click below
click below
Normal Size Small Size show me how
Antiarrhythmia
UVa med pharmacology block 3
Question | Answer |
---|---|
How do you treat AV nodal reentrant tachyarrythmias? | acute: vagal maneuvars, ADO, verapamil, ditizaem or esmolol chronic: surgical ablation, or nodal targets (beta blockers or Ca blockers, dig) or fast pathway blockers (clas Ia or III) |
How do you treat Vtach after MI or surgery? | acute - lidocain, procainamide, DC cardiovert chronic - amiodarone, ICD |
How do you treat Afib? | -rate cntrl-> acute tx w/IV drugs (dig, class IV, II, or adensoine)& maintence (beta or Ca blockers) -restore sinus -> DC cardioversion or IV procainamide or oral propafenone. maintence->amiodarone, sotalol> procainamide > flecainde, propafenone -antic |
T/F Like Class I drugs, Class III drugs work exclusively on the ventricular cells | F - work on all cardiac cells |
How does the action potential of nodal cells differ from ventricular cells? | phase 0 is entirely Ca as opposed to Na dependent in nodal cells thus have slower propogatio time than other cells |
T/F Class Ib drugs will alter the shape of the AP | F - only bind to Na fast channels in activated state, thus will lengthed ERP, which is unseen in the AP |
What are the beta blockers? | propranolol acebutolol esmolol |
What are the pharmocologic effects of amiodarone? | class III: blocks delayed rectifier also blocks Na & Ca channels and has beta blocking actiivity -> thus has alll class effects I-IV increases refractoriness in all cardiac cells, depresses automaticity, slows AV conduction, His and ventricular conducti |
How does acebutolol differe from propranolol? | B1 selective agen given orally to manage ventricular premature beats |
What are the different types of Class I drugs? | 1A - quinidine, procainamide 1B - Lidocaine 1C - flecainide, propafenone |
Why do some class I drugs cause widened QRS? | class Ia and Ic drugs slow phase 1 depolarzation, thus lengthen ventricular depolarization |
How do class III antiarrhythmic drugs generally work? | block K channel delayed rectifiers (Ik), thus increase ERP |
What drugs increase the PR interval? | drugs that slow the AV node phase 0 dV/dt: beta blockers Ca channel blockers digoxin adenosine |
How do class Ia,b, and c drugs differ in terms of half life and QRS elongation? | B -> fast (<1 s) half life and little to no QRS elongation A -> intermediate (1-10s) half life and small elongation C -> slow (>10 s) half life and 25% elongation |
What are the pharmocologic effects of dofelitidine? | selective blocker of one of the two main delayed rectifyers |
What are the side effects of propafenone? | new arrhymias excerbation of heart afailures increased entricualr rate in atrial flutter, sinus bardycardia |
What are the antiarrhythmic uses of beta blockers? | ventricular rate control in SVTs control of arrhymias due to excessive sympathetic tone digoxin indued arrthmias |
Why isn't ACh used for arrhthymias? What is used instead? | b/c local injection cauess hypotension -> increaesed HR use vagal maneuvers instead (carotid massage and Valsalva maneuer) |
What are the class IV drugs? | verapamil diltiazem Ca channel blockers |
What are the pharmological effects of propranolol? | non selective beta blocker w/ lidocaine effects at high dose slows HR by decreasing phase 4 repolarization in SA node increases PR interval by slowing phase 0 dV/dt in AV node increaes AV refractoriness |
What are the side effects of propanolol? | excessive AV block hypotension and aggravation of CHF withdrawal can cause rebound effect, thus withdrwa slowly decrease HDL/LDL reatio, worsen asthma and diabettis |
What is the ERP? | effective refractory period: the time it takes for at least 25% of Na channels to become reactivated |
What are the effects of NE on the AV node? | more rapid phase 4 dP/dt -> decrease refractoriness and more excitabile more rapid phase 0 dV/dt -> increae conduction velocity of AV node |
What are the side effects of lidocaine? | drowsiness, slurred speech, axiety, convulsions depression of heart contractility, automaticity and AV conduction |
What are the pharmocologic effects of flecainide? | class Ic drug thus widens QRS and reduces Ik (prolongs QT) depresses conduction velocity in atrial, ventricular and purkinje fibers |
How do class I antiarrhythmic drugs generally work? | block fast Na channels of non nodal cells: bind to the open and refractory states of the Na channels (more highly active cells), don't change shape of AP, just the length (longer) thus increase the ERP |
What aspect of the AV nodal AP controls "refractoriness"? What correlates to "conduction time"? | refractoriness -> phase 4 dV/dt conduction time -> phase 0 dV/dt |
What aer the side effects of sotalol? | torsades de pointes |
What is a DAD? | delayed after depolarization caused by any circumstance that produces intracellular Ca overload and subsequent depolarization by activation of Na/Ca exchange seen in structural V tach |
What are the effects of ACh on the AV node? | increase phase 0 threshold decrease phase 0 dV/dt decrase phase 4 dV/dt |
T/F adenosine produces a systemic wide vasodilation | F - everwhere but kidneys (vasoconstricition) |
What are the side effects of adenosine? | brief asystole and decreased contractlity constipation don't use in asthmatics |
What is amiodarone used for? | maintenance of sinus rhythm in Afib or flutter post operatively also prevents any Vtachs or Vfibs |
