardiogenic shock
adrenergic receptor agonists effect
stimulate cardiac contractility-->less tachy than other B-adrenergic agonists; Dobutamine=mild VD; Dopamine=renal & splanchnic VD
phosphodiesterase inhibitors uses
short term management of acute heart failure or acute exacerbations of chronic heart failure
phosphodiesterase inhibitors side effects
thrombocytopenia & ventricular arrhythmias
phosphodiesterase inhibitors MOA
inhibits type 3 phosphodiesterase & increases cAMP-->incr cardiac contractility & VD
adenosine use
DOC for diagnosing/abolishing AV nodal arrhythmia
potassium uses
depresses ectopic pacemakers, especially in digoxin toxicity
Magnesium uses
effective in TdP & digoxin toxicity
Ca channel blockers: Verapamil & Diltiazem MOA
primarily affects AV nodal cells; decreases conduction velocity, increases ERP, increases PR interval
Ca channel blockers: Verapamil & Diltiazem uses
prevention of nodal arrhythmias (SVT)
Ca channel blockers: Verapamil & Diltiazem side effects
constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
list antiarrhythmics that decrease HR
class 2, class 3 (exc Bret.), class 4, digoxin *note class1A +/-
list antiarrhythmics that increase PR interval
class IC, class 2, class 3 (except Bret.), class 4, digoxin, adenosine *note class 1A +/-
list antiarrhythmics that increase QRS duration
class 1A & C, Amiodarone
list antiarrhythmics that increase QT interval
class 1A & C, class 3 (exc.Bret.), *****Amiodarone is greatest prolongation
list antiarrhythmics that decrease QT interval
class 1B, digoxin
list antiarrhythmics that increase HR
list antiarrhythmics with increased ectopic automaticity
Bretylium & digoxin
list antiarrhythmics with no change to AV conduction velocity
Class IB, Bret., MgSO4

**note all other drugs in this chapter decrease AV conduction velocity & Increased AV refractory period
list antiarrhythmics with decreased His conduction velocity
Class I, Amiodarone; ***note all others in this chapter have no change (exc Bret may increase His conduction velocity)
list antiarrhythmics with increased His refractory period
Class I, class 3 **note IB may decrease
list antiarrhythmics with decreased His refractory period
digoxin, (& maybe class IB)
antiarrhythmics associated with torsade de pointes (TdP)
Quinidine, Ibutilide, Sotalol