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Pharm-Mini1
Mini 1 - Part I
| Question | Answer |
|---|---|
| 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
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