Cardio Meds Flashcards by Molly Szpakowski

MOA: inhibit angiotensin-converting enzyme from turning angiotensin I into angiotensin II

Pathophys: blocks vasoconstriction and sodium/water reabsorption -> vasodilate and decrease blood volume to lower B.P.

Notable Adverse Effects: angioedema (due to blocked bradykynin breakdown), hyperkalemia

Extra: prevents bradkynin breakdown
- Do NOT use when pregnant

Ace Inhibitors (-prils):
Lisinopril
Enalapril
Captopril

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MOA: block binding of angiotensin II to AT1 receptors

Pathophys: vasodilate and block sodium reabsorption -> lower BP

Notable Adverse Effects:

Extra:

Angiotensin Receptor Blockers (-tans)

Losartan
Valsartan
Telmisartan

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MOA:blocks renin from converting angiotensin to angiotensin I

Pathophys: allows for vasodilation, decreases kidney filtration

Notable Adverse Effects: hyperkalemia, GI upset, angioedema

Extra: NO use in pregnancy

Direct Renin Inhibitor - Aliskiren

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MOA: block Na-Cl symporter in distal convoluted tubule

Pathophys: decrease vascular resistance and blood volume, increase excretion of Na, Cl, K, Mg
Decrease excretion of Ca and uric acid

Notable Adverse Effects: erectile dysfunction, GOUT, dizziness, hypotension

Thiazide Diuretics

Hydrochlorothiazide
Chlorthalidone
Metolazone

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MOA: block epithelial Na channels in late distal tubule and collecting duct

Pathophys: Increase K+ retention and cause mild diuresis

Notable Adverse Effects: hyperkalemia, photosensitivity, and kidney stones (triamterene)

Potassium Sparing Diuretics

Amilioride
Triamterene

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MOA: block aldosterone from binding to mineralocorticoid receptors on late distal convoluted tubule and collecting duct

Pathophys: decreases Na+ reabsorption and increases K+ retention

Notable Adverse Effects: gynecomastia (spironolactone)

Extra:

Aldosterone Antagonists

Spironolactone

Eplerenone

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MOA: Block L Type calcium channels on smooth muscle of blood vessels

Pathophys: decreases TPR, increase peripheral vasodilation

Notable Adverse Effects: reflex tachycardia

Extra:

Dihydropyridines (Calcium Channel Blockers)

Amlodipine
Nifedipine

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MOA: inhibit effects of sympathetic n.s. at beta receptor, increase PR interval, decrease AV conduction and automaticity

Pathophys: SLOW HR, Decrease Contractility, inhibits renin release

Notable Adverse Effects: bradycardia, Raynaud’s
- Bronchoconstriction (nonselective)

Extra: caution for pts with asthma or DM, can exacerbate Heart Failure, do NOT use with Ca Channel Blockers

Beta Blockers

Atenelol, Bisoprolol, Metoprolol (B1 selective)

Nadolol, Propranolol, Timilol, Pindolol (Nonselective B1 B2)

Carvedilol, Labetalol (mixed alpha, beta)

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MOA: Fast sodium channel blocker

Pathophys: cardiotoxicity w/ wide QRS complex and tachycardia

Notable Adverse Effects: death

Cocaine

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MOA: block activation of post-synaptic alpha-1 receptors in smooth muscle and myocardium

Pathophys: atrial and venous dilation, decreases TPR, decreases preload and cardiac output -> lower BP

Notable Adverse Effects: orthostatic hypotension, nasal congestion

Extra:

Alpha-1 Antagonists (-zosin)

Prazosin
Doxazosin
Terazosin

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MOA: inhibit Na/K/Cl cotransporter in thick ascending loop of Henle
- increases Na K , and CL excretion
-Rapid diuresis and venodilation

Pathophys: decreases Blood vol. -> lower BP, decreases preload and afterload

Notable Adverse Effects: ototoxicity (hearing loss), hypokalemia

Extra: SEVERE hypotension when used with Beta-Blockers

Loop Diuretics

Furosemide
Bumetanide
Torsemide

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MOA: stimulates pre-synaptic alpha-2 adrenergic receptors in CNS
- decrease post-synaptic norepinephrine release

Pathophys: decrease HR and contractility, decrease TPR, decrease renin release

Notable Adverse Effects: rebound HTN w/ headache, anxiety, tremor, sweating, and tachycardia w/ sudden discontinuation

Extra: CHOICE for preganancy

Alpha 2 Agonists

Clonidine
Methyldopa

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MOA: interferes with Ca2+ mobilization in vascular smooth muscle, prevents arteriole contraction

Pathophys: arteriol vasodilation, increases HR & contractility

Notable Adverse Effects: lupus-like syndrome, vasculitis

Direct Vasodilator

Hydralazine

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MOA: Blocks open/active Na channels (and K+ channels), slows phase 0, prolongs action potential, QRS and QT interval

Pathophys: decrease contractility of atrial and ventricular myocytes and Purkinji fibers

Notable Adverse Effects: Cinchonism - headaches, tinnitus, blurry vision

Extra:

