Term
| Nonselective: Propanolol, Carvedilol, Nadolol, Pindolol, Labetolol / Beta 1-cardioselective: Acebutolol, Metoprolol, Atenolol, Esmolol |
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Definition
| beta-blockers MOA: block beta-1 receptors in heart PD: decrease myocardial oxygen consumption CI: post MI; anti-angina-combine with nitrates for exertional angina, combine with dihydropyridines to inhibit reflex tachycardia) AE: abrupt discontinuation can cause rebound symptoms, myocardial depression, bradycardia, bronchospams, exacerbates hypoglycemia in diabetics |
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Term
| Captopril, Lisinopril, Enalapril and Benazepril (prodrugs) |
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Definition
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Definition
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Term
| Nifedipine (primarily arteriolar); Verapamil and Diltiazem (primarily cardiac) |
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Definition
Ca2+ channel blockers
MOA: primarily SA/AV nodes-blocks Ca2+ channels, inhibits phase 0 in nodal tissue, inhibits phase 2 in muscle tissue, slows conduction through nodal tissue
CI: acute or chronic SVTs (helps with rate control)
AE: myocardial depression, severe sinus bradycardia, heart block, postural hypotension, reflex tachycardia
ECG: slowing of cardiac rate |
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Definition
Ca2+ channel blockers (primarily cardiac)
MOA: blocks Ca2+ channels, slows Ca2+ channel recovery time
CI: suppresses SA/AV nodal re-entrant activity
AE: myocardial depression, severe sinus bradycardia, heart block, postural hypotension, reflex tachycardia, GI disturbances-constipation
-diltiazem has less severe AEs than verapamil |
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Term
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Definition
Ca2+ channel blocker (primarily arteriolar)
MOA: inhibition of Ca2+ channels
PD: vascular smooth muscle (arteriolar vasodilation); cardiac cells (inhibit phase 2 in cardiac muscle and inhibits phase 0 in pacemaker cells)
PK: oral admin, liver metabolism, highly protein bound
CI: vasospastic angina (with a nitrate), exercise induced angina, AV nodal reentrant arrhythmia, hypertension
AE: worsening angina due to reflex tachycardia, negative inotrope, heart block, sinus bradycardia, hypotension/dizziness/heachache, edema due to venous pooling, constipation, coughing/wheezing |
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Term
| Hydralazine, Sodium Nitroprusside |
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Definition
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Definition
vasodilator
MOA: denitrated which releases NO -> smooth muscle relaxation/vasodilation
PD: decrease in preload and afterload, improved distribution of coronary blood flow, reduce work of heart
PK: absorption can be sublingual, buccal, transdermal, ointment, spray, IV; rapid 1st pass metabolism; rapid development of tolerance
CI: stable angina, variant angina, pulmonary congestion of CHF
AE: headache, dizziness, nitrate syncope, decreased coronary perfusion with excessive hypotension |
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Definition
nitrate
PK: oral admin, liver metabolism, onset of action in 30min
Overdose: methemoglobinemia |
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Definition
antiarrhythmic
MOA: moderate recovery (3 sec), Na+ channel blocker, K+ channel blocker, alpha receptor blocker, cholinergic receptor blocker (vagolytic)
CI: 2nd line treatment for chronic SVTs
AE: torsades de pointe tachycardia, paradoxical tachycardia, hepatic granulomas, GI upset and diarrhea, quinidine syncope, cinchonism (headache, dizziness, tinnitus)
PD: decreases automaticity-blocks Na+ channels, decreases conduction velocity through heart muscle, increases conduction velocity through nodes, lengthens duration of AP
PK: given IV or oral, 80% protein bound, metabolized by liver, inhibited by P450 system
ECG: prolonged QT, widened QRS |
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Definition
antiarrhythmic
MOA: moderate recovery (1.8sec), Na+ channel blocker, K+ channel blocker, active metabolite (NAPA) only has K+ channel blocking effects
CI: 2nd line treatment for sustained V-tach; acute or chronic SVTs
AE: lupus-like syndrome, torsades do pointe tachycardia, hypotension due to ganglionic blockade, bone marrow aplasia-agranulcytosis, GI upset
PD: decreases automaticity, decreases conduction velocity through heart muscles, lengthens duration of AP; esp. NAPA
PK: metabolized by liver, NAPA excreted by kidney |
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Definition
antiarrhythmic
MOA: rapid recovery (0.1sec), Na+ channel blocker, increases K+ conductance during phases 3&4
CI: 2nd line treatment for sustained V-tach or V-fib (try amiodarone first)
AE: CNS disturbances (nystagmus, tremor), seizures that are often refractory to treatment
PD: decreases automaticity, decreases conduction velocity through heart muscles, SHORTENS DURATION OF AP
PK: IV admin only, rapid 1st pass metabolism, redistibution to fat tissue increases ½ life
VAP: decreased slope and amplitude, shortened duration of AP
ECG: widened QRS, shortened QT |
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Definition
antiarrhythmic
-same as lidocaine, but in oral form |
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Definition
antiarrhythmic
MOA: slow recovery (11sec), Na+ channel blocker, K+ channel blocker, Ca2+ channel blocker
CI: atrial arrhythmias when no other structural heart disease is present (CAST)
AE: proarrhythmic agent, depress left ventricular function, heart block
PD: decreases conduction velocity through heart muscle, decreases conduction velocity through nodes, lengthens AP duration
PK: oral admin, metabolized by liver with renal excretion
ECG: widened QRS, prolonged QT |
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Definition
antiarrhythmic
MOA: Slow recovery (11sec), Na+ channel blocker, K+ channel blocker, beta-blocker
CI: chronic treatment of atrial tachyarrthymias
AE: proarrthymic agent (torsades de pointe), myocardial depression, sinus bradycardia, bronchospasm
PD: decreases conduction velocity through heart muscle, decreases conduction velocity through nodes, lengthens AP duration
PK: oral admin, metabolized by liver with renal excretion |
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Definition
beta-blocker/antiarrhythmic
MOA: non-selective beta-blocker, mild Na+ channel blocker at higher conc.
