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Arrythmiass Flashcards

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1
Q

What is arrhythmia?

A

A disturbance of normal rhythm.

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2
Q

Which node has the highest automaticity?

A

SA node.

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3
Q

What are subsidiary pacemakers?

A

Other pacemakers that take over when the SA node cannot generate impulses.

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4
Q

What is the main difference between fast and slow response action potentials?

A

Fast response action potentials have rapid depolarization, while slow response action potentials have gradual depolarization.

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5
Q

Fill in the blank: Phase 0 in fast response action potential is characterized by _______.

A

rapid depolarization.

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6
Q

Fill in the blank: Class III anti-arrhythmic drugs delay _______ repolarization.

A

Phase 3.

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7
Q

What is the effect of Class I anti-arrhythmic drugs?

A

Slow Phase 0 depolarization.

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8
Q

What do Class II agents target?

A

Beta-blockers.

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9
Q

What is the primary action of Class IV anti-arrhythmic drugs?

A

Calcium channel blockers.

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10
Q

What is the classification of anti-arrhythmic drugs based on Vaughan-Williams classification?

A

Class I, Class II, Class III, Class IV.

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11
Q

List the Class I anti-arrhythmic drugs.

A
  • Class IA: Procainamide, Quinidine
  • Class IB: Lidocaine, Mexiletine, Phenytoin
  • Class IC: Flecainide, Propafenone
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12
Q

What is the mechanism of action of Procainamide?

A

Blocks sodium channels and has Class III activity.

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13
Q

What are the adverse effects of Procainamide?

A
  • Hypotension
  • Lupus erythematosus-like syndrome
  • Nausea
  • Diarrhea
  • Rash
  • Fever
  • Agranulocytosis (rare)
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14
Q

What is the primary use of Quinidine?

A

To treat ventricular and supraventricular tachyarrhythmias.

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15
Q

What adverse effects are associated with Quinidine?

A
  • QT prolongation
  • Tachycardia
  • Hypotension
  • Diarrhea
  • Cinchonism
  • Thrombocytopenia
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16
Q

What is the effect of Lidocaine on action potential duration?

A

Shortens action potential duration and decreases QT.

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17
Q

True or False: Class IA drugs can have an anti-muscarinic effect.

A

True.

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18
Q

What is the mechanism of action of Class II anti-arrhythmic agents?

A

Reduce slope of spontaneous Phase 4 depolarization.

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19
Q

What effect do Class IV anti-arrhythmic drugs have on Phase 2?

A

Prolong Phase 2 repolarization.

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20
Q

Fill in the blank: Class II anti-arrhythmic drugs primarily act on _______ nodes.

A

SA and AV.

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21
Q

What is the main consequence of using Class III drugs?

A

Prolonged refractory period.

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22
Q

What is the effect of calcium channel blockers on conduction velocity?

A

Slows conduction velocity.

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23
Q

What does a ‘use-dependent’ blockade refer to?

A

The blockade of sodium channels that are active in highly active cells.

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24
Q

What is the metabolism route for Quinidine?

A

Hepatic metabolism by CYP3A4.

