pharm - cardiac.txt

"prils"

inhibit ACE, less angiotensin II produced (less vasoconstriction), less aldosterone secretion (less reabsorption), more bradykinin (vasodilation).

intermediate (12-24 hr) duration of action (except captopril).

HTN, CHF, MI, diabetic neuropathy

absolute hx of angioedema, pregnancy (cat D)

lithium (increased toxicity), azathioprine (increased toxicity). caution with NSAIDS in pts with poor kidney function (NSAIDS constrict, AA, ___ constrict EA).

cough (>women), angioedema (>blacks, women, smokers), hyperkalemia, proteinuria, dysguesia

Prinivil, Zestril

ACEI, 10-80mg PO qd (>40 rarely effective)

Lotensin

ACEI, 10-80mg PO qd (may give BID)

Vasotec

ACEI, 5-40mg PO qd (lower with diuretic)

ACEI. dosed BID/TID on empty stomach, is not a prodrug (hepatic impairment). Additional SE rash.

monitor K and SrCr as they begin or increase dose

"sartans"

blocks binding of angiotensin II to AT1 receptor (less vasoconstriction)

intermediate (12-24 hr) duration of action

HTN, CHF, pts who require an ACEI but cannot tolerate cough

absolute pregnancy (cat D). caution with volume depletion.

dizziness, hypotension, hyperkalemia, renal failure. [cough/angioedema less frequent]

Diovan

ARB, 80-320mg PO qd (lower with diuretic)

Benicar

ARB, 20-40mg PO qd

aliskiren (Tekturna)

inhibit renin, less angiotensin I produced, less angiotensin II produced (less vasoconstriction), less aldosterone secretion (less reabsorption), more bradykinin (vasodilation).

long (40 hr) half life

HTN

absolute pregnancy (cat D). caution with volume depletion, hyponatremia.

diarrhea, GERD, hyperkalemia.

renin concentrations will likely increase during administration (ATII negative feedback loop)

class 1a - procainamide, disopyramide, quinidine. Class 1b - lidocaine, mexitetene. Class 1c - propafenone, flecainide.

moderate Na+ channel blockers, increased ERP

weak Na+ channel blockers, decreased ERB

strong Na+ channel blockers, no ERB effect

block sodium channels, decreasing ion mvmt during phase 0. results in slower conduction, wider QRS. Phase 3 (and therefore QT interval) can be longer or shorter. also helps prevent after-depolarizations.

cardiac arrhythmia

pt does not have a life-threatening arrhythmia. lots of drug interactions (leading to QT prolongation, arrhythmias, other toxicities).

cardiac arrhythmias, including torsades de pointes

SCB class 1a. SE drug-induced lupis.

SCB class 1a. SE anticholinergic.

SCB class 1a. SE GI, bitter taste, cinchonism (vertigo, headache, tinnitus, psychosis)

SCB class 1b. orally active form of lidocaine (lidocaine is IV due to short half life).

SCB class 1c

SCB class 1c

class 2, "lols"

competitively antagonize the action of chatecholamines at beta receptors (beta-1 stimulation at SA/AV nodes leads to an increase in sodium currents/chronotropy/ionotropy). this reduces HR, contractility, and prevents after-depolarizations. can also block any compensatory increases in sympathetic activity.

atenolol, metoprolol selectivity

propanalol selectivity

labetalol, carvedilol selectivity

atenolol, (labetalol) distribution

propranolol, (metoprolol) distribution

HTN, CHF, angina, cardiovascular event protection, post-MI

absolute non-selective + asthma, 2nd degree heart block, bradycardia, acute heart failure. many cautions/interactions.

hypotension, Raynaud's, impotence, fatigue, hypoglycemia, insomnia, depression. **d/c taper (rebound HTN)

Tenormin

BB, 50-200mg PO qd

Lopressor

BB, 50-200mg PO BID

Toprol XL

BB, 25-400mg PO qd

Coreg

BB, 6.25-25mg PO BID

BB, 20-80mg PO qd

BB with class 2 and class 3 antiarrhythmic properties. start in hospital due to potential for serious arrhythmias/interactions/issues. CrCl prior to start.

