Pharm- Cardio

eesohbel's version from 2015-08-06 21:14


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Anti-arrhythmics 1

Question Answer
Class I anti-arrhythmics Na+ channel blockers - decrease slope of phase 0 (depolarization) of ventricular myocytes
Class II anti-arrhythmics ß-blockers - flatten out phase 4 of pacemaker cells - slows heart in general
Class III anti-arrhythmics K+ channel blockers - slow down phase 3 of ventricular myocytes - elongating effective refractory period; increase action potential duration
Class IV anti-arrhythmics Ca2+ channel blockers - decrease the slope of phase 0 of pacemaker cells - elongating effective refractory period - decrease in conduction of AV nodal cells
Class IAdisopyramide, quinidine, procainamide "double quarter pounder"
Class IBLidocaine, mexiletine, tocainide "mayo lettuce tomato"
Class ICFlecainide, propafenone "fries please"
Class IAIncrease action potential duration, effective refractory period, and QT interval. May also be proarrythmic
Drug with a side effect of cinchonismQuinidine
Dont take with quinidineantacids or opioids and take care with digoxin (need to decrease it)
Side effect of SLE-like syndromeProcainamide
Commonly used after MILidocaine class 1b
Class IBMost used of Class I
Class ICCan by PRO-arrhythmic esp. in post-MI state. Will prolong QRS more when HR is fast
Class IRaise the threshold potential of cardiac fast response tissues (cardiomyocytes)
Class IVRaise the threshold potential of cardiac slow response tissues (SA + AV nodes)
VerapimilClass IV Ca2+ channel blocker can decrease the amount of intracellular Ca2+ available for excitation-contration coupling within cardiomyocytes, reducing myocardial contractility
What patients should verapimil not be used inCHF because negative inotropic effects
Verapamil and diltiazemhave more selectivity for heart than "dipines" which have more selectivity for BV. Use verapamil and dilitazem to treat AV nodal arrythmias
A/E verapamilbradycardia, AV blocks. Constipation. Do not use in CHF
Class IA + IIIprolong repolarization + increase refractory period lead to long QT
A/E of 1Cproarrhythmic, especially post-MI. Contraindicated in strucutral and ischemic heart disease.
A/E of solatolclass III can cause torsades de points because of excessive beta blockafe
A/E of amiodaroneclass III. Remember to check PFTS, LFTS and TFTs. Very LONG half life.
Rate control in atrial fibrillationclass IV
drug of choice in diagnosing/abolishing SCTadenosine
a/e of adenosineflushing
Magnesiumeffective in torsades and digoxin toxicity.
Which class of 1 drugs can you give in someone with ischemic heart diseaseclass 1B
special about solatolclass III and beta blocker
CCB associated with increased progression of CHFverapimil because of its strong negative inotropic effects
of the class III and Ia antiarrythmic which has lowest risk of torsadesamiodarone

Anti-arrhythmics 2

Question Answer
Class IAQuinidine
Class IAProcainamide
Class IADisopyramide
Class IBLidocaine
Class IBMexiletine
Class IBTocainide
Class ICFlecainide
Class ICPropafenone
Class IIPropanolol
Class IIMetoprolol
Class IIIAmiadarone
Class IIISotolol, amiodarone, ibutilide and dofetillide
Class IVDiltiazem
Class IVVerapamil

Class 1 (Sodium channel blocking antiarrhythmics)

Question Answer
Class 1ADisopyramide, Quinidine, Procainamide (Double Quarter Pounder)
Class 1A inhibition of phase 0intermediate
effect of 1A length on action potential of ventricleprolonged
class 1bLidocaine, Tocainide, Mexeliteine (Lettuce, Tomato, Mayo)
Inhibition of phase 0 for 1bweak
effect on length of action potential for 1Bshortened
class 1cMoricizine, Flecainide, Propafenone (More Fries Please)
1C inhibition of phase O depolarizationweak
1C effect on length of action potentialno change

Antiarthymics on the action potential of ventricle

Question Answer
Phase 0 myocardiumNa channels open, rapid depolarization
Phase 1 myocardiumNa channels inactivated, outward K current and inward Cl- current
Phase 2 myocardiumplateau due to L-type Ca channels
Phase 3 myocardiumRepolarization phase due to potassium
Phase 4 myocardiumreturn to resting potential Na/K ATPase reestablishes Na/K gradient
Drugs that effect phase 0 of myocardiumClass I drugs
Drugs that effect phase 2 of myocardiumclass IB drugs can decrease the plateau and class III can prolong the plateau
Drugs that effect phase 3 of myocardiumclass III drugs and some class I drugs prolong repolarization by blocking phase 3
Drugs that effect phase 4 of myocardiumDigoxin can be proarrthyrmic through blocking phase 4
phase 4 in SA and AV nodepacemaker current. inward Na/Ca and outward K current. (baseline). Class III and IV block
phase 3 in SA and AV nodeK channels (downstroke). Class III block
Phase 0 in Sa and AV nodeactivation of L-type Ca channels responsible for upstroke. class IV drugs block

