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CRP > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

Slow response fibers

A
  • Found in SA and AV nodes
  • Resting potential -65 to -45mv
  • Phase 0 upstroke has less of a slope compared to fast response fibers due to slow inward movement of Ca2+
  • Repolarization is a combination of phases 1-3 and due to K+ efflux from the cell
  • Phase 4 slope due to increased influx of Na+ and Ca2+, and decreased efflux of K+
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2
Q

Fast response fibers

A
  • Found in atrial and ventricular muscle, and His/purkinje fibers
  • Resting membrane potential -80 to -95mv
  • Steep slope of phase 0 due to large Na+ influx via fast Na+ channels, up to +20 to +30mv
  • Plateau phase 2 due to slow Ca2+ channel influx
  • Atrial and ventricular muscle to not normally display phase 4 sloping (automaticity) but may do so under conditions of ischemia and sympathetic stimulation; His/purkinje fibers do display some phase 4 sloping and pacemaker behavior.
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3
Q

Excitability Definition

A
  • The measure of strength of the stimulus necessary to cause an action potential
  • It is inversely proportional to the difference b/w the resting potential and the threshold potential (E = 1 / (RP - TP)
  • Sympathetic increase, while parasympathetic decrease excitability
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4
Q

Responsiveness Definition

A
  • A measure of the slope of phase 0
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5
Q

Conduction Definition

A
  • The rate of movement of an impulse from one cell to the next or one tissue to the next
  • It is also related to the slope of phase 0
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6
Q

Conduction rates of different cardiac tissues

A
  • Atria: 1 m/sec
  • AV node: 0.1 m/sec
  • His/purkinje: 1-2 m/sec
  • Ventricle: 0.4 m/sec
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7
Q

Effective Refractory Period

A
  • Phase 1, 2 and part of 3, another stimulus at this time will not generate an action potential
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8
Q

Relative Refractory Period

A
  • From end of ERP to beginning of phase 4; larger than normal stimulus may produce another action potential
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9
Q

ERP/Action Potential Duration ratio

A
  • Useful for comparisons of normal and a arrhythmic tissues
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10
Q

Automaticity

A
  • The slope of phase 4
  • Sympathetic stimulation increases
  • Parasympathetic decreases
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11
Q

Mechanisms of Cardiac Arrhythmias

A
  • Abnormal automaticity
  • Triggered automaticity
  • Reentry
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12
Q

Abnormal Automaticity Mechanism of Cardiac Arrhythmia

A
  • SA node develops increased automaticity and heart rate increases, e.g. sinus tachycardia or the SA node develops decreased automaticity and heart rate decreases, sinus bradycardia
  • Latent pacemaker acquires increased automaticity and fires faster than the SA node- this is an ectopic beat that is premature in terms of normal rhythm, or the SA node develops function. These are referred to as escape beats, which terminate the pause caused, by cessation of, or slowing of, the normal firing rate.
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13
Q

Triggered Automaticity Mechanism of Cardiac Arrhythmia

A
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14
Q

Reentry Mechanism of Cardiac Arrhythmia

A
  • Reentry a common mechanism involving the development of a reentrant loop that is a self-sustaining electrical circuit which repeatedly depolarizes surrounding tissues. Reentry usually leads to tachyarrhythmias
  • Conduction block- fibrosis, ischemia or trauma may create a block where one part of the conduction system loses continuity w/ the remainder of the pathway. Escape beats usually result as more distal sites assume pacemaker function. AV conduction blocks are examples.
  • Bypass tracts- most commonly involves an additional or accessory tract that bypasses the AV node. The accessory tract conducts rapidly and the normal conduction delay at the AV node does not take place. A loop is created w/ the accessory tract serving as one limb and the normal AV pathway as the other. This may set the stage for reentry rhythms. The Wolff-Parkinson-White syndrome (WPW) involves this type of bypass tract at the AV node.
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15
Q

Types of Arrhythmias

A
  • Normal Sinus Rhythm
  • Sinus Bradycardia
  • Sinus Tachycardia
  • Atrial Flutter
  • Atrial Fibrillation
  • Paroxysmal (Supraventricular) Atrial Tachycardia (PAT)
  • Premature Ventricular Contraction (PVC)
  • Ventricular Tachycardia
  • Ventricular Fibrillation
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16
Q

Normal Sinus Rhythm

A
  • SA node controls the heart
  • 70 beats/min
  • PQRST connected
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17
Q

Sinus Bradycardia

A
  • SA node controls the heart
  • <60 beats/min
  • Caused by athletic conditioning, hypothermia
  • PQRST still connected, just beating more slowly
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18
Q

