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Pharma of antiarrhythmic
Pharmacy 412 with Roseburg at Roseman University of Health Sciences
About this deck
By: Nyssa Stant
Created: 2012-01-03
Size: 34 flashcards
Views: 4
Created: 2012-01-03
Size: 34 flashcards
Views: 4
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arrhythmia
Disorder of rate
rhythm
impulse generation
conduction of electrical impulse w/in the heart
Resting membrane potential
- -85 to -90 mV
- determine by K+ ions
Voltage gated Na+ Channels
- Open - intracellular environment is less negative
- Closed - intracellular environment is negative
- Conformational States
- Resting - Activated - Inactivated
Depolarization Phase
- Na+ permeability increases: membrane potential reverses
- Na+ gates are opened: K+ gates are closed
- Threshold (-55 to -50 mV)
- depolarization becomes self-generating once threshold reached
Repolarization Phase
- Na+ gates close - K+ gates open
- membrane permeability to Na+ declines to resting levels
- K+ exits cell restoring internal negativity
Effect of K+ channel blockade
Will prevent the release of K+ from cell increasing the time cell is depolerized.
Effect of Ca++ channel blockade
Will prevent the entry of Ca++ into the cell
Conduction velocity slowed
Electrical Conduction System of Heart
SA Node -> AV Node -> Bundle of HIS -> Purkinje fibers -> Ventricles
P wave
SA Node send the signal to depolarize and contract atria
Absolute Refractory Period (ARP) See slide on page 10
regardless of the strength of a stimulus, the cell cannot be depolarized
occurs from phase 0 to phase 3
Relative Refractory Period (RRP)
stronger than normal stimulus can induce depolarization
occurs in phase 3
Refractoriness is determined by
voltage-dependent recovery of Na+ channels
Causes of Arrhythmias
- Ischemia
- Electrolyte abnormalities (K+ and Mg+)
- Excessive Sympathetic nervous System stimulation
- Hypertrophy of cardiac cells, scarred or diseased tissue
DAD abnormal Impluse
- Delayed after depolarization
- altered phase 4
- results from increased intracellular Ca++
- Exacerbated by fast heart rate
- Digitalis, catecholamine, myocardial ischemia
EAD abnormal Impuse
- early after depolarization
- altered phase 3
- slow heart rate
- Contribute to development of Long QT arrhythmias
AV Block
delay in AV node
Ectopic Foci
- Abnormal pace maker sites w/in the heart displaying automaticity
- Conduction systme doesn't follow normal fast conducting path
- shape chage
- longer duration of QRS complex
- Ventricles take more time to depolarize
QT Prolongation
- due to prolongation of action potential during depolarization
- Torsade de pointes
- Bradycardia increases risk
- Usually caused by drugs that affect K+ channels
- Congenital abnormality of K+ channels increases risk
Torsades de Pointes
- potentially fatal ventricular arrhythmia
- twisting of the point
- twist of QRS complex around the isoelectric baseline (think party streamer)
Torsades de Points antiarrhythmic drugs
Amiodarone, sotalol, quinidine, disopyramide
Hyperkalemia arrhythmia
- Reduced action potential duration (resting membrane mV less negative than normal)
- Slowed conduction
- Decreased pacemaker rate
- Decreased pacemaker arrhythmogenesis
4 ways to reduce spontaneous discharge in automatic tissue
- Increase max diastolic potential
- Decrease phase 4 slope
- Increase Threshold potential
- Increase action potential duration
2 ways to block arrhythmias due to DAD
- Inhibition of development of after depolarization
- Interference with inward current
- Na+ or Ca++ channel
Block arrhythmias due to EAD
- Shortening action potential duration
- Mg++
Block arrhythmias due to reentry circuit
- Block propagation of action potential
- CCBs, Digitalis, beta blockers, etc. with caution
- Prolongation of refractoriness
- Fast response tissue
- delaying recovery of Na+ Channels
- Slow response tissue
- block Ca++ channels
- Acceleration of conduction
Antiarrhythmic Drugs
- Modify impulse generation of conduction to reduc arrhythmia
- 4 classes + some non-specific agents
- some can cause arrhythmia
Class 1A antiarrhythmic Drugs
- Membrane stabilizing agents
- A - Quinidine like agents: Quinidine, Procainamide, Disopyramide
Class 1B antiarrhythmic Drugs
- Membrane stabilizing agents
- B - Lidocaine, Phenytoin
Class 1C antiarrhythmic Drugs
- Membrane stabilizing agents
- C- Flecainide, Propafenone, Encainide, Lorcainide
Class II antiarrhythmic Drugs
- Beta-blocking agents
- Propranolol, Sotalol
Class III antiarrhythmic Drugs
- Agents which prolong the action potential (major effect)
- C - Amiodarone, Bretylium, Sotalol, Dofetilide, Ibutilide, others
Class IV antiarrhythmic Drugs
- Calcium Channel Antagonsits
- 4 - Verapamil, Diltiazem
About this deck
By: Nyssa Stant
Created: 2012-01-03
Size: 34 flashcards
Views: 4
Created: 2012-01-03
Size: 34 flashcards
Views: 4
About StudyBlue
STUDYBLUE makes things that make you better at school.
Things like online flashcards with photos and audio.
Things like personalized quizzes and friendly reminders about when (and what) to study next.
Think of it as a digital backpack™: access to all of your study materials online and on your phone.
STUDYBLUE exists to make studying efficient and effective for every student, for free. Join us.
“I have used this website for three exams, and I see a huge difference in my test results.”
Naj
Naj