Antihypertensive therapy

Question Answer
Treatment for essential hypertensionthiazides, ACE-inhibitors, ARBS, dihydropyridine Ca channel blockers
Treatment for patients w hypertension and HFdiuretics, ACE/inhibitors/ARBs, B blockers (compensated HF), aldosterone antagonists
Treatment for hypertension and diabetesACE inhibitors/ARBs, Ca channel blockers, thiazides diuretics and beta blockers
Decrease in arteriolar resistance, decrease in cardiac work, decrease in afterloadACE inhibitors, ARBs and CCB
Mnemonic for hypertension and pregnancyHypertensive Moms Love Nifedpine (Hydralazine, Methyldopa, Labetolol, Nifedipine)
Dihyropyridine CCBsamlodipine, felopidine, nicarpidipine, nifedipine, nisoldipine
Dihydropyrine CCB MOAacts on vascular smooth muscle to cause vasodilation
Clinical use of dihyropyridine CCBhypertension, angina, vasospasm, esophageal spasm, migraine prophylaxsis
A/E of dihydropyridine CCBperipheral edema, flushing, dizziness, and reflex tacycardia
Non-dihyropyridine CCBsdilitazem, verapamil
MOA of non-dihyropyridine CCBblock Ca channels at pacemaker cells, decreases O2 demand
Clinical use of non-dihydropyridine CCBhypertension, angina, arrhthymyias
A/E of non-dihydropyridine CCBcardiac depression, AV block, flushing, dizziness, constipation. Verapamil causes gingival hyperplasia. Avoid in CHF
MOA of hydralazineincreases cGMP leading to smooth muscle relaxation. vasodilates arterioles and reduces afterload.
Clinical use hydralazinesevere hypertension (particularly acute), HF. Safe to use during pregnancy. Can give give with beta blocker to prevent reflex tach.
Toxicity of hydralazinetachycardia, drug induced lupus! Remember SHIPP
Drugs in hypertensive emergencyclevidipine, fenoldopam, labetalol, nicardipine, nitroprusside
MOA of nitroprussideshort acting. increases cGMP via release of NO.
Toxicity of nitroprussidecyanide toxicity
FenoldopamDopamine D1 agonist
MOA of nitratesvasodilate by increasing NO in vascular smooth muscle leads to an increase in cGMP and smooth muscle relaxation. dilates veins more than arteries decreases preload.
Clinical use of nitratesangina, ACS, pulmonary edema
Toxicity of nitratesflex tachycardia, hypotension, flushing, headache.
MOA digoxindirect inhibition of Na/K/ATPase leads to indirect inhibition of Na/Ca exchanger leads to increased Ca leads to positive inotropy. Stimulates vagus nerve decreases HR ,
Digoxin's effect in atrial fibrillationdecreases conduction at AV nodes
Digoxin's effect in HFincreases contractility (inotropy)
Toxicity of digoxincholinergic because of increased parasympathetic nausea, vomiting, diarrhea; blurry yellow vision, arrhthymias, AV block. Very low therapeutic index. Bradycardia! Hyperkalemia indicates poor prognosis
antidote to digoxin toxicitiyslowly normalize K+, cardiac pacer, anti-dig FAB fragmens, MG.
digoxin clinical useHF (increases contractility) and atrial fibrillation (decreases conduction at AV node and depression of SA node)
what anti-hypertensive causes arteriolar dilation and natriuresis and improves renal perfusionfenoldopam

Antianginal therapy of Nitrates and Beta blockers and together

Question Answer
lowers end-diastolic volumenitrates (decrease preload by dilating venous system)
lowers BPnitrates, beta blockers, nitrates and beta blockers
decreases contractilitybeta blockers
increases HRnitrates (reflex response)
decreases HRbeta blockers, and beta blockers and nitrates (beta blocker effect is strong)
decreases ejection timenitrates
increases ejection timebeta blockers
decreases MVO2nitrates, beta blockers and nitrates plus beta blockers
main contributor to nitrate effect in patients with stable anginadecreased cardiac preload (left ventricular volume during diastole)

Lipid Lowering Agents

Question Answer
Greatly decreases LDLstatins otherwise known as HMG-COA reductase inhibitors
Toxicity of statinsmyalgias, myositis, rhabdo, hepatotoxicity
Bile acid resinscholestyramine, colestipol, colevelam
MOA bile acid resinsprevents intestinal reabsorption of bile acids, liver must use cholesterol to make more decreases LDL
Toxicitiy of bile acid resinsGI upset and increase blood triglyceride levels!!!!
Binds C-diff toxincholestyramine
Decreases triglyceridesfibrates
Fibratesgemfibrozil, clofibrate, bezafibrate, fenofibrate
MOA fibratesupregulate LDL and increae TG clearance. Activate PPAR-alpha which increases lipoprotein lipase activity
Toxicity of fibratesmyopathy increases risk with statin and fibrates and gallstones. suppresses 7 alpha hydroxylase which reduces conversion of cholesterol to bile acids.
Drug of choice to raise HDLniacin
Mechanism of action of niacininhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis
Toxicity of niacinred flushed face which is decreased long term by NSAID use, hyperglycemia, hyperuricemia
omega 3 fatty acidsdecrease triglycerides
increase risk of gallstonesbile acid resins and fibrates
Liver makes more bile acid because of drug administration and uses up cholesterolbile acid resins
inhibits transport of cholesterol through intestinal wallezetimibe (decreases LDL)
treatment with statinscause hepatocytres toincrease LDL receptor density as a way of increasing their means of uptaking circulating LDL