class 3, amiodarone (also shows class 4 properties), dronedarone, ibutilide, dofetilide, azimilide

blocking K channels in phase 3 of the action potential slows the efflux of K, increasing the refractory period.

prolonged QT interval

"darones" are inhibitors of CYP3A4/P-glycoprotein, so numerous interactions.

very long half-life (58 days), variable and slow elimination from plasma/tissues (so proarrhythmic effect, potential for interactions is prolonged). requires a loading dose.

shorter half-life than other "darone" (loading dose not needed). Is also less lipophilic, and lacks an iodine group.

treat/prevent a-fib/flutter, VF/VT

absolute with 2/3 degree heart block (suppresses conduction/escape beats). caution with amiodarone in pts with hypotension.

fatal pulmonary toxicity (report SOB/cough), eye issues, hepatotoxicity, blue-grey skin, thyroid issues. "beta blocker blues"

class 4 = verapamil, diltiazem. also in this category are the "pines"(dihydropyridines)

binds to various sites on L-type calcium channels (V, D, or N) blocking Ca influx. non-DHPs are cardiac depressants (chronotropy/ionotropy) with some vasodilator activity. DHPs are primarily vasodilators, which can lead to a potential reflex increased chronotropy/ionotropy.

much longer (40 hr) half life than nifedipine (4 hr), helping to mitigate reflex tachycardia.

has the highest affinity of the dipines, therefore causes the most dilation but also the most side effects

non-DHPs angina, tachycardia, HTN (diltiazem only). DHPs HTN, vasospasm (eg. Prinzmetal's).

non-DHPs end stage CHF. DHPs conditions where tachycardia might be undesirable.

metabolized by CYP3A4, so numerous potential interactions. grapefruit is also an issue (except with amlodipine).

verapamil constipation (blocks Ca channels in bowel), diltiazem less so. DHPs HA, hypotension, peripheral edema.

CCB, 80-120mg PO TID

CCB, 120-480mg PO qd

CCB, 5-10mg PO qd

IV CCB, avoid in pts allergic to soy/eggs

atropine (cardiac), glycopyrrolate (surgical), scopolamine (surgical, motion sickness)

block activity of ACh on parasympathetic muscaric receptors. in heart, SA/AV nodes increase pacemaker rate, sometimes increase conduction through blocks

SB with hypotension, 2 degree heart block with bradycardia (can be tried in 3 degree).

symptomatic bradycardia, slow PEA, asystole

caution in situations where tachycardia can be dangerous

tachycardia, hyperthermia, delirium, other decreased parasympathetic issues

anticholinergic, 0.5mg IV q5min max 3mg

quartet: red, hot, dry, confused

stimulates A1 receptors in AV note, decreasing K efflux, Ca influx, and Na influx. Hyperpolarization renders the cell refractory (essentially causing a 3 degree heart block for a few seconds).

1) reentry circuits terminated and NSR resumes, 2) QRS eliminated so atrial tachycardias can be more easily diagnosed

half life of 10 seconds, so double-push.

caffiene acts on the same receptors and can block its action.

SVT

short-lived angina/extreme discomfort (endogenous adenosine is typically released with ischemia: decreased o2 --> decreased ADP change to ATP --> increased adenosine levels)

6-12 mg IV q1-2min, max 3 doses. pts taking carbamazepine, dipyridamole, heart transplant, central line initial dose is 3mg.

digoxin, digitalis (foxglove plant, longer T1/2)

decreased Na/K pump action. Increased intracellular Na decreases electrochemical gradient for Na-Ca exchanger, less Ca exits cell and intracellular levels rise. Net result is increased contractility. Indirectly decreases need for sympathetic compensation.

direct increase in parasympathetic tone via baroreceptors/brainstem vagal nuclei. net result is a decrease in HR (also useful in pts with a-fib due to increased PNS tone at AV node)

half-life is 30 hrs

therapeutic index 0.8-2ng/mL, 2.6 probable toxicity, 3 guaranteed toxicity (higher in children). Draw levels away from dose administration. 20% will experience toxicity, especially those with hypokalemia/electrolyte imbalances.

