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88 Cards in this Set
- Front
- Back
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what are the four main classes of antidysrhythmic drugs?
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Class I: Na+ channel blockers
Class II: Beta-blockers Class III: K+ channel blockers Class IV: Ca++ blockers |
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what are the 3 antidysrhythmic drugs which do not fit into the regular classifications that we need to know?
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1. Adenosine
2. Digitalis 3. Magnesium |
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what do class IA drugs do to APD?
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lengthen action potential duration (QT-interval)
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what do class IB drugs do to APD?
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shorten action potential duration (QT-interval)
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what do class IC drugs do APD?
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no effect on APD
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which class of antidysrhythmic drugs is the most potent and why?
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Class IC because it both decreases the rate of depolarization (more than any other class) and increases the absolute refractory time
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describe the channels blocked by Class IA drugs and the effect this has on cardiac cells?
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Na+ block (phase 0) decreases conduction velocity of depolarization
K+ block (phase 2) - increases the threshold potential and decreases the slope of phase 4 for slow-response tissue - increases the ERP of fast-response tissue |
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what are the cardiac effects of quinidine?
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prolongs ERP and ARP (Na+ and K+ channel blocker)
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what extracardiac effects of quinidine?
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mainly mediated by alpha-blockade which results in hypotension and relfec tachycardia
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the following ECG effects are characteristic of which class of antidysrhythmic drug?
widens QRS complex and prolongs QT/QTc |
Class IA drugs and class IC drugs
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the prolonged QT seen with the use of Class IA antidysrhythmics leads to what effect?
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increased ERP
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which antidysrhythmic drug profile includes:
1. Proarrhythmic effect (Torsades de Pointes) 2. Cinchonism 3. Precipitates Digoxin toxicity |
Quinidine
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what is the best indication for quinidine use?
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chemical cardioversion of atrial fibrillation and flutter into sinus rhythm
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how does quinidine increase AV nodal conduction?
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it has anticholinergic effects which block parasympathetic input which would delay AV node conduction
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what is different about procainamide as compared to quinidine? (3)
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1. less antimuscarinic (less anticholinergic) -> more SA/AV nodal depression
2. is a ganglionic blocker 3. less QTc prolongation which decreases ERP |
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what 2 patients would you really not want to give procainamide to?
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a patient with CHF because procainamide has more cardiac depression than other Class IA drugs
a patient with hypotension because procainamide has a hyoptensive effect |
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a patient of yours is on digoxin, what antidysrhythmic drug would you want to avoid?
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Quinidine
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what are the 3 class IA antidysrhythmic drugs?
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1. Quinidine - proarrhythmic and don't use with digoxin
2. Procainamide - precipitates CHF and hypotension 3. Disopyramide - increased anticholinergic effect |
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what are the channels blocked by Class IB antidysrhythmic drugs?
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Na+ only
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what is the cardiac effect of Class IB drugs? (3)
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1. prolongs ERP but shortens ARP
2. blocks K+ channels in ischemic myocardium 3. shortens QT interval which reduces RRP |
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even though the QT-time is reduced why do class IB drugs still give a antidysrhythmic effect?
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they increase the ERP time which blocks fast, abnormal action potentials from spreading throughout the heart between regular beats
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what are the two class IB drugs?
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1. Lidocain
2. Phenytoin |
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what are the adverse effects of lidocain? (3)
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1. liver dysfunction
2. CHF 3. confusion and CNS effects especially in the elderly |
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what is the indication for lidocain?
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ventricular dysrhythmia DOC
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what might be a good drug to use for someone with ventricular arrythmia do to digoxin toxicity?
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phenytoin
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why is phenytoin not frequently used?
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it is limited by extensive CNS disturbances and hypotensive effects
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what channels are blocked by Class IC drugs?
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potent Na+ channel blockade
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what is the effect of class IC drugs? (3)
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1. prolongs ERP but not APD or QT interval
2. increases ERP and decreases RRP 3. depresses myocardial function |
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describe the change to QT interval seen with Class IC drugs?
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there is none, the increase in ERP is directly offset by the decrease in RRP
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what class I drug type increases the QRS complex but not the QT interval?
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Class IC
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what is the most common class IC agent that also serves as a Ca++ blocker and Beta-blocker?
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Propafenone
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what are the 3 major adverse effects of Class IC agents?
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1. proarrhythmic
2. HF 3. AV block |
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Atrial dysrhythmias and and ventricular dysrhythmias are indications for the antidysrhythmic drug?
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Propafenone or other Class IC drugs
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how do beta-blockers (class II agents) control HR?
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they are Ca++ channel blockers that decrease Ca++ influx and increase the refractory time of slow-phase cells (such as those in AV and SA nodes)
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what two effects do beta-blockers (class II agents) have on the AV node?
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1. reduce AV node conduction
2. increase AV node ERP |
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which phase of pace-maker cells do beta-blockers work on?
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phase 4 (decrease slope) and the repolarization by increasing ERP
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what is the prototypic beta-blocker?
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propranolol
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what is the extremely short acting beta-blocker which is given IV, is selective for B1 and has a T1/2 of 10 minutes?
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esmolol
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what is the most commonly used beta-blocker - B1 specific?
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Metoprolol
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what are the adverse cardiac effects of Beta-blockers? (3)
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1. SA and AV block
2. Hypotension 3. Heart Failure |
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what are the adverse systemic effects of beta-blockers?
