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Pharm-Mini1

Mini 1 - Part I

QuestionAnswer
The fast response is mediated by what ion? Where does it occur? Na2+. Everywhere but the SA and AV nodes
The slow response is mediated by what ion? Where does it occur? Ca2+. Only in the SA and AV nodes, and abnormal myocardial tissue'.
What is represented by the slope of phase 0? Conduction velocity
What is represented by the slope of phase 3? Refractoriness.
What is represented by the slope of phase 4? Automaticity
What is represented by the duration of phase 2? Refractoriness (also represented by slope of phase 3).
Refractoriness is represented by what part of the action potential? Slope of phase 3 ans duration of phase 2.
What is the most common mechanism for arrhythmia? re-entry. (continuous propagation of an excitement wave in a closed circuit
Most effective drug to control RATE in A-fib? Any drug that will reduce conduction. Digoxin, Ca 2+ blocker, or Beta blocker
Key differences between procainamide and quinidine? Procainamide does not have antimuscarinic fx, no effect on Ca2+ chnnel, and no alpha blocking activity. Also: It is activated by ACETYLATION (slow acetylators need LOWER dosage)
Rate of acetylation plays a key role in the metabolism of what antiarrhythmic? Procainamide.
Lupoid syndrome has high incidence with what two drugs? Procainamide (antiarrhythmic) and Hydralazine (vasodilator)
Actions common to both class 1a drugs (name the drugs) Quinidine and procainamide...Blockage of ACTIVATED Na+ channels (main effect) and K= channels
DOC of WPW syndrome procainamide
Actions of quinidine Blockade of activated Na + channels, inactivated Na+ channels, K+ channels, Ca++ channels, and alpha-1 receptors. Results in decreased conduction (phase 0), increased refractoriness (increased slope of phase 2+3), and decreased automaticity (phase 4)
What antiarrhythmic can have varying effects on conduction? Why is this? Quinidine. This is due to its ANTIMUSCARINIC EFFECTS (similar to atropine) (INCREASED CONDUCTION!) These effects vary (unpredictable)
What drugs are associated with causing cinchoism? aspirin and quinidine.\
Rhythm control of chornic A-fib after cardioversion to maintain normal rhythm quinidine, flecainide (and ibutilide? Also use ibutilide for cardioversion if DC is not avail)
What is the mechanism of lidocaine? blockage of INACTIVATED Na channels. Causes DECREASED refractoriness in NORMAL cells and INCREASED recractoriness in DEPOLARIZED cells.(injured cells are always depolarized)
What drug is most effective in arrhythmia due to MI Lidocaine
What is the least cardiotoxic antiarrhythmic? lidocaine.
Side effects of lidocaine with normal doses anxiety and feeling of dissociation are common. With toxic does restlessness, slurred speech, halluc, and blutted vision may occur.
Digitalis induced arrhytmia DOC lidocaine or phenytoin
Ventricular arryhthmia DOC lidocaine or amiodarone (both very commonly used)
drug given PO for prevention of V-TAC mexiletine or amiodarone
Mechanism of phenytoin blockade of inactivated Na+ channels in heart and brain (this is a class 1b drug). Use for digitalis induced arrhythmia.
What is the class and mechanism of flecainide? Blockade of activated Na+ channels and K+ channels. MARKED decrease in conduction with slight decrease in refractoriness.
What are the key adverse effects of flecainide? Decreased cardiac contractility (worsens congestive HF) and may act as a pro-arrhythic.
Flecainide is absolutely contraindicated in pt with ... Congestive HF
What are the main indications for flecainide ? 1) chronic control of RHYTHM in A-FIB and A-flutter. 2) chronic control of SVT in pts without structural heart abnormalities when other drugs have failed
What is the mechanism of beta blockers as antiarrhytmics reduction of SNS tone in pts with tachycardia. Ie; tachcardia spikes when they start moving or hyperthyroid)
DOC for prophylaxis of V-FIB in pt with hx of MI Beta BLOCKERS
What is the mechanism of amiodarone? Blockade of K+ channels and INACTIVATED Na+ channels only (INCREASED refractoriness with no chance in velocity)
What antiarrhytmic increase refractoriness with no changes in conduction velocity? amiodarone. decreased slope of phase 2 and 3
THis antiarrhythmic causes decreased TPR due to vasodilation (via Alpha block plus Ca2+ block). Also causes increase coronary blood flow Amiodarone
What antiarrhythmic has a very long half life (26 days) amiodarone
Any drug that increase the refractoriness will have what effect on ECG? increase QT interval
Amiodarone is DOC for pretty much all arrhythmias, unless there is a contraindication.(mainly used for chronic control of a-fib, a-flutter, svt prophylaxis, v-fib prophylaxis, sustained V-tac.
Patient with arrhytmia due to hypertrophic cardiomyopathy with an allergy to beta blockers. Rx? amiodarone.
Mechanism of ibutilide? Blockade of K+ channels, also seems to in Na + inflow. Results in prolonged AP.
Prolongation of action potential due to K+ channel blocking is a mechanism of ?? Ibutilide
This drug is used only to convert to sinus rhythm in A-fib or A-flutter? ibutilide
Decreased conduction and increased refractoriness in SLOW fibers is the effect of what drug group? Ca++ channel blockers.
What are the effects (electrophysiological) of Ca++ blockers in arrhythmias. Decreased automaticity, conduction and INCREASED refractoriness in SLOW fibers only.
Ca2+ blockers are absolutely c/id in... WPW syndrome
What are Ca2+ blockers used for as antiarrhythmics? acute tx of SVT, acute tx / chronic control of a-flutter and a-fib.
Pt with WPW is given a drug and dies of V-tac. What drug was given? Ca2+ blocker.
