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148 Cards in this Set
- Front
- Back
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What are the Vaughan-Williams classes of antiarrhythmic drugs?
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1. class IA, IB, and IC (Na+ channel blockers)
2. class II (beta-blockers) 3. class III (K+ channel blockers and others that prolong repolarization) 4. class IV (CCB's) 5. miscellaneous |
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During which phase of the myocardial cell AP does Na+ influx occur? Ca++ influx? K+ efflux?
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1. phase 0
2. phase 2 3. phase 3 |
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What 2 things happen when you block Na+ channels during phase 0?
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1. decrease conduction velocity
2. decrease slope of phase 0 |
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What 2 things happen when you block K+ channels during phase 3?
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1. prolong phase 2
2. increase ERP |
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During which phase of the nodal cell AP does Ca++ influx occur? K+ efflux? I-sub-f influx?
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1. phase 0
2. phase 3 3. phase 4 |
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Diastolic depolarization is what phase? This occurs at what voltage in nodal cells?
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1. phase 4
2. -60 mV |
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What is the treatment for chronic bradycardia?
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pacemaker
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What are the 2 main mechanisms of cardiac arrhythmias?
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1. abnormal impulse formation
2. abnormal impulse conduction |
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What are the subclasses for the 2 main mechanisms of cardiac arrhythmias?
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1. class-abnormal impulse formations (subclasses- abnormal automaticity and triggered automaticity)
2. class-abnormal impulse conduction (subclass-reentry) |
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How does abnormal automaticity occur?
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ischemia or damage to non-nodal tissue causes abnormal ion movement through the na-k-atpase pump->more Na+ influx occurs->phase 4 slope increases->threshold is reached sooner->AP develops sooner than in nodal tissue->non-nodal tissue becomes new pacemaker
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How can you eliminate arrhythmias due to increased automaticity?
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1. decrease phase 4 slope
2. make the diastolic potential more negative 3. make the threshold more positive |
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What are the major effects of Na+ channel blockers (SCB's)?
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1. decrease phase 4 slope
2. decrease excitability 3. increase threshold |
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How can you prevent v-tach from a rapidly firing ectopic pacemaker?
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give a SCB
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How does triggered automaticity occur?
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it occurs when the repolarization phase is interrupted by an EAD or DAD
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What causes a DAD?
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Ca++ overload will cause spontaneous Ca++ release from the SR
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What antiarrhythmic can cause a DAD?
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digoxin
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What causes an EAD?
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small depolarization in phase 3->prolongs plateau->can cause torsades
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What can prolong plateau phase of an AP?
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1. anything that increases net inward current during repolarization
2. K+ channel blocker (PCB) will delay repolarization->prolongs plateau->can develop EAD->can develop torsades |
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What ion can suppress EAD's? How? What is this used to treat?
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1. Mg++
2. shortens plateau 3. torsades |
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What are the 3 requirements for reentry to occur?
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1. 2 pathways for impulse conduction
2. unidirectional block in 1 pathway 3. slow conduction through the loop of tissue |
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What causes a unidirectional block?
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the block results from the pathway still being refractory from the previous impulse
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In reentry, how can an impulse move retrogradely after a unidirectional block has been established?
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the pathway that was refractory during antegrade impulse conduction is no longer refractory
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How can you stop reentry? How is this done?
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1. convert unidirectional block into a bidirectional block
2. slow conduction velocity or increase ERP |
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How can you decrease conduction velocity of fast response tissue?
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block fast Na+ channels in phase 0
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How does increasing the ERP stop a reentry?
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impulse that attempts to move retrogradely will encounter refractory tissue and the impulse will die
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How can you increase the ERP to stop reentry? Why is this potentially dangerous?
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1. block K+ channels->delays repolarization
2. can cause EAD->can cause torsades |
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What can cause a-flutter?
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reentry circuit over large anatomically fixed circuit
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What 2 things can cause a-fib?