Quinidine (Class Ia Na+ Channel Blocker)

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MOA: Blocks open/active Na channels (and K+ channels), slows phase 0, prolongs action potential, QRS and QT interval

Pathophys: decrease contractility of atrial and ventricular myocytes and Purkinji fibers

Notable Adverse Effects: lupus-like syndrome and rash, pancytopenia

Extra: use in WPW syndrome

Procainamide (Class Ia Sodium Channel Blocker)

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MOA: Blocks open/active Na channels (and K+ channels), slows phase 0, prolongs action potential, QRS and QT interval

Pathophys: decrease contractility of atrial and ventricular myocytes and Purkinji fibers

Notable Adverse Effects: anticholinergic affects - dry eyes, dry mouth, urinary retention

Disopyramide (Class Ia Sodium Channel Blocker)

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MOA: Block inactivated NA channels, prolong phase 3 repolarization, shorten action potential, act on Purkinji fibers and ventricular myocytes

Notable Adverse Effects: CNS toxicity (seizure, tremos, confusion)

Extra: USE POST M.I.

Lidocaine (Class Ib Sodium Channel Blocker)

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MOA: Block inactivated NA channels, prolong phase 3 repolarization, shorten action potential, act on Purkinji fibers and ventricular myocytes

Notable Adverse Effects: hypersensitivity syndrome

Extra: USE POST M.I.

Mexiletine (Class Ib Sodium Channel Blocker)

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MOA: Block open/activated Na channels, strong phase 0 depression -> LONG QRS, no change in action potential

Notable Adverse Effects: 1st or 2nd Degree AV Block

Flecainide (Class Ic Sodium Channel Blocker)

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MOA: Block open/activated Na channels, strong phase 0 depression -> LONG QRS, no change in action potential

Notable Adverse Effects: 1st or 2nd Degree AV Block, Metallic Taste

Propafenone (Class Ic Sodium Channel Blocker)

MOA: blocks K channels (cardiac delayed rectifier K Channels IKr), prolongs repolarization, increase QT interval and refractory period
- also affect Na, Ca, and Beta receptors

Notable Adverse Effects: Pulmonary Fibrosis, Thyroid dysfunction, hepatotoxicity (increased LFTs), corneal deposits, Blue-grey skin, sun sensitivity

Extra: contains iodine, very lipophilic, likes ot get into various tissues

Amiodarone (Class III K Channel Blocker)

MOA: blocks K channels (cardiac delayed rectifier K Channels IKr), prolongs repolarization, increase QT interval and refractory period

Notable Adverse Effects: TdP

Extra: Ibutilide can be used in chemical cardioversion

Sotalol
Dofetilide (p.o)
Ibutilide (IV)
Dronedarone

MOA: Block L-Type calcium channels and increase refractory period in pacemaker cells, decreases AV ode conduction, Negative inotrope, Non-dihydropyridine

Notable Adverse Effects: Constipation, hypoprolactinemia

Extra: use in supraventricular tachycardia (A-fib/flutter)

Class IV Ca2+ Channel Blockers

Verapamil
Diltiazem

MOA: inhibits Na/K ATPase
- increases intracellular Ca

Pathophys: Increases contractility, decreases AV Conduction

Notable Adverse Effects: AV Block, Yellow Halos (vision disturbances), nausea/vomiting

Extra: Pts w/ HYPOkalemia are at increased risk of drug toxicity, pts. w/ HYPERkalemia indicative of drug toxicity

Digoxin (Cardiac Glycoside)

MOA: activates acetylcholine-sensitive K current Pathophys: hyperpolarizes AV node Notable Adverse Effects:dyspnea, chest pain Extra: use for acute termination of reentrant supraventricular tachycardia

Adenosine

MOA: inhibits late phase inward Na+ current during repolarization-> Ca2+ overload and myocardial O2 demand Pathophys: decreases ventricular wall tension, NO decrease in HR or BP Notable Adverse Effects: palpitations, syncope, dizziness, Extra:

Ranolazine

MOA: releases NO, leads to cGMP mediated vasodilation -> decreases L Ventricular Well Tension Pathophys: Decreases PReload and myocardial O2 demand, decreases TPR Notable Adverse Effects: hypotension, flushing, bradycardia, headache, paresthesia Extra: do NOT co-administer w/ PDE-5 inhibitors

Nitrates: Nitroglycerin ISDN ISMN Sodium Nitroprusside (direct NO donor)

MOA: irreversibly inhibits thromboxane-synthesizing cyclooxygenase (COX-1) in platelets Pathophys: prevents platelet aggregation and thrombus formation Notable Adverse Effects: bleeding, gastric ulcers, tinnitus, renal injury Extra: interactions alcohol, NSAIDs

Aspirin

MOA: Prodrug, P2Y12 receptor antagonist, blocks ADP-mediated platelet aggregation - No GPIIb/IIa receptors expressed Notable Adverse Effects: TTP, Bleeding