CHF, a-fib

absolute in pts with VF. relative in pt with ventricular arrhythmias/PVCs (exacerbate them).

diuretics (spironolactone), antiarrhythmics (quinidine), calcium antagonists (verapamil), statins (atorvastatin) increase levels

GI (N/V/D, anorexia), CNS (confusion, dizziness, agitation), CV (arrhythmias/blocks), visual (orange-tinted vision, visual disturbances)

long PR interval, AV block, scooping of ST-segment, upslope into R wave

inhibit HMG-CoA reductase, mediator in the first step in the biosynthesis of cholesterol. reduced synthesis increases number of LDL receptors (via SREBPs), increasing catabolic rate of LDL and liver extraction of LDL precursors.

major LDL. minor HDL/trigs.

lovastatin/simvastatin/atorvastatin/rosuvastatin have active metabolites

cyclosporine, macrolides, anti-fungals. pravastatin is the only one not metabolized by CYP450 enzymes (reduced risk of interactions)

absolute pregnancy (cat X), liver disease

generally well tolerated. myalgia 10%. rare include myositis/rhabdomyolysis, hepatotoxicity. possibly increase glucose.

Zocor

10-80mg PO qd

Lipitor

10-80mg PO qd

Pravachol

10-80mg PO qd

Mevacor

20-80mg PO qd

Crestor

5-40mg PO qd

Vytorin

20-40mg/10mg PO qd

monitor liver enzymes, blood sugar

gemfibrozil, fenofibrate, clofibrate

activate transcription factors (PPARs). reduces production of VLDL and speeds up removal of triglycerides, increases HDL levels (apo A1/A2 expression increased).

major HDL/trigs. minor LDL.

gemfibrozil inhibits glucoronidation of statins (increased liklihood of muscle breakdown/pain with coadministration). Interact with warfarin (potentiate anticoag - monitor INR).

rash, gallstones, liver enzyme elevation. rare pancreatitis, reversable decreased renal function, myositis/myopathy/rhabdomyositis.

Fenoglide

fibrate, 50-200mg PO qd

Lopid

fibrate, 600-1200mg PO qd

cholestyramine, colestipol, colesevelam

bile acids facilitate fat digestion/absorption, and are normally enterohepatically recycled. sequestrants are large and carry a positive charge, so they bind negatively charged bile acids and are excreeted together. the body needs to create more bile acids (which takes cholesterol) and less fat is absorbed.

major LDL. no HDL. hurt trigs.

never leave GI tract, so are OK to use in disease/pregnancy. reduce absorption of fat-soluble vitamins (A,D,E,K)

hypertriglyceridemia (interruption of enterohepatic recycling increases enzyme activity of phospatidic acid phosphatase, which is involved in triglyceride formation)

bind to negatively charged molecules, so interfere with absorption of thiazides, furosimide, propranolol, digoxin, warfarin, OCPs (can be overcome simply by seperating administration)

GI. rare hyperchloremic acidosis (bile acid resins are chloride salts, can result in increased chloride/decreased bicarb levels)

Questran

BAS, 8g powder dissolved in liquid PO TID

most often used in combo with statins because their use alone results in upregulation of HMG-CoA reductase

Niacin

unknown. does reduce liver synthesis of VLDL.

major HDL/trigs. moderate LDL.

arterial bleeding (can cause slight decrease in platelets/increased prothrombin times), hepatic issues (increased LFTs dose related)

skin flushing, itching, dryness, rash (offset with ASA/ibuprofin 30 min prior). hyperglycemia, hyperuricemia, upper GI distress (offset by taking with food).

nicotinic acid, 0.5-2g PO TID

ezetimibe

selectively inhibit absorption of cholesterol by small intestine (NPC1L1 transporter) by up to 50%

moderate LDL. no HDL/trigs.

Zetia

CAI, 10mg PO qd

omega-3 fatty acids (eicosapentaenoic acid/docosahexaenoic acid; EPA/DHA)

thought to inhibit triglyceride synthesis in the liver.