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1. multiple wandering reentry circuits
2. rapid ectopic focal discharge |
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What are the 2 ways to treat a-fib and a-flutter?
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1. rate control->slows AV conduction->slows ventricular rate
2. rhythm control->stops reentry->cardioverts to NSR |
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What 3 drug classes will slow AV conduction to treat a-fib? Why are these effective?
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1. Non-DHP CCB's, BB's, and digoxin
2. these will deal with the main phase 0 ion (Ca++) |
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What 2 drug classes will stop reentry to cardiovert a-fib?
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1. SCB's
2. PCB's |
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What is monomorphic v-tach? What can cause this?
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1. structural abnormality that causes reentry
2. old infarction |
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How can you treat pulseless v-tach or pulseless v-fib?
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electrical cardioversion
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What are 2 ways to treat v-tach or v-fib?
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1. pacemaker
2. give drugs to stop reentry |
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Blocking what channels will stop reentry to help treat/prevent ventricular tachycardia or fibrillation?
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1. SCB's
2. PCB's |
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What are the 2 classes of paroxysmal supraventricular tachycardias? Which of these is the most common?
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1. AV nodal reentrant tachycardia (AVNRT)
2. atrioventricular reentrant tachycardia (AVRT); WPW most common of this class 3. AVNRT is the most common class of PSVT's |
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What is the conduction path for AVNRT?
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1. one path shows fast conduction and slow recovery time
2. other path shows slow conduction and fast recovery time |
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T or F: unless a premature atrial impulse occurs, AVNRT will show NSR on ECG.
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true
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How does an arrhythmia develop in AVNRT?
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premature atrial impulse occurs->impulse encounters unidirectional block at fast conduction pathway due to slow recovery time->impulse will conduct along slow pathway->if retrograde impulse meets refractory tissue in fast pathway, reentry circuit develops
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How can you eliminate AVNRT?
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1. break reentry circuit in AV node (most important)
2. prevent premature atrial impulse |
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What 2 methods can be used to convert AVNRT?
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1. vagal maneuvers-blocks AV node (slow path)
2. SCB/PCB-cardioverts to NSR (fast path) |
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What is the key feature of WPW on ECG?
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delta waves
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What can trigger AVRT arrhythmia in WPW patient?
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premature atrial impulse
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What are the 2 kinds of AVRT that can develop?
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orthodromic and antidromic
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Which ERP is longer in orthodromic AVRT? Antidromic AVRT?
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1. accessory pathway
2. AV nodal pathway |
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Which form of AVRT is more commonly seen in WPW?
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c-O-mm-O-n=O-rth-O-dromic
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Antidromic AVRT is difficult to distinguish from what other arrhythmia?
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v-tach
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What is the treatment for antidromic AVRT?
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radioablation
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Orthodromic or antidromic: which AVRT will show a wide QRS? Narrow QRS? Why is this not a good way to tell?
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1. ortho-O-dromic=narr-O-w QRS
2. ant-I-dromic=w-I-de QRS 3. WPW all show wide QRS |
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How can you treat an orthodromic AVRT?
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1. slow conduction velocity (SCB) or increase ERP (PCB)
2. slow the AV node |
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Why is AVRT with a-fib or a-flutter a problem?
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too many impulses will pass through the accessory pathway (HR~220 BPM)
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What is the treatment for AVRT with a-fib or a-flutter? Why is slowing the AV node bad in this situation?
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1. SCB/PCB
2. slowing the AV node with a CCB will shorten Ca++ influx phase->decrease ERP->increase excitability->early AP conduction |
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What is the biggest problem with ALL antiarrhythmic drugs?
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they can be anti-arrhythmic and pro-arrhythmic
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SCB's will block fast Na+ channels in what configuration?
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1. open state (phase 0)
2. inactive state (phase 2) |
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When do SCB's work better?
