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Pharm. Cardio

Things that determine O2 demand heart rate, myocardial contractility, intramyocardial wall tension (preload and afterload)
Things that determine O2 supply myocardial blood flow (can increase flow or increase blood oxygen content- Hgb)
2 Goals of drug therapy for angina 1) Prevention of MI and death 2) Prevention of ischemia and pain
Drugs used to prevent MI and death for angina patients (CV prophylaxis) antilipemics and antiplatelets, ACE inhibitors
Drugs used to prevent ischemia and pain for angina patients nitrates, beta blockers, calcium channel blockers
Stable angina usually triggered by physical activity, emotional excitement, large meal, cold exposure. CAD is underlying cause; partial obstruction (>70%) deposition of fatty plaque in arterial wall. coronary arteries cant dilate during exertion b/c of plaque.
Therapy for Stable Angina Reduce oxygen demand by decreasing HR, contractility, afterload and preload. 1) Organic Nitrates 2) Beta Blockers 3) Calcium Channel blockers 4) Renolazine (Ranexa)
Ranolazine (Ranexa) blocks late sodiun (and K+ and Ca2+), weak alpha and beta antagonist activity (antiarrythmic qualities), increases exercise performance and reduces angina frequency
Adverse effects of Ranolazine (Ranexa) prolongs QT interval
Unstable Angina medical emergency! Angina at rest, ne onset exertional angina, intensification of existing angina. Plaque rupture leads to platelet aggregation and thrombus formation = severe stenosis
treatment of unstable angina anti-ischemic therapy AND antiplatelet therapy AND anticoagulant therapy
Antiischemic therapy for unstable angina (NTG, betablocker, supplemental O2, IV morphine sulfate)
antiplatelet therapy for unstable angina aspirin, clopidogrel (Plavix), GP IIb-IIa antagonists (abciximab, integrilin, aggrastat)
anticoagulant therapy for unstable angina heparin or LMWH
Variant Angina (prinzmetals/vasospastic) caused by coronary artery spasm; pain not exertion related
treatment of variant angina calcium channel blockers and nitrates
CABG more expensive than PCI, longer hospital stay, slower recovery but better coronary blood flow, angina relief, exercise tolerance. Should consider for multivessel disease
PCI usually balloon angioplasty- higher initial reperfusion, less residual stenosis, lower reccurence rates, no intracranial bleeding. Use heparin, antiplatelets, for adjuncts
3 major vasodilator classes ACE inhibitors/ARBs, nitrates, Calcium Channel Blockers
Adverse effects of vasodilators postural hypotension, reflex tachycardia, increase blood volume??
Nitrates (Nitroglycerin)- MOA in endothelium, NTG is denitrated and nitric oxide is released. NO stimulates guanylyl cyclase to produce cGMP, dephosphorylation of myosin, relaxation of vascular smooth muscle and vasodilation
Nitroglycerin for use during stable angina decreases oxygen demand by reducing preload - primary effect is on VEINS
Nitroglycerin for use during variant angina increases cardiac O2 supply by dilating arterioles
Adverse effects of nitroglycerin secondary to vasodilation: headache, orthostatic hypotension, reflex tachycardia
Drug interactions of NTG other hypotensive drus, especially sildenafil
tolerance of nitroglycerin rapid- within a day complete tolerance or tachyphylaxis can occur
prevention of tolerance to NTG low dose, long acting formulations, intermittent schedule that allows 8 drug free hours every day; can also withhold nitrates for a while
sublingual NTG rapid onset, short duration
transmucosal (buccal) tablets of NTG rapid onset, long duration (3-5 hours)
transdermal patches of NTG slow onset, long duration (24 hr)
oral NTG sustained release, taken q 6-12 h (dont take at night to avoid tolerance)
intravenous infusion of NTG short half life; rarely used for angina, may be used for MI or acute HTN