How is drug induced torsades treated? | discontinue drug administer MgSO4 IV (Ca channel blocker) thus reducing exctabliilty adust K to within 4.5 to 5 if hypokalemic -> will stabilize the ventricle |
What are the effects of ACh on the SA node? | decrease phase 4 dV/dt |
What are the pharmocologic effects of sotalol? | Class III thus blocks delayed rectifyer beta blocker as well same effects as amiodarone except does not affect conduction velocity in fast respone tissue b/c doesn't block Na channels |
How does esmolol differ from propranolol? | selective B1 blocker given only IV for acute ventriular rate control caused by SVTs |
What are the pharmocological effects of lidocaine? How is it used? | class Ib drug -> mild Na blockade w/ no QRS widening increases refractoriness and slows conduction in ischemic cells ONLY USED IV for acute treatment of Vtach or Vfib in surgery or MI |
What is sotalol used for? | sustained Vtach and prevents recurrence of Afib |
What are the pharmocoloigc effects of class IV drugs? | slow conduction only in slow respone (nodal) tissue to increase the PR interval increase AV refractoriness to slow ventricular rate redue calcium entry in ventrcile and inhibit calcium mediate slow response in ventricles (good for Vtach) |
How do class IV antiarrhythmic drugs generally work? | block Ca channels thus: SA: decrease phase 4 dV/dt increase phase 0 threshold AV: increase phase 0 threshold decrease phase 0 dV/dt decrease phase 4 dV/dt |
How do class IA antiarrhythmic drugs generally work? | same as class I (bind to open and inactivated Na channels) to prolong the ERP ALSO slow phase 0 dV/dt, thus mkaing the AP last even longer can cause more arrhythmias... |
What is Torsade de Pointes? | rapid ventricular rhythm caused by two competeing irritable ventricular foci or drugs "twisted ribbon" |
What are the therapeutic uses of class IV drugs? | IV for acute treatment or orally for chronic care useed for rate control in SVTs or Vtach due to DADs |
What are the side effects of quinidine? | new arrthymias - torsades de pointes, long qt, AV conduction problems GI distress, hypotension, others.. |
How do class II antiarrhythmic drugs generally work? | beta AR antagonists thus: SA: increase phase 0 threshold decrease phase 4 dV/dt AV: decrease phase 0 dV/dt decrease phase 4 dV/dt |
What is Procainamide used for? | injected IV as alternative to electric cardioersion in Afib or Aflut can be used to maintain sinus rhythym in SVTs |
What are the effects of NE on the SA node? | decrease phase 0 threshold increase phase 4 dV/dt |
What are the side effects of class IV drugs? | excessive bradycardia AV block negative inotropic efects constipation |
What is ibulitide used for? Risks? | given IV to convert recent onset of Afib or Aflut may cause torsade |
What are the pharmocological actions of procainamide? | Ia drug, thus similar to quinidine except: less vaglolytic and alpha-blocking (thus won't increase AV conduction / pro arrthymatic) |
What are the pharmocologic effects of adenosine? | similar to ACh -> activates K chanels in SA/AV nodes to resut in bradycardia and reduce AV nod excitability also reduces ventcrular contractlity |
What is adeonsine used for? | IV treament for acute control of ventciular rate in SVTs also fordiagnosis of Afib and Aflut with increased ventricular rate |
What is propfenone used for? | taken orrally to maintain sinus rythym in SVTs and in conjunction w/ AV blockerin treating ventricular arrythmias |
What is dofelitide used for? | taken orally to convert Afib or Aflut and to prevent recurrences |
What are the pharmocologic effects of ibutilide? | prolongs AP duration by turning on a slow Na current |
What is digoxin used for? | used IV or orally to control ventricular rate in AFib or flut associated w/ heart failure |
What is quinidine typically used for? | chroinc maintenance of sinus rhythm in Afib or Aflut most coadminister AV nodal blocking agent b/c of increased AV conduction / decreased refractoriness (alpha blocking effects and anticholinergic effect) |
What are hte pharmacological actions of Quinidine? | class Ia block Na chanels increase ERP AND widen QRS reduces Ik: increases ERP further and may cause Torsades de pointe anti muscarinic effect - increase HR and excitability of AV node (proarrhythmatic) mild alpha blocker - drop in BP cause reflex tach |
What are the side effects of flecainide? | new arrhythmias excerbation of heart failrue |
What aer the side effects of dofelitide? | torsades renal inssuficiency |
What are the side effects of Procainamide? | lupus like syndrome CNS side effects (confusion) rash, hypotension, torasdes de points heart block if IV |
What are the pharmocolgic actions of propafenone? | Ic drug, thus Na channel blocker that slows conduction of fast pathways some K blocking activity and is bild beta blocker |
What are the side effects of amiodarone? | pulmonary fibrosis cardiac and GI problems no Torsades.... unless hypoMg/K |
What are the pharmocological effects of digoxin? | inibhitis Na/KATPase everywhere to increase intracellular Ca, thus resting potential, thus making it easier to dpolarize, thus facilitates pressure sensor to increase parasympathetic input to heart |
What is flecainide used for? | maintenace of sinus rhym in Afib or other SVTs in pts w/ no structural heart diseae |