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70 Cards in this Set
- Front
- Back
What current constitutes the phase 0 of the action potential?
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Fast inward sodium (depolarization)
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What currents are present at phase 1 of the action potential?
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fast inward sodium is closing
transient outward potassium current briefly depolarizes cell |
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What currents are present at phase 2 of the action potential?
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slow inward calcium current causes plateau of membrane potential
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What current is responsible for phase 3 of the action potential?
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special outward potassium channels open
slow inward calcium channels close |
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What current is responsible for the phase 4 of the action potential?
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normal outward current of potassium
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What accounts for automaticity?
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automatic phase 4 depolarization
seen in the SA node, AV node, and His-Purkinje Not seen in cardiac muscle |
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What are some factors that alter automaticity and excitability?
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slower rate of phase 4 depolarization
altered threshold potential Altered maximum diastolic potential altered action potential duration |
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What can alter rate of phase 4 depolarization?
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muscarinics decrease rate causing longer duration between action potentials
Beta1 increase rate of phase 4 depolarization which decreases time between action potentials |
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What can alter the threshold potential?
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Opening of sodium or calcium channels will increase the threshold for action potential firing
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What can alter the maximum diastolic potential?
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if potassium channels stay open longer or increase in number it can cause the diastolic threshold to be excessivly repolarized ("overshoot")
Muscarinic activation |
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What can increase action potential duration?
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longer plateau periods caused by calcium/potassium balance
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What is the relationship between slope of phase 0 and conduction velocity?
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increased slope of phase 0 leads to an increase conduction velocity
cardiac tissue -Na channels SA and AV nodes - calcium channels |
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What determines the ERP?
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It is determined by the recovery of channels in phase 3 of the action potential
it is the minimum interval between propogating action potentials |
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What is closely linked with ERP?
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action potential duration
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What are some causes of developing abnormal automatic mechanisms?
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-Increased rate of phase 4 depolarization
-less negative max diastolic potential -afterdepolarizations (require initial impulse, nerve or muscle fibers, may or may not intial and action potential) |
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What is Delayed Afterdepolarization?
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spontaneous depolarization after phase 3 return to baseline (phase 4)
due to an increase in extracellular calcium induced by ischemia, digoxin, catecholamines |
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What is Early Afterdolarization?
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associated with a prolonged APD
Hypokalemia - slow HR induced by drugs that prolong APD like quinidine |
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What are the effects of sympathetic stimulatiton on the heart?
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increase the rate of phase 4 depolarization
increase automaticity increase conduction velocity decrease in APD and ERP can lead to afterdelpolarizarion increase in contractility |
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What are the parasympathetic effects on the heart?
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decrease automaticity
decrease conduction velocity decrease APD and ERP in Atria Increase APD an ERP in AV node decrease contractility in atrial muscle |
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What are the class 1A antiarrythmic drugs?
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Quinidine, Procainamide, Disopyramide
cause modest dissociation from Sodium channels moderate depression of phase 0 and conduction velocity increases APD and ERP |
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What are the class 1B antiarrythmic drugs?
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lidocaine, Mexiltine
fast dissociation from sodium channels little to no depression of phase 0 and conduction velocity minimal change to APD and ERP |
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What are the class 1C antiarrythmic drugs?
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flecainide, propafenone
slow dissociation from sodium channel marked depression of phase 0 and conduction velocity increase in APD and ERP |
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What is the MOA of Class 1 antiarrythmics?
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state dependent block of sodium channels
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What is the MOA of Class II antiarrythmics?
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inhibition of beta andrenergic receptors
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What are the Class II antiarrythmic drugs?
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Propranolol
Esmolol |
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WHat is the MOA of class III antiarrythmics?
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homogenous prologation of APD and ERP
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What are the class III antiarrythmics drugs?
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Amiodarone
Dronedarone Ibutilide Dofetilide Sotolol |
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What is the MOA of class IV antiarrythmics?
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inhibition of Calcium channels
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What is a class IV antiarrythmic drug?
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Verapamil
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What are the effects of quinidine, procainamide, and disopyramide (I)?
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decrease automaticity
decrease conduction velocity increase APD and ERP anticholinergic effects - disopyramide is worst avoid with people in torsades de pointes (prolonged QT) |
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What are the indications of Quinidine?
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conversion of A fib after AV block
maintainance of sinus rhythym in A flutter and A Fib prevent recurrence of VT and V fib |
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What are the adverse effects of quinidine?
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GI distress
torsades de pointes tinitus thrombocytopenia hypotension decreased contractility from conduction block |
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What are the major contraindications for quinidine?