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in depolarized/damaged tissue
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How do SCB's affect reentry tissue alone?
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damaged tissue will have a prolonged recovery from block->SCB's will still be on some Na+ channels during phase 4->this will cause Na+ channels to be blocked just before phase 0->this will more effectively block Na+ channels->increased steady state blocking
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What happens if you have a high steady state block of fast Na+ channels in normal tissue?
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arrhythmia can develop because Na+ channels throughout the heart have their conduction velocity messed up
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What are the recovery-from-block rates of Class IA, Class IB, and Class IC SCB's?
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1. 1A-intermediate
2. 1B-very fast 3. 1C-very slow |
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Which is most pro-arrhythmic: drugs with slow recovery rates from block or drugs with fast recovery rates from block?
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slow recovery from block are most pro-arrhythmic
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What are the 3 Class IA SCB's?
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1. quinidine
2. procainamide 3. disopyramide |
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Quinidine, procainamide, and disopyramide are all Na+ and K+ channel blockers. What other things do they block?
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1. quinidine-also blocks alpha and muscarine receptors
2. procainamide-also blocks ganglia 3. disopyramide-also blocks muscarine receptors |
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How do SCB's prevent reentry in fast response tissue?
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decrease phase 0 slope->decrease conduction velocity
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How do SCB's prevent reentry in ectopic foci?
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1. increase threshold->decrease rate of firing from ectopic foci
2. decrease phase 4 slope->decrease rate of firing from ectopic foci |
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How does quinidine work to treat a-fib and v-tach?
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increased ERP and decreased conduction velocity in reentrant circuit terminates/prevents arrhythmia
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How does quinidine work in treating orthodromic AVRT?
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1. in ectopic foci-decreases phase 4 slope (will not terminate arrhythmia)
2. in accessory pathway-decreases conduction velocity and prolongs ERP |
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What 5 arrhythmias will quinidine treat?
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1. a-fib
2. a-flutter 3. v-tach 4. orthodromic AVRT 5. AVNRT |
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What are the major adverse effects of quinidine?
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1. GI effects
2. inhibits vagal effect on heart 3. torsades 4. non-selective depression of heart functions 5. hypotension (especially IV) 6. cinchonism (CNS toxicity) |
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What will happen if you give quinidine without cardioverting for a-fib? How can this be prevented?
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1. quinidine will stop reentry, but will increase AV nodal conduction via its antimuscarinic properties
2. must block AV node first |
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Quinidine is only given via which route?
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PO
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Which is more effective at suppressing abnormal ectopic pacemaker activity: quinidine or procainamide?
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quinidine
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What is the half life of procainamide?
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3-5 hours
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Procainamide is only given via which route?
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IV over 2 minutes to prevent hypotension
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What is procainamide used to treat?
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1. most supraventricular and ventricular arrhythmias
2. v-fib or pulseless v-tach |
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What are the adverse effects of procainamide?
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1. GI problems
2. non-selective depression of heart functions 3. lupus-like syndrome 4. hypotension from ganglionic blockade |
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Which Class IA SCB has the most antimuscarinic effects?
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disopyramide
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What is disopyramide used to treat?
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1. prevents a-fib or a-flutter
2. prevents ventricular arrhythmias 3. prevents AVNRT |
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What are the adverse effects of disopyramide?
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1. torsades
2. negative inotropic effect 3. urinary retention 4. dry mouth |
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What are the Class IB SCB's?
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1. lidocaine
2. mexiletine |
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Lidocaine will have its greatest effect on what kind of tissue?
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depolarized and/or rapidly driven tissue
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What is the MOA of Class IB SCB's?
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1. decrease upstroke velocity
2. shortens AP duration (continued Na+ channel blocking during phase 2) |
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Does lidocaine block K+ channels?
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no
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In addition to prolonging the AP duration and ERP, how else does lidocaine work?
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decreases phase 4 slope
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Lidocaine only works in the ___, and will not work well in the ____.