Beta Blockers- MOA used for stable angina (not effective for variant) reduce angina pain by decreasing O2 demand via blockade of B1 receptors in heart, decreasing HR and contractility. Also decrease arterial pressure (dec. afterload), increase O2 supply
adverse effects of beta blockers bradycardia, AV block, bonchoconstriction, CNS effects (insomnia, bizarre dreams, depression, sexual dysfunction)
Calcium channel blockers decreased calcium influx inhibits smooth muscle contraction in vessel, diltiazem and verapamil also decrease heart rate and contractility [decrease O2 demand by dilating arterioles]--- used to treat variant angina (works on arterioles)
calcium channel blockers- dihydropyridines nifedipine and amlodipine; act on smooth muscle of arterioles, no conduction effects
calcium channel blockers- non dihydropyridines verapamil, diltiazem; act on aretrioles and on heart, lowers HR, decreases AV conduction, decreases force of contraction
adverse effects of calcium channel blockers cardiac depression (arrest, bradycardia, AV block), reflex tachycardia with nifepidine
Myocardial Infarction- STEMI complete interruption of regional blood flow to myocardium, ST elevation. Cell death within 20 minutes, scar formation by 4-6 weeks. Injury triggers ventricular remodeling, which increases risk of heart failure and death- Troponin I/T and CPK-MB
7 drug classes for treatment of MI oxygen, aspirin, IV morphine sulfate, beta blockers, NTG, ACE inhibitors, thrombolytics
Purpose of oxygen therapy in MI tx increases oxygen supply
purpose of aspirin in tx of MI suppresses platelet aggregation, producing antithrombotic effect
purpose of IV MS in tx of MI for pain, modest arterial and venous dilation so improves preload and afterload to lower oxygen demand
purpose of beta blocker in tx of MI reduce short term mortality rate and infarct size, also long term survival
purpose of NTG in tx of MI does not reduce mortality, but offers hemodynamic properties and relieves pain
purpose of ACE inhibitors in tx of MI decrease short term mortality in MI and decrease long term mortality if reduced LV function
purpose of thrombolytics in tx of MI if present early (3 hours or less after signs and symptoms of MI)
Heart Failure progressive disorder characterized by left ventricular dysfunction, decreased cardiac output, decreased tissue perfusion and s/s of intravascular and interstitial volume overload
4 things the body does to adapt to reduced CO in heart failure 1) cardiac dilation, 2) increased sympathetic tone, 3) water retention and increased blood volume, 4) natriuretic peptides
HF compensation- Cardiac dilation heart expands, initially improves cardiac output (contractility increases), BUT maximal contractile force of failing heart not enough to drive new muscle mass (causes further decrease in CO)
HF compensation- Increased Sympathetic tone heart failure causes decrease in arterial pressure, so baroreceptor reflex increases sympathetic output to heart and arterioles - increased HR, increased contractility, increased venous tone, increased arteriolar tone
problem with increased heart rate during HF if Hr increases too much, there will be insufficient time for complete ventricular filling and CO will fall
problem with increased contractility in HF increases myocardial oxygen demand
problem with increased venous tone in HF increases venous pressure, which increases ventricular filling, which increases stroke volume, preload. If venous pressure is excessive, blood will back up behind failing ventricle, causing edema.
problem with increased arteriolar tone in HF increased arteriolar pressure increases perfusion of organs, BTU heart must pump against greater resistance
HF compensation- Water Retention and Increased blood volume reduction in renal blood flow and glomerular filtration causes activation of RAA, which promotes water retention.