***DOC for attack of SVT adenosine****
Mech of adenosine? OPENS Ach sensitive K+ channels which hyperpolarizes the SA and AV node (slowed conduction). This is equivalent to the effect of Ach on M2 receptors (slowed conduction and rate. (PNS TONE IS INCREASED)
Drug of choice for prevention of recurrent of TDP MgSO4
What antiarrhythmic is C/I in constipated pt? Ca2+ blocker
What antiarrhytmic is C/I in pt with respiratory problems? amiodarone
What drug is C/I in a pt with hx of MI? flecainide (also CI in HF)
What antiarrhytmic is c/i in pt with diarrhea ? quinidine
What antiarrhytmmic is c/i in pt with WPW? digoxin and ca2+ blockers
What antiarrhytmic is c/i in pt with diabetes? beta blockers.
What antiarrhytmic is c/i in pt with asthma? beta blocker
pt with chest pain, high BP, tachcardia, and T-wave inversion indicates? What should be used to treat this?
What diuretic drug is absolutely c/i in a pt with pulm edema? mannitol
What electrolyte imbalance is caused by losartan? Why? hyperkalemia. Losartan is an ANG II antagonist. So it prevents aldosterone from being release, thus decreasing K+ secretion.
DOX for HTN in a pt with gout and AV block losartan. It increases uric acid in urine.Hydrochlorothiazide in counterindicated becauseit cause uric acid build up.
What is the treatment for an acute MI (list all drugs given in emergency tx Nitroglycerine (to reduce angina/large venous dilation to REDUCE PRELOAD, alteplase (fibronolyrtic), aspirin, heparin (anticoag)
What is the purpose of nitro in tx of acute MI venous dilation to reduce preload
What antihyperlipidemic is used in young women of fertile age or pregnant women? Cholestyramine.
What antihyperlipidemic decrease LDL but may increase TG? Cholestyramine.
What is the mechanism by which atropine correct the bradycardia seen in post MI pt? (w/ regard to ions) Decrease K+ efflux from cell of SA node.This counteracts the effects of ACh
DOC for variant angina? Calcium channel blockers (nifedipine, diltiazam, and verapamil are all effective)
DOC for ascites in cirrhotic patients? Why? SpironolactonePatients with ascites have secondary hyperaldosteronism. a thiazide or furosemide can be added if diuresis is not adequate.
When is clopdigrel given to a patient w/ MI? When they cannot receive aspirin. Clopdigrel is an antiplatelet. Aspirin is c/i in patients with asthma (due to risk of hypersensitivity), nasal polyps, and chronic urticaria.
What patients cannot receive aspirin when being tx'd for acute MI. pts with asthma, nasal polyps, and chronic urticaria.
DOC for sustained v-tac when first line drugs are c/i'd? What are the first line drugs? First line drugs for v-tac = amiodarone or lidocaine. If these are c/i'd, use procainamide.
Ca++ blockers and beta blockers are used for what type of arrhythmia? supreventricular arrhythmias.
Fenoldopam is c/i in pt with ? glaucoma
Nitro is c/i in patients with ? toxic amblyopia, hypotension, and others
Patients with toxic amblyopia cannot receive what CVS drug ? nitro
Pt in htn crisis, who has diastolic dysfunction, diabetes, glaucoma, and toxic amblyopia. labetalol is the DOC for pt in hypertensive crisis who has diastolic dysfunction. Beta blockers and fenoldopam are c/i due to diabetes, nitro is c/i due to amblyopia, and diazoxide is also c/i due to diabetes.
What is the mechanism of minoxidil? arteriolar vasodilator that works by opening K+ channels in smooth muscle. ALways given concomitantly with a beta blocker and diuretic due to the associated fluid retention (due to renin) and incr. CO. These a/e are due to relflex SNS activation.
When is minoxidil given? when other drugs fail (3rd or 4th line drug). Always given with a B-blocker and diuretic.
what drug is used in prevention of delayed reactive vasospasm due to SUbarrachnoid hemorrhage dihydropyridines (ie; nimodipine)
Therapy for extertional angina ? beta blockers + nitrates
DOC for variant angina: Ca++ blockers.
Prevention of reynauds phenomenon? (prevents peripheral vasospasm) ca2+ channel blockers
DOC for hypertrophic cardiomyopathy (diastolic HF) diltiazem + beta blocker
What effect do each of the following have on EDV? 1) nitro, 2)Ca++ blocker, 3) beta blocker Nitro: decrease EDV, beta blocker and ca++ blocker incread EDV because they increase duration of diastole. These three drugs all have the common action of decreasing arteriar pressure
What drug can be coadministered with nitro to recude reflex tachycardia and reflex increase in contractility? Beta blocker or ca++ blocker
Sildenifil should never be given with what drug? nitro
What CVS drug is c/i in gerd? Ca++ blocker. due to its ability to relax lower the lower esoph. sphincter
Ca++ blocker with high affinity for cerebral vessels? Nimodipine
Mechanism of nitro? Nitrate is converted to Nitrite then to NO, No activiates guanylyl cyclase, which cause a dephosph of the myosin light chain... this prevents myosine and actin from interacting--> vasc muscle relaxation
In prevention of exertional angina, COPD c/i's what drug from being used? propanolol.
What drug should be used in the prevention of exertional angina in a pt with severe constipation and COPD? isosorbide mononitrate. Ca++ block is c/i due to constipation and propanolol is c/i due to COPD.
How long should beta blockers be taken following MI to prevent further infarction. indefinitely
What is the mech by which Ca++ and B blockers (alone or together) treat hypertrophic cardiomyopathy ? decrease contractility leads to increase ventricular compliance -- > decreased outflow obstruction. These drugs also slow HR, allowing longer diastolic filling
Created by: rkirchoff