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1. ventricles
2. atria |
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How does lidocaine work in v-tach?
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in the reentrant circuit, it will decrease conduction velocity and decrease ectopic focus
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In ACLS, what is lidocaine used to treat?
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v-tach or v-fib
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Can you use lidocaine to treat PVC's?
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no
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Can lidocaine be used for chronic therapy?
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no
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How is lidocaine given?
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IV (extensive 1st pass metabolism)
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What are the adverse effects of lidocaine?
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1. bad heart problems
2. CNS problems 3. low pro-arrhythmic effects |
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What drug does mexiletine resemble? What is the main difference?
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1. lidocaine
2. lidocaine-IV and mexiletine-PO |
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What are the adverse effects of mexiletine?
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1. low pro-arrhythmic effect
2. CNS problems 3. bad GI problems |
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What are the Class IC SCB's?
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1. flecainide
2. propafenone |
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T or F: Class IC SCB's will effect ERP.
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false
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What is flecainide used to treat?
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1. most arrhythmias
2. pocket pill for a-fib 3. only given when there is no structural disease |
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What are the adverse effects of flecainide?
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1. cardiac problems
2. CNS problems |
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When is flecainide contraindicated?
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1. MI
2. HF 3. AV block or BBB |
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Flecainide and propafenone are similar drugs with what exception?
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propafenone blocks beta receptors
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BB's are what class of antiarrhytmics?
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Class II
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What happens to the heart when you give BB's?
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1. SA node-negative chronotropic effects
2. AV node-delayed conduction 3. prevents arrhythmias from excess catacholamines |
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What are the clinical uses of BB's for arrhythmias?
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1. prevents sudden cardiac death in post-MI patients
2. controls ventricular rate in a-fib and a-flutter 3. AVRT 4. stress induced arrhythmias (includes prolonged QT syndrome) |
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How will BB's work in a-fib?
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prolongs AV nodal conduction and refractoriness->slows rate
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How will BB's work in orthodromic AVRT?
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prolongs AV nodal conduction and refractoriness->terminates arrhythmia
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Should BB's be given alone with a-fib combined with AVRT?
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no-it won't cardiovert the a-fib->more impulses will go through accessory pathway now
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What are the genetics of long QT syndrome? What can long QT cause?
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1. faulty HERG gene->IKr channel is aberrant->phase 3 is prolonged->long QT interval
2. torsades |
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What are the Class III antiarrhythmic drugs?
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1. amiodarone
2. dronedarone 3. sotalol 4. ibutilide 5. dofetilide |
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What is the MOA for Class III antiarrhythmics in general?
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1. prolong AP duration
2. increase ERP |
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In what 4 ways does amiodarone have its effects?
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1. blocks K+ channels
2. blocks inactive Na+ channels 3. blocks Ca++ channels 4. non-competitive alpha and beta blocker |
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What does the Ca++ blocking effect of amiodarone do?
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1. decreases phase 4 slope in SA node
2. coronary and peripheral vasodilation |
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What are the end results of amiodarone?
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1. inhibits abnormal automaticity
2. increases atrial, AV node, and ventricular ERP 3. decreases AV conduction and conduction in atria and ventricles 4. sinus bradycardia |
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What is the 1/2 life of amiodarone?
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13-103 days
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What is amiodarone used for?
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1. a-fib and a-flutter
2. v-tach and v-fib 3. ACLS for v-fib and pulseless v-tach |
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T or F: amiodarone improves mortality rates
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false
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How does amiodarone prevent reentry?
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1. slows conduction velocity by blocking Na+
2. increases ERP in reentrant pathway by blocking K+ channels |
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T or F: amiodarone is used in AVNRT and AVRT.
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true (can either slow rate or stop reentry)
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What are 2 advantages of using amiodarone?
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1. no negative inotropy
2. very low proarrhythmic effect |
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What is a drug of choice in treating arrhythmias in patients with HF?