benefits of water retention and increased blood volume in HF increased blood volume increases venous pressure and venous return- ventricular filling increases and SV increases. increases CO and tissue perfusion
harms of water retention and increased blood volume increased blood volume= increased venous pressure= blood back up and edema
HF compensation- Natriuetic Peptides in response to stretching of fibers and dilation, heart releases atrial natriuetic peptide and B natriuetic peptide to promote dilation of arterioles and veins and to promote loss of Na+ and H20 to counterbalance SNS and RAA effects
5 drug classes for treatment of heart failure 1) diuretics 2) ACE inhibitors 3) aldosterone antagonists 4) Beta blockers 5) Digoxin
Diuretics for HF reduce blood volume, decrease arterial pressure (preload), edema, cardiac dilation. Thiazides, Loop, and K+ sparing (spironolactone prolongs survival by blocking recpetors for aldosterone)
ACE inhibitors for HF blocks conversion of AT1-AT2. Dilates arterioles and veins and decreases aldosterone release. Dilation counteracts sympathetic outflow, increases CO, and decreases edema. Aldosterone suppression= less sodium and water retention, decreases preload
Adverse effects of ACE inhibitors hypotension, hyperkalemia, dry cough, angioedema
aldosterone anatgonists for HF Spironolactone and Inspra. Reduce symptoms, decreased hospitalizations, prolong life. Block aldosterone receptors: supress cardiac remodeling and fibrosis, prevents SNS activation, prevents vascular fibrosis
Beta Blockers for HF contraindicated until 1990s because they reduce contractilit. Now: can improve LV ejection fraction, increase exercise tolerance, slow progression, decrease hospitalization, and prolong survival
Digoxin- MOA cardiac glycoside, increases contractility and CO by inhibition of Na+/K+ ATPase (sodium potassium pump)
Normal Action of the Na+K+ATPase pump during action potential, Na+ and Ca++ enter the cardiac cell and K+ exits. Following the action potential, Na+K+ATPase pumps Na+ out of cell and takes up K+ to restore ion concentrations. Ca+ leaves the cell in exchange for uptake of Na+
Inhibition of Na+K+ATPase by digoxin digoxin prevents extrusion of Na+ from cell and take up of K+ to restore balance after AP. Na+ accumulates inside cell. Calcium cant be exported outside cell b/c theres too much sodium inside(no way to exchange). Result = increase in calcium concentration
Pharmacokinetics fo Digoxin enterohepatic circulation contributes to long half life (50 hr), but 2/3 excreted unchanged by kidney. Loading dose usually given b/c of long half life. Narrow therapeutic range
Electrical Effects of Digoxin resting membrane potential reduced(less k+ inside due to sodium pump inhibition) eventually leading to premature depolarization. May lead to arrythmia
neurohormonal effects decreased sympathetic tone, increased renal blood flow and urine output, decreased renin release
Adverse Effects of Digoxin arrythmias (caused by hypokalemia), GI, CNS (fatigue, visual disturbances)
digoxin- K+ levels K+ levels must be kept within physiologic range because K+ competes with digoxin for binding to the ATPase. too much K+ interferes with digoxin efficacy and too low K+ can cause dig toxicity
Digoxin Toxicity diarrhea, loss of appetite, nausea, vomiting, headache, visual disturbances, or cardiac dysrhythmia
Reversing Digoxin toxicity IV antidigoxin fab fragments (total neutralization not necessary
which classes have been shown to prolong survival in heart failure patients? ACE Inhibitors, aldosterone antagonists, Beta Blockers
Nesiritide (Natrecor)- MOA recombinant form of BNP (hormone secreted from ventricles in response to inc. volume and pressure overload)- vasodilation via increased cGMP in smooth muscle and decreases venous and arterial tone and diuresis, suppress RAA, suppress sympathetic outflow
Nesiritide (Natrecor)- Uses addition to standard care for decompensated heart failure, more rapid and sustained hemodynamic actions compared to NTG/dobutamine/milrinone; effective IV when patient has dyspnea at rest
sildenafil- MOA inhibits breakdown of cGMP by phosphodiesterase (5), resulting in vasodilation.Relaxation of smooth muscle of corpus cavernosa, fills with blood= erection. NO/nitrates activate guanylyl cyclase, increase cGMP and cause vasodilation too- dont take together
Arrhythmia abnormality in site of origin of impulse, its rate or regularity or its conduction
refractory period lenght of time between phase 0 and sufficient recovery of Na+ channels to permit a new propagated response (cell will not respond to stimulus)
P wave atrial depolarization
QRS ventricular depoolarization
T wave ventricular repolarization
Phase 0 rapid rise that represents depolarization following rapid sodium entry into cell
Phase 1 overshoot; early fast repolarization as sodium gates inactivate
Phase 2 plateau; slower calcium current- calcium enters cell and promotes contraction of atrial and ventricular muscle (drugs that reduce calcium entry during phase 2 dont influence cardiac rhythm, but reduce contractility)
Phase 3 repolarization, completion of Na and Ca channel inactivation and increase K permeability (K+ leaves cell)- can be delayed by drugs that block calcium channels(prolongs AP duration and prolongs effective refractory period)
Phase 4 membrane potential may remain stable or membrane can undergo spontaneous depolarization (phase 0 starts, starting new AP= automaticity) - pathological conditions, membrane may depolarize spontaneously and initiate dysrhythmia
how do dysrhythmias form? 1) disturbances in impulse FORMATION (automaticity) and 2) disturbances of impulse CONDUCTION
Disturbances of Automaticity 1) Cell normally capable of automaticity (SA/AV/HIS/ purkinje)produce dysrhytmias if normal rate of discharge changes 2) dysrhythmias occurif tissues that dont normally express automaticity (atria/ventricle muscle) develop spontaneous phase 4 dep.