Clopidogrel

MOA: block fibrinogen (Xa) binfing to GP iib/iia receptor -prevents platelet aggregation Notable Adverse Effects: Thrombocytopenia, Bleeding

Xa Inhibitors: Abciximab Eptifibatide Tirofiban

MOA: converts plasminogen to active plasmin, promotes fibrinolysis Notable Adverse Effects: significant bleeding, hypersensitivity rxns. Extra: use for acute stroke, STEMI, P.E.

tPa

MOA: selective B1 Blocker, DECREASE HR, myocardial O2 demand, Negative inotropic effects Pathophys: Decrease Cardiac Output - Increase TPR and LVEDP Notable Adverse Effects: initially worsening H.R. Extra: do NOT give w/ Ca Blockers

Selective B1 Blockers: Bisoprolol Metoprolol Succinate

MOA: non-selective Beta and Alpha Blocker Pathophys: Decrease AFTERLOAD, decrease C.O. and increase TPR and LVEDP Notable Adverse Effects:bradycardia, Extra:increase TPR due to (MAP = CO * TPR)

Carvedilol

MOA: inhibits Na-K-2Cl transporter in thick ascending limb Pathophys: decrease blood volume, decrease LAP, decrease C.O., decrease B.P. - Increase: TPR Notable Adverse Effects: hypokalemia, ototoxicity, photosensitivity Extra: do not give with Digoxin, NSAIDs, lithium

Furosemide (lasix)

MOA: neprilysin inhibitor + ARB Pathophys: increases ANP and BNP, decreases RAAS, promotes vasodilation, diuresis, and natriuresis Notable Adverse Effects: angiodema, hypotension, hyperkalemia, increased SCr Extra: NO preganacy or use w/ ACE inhibitors

Sacubitril / Valsartan (Entresto)

MOA: decrease afterload and preload Notable Adverse Effects: lupus like syndrome, headache, dizziness, tachycardia Extra: NO PDE-5 inhibitors

Hydralazine / Isosorbide Dinitrate

MOA: inhibits If (funny current) in SA node Pathophys: Decrease HR w/OUT reducing contractility or BP Notable Adverse Effects: bradycardia, hypertension, a-fib, phosphenes, halos

Ivabradine

MOA: small molecule sln. for reperfusion Notable Adverse Effects: edema, electrolyte abnormalities

Crystalloid

MOA: large moecule slns. proteins Notable Adverse Effects: allergic rxn, coag. rxn Extra: use in refractory shock

Colloid

MOA: non-selective, direct acting adrenergic agonist - Low dose: more Beta -High dose: more alpha Pathophys: INCREASE SV, (+) inotropic and chronotropic effects, increase HR and C.O. Notable Adverse Effects: tachycardia, increased BP Use: septic shock, cardiac arrest, anaphylaxis

Epinephrine

MOA: PRIMARILY alpha 1, small B1 and B2 stimulation Pathophys: Increases SVR and BP, IMPROVE MAP, decrease HR due to increased vagal activity Notable Adverse Effects: HTN, decreased renal function Extra: use in septic and cardiogenic shock

Nor-epinephrine

MOA: natural precursor to nor-epi and epi, Lw dose: D1/2 vasodilates renal and coronary arteries Med dose: (+) inotropic effects, increase HR High dose: vasoconstriction Pathophys: increase C.O., HR, and MAP at medium dose Notable Adverse Effects: arrhythmias Extra: akes longer to reach steady dose in kids, use is septic and cardiogenic shock

Dopamine

MOA: Antidiuretic hormone analog Pathophys: increases SVR and BP, decreased HR due to baroreceptor activation Notable Adverse Effects: bradycardia, HF exacerbation Extra: adjunct therapy in refractory shock

Vasopressin

MOA: inotrope w/ vasodilator properties, selective B1 agonist Pathophys: increases C.O. (via B1), decrease BP and afterload, decreases SVR (vasodilation) Notable Adverse Effects: tachycardia, arrhythmias, headache Extra: use in patient with LOW CO and HIGH LVEDP

Dobutamine

MOA: non-selective Beta agonist, Pathophys: increases HR and CO, decreases BP and MAP, DECREASE SVR Notable Adverse Effects: palpitations, tachycardia, headache, flushing Extra: use in evere bradycardia, AV block, arrhythmia, use in cardiogenic shock w/ norepi

Isoproterenol

MOA: PDE-3 Inhibitor, increases intracellular cAMP -> increase contractility of myocytes and vasodilation Pathophys: Notable Adverse Effects: arrhythmia, hypotension, headache, tremor Extra: use w/ low cardiac idex and hypotension

Milrinone

MOA: alpha 1 agonist Pathophys: increase SVR w/ little to no impact on the heart Notable Adverse Effects: supine hypertension Extra: IV administration

Phenylephrine, Midodrine

MOA: bind to mineralocorticoid receptors in distal convoluted tubule, increase expression of Na/K ATPase, increase Na and water reabsorption Notable Adverse Effects: edema, fluid retention, hypertension, hypokalemia, HPA axis suppression Extra: it's a corticosteroid

Fludrocortisone