Major trigs. No HDL, hurt LDL.

caution with anticoagulation (can inhibit platelet aggregation)

Lovaza

EFA, (EPA 465mg/DHA 375mg) 4g PO qd (can divide dose)

dobutamine; norepinephrine, phenylephrine; epinephrine, dopamine

act on adrinergic receptors. alpha-1 receptors increase IP3 which increases vascular tone (vasoconstriction). beta-1 receptors activate G proteins that increase cAMP levels, resulting in increased myocardial contractile force.

dobutamine (also a vasodilator)

norepinephrine, phenylephrine (pure)

epinephrine, dopamine

very short half lives, so IV infusions (or boluses in ACLS)

hypotension, shock, acute CHF (dobutamine/dopamine)

1mg IV q3-5min

amrinone/inamrinone, milrinone

PDE breaks down cAMP/cGMP. Inhibitors increase cAMP/cGMP, causing increased intracellular Ca. Cardiac tissue = stronger contraction, smooth muscle = decreased afterload due to smooth muscle relaxation. Also theoretically improves diastolic functioning (decreased end diastolic pressure).

long half life even though administered IV, can make it tricky to find correct dose (often levels get too high) -- Swang Ganz monitoring of CO can help titrate to correct dose

CHF (increased risk of mortality)

hypotension secondary to vasodilation (can last for hours due to long half life), thrombocytopenia (much less often with milrinone).

PDE-3 not direct positive chronotropes (better for tachy pts/CAD). In CHF b-receptors are frequently down-regulated to to high endogenous chatecholamine compensatory mechanisms, so PDE-3 inhibitors are clinically much stronger.

nitroglycerin, isosorbide dinitrate (ISDN), isosorbide-5-mononitrate

release NO (EDRF), inducing vasodilation primarily on venous side (reduces venous return, preload, end diastolic pressure). Lower ventricle wall tension reduces stress/o2 demand; lower intraventricular pressure means higher coronary perfusion grandient and increased o2 supply. minor effects include coronary vasodilation, arterial vasodilation (decreased SVR) decreasing afterload.

those that release NO spontaneously (sodium nitroprusside), those that require an enzymatic process (S-nitrosothiol; organic nitrates)

oral availability is low (10%) due to reductase enzyme in liver. sublingual route avoids this first pass effect, as does patch/ointment.

ISDN/IS5M have a longer duration of action, thus are useful for long-term prophylaxis.

nitrate tolerance can develop particularly with long-acting agents, therefore they need a nitrate free period to remain effective (typically 12 on, 12 off)

angina, acute coronary syndromes, CHF, hypertensive emergencies

absolute concurrent use with PDE-5 inhibitors, increased ICP, severe anemia

HA, flushing, hypotension, dizziness

20mg PO BID

prevents reflex tachlycardia, nitrates prevent coronary vasospasm of b-blockers, nitrates prevent preload increases resulting from the negative ionotropic effects produced by b-blockers

sodium nitroprusside, Hydralazine

dilation of arterioles. SNP (prodrug) also slighly venodilates, Hydralazine is artery selective. exact mechanism is unknown.

very short half life, only available IV, rapid onset

severe hypertensive emergencies, severe heart failure

caution where reflex tachycardia/increased contractility would be harmful (CAD,AS,MS)

HA, flushing, tachycardia, lupus-like syndrome (~10%)

Nesiritide (recombinant form of BNP)

endogenous serve as a counter-regulatory system for RAAS, causing vasodilation, natriuresis, and inhibition of renin and aldosterone. This reduces preload/afterload.

short half life (initial bolus followed by continuous infusion)

advanced decompensated acute heart failure

prolonged hypotension

clonidine, guanabenz, guanfacine, methyldopa (prodrug)

agonize central alpha-2 receptors (inhibits adenylyl cyclase activity), producing a decrease in peripheral resistance, HR, BP.

HTN (not first line)

sedation, dry mucus membranes, bradycardia, hypotension, constipation, nausea

selective = prazosin, terazosin, doxazosin. non-selective (used in mgmt of pts w/ pheochromocytoma) = phentolamine, phenoxybenzamine

antagonize peripheral alpha-1 adrinergic receptors (stimulate phospholipase C activity), causing vasodilation

HTN (not first line), benign prostatic hypertrophy

orthostatic hypotension, HA, somnolence, palpitations (reflex tachycarda), nasal congestion, dizziness