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25
Fill in the blank: The dominant mode of action of Procainamide is due to _______ and _______ channel block.
Na+ and K+.
26
What is a key characteristic of Class IB anti-arrhythmic drugs?
They have a weak effect on action potential duration.
27
What is the primary mechanism of action of Lidocaine?
Blocks sodium channels, affecting both open activated and inactivated states ## Footnote Greater effect on ventricular cells due to longer action potential
28
What are the cardiac effects of Lidocaine?
Increases threshold for excitability, decreases automaticity, shortens Phase 3 repolarization, APD, ERP, and QT ## Footnote Can prevent arrhythmias post-myocardial infarction
29
What is the preferred route of administration for Lidocaine?
Parenteral (IV) route ## Footnote Oral route is avoided due to extensive first-pass metabolism
30
List the common neurologic adverse effects of Lidocaine.
* Paresthesia * Tremor * Nausea * Lightheadedness * Hearing disturbances * Slurred speech * Convulsions ## Footnote These effects are more common in the elderly or during rapid IV administration
31
What is the mechanism of action of Mexiletine?
Analogue of Lidocaine with similar mechanisms and anti-arrhythmic actions ## Footnote Used primarily for ventricular arrhythmias
32
What are the adverse effects of Phenytoin?
* Acute: Nystagmus, diplopia, ataxia * Chronic: Gingival hyperplasia, hirsutism ## Footnote Commonly used as an anti-epileptic drug with Class IB activity
33
What distinguishes Class IC agents like Flecainide?
Potently blocks sodium channels, slows Phase 0 depolarization and conduction velocity, minimal effect on APD, ERP, and QT ## Footnote Reduces automaticity by raising the threshold potential
34
What is the major use of Propafenone?
Supraventricular arrhythmias ## Footnote Has structural similarity to propranolol and includes beta-blocker activity
35
What are the effects of Class II beta-blockers?
Block adrenergic effects on SA and AV nodes, reduce heart rate and contractility ## Footnote More effective in arrhythmias due to sympathetic stimulation
36
Which beta-blocker is most commonly used for treating arrhythmias?
Metoprolol ## Footnote It is a selective beta-blocker
37
What are the contraindications for beta-blockers?
* Bronchospasm in respiratory diseases * Wolf-Parkinson-White syndrome * SA nodal disease or AV block ## Footnote Can precipitate arrhythmias
38
What are the mechanisms of action for Amiodarone?
* Potassium channel blocker * Sodium channel blocker (inactivated channels) * Adrenergic and calcium channel blockade ## Footnote Leads to reduced SA node automaticity and marked ERP prolongation
39
List the key advantages of Amiodarone.
* Broad spectrum of actions * High efficacy * Low incidence of torsades de pointes despite QT prolongation ## Footnote Accumulates in various tissues leading to unique side effects
40
What are the common adverse effects of Dronedarone?
* Nausea * Vomiting * Diarrhea * Liver failure (hepatotoxicity) ## Footnote Benzofuran derivative of amiodarone with fewer adverse effects
41
What is the mechanism of action of Dofetilide?
Selective Class III activity, pure K+ channel blocker ## Footnote Prolongs ERP and QT interval; pro-arrhythmogenic properties require hospital initiation
42
What distinguishes Ibutilide from Dofetilide?
Ibutilide has mixed Class III and IA actions ## Footnote Indicated for chemical conversion of atrial flutter
43
What is the mechanism of action of Sotalol?
Combination of beta-blocking and K+ channel blocking properties ## Footnote Prolongs Phase 3 repolarization and ERP
44
What are the main uses of Sotalol?
Treats atrial, supraventricular, and ventricular tachyarrhythmias ## Footnote Effective on both SA/AV nodes and ventricular muscle
45
What is the mechanism of action of Class IV calcium channel blockers?
Prolong Phase 2 repolarization and slow conduction ## Footnote Also reduce slope of spontaneous Phase 4 depolarization in SA and AV nodes
46
What are Class IV agents in cardiology?
Calcium channel blockers (CCBs)
47
What is the primary effect of non-dihydropyridine CCBs?
They have Class IV anti-arrhythmic properties
48
Which two drugs are examples of non-dihydropyridine CCBs?
* Verapamil * Diltiazem
49
What is the mechanism of action of Verapamil?
Blocks both activated and inactivated L-type calcium channels
50
In which conditions are non-dihydropyridine CCBs more useful?
Atrial and supraventricular tachycardia
51
How do CCBs affect Phase 2 of the cardiac action potential?
Prolong Phase 2 repolarization
52
What effect do CCBs have on automaticity and heart rate?
Reduce automaticity and decrease heart rate
53
What is the effect of CCBs on the effective refractory period (ERP)?
Increases the effective refractory period
54
What is the metabolism pathway for Verapamil and Diltiazem?
Both are metabolized by CYP3A4
55
What are the adverse effects associated with CCBs?
* Reduced force of contraction * Heart failure * Constipation * Lassitude * Nervousness * Peripheral edema
56
What are the contraindications for using CCBs?
* SA nodal or AV nodal disease * Wolff–Parkinson–White syndrome
57
What is the mechanism of action of Digoxin?
Enhances vagal tone at the AV node and inhibits Ca2+ influx
58
What are the adverse effects of Digoxin?
* Induces arrhythmias * Ectopic ventricular beats * Nausea * Vomiting * Yellow vision
59
What is the mechanism of action of Adenosine?
Binds to A1 adenosine receptors, promoting K+ influx and inhibiting Ca2+ influx
60
What is the duration of action of Adenosine?
Ultra-short acting, ~10-15 seconds
61
What are the uses of Magnesium in cardiology?
* Treatment of digitalis-induced arrhythmias * Treatment of Torsades de pointes
62
What is the role of potassium in arrhythmias?
Alterations in serum potassium levels can cause arrhythmias
63
What is the mechanism of action of Vernakalant?
Targets specific K+ channels in the atria, prolonging atrial refractoriness
64
What are the side effects of Vernakalant?
* Taste disturbance * Sneezing * Paraesthesia
65
What is the mechanism of action of Atropine?
Non-selective muscarinic receptor antagonist that increases heart rate
66
What are the drugs used in the management of bradycardia?
* Atropine * Dopamine * Epinephrine * Glucagon * Isoproterenol
67
What defines ectopic foci in cardiac physiology?
Abnormal impulse generation that can lead to arrhythmias
68
What phases are part of the cardiac action potential?
* Phase 0: Rapid depolarization * Phase 1: Early repolarization * Phase 2: Plateau phase * Phase 3: Rapid repolarization * Phase 4: Resting phase
69
What is the primary action of Class III anti-arrhythmic agents?
Delay Phase 3 repolarization and prolong refractory period
70
How do Class II agents affect cardiac function?
Reduce slope of spontaneous Phase 4 depolarization, reducing automaticity
71
What is the effect of hypokalemia in cardiac function?
Increases the risk of triggered activity after depolarizations
72
What does the PR interval represent in an ECG?
Time taken for atrial impulses to reach the ventricle
73
What is the consequence of high calcium levels in cardiac cells?
Can lead to triggered activity due to delayed after depolarizations (DADs)

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