Sinus tachycardia excessive discharge of sympathetic neurons that innervate the SA node can augment automaticity to such a degree that tachycardia results (inc. sympathetic stimulation= sinus bradycardia)
Disturbances of Conduction AV block, Reentry
Atrioventricular Block impaired conduction through the AV node produces varying degrees of AV block
First degree AV block if impulse conduction is delayed (but not prevented completely)
Second degree block if some impulses pass through the node, but others do not
third degree AV block if all traffic throguht he AV node stops
Reentry (Recirculating Activation) causes dysrhythmias by establishing a localized, self sustaining circuit capable of repetitive cardiac stimulation
Normal Conduction impulses from purkinje fiber stimulates the strip of ventricular muscle in 2 places. Within the muscles, waves of excitation spread from both points of excitation, meet between the purkinje fibers, and cease further travel
One Way Block strip of muscle excited at only one location. impulses spreading from this area meet no impulses from other side, can travel to stimulate other branch of purkinje fiber. Stimulation passes back up fiber, past block, then stimulate first branch again
Drugs for One way Block (reentrant conduction) 1) convert unidirectional block to bidirectional 2) improve conduction in block (eliminate block) 3) increase refractory period
4 antidysrhythmic classes 1) Sodium Channel Blockade 2) Beta Blockers 3) Action potential blocking agents 4) Calcium Channel Blockers
Class IA Antidysrhythmics Quinidine, Disopyramide, Procainamide
Quinidine (class IA)- MOA blocks sodium channels- slows impulse conduction in atria, ventricles, and HIS/Purkinje system. Also delays repolarization.
Quinidine (class IA)- Uses broad spectrum use against supraventricular and ventricular dysrhythmias. Long term suppression of dysrhythmias
Quinidine (Class IA) Adverse Effects diarrhea, GI upset, cinchonism, cardiotoxicity, arterial embolis,
Class 1B antidyrhythmics Lidocaine
Lidocaine (class IB)- MOA blocks sodium channels and reduces automaticity, accelerates repolarization; no effects on EKG
Lidocaine (class IB)- uses short term treatment of ventricular dysrhythmias, local anesthetic
Lidocaine (class IB)- Adverse Effects generally well tolerated, may cause CNS effects (drowsiness, confusion, paresthesias), toxic doses can cause convulsions and respiratory arrest
Class IC Antidyrhythmics Propafenone (Rhythmol), Flecainide (Tambocor)
Class IC (flecainide/propafenone) - MOA block Na channels and delay ventricular repolarization (increases effective refractory period)
Flecainide (uses and warnings) twofold increase in mortality for asymptomatic ventricular tachycardia after Mi, reserved fro severe refractory ventricular dysrhythmias
Class II Antidysrhytmics Beta Blockers
Beta Blockers (Class II) reduce calcium entry and depress phase 4 depolarization, reduce automaticity, slow conduction velocity, reduce contracitlity
Class III Antidyrhythmics Action Potential Prolonging Agents (AMIODARONE)
Amiodarone (Class III)- MOA K+ channel blocker that delays repolarization, but also blocks inactivated sodium channel and is a weak adrenergic and Ca++ channel blocker
Effects of Amiodarone (class III) slowed HR, AV conduction, QT prolongation
Amiodarone (Class III)- uses highly effective for atrial and ventricular dysrhytmias, only used/approved for refractory life threatening ventricular dysrhythmias
Amiodarone (class III)- adverse effects Pulmonary toxicity, hepatic function must be monitored, corneal microdeposits, photophobia, blurred vision, photosensitivity, blue gray discoloration of the skin, CYP interactions
Class IV Antidysrhythmics Calcium Channel Blockers
Effects of Calcium Channel blockers reduce automaticity in SA node, delay conduction throguh AV node, reduction of myocardial contractility
Prodysrhytmics effects all antidyrhythmic drugs can worsen existing dysrhythmias and generate new ones
