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70 Cards in this Set

  • Front
  • Back
What current constitutes the phase 0 of the action potential?
Fast inward sodium (depolarization)
What currents are present at phase 1 of the action potential?
fast inward sodium is closing

transient outward potassium current briefly depolarizes cell
What currents are present at phase 2 of the action potential?
slow inward calcium current causes plateau of membrane potential
What current is responsible for phase 3 of the action potential?
special outward potassium channels open

slow inward calcium channels close
What current is responsible for the phase 4 of the action potential?
normal outward current of potassium
What accounts for automaticity?
automatic phase 4 depolarization

seen in the SA node, AV node, and His-Purkinje

Not seen in cardiac muscle
What are some factors that alter automaticity and excitability?
slower rate of phase 4 depolarization

altered threshold potential

Altered maximum diastolic potential

altered action potential duration
What can alter rate of phase 4 depolarization?
muscarinics decrease rate causing longer duration between action potentials

Beta1 increase rate of phase 4 depolarization which decreases time between action potentials
What can alter the threshold potential?
Opening of sodium or calcium channels will increase the threshold for action potential firing
What can alter the maximum diastolic potential?
if potassium channels stay open longer or increase in number it can cause the diastolic threshold to be excessivly repolarized ("overshoot")

Muscarinic activation
What can increase action potential duration?
longer plateau periods caused by calcium/potassium balance
What is the relationship between slope of phase 0 and conduction velocity?
increased slope of phase 0 leads to an increase conduction velocity

cardiac tissue -Na channels
SA and AV nodes - calcium channels
What determines the ERP?
It is determined by the recovery of channels in phase 3 of the action potential

it is the minimum interval between propogating action potentials
What is closely linked with ERP?
action potential duration
What are some causes of developing abnormal automatic mechanisms?
-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)
What is Delayed Afterdepolarization?
spontaneous depolarization after phase 3 return to baseline (phase 4)

due to an increase in extracellular calcium

induced by ischemia, digoxin, catecholamines
What is Early Afterdolarization?
associated with a prolonged APD

Hypokalemia - slow HR

induced by drugs that prolong APD like quinidine
What are the effects of sympathetic stimulatiton on the heart?
increase the rate of phase 4 depolarization
increase automaticity
increase conduction velocity
decrease in APD and ERP
can lead to afterdelpolarizarion
increase in contractility
What are the parasympathetic effects on the heart?
decrease automaticity
decrease conduction velocity
decrease APD and ERP in Atria
Increase APD an ERP in AV node
decrease contractility in atrial muscle
What are the class 1A antiarrythmic drugs?
Quinidine, Procainamide, Disopyramide

cause modest dissociation from Sodium channels
moderate depression of phase 0 and conduction velocity

increases APD and ERP
What are the class 1B antiarrythmic drugs?
lidocaine, Mexiltine

fast dissociation from sodium channels

little to no depression of phase 0 and conduction velocity

minimal change to APD and ERP
What are the class 1C antiarrythmic drugs?
flecainide, propafenone

slow dissociation from sodium channel

marked depression of phase 0 and conduction velocity

increase in APD and ERP
What is the MOA of Class 1 antiarrythmics?
state dependent block of sodium channels
What is the MOA of Class II antiarrythmics?
inhibition of beta andrenergic receptors
What are the Class II antiarrythmic drugs?
Propranolol
Esmolol
WHat is the MOA of class III antiarrythmics?
homogenous prologation of APD and ERP
What are the class III antiarrythmics drugs?
Amiodarone
Dronedarone
Ibutilide
Dofetilide
Sotolol
What is the MOA of class IV antiarrythmics?
inhibition of Calcium channels
What is a class IV antiarrythmic drug?
Verapamil
What are the effects of quinidine, procainamide, and disopyramide (I)?
decrease automaticity
decrease conduction velocity
increase APD and ERP

anticholinergic effects - disopyramide is worst

avoid with people in torsades de pointes (prolonged QT)
What are the indications of Quinidine?
conversion of A fib after AV block
maintainance of sinus rhythym in A flutter and A Fib
prevent recurrence of VT and V fib
What are the adverse effects of quinidine?
GI distress
torsades de pointes
tinitus
thrombocytopenia
hypotension
decreased contractility from conduction block
What are the major contraindications for quinidine?
prolonged QT -> torsades de points
increase digoxin toxicity
hypokalemia ->torsades de pointes
What are the indications for Procainamide?
conversion of A fib after AV block
maintainace of sinus rhythym in A flutter/fib