Question Answer
MOA of digoxindirect inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger. Leads to increased CA in the cell increases inotropy. Stimulates vagus nerve and decreases HR
Clinical use of digoxinHF, atrial fibrillation
Digoxin toxicitycholinergic, blurry yellow vision, arrthymias, AV block
Clearance of digoxinrenal
Factors predisposing to digoxin toxicityrenal failure, hypokalemia (drugs that cause hypokalemia such as loops!) verapamil, amiodarone, quinidine (decreased digoxin clearance)
Antidote for digoxinslowly normalize potassium, cardiac pacer, anti-digoxin Fab fragments and magnesium

beta blockers

Question Answer
non-selective beta blockersN to Z
beta 1 blockersA to M with exception of C and L which are alpha 1 and beta 1
glaucoma drugstimolol, nadolol
non-selective beta 1, beta 2, alpha antagonistlabetalol and carvedilol
partial beta agonistpindolol, acebuetolol
do not use in anginabeta 1 and beta 2 weak agonists
selective antagonistsA to M
nonselective antagonistsN to Z


Question Answer
beta-1 selective blockersnames usually start with A-M (acebutolol, betaxolol, esmolol, atenolol and metoporolol)
PDE inhibitors and nitratesabsolutely contraindicated because both increase cGMP too much hypotension
HTN in pregnancy?Hydralazing, Methyldopa, Labetalol, Nifedepine
non-dihydropyridine on heartverapamil, diltiazem (block L type calcium channels)
cause AV blockverapamil and diltiazem
gingival hyperplasiacalcium channel blockers
drug induced SLEhydralazine, procainamide
decreaed afterloadhydralazine
cyanide toxicitynitroprusside
HTN emergency medsnitroprusside, fenoldopam
decreases prelaodnitrates
nitrate with highest bioavailabilityisosorbide mononitrate
Monday diseaseindustrial exposure to nitrates develop tolerance during work week, then lost over weekend, reexposure on monday causes tacky, dizzy, headache
lowers LDL the moststatins
lowers TG the mostvibrates
lower LDL while slightly increasing HDL and TGbile acid resins
lowers LDL aloneezetimibe
best at increasing HDLniacin (B3)
how to decrease side effect of niacin?NSIADS or long term use can decrease the red flushed face seen in niacin use
niacin flushing is mediated byprostglandins
histamine flushing is mediated byhistamine
GI upset and decreased absorption of fat soluble vitaminsbiel acid resins
decrease TG but not the greatest at itomega III fatty acids
cardiac glycoside side effectsdigoxin! N/V, diarrhea, blurry yellow vision, arrhythmia, AV block, hyperkalemia
antidote for cardiac glycosidefor digoxin! anti-digoxin Fab fragments, Mg++, cardiac pacer, normalize K+ slowly
side effect of thrombocytopenia, tornadoes, cinchonismquinidine
side effect of AV block / bradycardiabeta blockers
side effect of masking hypoglycemiabeta blockers
best post-MIClass IB --> Lidocaine, Mexiletine, Tocainamide
contraindicated post-MIClass IC --> Flecainide, Propafenone
decrease slope of phase 0class 1 sodium channel blockers
decrease SA and AV node activity and decrease slope of phase 4class II beta blockers
beta blocker overdose treatmentglucagon, atropine, saline
shortest acting beta blockeresmolol
elongate phase III refractory periodclass III K+ channel blockers
this has the most side effectsamiodarone
corneal deposits and gray skin depositsamiodarone
what to monitor with amiodaronePFTs, LFTs, TFTs, (K+ channel blocker) . it causes a restrictive lung picture
decrease phase O and AV node conductionclass IV calcium channel blockers (verapamil, diltiazem)
abolish supra ventricular tachycardia?adenosine
sense of impending doomadenosine
short acting about 15 secondsadenosine
what blunts the effects of adenosine?theophylline and caffeine
causes bradycardia and prolonged QTsotalol (class III and beta blocker)
gingival hyperplasia and constipationverapamil (class IV)
S/E of lidocaineneurologic symptoms
slow AV conduction and cause PR interval prolongationBeta blockers
long QT1a and III (such as solatol)
CCBs prolong what part of the EKGPR interval
what beta blockers are contraindicated in anginaacebutolol and pindolol which have intrinsic sympathomimetic activity and thus acts as a partial beta-1 agonist
what antihypertensives can cause lipid abnormalitiesthiazides and metropolol
what drug slows HR but has no effect on contractility or relaxationdrug ivabradine that slows heart rate by sleective inhibition of funny sodium channels

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