Supraventricular Dysrhythmias arise in areas of the heart above the ventricles (atria, SA node, AV node)- includes atrial fibrillation, atrial flutter, sustained supraventricular tachycardia
Atrial fibrillation multiple ectopic foci fire randomly and stimulates a small area of atrial muscle. Highly abnormal atrial rhythm but rapid or normal ventricular rate. Sometime benign
Main risk with Atrial fibrillation STROKE- blood can be trapped in atria, permitting formation of a clot. when normal sinus rhythm is restored, the clot may become dislodged and can travel to brain
Treatment goals of Atrial fibrillation 1) improvement of ventricular pumping 2) prevention of stroke
1) Improvement of ventricular pumping in A Fib 1) restoring normal sinus rhythm (DC cardioversion, short term tx with drugs, RF ablation of dydrhythmic source) 2) Slowing ventricular Rate: beta blocker, cardioselective CCB
2) Prevention of Stroke in A Fib Warfarin therapy or new oral agent dabigatrin (pradaxa)
What do you treat infrequent episodes of A Fib with? PRN flecainide or propafenone, "pill in pocket"
Atrial Flutter caused by an ectopic atrial focus discharging at a rate of 250-350 times per minute. Ventricular rate is slower (~150) because AV node cant transmit impulses at such a high rate (creates saw tooth pattern)
Treatment of choice for atrial flutter DC cardioversion
Long term therapy of atrial flutter class IC (flecainide or propafenone) of Class II (amiodarone)
Alternatives to cardioversion for atrial flutter RF ablaiton of focus, ventricular rate control (beta blocker, cardioselective CCB)
supraventricular tachycardia usually caused by an AV nodal reentrant circuit; HR increases to 150-250 bpm
Interventions (non pharmacological) for Supraventricular tachycardia interventions that increase vagal tone= carotid sinus massage or Valsava maneuver). Catheter ablation of focus (transect reentrant circuit)
Drugs for Supraventricular tachycardia IV beta blocker or calcium channel blocker to slow the rate, IV adenosine for paroxysmal SVT
Ventricular dysrhythmias NOT benign, affect cardiac output, common cause of sudden cardiac death, may be paroxysmal
sustained ventricular tachycardia arises from single, rapidly firing ventricular ectopic focus, typically located at the border of an old infarction. Focus drives ventricles at a rate of 150-250 bpm
Treatment of choice for ventricular tachycardia cardioversion
What do you give a patient in V Tach if Cardioversion fails? IV amiodarone (lidocaine and procainamide are alternatives)
long term management of Ventricular tachycardia amiodarone, sotalol OR implantable cardio defibrillator (ICD)
Ventricular Fibrillation asynchronous discharge of multiple ventricular foci- localized twitching all over ventricles. Pumping of heart stops, patient becomes unconscious and cyanotic, death follows if heartbeat is not restored quickly
Immediate treatment for Ventricular Fibrillation electrical countershock (defibrillation)
Drugs to enhance effects of defibrillation in V Fib IV lidocaine, procainamie, bretylium
Long term suppression of ventricular fibrillation amiodarone, ICD
Tosades de Pointes caused by prolonged prolongation of QT interval by a variety of drugs (Class 1A and II)
High Risk Patients: LDL goals has CAD or CAD risk equivalents, 10 year risk >20%. GOAL: <100 mg/dL. DRUG THERAPY if LDL >130
Moderate Risk Patients: LDL goals has 2 or more risk factors, doesn’t have CAD yet, 10 year risk is <10% o Goal is <130 mg/dL o Start therapeutic lifestyle changes if 10 year risk 10-20%, or LDL >130 o Start drug therapy if LDL >160
Low to Moderate Risk Patients: LDL goals has 0-1 risk factor o goal is <160 o TLCs at >160 o Drug therapy at >190
Lipoproteins (Chylomicrons) serve as carriers for transporting triglycerides and cholesterol in blood (hydrophobic core of TG/cholesterol and hydrophilic shell of phospholipids)