Sinus Tachycardia

A
  • SA node controlling
  • >100 beats/min
  • Caused by excessive catacholaminergic activity
  • Ex: pheochromocytoma, anxiety and fever
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19
Q

Atrial Flutter

A
  • Atria beating rapidly, >300 beats/min
  • 2 P-waves/ORS complex
  • AV node is protecting the ventricles by only letting every other impulse through
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20
Q

Atrial Fibrillation

A
  • No effective contraction of atria, blood move passively into ventricles AV node protects ventricle from rapid beating
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21
Q

Parosyxmal (Supraventricular) Atrial Tachycardia (PAT)

A
  • Ectopic foci takes over in atria
  • Sudden starts and stops
  • Tachycardia
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22
Q

Premature Ventricular Contraction (PVC)

A
  • An ectopic focus from ventricle takes over
  • Ventricular beat followed by a pause, then goes back to sinus rhythm
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23
Q

Ventricular Tachycardia

A
  • Ventricles completely take over
  • Torsade de Pointes
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24
Q

Ventricular Fibrillation

A
  • Worst case scenario
  • No effective contraction of ventricles
  • Incompatible w/ life
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25
Q

Antiarrhythmic Drugs Classification Chart

26
Q

Class 1A Antiarrythmic Main Cardiac Effects

A
  • Prolong QRS wave (decrease slope phase 0)
  • Prolong ventricular repolarization (increase phases 1-3 of RP)
  • Prolong QT interval
  • Decrease automaticity, slow fast fibers
  • Inc. ORS and OT intervals, PR variable due to initial anticholinergic effect of IA’s to inc HR/AV conduction
27
Q

Class 1A Antiarrythmic Drugs Toxicity

A
  • Widening of QRS may lead to ventricular tachycardia
  • Torsades de Pointes (type of proarrythmia), caused by drugs that prolong QT interval; tachycardia and fainting
  • Hyperkalemia increases toxicity
28
Q

Class 1A Antiarrythmic Drugs Clinical Indications

A
  • Supraventricular arrythmias, atrial flutter, fibrillation
  • Ventricular arrythmias
29
Q

Quinidine

A
  • Class 1A antiarrhythmic
  • From bark of cinchona tree, isomer of quinine
  • Hepatic metabolism to several active metabolites
  • Antimalarial, antipyretic, oxytocic actions
  • Dose-related toxicity, cinchonism (tinnitus, headache)
  • GI disturbances, immune-based hepatitis and thrombocytopenia
  • Torsades de Pointes
  • Drug interactions: digitalis, bile acid absorbants, diuretics (K loss)
30
Q

Disopyramide

A
  • Class 1A antiarrhythmic
  • Marked anticholinergic effect
  • Clinical indications similar to quinidine/procainamide, only used when other drugs are not effective
31
Q

Procainamide

A
  • Class 1A antiarrhythmic
  • Undergoes N-acetylation (fast and slow acetylators) to NAPA, N-acetylprocainamide, active metabolite, class III actions
  • GI disturbances, lupus-like syndrome (malaise, rash, arthralgias)
  • Clinical indications similar to quinidine
32
Q

Class IB Antirarrythmic Drugs Main Cardiac Effects

A
  • Shortens QT inteval, slight decrease slope phase 0
  • Decreases ventricular automaticity, especially ischemic cardiomyocytes
33
Q

Class 1B Side Effects

A
  • Dose-related CNS effects, dizziness, tremor, psychosis, convulsions >> CNS depression (anesthetic action)
34
Q

Class 1B Antiarrythmic Drugs Clinical Indications

A
  • Ventricular arrhythmias only, especially post MI to reduce ventricular fibrillation
35
Q

Lidocaine

A
  • Class 1B antiarrhythmic
  • Extensive 1st pass metabolism, no PO
  • IV loading/maintenance dosing; follows 2-compartment model, t1/2 1-2 hrs.
  • Hepatic metabolism to active metabolites
36
Q

Orally Active Lidocaine Analogs

A
  • Mexiletine
  • Tocainide
37
Q

Class 1C Antiarrhythmic Drugs Main Cardiac Effects

A
  • Widening of QRS and PR interval, minimal QT
38
Q

Class 1C Antiarrhythmic Drugs Toxicity

A
  • Aggravation of AV block, ventricular tachycardia
  • Increased mortality in CAST w/ encainide, flecainide
39
Q