WPW - prolongs refractory period
Which class I antiarrythmic agent is best for IV use?
procainamide
What is unique about the metabolism of procainamide?
active metabolite formation
What are the adverse effects of procainamide?
+ANA in chronic treatment
agranulocytosis
proarrhythmic effect
conduction block
less GI than quinidine
What are the major contraindications for procainamide?
SLE

prolonged Q-T
What are the indications for Disopyramide?
conversion of A fib after AV block
Maintanance of sinus rhythym in A flutter and A fib
Prevent recurrence of VT and V fib
What are the adverse effects of disopyramide?
precipitates CHF
anticholinergic
proarrythmic
conductions block
What are the contraindications for disopyramide?
CHF, BPH, glaucoma,
torsades de pointes
What are the indications for Lidocaine?
Acute suppression of V fib
digoxin induced arrythmia
What is the admin route for lidocaine?
IV only
What are the adverse effects of lidocaine?
CNS
seisures
hypotension
What are the contraindications of lidocaine?
hypersensitivity
hepatic dysfunction
history of seisures induced by lidocaine
What are the major differences between mexilitine and lidocaine?
mexilitineis effective orally

mexilitine has thrombocytopenia as an adverse effect
What are the indications for class IC antiarrhythmic drugs (Flecainide)?
life threatening ventricular arrhythmias in abscence of heart disease

disabling supraventricular arrhythmias in abscence of heart disease
What are the adverse effects of Flecainide?
if there is an preexisting heart disease, it increases mortality

precipitate CHF
AV block
Proarrhythmic effect
What are the contraindications of Flecainide?
pre-existing heart disease
What are the effects of class II - beta blocker antiarrhythmic drugs?
decreases automaticity and conduction velocity at SA and AV nodes
Increases the refractory period
decreases myocardial contractility
What are the indications for class II beta blockers?
post MI
CHF
Supraventricular arrhythmias
control of ventricular rate in A flutter/fib
symptomatic PVC's
What is esmolol?
cardioselective beta blocker
short t1/2
short term use
controls ventricular rhythm in atrial flutter/fib
controls sinus tachycardia
What are the effects of the class III antiarrhyhtmic drugs?
increase APD and ERP

can cause torsades de pointes
What are the indications of Amiodarone?
class III
drug of choice for acute supression of ventricular arrhythmias?
What are the adverse effects of amiodarone?
pulmonary fibrosis
thyroid dysregulation
hepatic dysfunction
--must monitor--
AV block
sinus bradycardia
corneal deposits
photosensitivity
blue grey cheeks
drug interactions
Some class III antiarrhythmic have addition MOA's. What are they?
amiodarone - class III action and class I and IV

dronedarone - class II action and class I
What are the indications for dronedarone?
prevent atrial fibrilation/flutter
What is the main difference in the metabolism of amiodarone and dronedarone?
amiodarone has very long half life
What are the adverse effects of dronedarone?
increase mortality in patients with CHF
What is the MOA of Ibutilide and Dofetilide?
inhibits Ikr
What are the indications of ibutilide and dofetilide?
terminate A flutter and A fib
What are the effects of Verapamil?
Class IV
decrease conductance and increase ADP at SA and AV nodes
decrease HR
Decrease muscle contractility
decrease TPR
What are the indications of Verapamil?
supraventricular tachyarrhythmias
PSVT due to AV nodal reentry
controls ventricular rate when there is atrial problems
What is the MOA of Verapamil?
Calcium channel blocker
Which Antiarrhythmic drug(s) has no effect on PR interval?
Lidocaine and Quinidine (may also increase or decrease)
Which drugs increase the QRS interval?
Flecainide (greatest)
Quinidine
Amiodarone
Which drugs increase the QT interval?
Quinidine
Amiodarone
How is Adenosine used to control arrhythmias?
decrease automaticity
terminate PSVT

DO NOT USE WITH ASTHMA
How are Vagomimetics used to control arrhythmias?
decrease AV nodal conduction which terminate PSVT

include carotid sinus massage
digoxin
What drugs are used to control bradyarrhythmias?
atropone - vagolytic

isoproterenol - increase in AV conduction