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bronchospasm (B2 block)
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what is the main indication for beta-blockers as far as antidysrhythmic uses and why?
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atrial dysrhythmias because beta-blockers facilitate AV node block and help protect the ventricles from reentry depolarizations
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why are beta-blockers especially effective in preventing ventricular dysrhythmias after an MI?
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the block the effect of catecholamines which are released in the dead and dying tissue
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what effect on the phases of the cardiac cycle do Class III drugs have?
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prolong ERP thus increase phase 2 and phase 3
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what are the 4 agents which are considered to be class III drugs?
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1. Bretylium
2. Sotalol 3. Amiodarone 4. ibutalide |
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what is the prototype class III agent?
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Bretylium
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what is special about amiodorone?
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it blocks beta-receptors, sodium channels, potassium channels, and calcium channels (does it all)
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in addition to increasing QT-interval, amiodarone also increases ___ which effectively increases the time between heart beats?
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PR-interval
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what effect does bretylium have on an ECG?
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none
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what are the adverse effects which bretylium can have? (2)
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1. hypertension
2. hypotension |
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what are the ECG effects of Amiodarone? (2)
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1. prolongs QT/QTc interval
2. Prolongs PR interval |
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which antidysrhythmic drug has the longest half life and what is it?
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10 days, 53 before the drug is effectively cleared = amiodarone
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what limits the use of amiodarone?
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noncardiac toxicities
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what is amiodarone indicated for? (2)
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1. atrial dysrhythmias
2. ventricular dysrhythmias = DOC for acute settings and given as IV therapy |
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what are the ECG effects caused by sotalol?
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prolongs QT/QTc interval
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which of the class III drugs also has beta-blocker effects?
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sotalol
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what are the indications for sotalol? (2)
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1. atrial dysrhythmia
2. ventricular dysrhythmia |
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which of the class III drugs does not prolong PR-interval?
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1. Sotalol
2. Ibutalide |
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what is the major toxicity of ibutalide?
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causes Torsades de Pointes (proarrhythmic)
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what is the indication for ibutalide?
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to convert atrial flutter/fibrillation to NSR
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what effect do class IV drugs have at the SA and AV nodes?
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increase the time the cells are unable to fire by decreasing the slop of phase 0 and increase the length of phase 2 in slow-response tissue, which increases ERP
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what is the ECG effect of class IV drugs?
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none
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what are the 2 class IV agents?
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1. verapamil
2. diltiazem - most commonly used |
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heart failure, hypotension, and AV nodal blockade are all examples of adverse effects of which class of antidysrhythmic drugs?
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Class IV
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what are the indications for class IV drugs? (1)
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1. atrial dysrhythmias
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of all the antidysrhythmic drugs which has the shortest half-life?
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Adenosine T1/2 = 10 seconds
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what effects does adenosine have on the heart? (3)
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1. decreases AV and SA node conduction
2. Inhibits cAMP-mediated Ca+ influx 3. Enhances K+ conductance |
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what ECG effect does adenosine have?
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transient PR-interval prolongation
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what is the major toxicity of adenosine?
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3rd degree heart block
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what is the drug of choice for super-ventricular tachycardia?
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adenosine
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what effect does digoxin have on HR and contractility?
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increases contractility and decreases HR
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what is the mechanism of action for digoxin?
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increases Na+ and Ca++ within heart cells by inhibiting the Na+/K+ ATPase pump
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what effect does digoxin have on automaticity of pacemakers in the heart?
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slows SA discharge
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describe the effect of digoxin at the AV node?
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1. slows AV nodal conduction
2. increases vagal response |
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what effect does digoxin have on cardiac cell refractory period and what cells are effected?
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prolongs ERP in AV nodal cells
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what are the antidysrhythmic indications of digoxin? (2)
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1. atrial flutter and fibrillation
2. atrial tachycardia/SVT (reentry arrhythmias |
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what is the most common adverse effect of digoxin?
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GI upset
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what is the most concerning adverse effect of digoxin?
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proarrhythmic and can cause AV block
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what are the 3 indications for magnesium?
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1. Torsades de Pointes
2. Resistant VT/VF 3. Digoxin toxicity |
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if a patient has SVT/Atrial tachycardia and is unstable what is the first thing that needs to be done?
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Synchronized electrical cardioversion
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what is the DOC for stable SVT/Atrial Tachycardia?
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adenosine
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what is the minimum BPM in the ventricles for synchronized electrical cardioversion in atrial flutter/fibrillation?
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150
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If atrial flutter/fibrillation is stable, what 3 drugs are indicated to control HR? (list in order of importance)
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1. Ca++ channel blockers
2. Digoxin 3. Amiodarone |
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what agents can be used for chemical cardioversion to NSR with atrial flutter/fibrillation? (3)
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1. quinidine
2. ibutalide 3. sotalol |
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if patient is in VT without a pulse what needs to be done?
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electrical defibrillation
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if a patient is in VT (has a pulse) and is unstable (hypotension), what should be done?
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synchronized electrical cardioversion
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if a patient is in VT (has a pulse) and is stable, what should be done? (list in order of importance)
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1. amiodarone
2. lidocain 3. procainamide |
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what is the MOST IMPORTANT thing to do before using a defibrillator on a patient?
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check for a pulse
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