Class 1C Antiarrhythmic Drugs Clinical Indications

A
  • AV nodal reentry, WPW
  • Ventricular arrhythmias
40
Q

Class 1C Antiarrhythmic Drugs

A
  • Flecainide
  • Propafenone/ Moricizine
41
Q

Class II Antiarrhythmics - Beta Blockers

A
  • Propranolol
  • Metoprolol
  • Esmolol
  • Atenolol
42
Q

Propanolol

A
  • Pacemaker cells: SA, AV, purkinje fibers affected
  • Decrease HR, slowed AV conduction, increase PR, decrease automaticity, especially related to SNS
  • Decreased cardiac work and oxygen consumption
  • Post MI reduction of reinfarction and sudden death
43
Q

Esmolol

A
  • Class II antiarrhythmic - Betal blocker
  • Used IV emergency treatment (atrial flutter/fib, sinus tachy) to dec ventricular rate; t1/2 - 9min., metabolized by RBC esterases
44
Q

Class III Antiarrhythmics - K Channel Blockers Effects

A
  • Increase effective refractory period - decrease reentry
  • Amiodarone only: decrease conduction velocity - decreast reentry
  • Decrease rate of firing (phase 4 slope) - decrease automaticity
  • Prolong RP (phases 1-3) and AP duration, w/o significant Na channel blockade
45
Q

Class III Antiarrhythmics

A
  • Amiodarone
  • Bretylium
  • Sotalol
  • Ibutilide
  • Dofetilide
46
Q

Amiodarone Main Cardiac Effects

A
  • Class I effect
  • Class II effect
  • Class IV effect
  • ECG - increased PR, QRS, QT intervals
  • vasodilation, due to b and c above
47
Q

Amiodarone Pharmacokinetics

A
  • Long half-life (i.e. 50 hrs.), use of loading doses
48
Q

Amiodarone Clinical Indications

A
  • Broad spectrum use atrial, nodal, ventricular arrhythmias
49
Q

Amiodarone Adverse Effects

A
  • Microdeposits in cornea, skin, and other tissues
  • pulmonary toxicity - fibrosis
  • Peripheral neuropathy and myopathy
  • Abnormal liver function
  • Thyroid dysfunction
  • Photosensitivity, blue-gray skin discoloration over sun-exposed areas
50
Q

Sotalol

A
  • Class III antiarrhythmic
  • A nonselective beta blocker w/ class III properties, inc. RP, indicated for vent arrhythmias, usu well tolerated but risk of proarrhythmias
51
Q

Class II Antiarrhythmics ECG Effects

A
  • Decrease phase 4 slope
  • Decrease rate of firing
  • Decrease automaticity
  • Prolonged repolarization of AV node - increase effective refractory period - decrease re-entry
52
Q

Class I Antiarrhythmic ECG Effects

A
  • Na+ channel blockade - decrease phase 0 upstroke velocity - decrease conduction velocity - decrease re-entry
  • Prolonged repolarization - increased effective refractory period - decreased re-entry
  • Decrease rate of firing - decrease automaticity
53
Q

Class IV Antiarrhythmics - Calcium Channel Blockers ECG Effects

A
  • Decrease conduction velocity of AV node - decrease re-entry
  • Increase Effective refractory period of AV node - decrease re-entry
54
Q

Class IV Antiarrhythmics - Calcium Channel Blockers

A
  • Verapamil
  • Diltiazem
55
Q

Verapamil

A
  • Antiarrhythmic effects on slow fibers SA/AV
  • Decreased myocardial contractility due to CA block during phase 2
  • Clinical indication for atrial fib/flutter, AV nodal reentry
  • Adverse effects: Cardiac, GI
56
Q

Magnesium Sulfate

A
  • Adm IV for Torsade de Pointes, digitalis-induced ventricular arrhythmias, and arrhythmias assoc. w/ Mg deficiency
57
Q

Cardiovascular Drug Effects on ECG Chart

58
Q

Bretylium

A
  • Class III antiarrhythmic
  • Class III drug that also depletes neuronal release of catecholamines, inc RP and AP, used IV to treat emergency vent. fibr.
59
Q

Ibutilide

A
  • Class III antiarrhythmic
  • IV for rapid conversion atrial fib/flutter to normal sinus rhythm
60
Q

Dofetilide

A
  • Class III antiarrhythmic
  • PO to maintain sinus rhythm pts w/ atrial fibrillation
61
Q

Adenosine

A
  • Used rapid bolus IV to halt reentrant paroxysmal supraventricular tachycardia (PSVT) during emergencies
  • Decrease automaticity and conduction thru AV node

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