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amiodarone
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T or F: due to its K+ channel blocking effect, amiodarone frequently causes torsades.
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false-this causes almost no torsades
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What are the adverse effects of amiodarone?
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1. GI problems
2. deposits in cornea 3. deposits in skin (bluish) 4. hepatotoxicity 5. hypo-/hyperthyroidism 6. pneumonitis leading to PF 7. peripheral neuropathy 8. bradycardia 9. prolonged QT |
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What drugs will interact with amiodarone?
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1. any drug that prolongs QT
2. digoxin-low TI 3. warfarin-low TI |
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Amiodarone is similar to what drug? What is the main difference between the two?
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1. dronedarone
2. dronedarone has no iodine->less lipophilic->shorter 1/2 life |
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What is dronedarone currently used for?
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a-fib
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T or F: the use of dronedarone is indicated in mild HF.
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true (not in severe HF though)
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Because of the potential for serious adverse effects, the FDA requires that a Medication Guide be given to patients that are prescribed what drug?
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amiodarone
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Which antiarrhytmic drug has a black box warning?
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dronedarone
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What is the black box warning on dronedarone?
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contraindicated in patients with NYHA Class IV heart failure or NYHA Class II – III heart failure with a recent decompensation requiring hospitalization or referral to a specialized heart failure clinic
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When would you see more side effects in amiodarone?
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higher dose
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Which Class III antiarrhythmic is not used to treat HF?
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sotalol
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Which Class III antiarrhythmic drug is IV only?
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ibutilide
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Which Class III antiarrhythmic drugs are used for all arrhythmias? A-fib/a-flutter only?
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1. amiodarone and sotalol
2. ibutilide and dofetilide |
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Which Class III antiarrhythmic drug blocks only K+ channels? K+ channels and beta receptors? All channels?
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1. ibutilide and dofetilide
2. sotalol 3. amiodarone and dronedarone |
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How does sotalol stop reentry in atria or ventricles?
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blocks K+ channels (blocking beta receptors won't help reentry)
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What effect would sotalol have on conduction velocity in fast response tissue?
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none (not a SCB)
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What are some adverse effects of sotalol?
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1. torsades
2. beta blocking effects |
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How does ibutilide work?
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1. blocks K+ channels
2. promotes Na+ influx through slow inward Na+ channels |
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How is ibutilide used?
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1. given IV to convert a-fib/a-flutter
2. increases efficacy of DC cardioversion of a-fib/a-flutter |
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What are the adverse effects of ibutilide?
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1. torsades
2. ventricular arrhythmias 3. BBB, AV block, bradycardia |
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T or F: amiodarone is given IV or PO.
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true
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What are the adverse effects of dofetilide?
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1. torsades
2. v-tach |
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How can you minimize the chance of getting dofetilide-induced torsades?
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1. therapy is initiated in the hospital
2. dose is calculated based on creatinine clearance effect on QT interval |
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What is the MOA of CCB's as antiarrhythmics?
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1. blocks activated and inactivated Ca++ channels
2. effects mainly the SA node and the AV node |
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CCB's treat the same conditions as what drugs?
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BB's
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Why wouldn't you give a CCB in ventricular arrhythmias?
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causes vasodilation->increases SNS stimulation->causes v-fib
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What does adenosine cause?
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AV nodal block
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Which antiarrhythmics will cause AV nodal block?
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1. adenosine
2. BB's 3. non-DHP CCB's 4. digitalis |
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Is adenosine given via IV bolus or slow infusion?
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bolus-short 1/2 life
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What is the major indication for giving adenosine?
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AV nodal reentry or WPW
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What is the advantage of giving adenosine?
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adverse effects only last a minute
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What are the adverse effects of adenosine?
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1. transient asystole
2. dyspnea 3. chest pain (from bronchospasm) 4. facial flushing |