Apolipoprotein constitute protein in lipoprotein. Serve as recognition sites for cell receptors and allow cells to bind with and ingest lipoproteins, activate enzymes that metabolize lipoproteins, increase structural stability of lipoproteins
Apolipoprotein B-100 lipoproteins that deliver triglycerides and cholesterol to nonhepatic tissues contain B-100
Apolipoprotein A-I Lipoproteins that transport lipids from nonhepatic tissues to liver contain A-1
LDL contain cholesterol as primary core lipid and account for 70% cholesterol in blood. Deliver cholesterol to nonhepatic tissues(cells use receptor mediated endocytosis by binding to B-100 apolipoprotein)
HDL contain cholesterol as primary core lipis and account for 20-30% of blood cholesterol. carry cholesterol form peripheral tissues back to liver and promote cholesterol removal from blood. Contain apolipoprotein AI and A-II
Antilipemic Therapy classes (4) Statins, Niacin, Fibric Acid Derivatives, Bile Acid binding resins
Statins- MOA competitive inhibition of HMG CoA reductase (enzyme that catalyzes hepatic cholesterol synthesis). Causes hepatocytes to synthesize more LDL receptors so they are able to remove more LDL from blood. Also decrease production of apolipoprotein B-100
statins- effects Raises HDL by 5-22%, Reduce LDL by 25-63%. Promote plaque stability, reduce inflammation, improve endothelial function, enhance dilaiton, lower the risk of AF, reduce risk of thrombosis, increase bone formation
Statins- Indications hypercholesteorlemia, primary and secondary prevention of CV events, post MI therapy, diabetes
Statins- drugs Lovastatin, Simvastatin (prodrugs), Atorvastatin, Fluvastatin, Rosuvastatin - given at night b/c cholesterol biosynthesis is at night, contraindicated in pregnancy and children
Statins- Adverse effects myopathy, rhabdomyolysis, liver injury, CYP3A4 Inhibitors raise statin levels (grapefruit juice)
Niacin - MOA inhibits VLDL production, which decreases LDLs (byproducts of VLDL degradation)
Niacin- effects decreases LDL by 14-17% alone, but 40-60% when combined with a resin. Triple combination of niacin/statin/bile resin can lower LDL by 70% or more. Most effective for increasing HDL (combo with statin raises by 41%)
Adverse effects of Niacin harmless cutaneous vasodilation and headache (flushing of face, neck, ears), Hepatotoxic
what should you do to reduce flushing with use of niacin? pretreatment with aspirin 325 mg or 200 mg ibuprofen. tolerance also helps
Fibric Acid Derivatives (Fibrates)- MOA increase lipolysis via Lipoprotein lipase (LPL) and decrease VLDL secretion
Fibric Acid- effects lower levels of triglycerides by 50% or more, raises HDL, little effect on LDL
Fibric Acid Derivatives- drugs Gemfibrozil, Fenofibrate
Fibric Acid Derivatives- Indications useful in hypertriglyceridemia when VLDL predominates, also useful for increased triglycerides from viral protease inhibitors
Fibric Acid derivatives- adverse effects well tolerated, rash and GI disturbances, can cause gallstones, myopathy, and liver injury
Bile Acid Binding Resins- MOA bind bile acids in intestine and prevent reabsorption and reuse. Liver must increase cholesterol uptake from plasma, so plasma LDL decreases
Bile Acid Binding Resins- drugs Colesevelam (Welchol)- produces 20% reduction in LDL, 50% in combo with statin
Bile Acid Binding Resins- indications hypercholesterolemia
Bile Acid Binding Resins- adverse effects constipation and bloating, interfere with absorption of other drugs (give 1 hr before or 2 hr after resins)
Ezetimibe (zetia) inhibits intestinal absorption of cholesterol, 18% avg. cholesterol reduction, decreases LDL by 25% beyond statin alone (synergistic) --> Vytorin= simvastatin+zetia
Fish Oil omega 3 fatty acids- decrease risk for CHD and thrombotic stroke
Lovaza : contains a combination of EPA and DHA. Approved as adjunct to dietary measures to reduce triglycerides (can decrease by 20-50%)
Created by: alexadianna