CI: acute and chronic management of atrial flutter and fib, prevent post-MI ventricular arrhythmias
AE: myocardial depression, bronchospasm (exacerbates asthma)< augments hypoglycemia in diabetics, rebound sympathetic effects following abrupt withdrawal
PD: decreases automaticity, decreases conduction velocity through nodes
PK: oral admin, metabolized by liver
AP: see more effect in nodes than in muscle
ECG: bradycardia |
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Definition
antiarrhythmic
MOA: K+ channel blocker, Na+ channel blocker, beta-blocker, Ca2+ channel blocker (weak)
CI: acute and chronic treatment for atrial and ventricular arrhythmias; may be combined with ICD to help with stabilization
AE: corneal deposits; liver, lungs, thyroid dysfunction, postural hypotension, photosensitivity, blue-gray skin discoloration
PD: decreases automaticity, decreases conduction velocity through heart muscle, decreases conduction velocity through nodes, lengthens AP duration
PK: oral or IV admin, highly lipophilic, LONG ½ LIFE (55 days)
ECG: very similar to quinidine (prolonged QT, widened QRS) |
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Definition
antiarrhythmic
MOA: K+ channel blocker, non-selective beta-blocker
CI: chronic management of atrial arrhythmias
AE: torsades do pointe tachycardia, myocardial depression, bronchospasm, augments hypoglylcemia in diabetics, rebound sympathetic effects following abrupt withdrawal
PD: decreases automaticity, decreases conduction velocity through nodes, lengthens AP duration
PK: oral admin, RENAL EXCRETION |
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Term
| Ibutilide, Dofetilide (Class III) |
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Definition
MOA: K+ channel blocker
CI (ibutilide): acute managemet of atrial arrhythmias
CI (dofetilide): chronic management of atrial arrhythmias
AE: torsades de pointe arrhytmia
PD: lengthens duration of AP
PK: dofetilide-oral; ibutilide-IV
-patients must be hospitalized to initiate therapy with dofetilide
AP: prolonged AP
ECG: long QT |
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Term
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Definition
antiarrhythmic
MOA: binds to adenosine receptors (G-protein coupled), opens ACh sensitive K+ channels
CI: acute termination of atrial flutter and fibrillation
AE: transient asystole, dyspnea, a-fib
PD: decreases automaticity, shortens AP duration in atrial muscle, lengthens AP duration in nodes, slows nodal conduction velocity (Ca2+ inhibition)
PK: IV admin, eliminated by cellular uptake (1/2 <10sec)
AP: shortened duration
ECG: slowing of HR |
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Term
| Digoxin/Digitoxin (Digitalis) |
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Definition
cardiotonic/antiarrhythmic
-digoxin shorter effects than digitoxin (except digitoxin has greater volume of distribution than digoxin)
MOA: reversible inhibition of Na+/K+ ATPase, binding affinity greater to phosphorylated E2 conformation
PD: mechanical effects (increase tension development, improvement in cardiac function); direct electrical effects (increased automaticity, decreased conduction velocity, shorter duration of AP); indirect electrical effects (increase in vagal tone -> bradycardia and heart block)
PK: narrow therapeutic window, oral admin
CI: CHF, AV nodal reentrant arrhythmias, a-fib
AE: altered serum electrolytes, acidosis inhibits Na/K pump, altered thyroid status, renal disease impairs elimination, increased sympathetic tone, respiratory disease/hypoxia
AE (neurological and GI signs): malaise, dizziness, confusion, delirium; anorexia, nausea, vomiting, abdominal pain; disturbed color vision -> adjust dose
AE (early cardiac signs): sinus bradycardia, 1st degree AV block, AV pacemaker or ectopic impulses orginiating from AV node -> adjust dose
AE (serious cardiac signs): marked sinus bradycardia, SA node arrest, 2nd or 3rd degree AV block -> give atropine and K+
AE (most serious cardiac signs): any of above signs + premature ventricular arrhythmias (PVCs), worsening ventricular arrhythmias -> DIGIBIND (Fab immunoglobulin against digoxin)
DI: decreases absorption (cholestyramine, bran); increase plasma levels (antiarrhythmics), increase absorption (antibiotics); increase automaticity due to electrolyte alteration (furosemide, chlorothiazide); exacerbate AV node inhibition (verapamil, diltiazem)
ECG: bradycardia and prolonged PR, shortened QT interval |
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Definition
B1 agonist/cardiotonic
MOA: stimulated beta-1 adrenergic and dopamine receptors
PD: positive inotropic effect, at low doses causes dilation of renal vessels via D1 receptors
AE: tachycardia, proarrhythmogenic |
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Term
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Definition
b1 agonist//cardiotonic
MOA: stimulates beta-1 and -2 adrenergic receptors
PD: positive inotropic effect (beta-1); vasodilation of vasculature (beta-2)
AE: tachycardia and proarrhythmogenic (but less than dopamine), tolerance after several days |
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Term
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Definition
phosphodiesterase inhibitor/cardiotonic
MOA: phosphodiesterase inhibitor
PD: positive inotropic effect, vasodilation
AE: proarrhythmogenic with prolonged used (few days), thrombocytopenia and liver damage |
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Term
| Ca2+ channel blockers, beta-blockers, nitrates |
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Definition
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