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prolonged QT -> torsades de points
increase digoxin toxicity hypokalemia ->torsades de pointes |
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What are the indications for Procainamide?
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conversion of A fib after AV block
maintainace of sinus rhythym in A flutter/fib WPW - prolongs refractory period |
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Which class I antiarrythmic agent is best for IV use?
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procainamide
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What is unique about the metabolism of procainamide?
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active metabolite formation
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What are the adverse effects of procainamide?
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+ANA in chronic treatment
agranulocytosis proarrhythmic effect conduction block less GI than quinidine |
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What are the major contraindications for procainamide?
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SLE
prolonged Q-T |
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What are the indications for Disopyramide?
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conversion of A fib after AV block
Maintanance of sinus rhythym in A flutter and A fib Prevent recurrence of VT and V fib |
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What are the adverse effects of disopyramide?
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precipitates CHF
anticholinergic proarrythmic conductions block |
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What are the contraindications for disopyramide?
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CHF, BPH, glaucoma,
torsades de pointes |
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What are the indications for Lidocaine?
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Acute suppression of V fib
digoxin induced arrythmia |
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What is the admin route for lidocaine?
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IV only
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What are the adverse effects of lidocaine?
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CNS
seisures hypotension |
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What are the contraindications of lidocaine?
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hypersensitivity
hepatic dysfunction history of seisures induced by lidocaine |
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What are the major differences between mexilitine and lidocaine?
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mexilitineis effective orally
mexilitine has thrombocytopenia as an adverse effect |
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What are the indications for class IC antiarrhythmic drugs (Flecainide)?
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life threatening ventricular arrhythmias in abscence of heart disease
disabling supraventricular arrhythmias in abscence of heart disease |
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What are the adverse effects of Flecainide?
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if there is an preexisting heart disease, it increases mortality
precipitate CHF AV block Proarrhythmic effect |
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What are the contraindications of Flecainide?
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pre-existing heart disease
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What are the effects of class II - beta blocker antiarrhythmic drugs?
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decreases automaticity and conduction velocity at SA and AV nodes
Increases the refractory period decreases myocardial contractility |
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What are the indications for class II beta blockers?
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post MI
CHF Supraventricular arrhythmias control of ventricular rate in A flutter/fib symptomatic PVC's |
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What is esmolol?
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cardioselective beta blocker
short t1/2 short term use controls ventricular rhythm in atrial flutter/fib controls sinus tachycardia |
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What are the effects of the class III antiarrhyhtmic drugs?
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increase APD and ERP
can cause torsades de pointes |
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What are the indications of Amiodarone?
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class III
drug of choice for acute supression of ventricular arrhythmias? |
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What are the adverse effects of amiodarone?
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pulmonary fibrosis
thyroid dysregulation hepatic dysfunction --must monitor-- AV block sinus bradycardia corneal deposits photosensitivity blue grey cheeks drug interactions |
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Some class III antiarrhythmic have addition MOA's. What are they?
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amiodarone - class III action and class I and IV
dronedarone - class II action and class I |
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What are the indications for dronedarone?
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prevent atrial fibrilation/flutter
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What is the main difference in the metabolism of amiodarone and dronedarone?
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amiodarone has very long half life
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What are the adverse effects of dronedarone?
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increase mortality in patients with CHF
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What is the MOA of Ibutilide and Dofetilide?
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inhibits Ikr
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What are the indications of ibutilide and dofetilide?
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terminate A flutter and A fib
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What are the effects of Verapamil?
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Class IV
decrease conductance and increase ADP at SA and AV nodes decrease HR Decrease muscle contractility decrease TPR |
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What are the indications of Verapamil?
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supraventricular tachyarrhythmias
PSVT due to AV nodal reentry controls ventricular rate when there is atrial problems |
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What is the MOA of Verapamil?
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Calcium channel blocker
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Which Antiarrhythmic drug(s) has no effect on PR interval?
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Lidocaine and Quinidine (may also increase or decrease)
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Which drugs increase the QRS interval?
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Flecainide (greatest)
Quinidine Amiodarone |
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Which drugs increase the QT interval?
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Quinidine
Amiodarone |
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How is Adenosine used to control arrhythmias?
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decrease automaticity
terminate PSVT DO NOT USE WITH ASTHMA |
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How are Vagomimetics used to control arrhythmias?
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decrease AV nodal conduction which terminate PSVT
include carotid sinus massage digoxin |
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What drugs are used to control bradyarrhythmias?
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atropone - vagolytic
isoproterenol - increase in AV conduction |