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Pharmacology II > Cardiac antiarrhythmic drugs > Flashcards

Cardiac antiarrhythmic drugs Flashcards

1
Q

What is the heart rate regulated by?

A

SA node

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2
Q

What is the sino-atrial node?

A

pacemaker within right atrium

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3
Q

How does Sino-atrial node regulate HR?

A

electrical impulses

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4
Q

What innervates the heart to affect HR?

A

sympathetic & parasympathetic

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5
Q

What causes heart contraction?

A

spontaneous action potential generated by SA node & AV node

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6
Q

What type of potential does the SA node generate?

A

slow potential

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7
Q

Why is the SA node the primary pacemaker?

A

has faster rate than AV node

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8
Q

How does the electric impulse of the heart travel?

A

SA node —> atrium —> AV node —> bundle of HIS —> ventricles

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9
Q

How are the impulse from SA node & AV node generated?

A

ion influxes (slow potential)

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10
Q

How does SA node & AV node maintain cell’s negative polarization?

A

continuous efflux of K ion

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11
Q

Depolarization of slow potential of the SA & AV node

A

the increase in influx rate of the Ca2+ and decreased K+ efflux rate

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12
Q

What can affect the rate of impulse generation at the SA node?

A
  • sympathetic beta1 receptor
  • parasympathetic muscarinic receptor
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13
Q

How does sympathetic beta1 receptor alter the rate of SA node?

A

increase Na+/Ca2+ influx enhancing signal generation & increase rate of depolarization

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14
Q

How does parasympathetic muscarinic receptor alter the rate of depolarization

A

stimulates K+ efflux and decrease Na+ influx (decrease rate of signal generation)

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15
Q

Process of signal transduction & heart contraction

A
  • SA generates impulse and causes atrium to contract
  • signal travels to AV node
  • signal pause for filling of ventricles
    -signal travels through bundle of HIS and bundle branches and purkinje fiber
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16
Q

What type of potential does bundle of HIS & purkinje fiber generate?

A

fast potential

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17
Q

How are the fast potentials generated?

A

stimulation above threshold causes rapid Na+ voltage-gated ion channels to open

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18
Q

What is the difference between slow potential and fast potential?

A

Slow potential:
- SA node & AV node
- have constant K+ efflux
- depolarization involves mainly Ca2+ influx (some Na influx) and slow K+ efflux
Fast potential:
- HIS/ Purkinje fiber system
- rapid depolarization due to Na+ voltaged gated channel opening ( Na+ influx)
- no constant loss of K+

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19
Q

Process of fast potential

A
  • stimulation of potential above threshold causes Na+ voltage-gated channels to open (Na+ influx)
  • Cell depolarize & becomes sufficiently positive and rapid Na+ channel close and K+ channels open & efflux
  • Ca2+ then influx for contraction & Na+ influx
  • rapid repolarization & K+ efflux
  • slow spontaneous depolarization K+ efflux and Na+ influx
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20
Q

Definition of arrhythmia

A

disruption of normal HR & rhythm

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21
Q

What causes arrhythmia?

A

abnormal impulse formation, conduction or both

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22
Q

Underlying causes that causes arrhythmia

A
  • cardiac structure or physiological remodeling
  • external influence increases triggering (catecholamine, toxins & electrolytes)
  • unknown
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23
Q

Effects of arrhythmia

A

Decrease cardiac output:
1. bradycardia: decreases cardiac output due to decreased HR
2. tachycardia: insufficient time to fill ventricles with blood & irregular contraction

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24
Q

How does class I anti-arrhythmic drug combat arrhythmia?

A

block Na+ channel and decrease Na+ influx

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25
Q

General characteristics of class I antiarrhythmic drugs

A
  • “use dependency”: tend to bind more readily to Na+ channels in the opened or refractory state
  • only affect abnormal cells (abnormal cells opens more frequently)
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26
Q

What does Class I antiarrhythmic drug do?

A
  • suppress excitable tissues
  • decrease conduction velocity through atria, ventricles and HIS purkinje fibers
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27
Q

Indications for Class I antiarrhythmic drugs

A
  • ventricular arrhythmia
  • supraventricular arrhythmia
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28
Q

Name some Class I arrhythmic drugs

A

Lidocaine, Mexiletine, Quinidine, procainamide

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29
Q

Features of Lidocaine

A
  • Class I drug
  • blocks mostly Na+ channels (some Ca2+ channels)
  • more effective on ventricular cells
  • rapid association/dissociation rate
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30
Q

What is lidocaine used for?

A

Reverting ventricular arrhythmias ( decrease AP amplitude & automaticity

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31
Q

How are Lidocine administered & why?

A

CRI due to short half-life and high first pass effect

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32
Q

Adverse effects of Lidocaine

A

nausea, vomiting, skeletal fasciculation, CNS excitement/ seizure

33
Q

Drug interaction of lidocaine

A
  • metabolized in liver
  • affected by drugs that affect hepatic blood flow & metabolism
  • hepatic enzyme inhibitor/ hepatic enzyme inducer
34
Q

What is Mexiletine

A
  • non-selective blocker of NA+ channels
  • oral administration
  • long-term treatment for ventricular arrhythmia
35
Q

What drug is Mexiletine commonly given with?

A

beta blockers

36
Q

Adverse effects of Mexiletine

A

tremors, bradycardia, vomiting

37
Q

General features of Quinidine

A
  • class I drug
  • affect atrial, ventricular & HIS Purkinje fibers
  • cytochrome P450 inhibitor
  • can increase HR
38
Q

What are the effects of quinidine?

A

Affect atrial, ventricular & HIS Purkinje fibers:
- inhibit Na+, K+ channels, alpha1 receptors
- markedly prolong effective refractory period
- vagolytic effect (increase impulse through AV node)

39
Q

What drug is usually given with quinidine and why

A
  • Negative chronotropic drug
  • decrease HR to combat vagolytic effect og quinidine
40
Q

Clinical use of quinidine

A
  • mainly horses (due to high vagal tone)
  • used to convert atrial fibrillation
41
Q

Adverse effects of quinidine

A
  • hypotension due to alpha 1 blockage
  • AV block
  • ventricular tachycardia
    -LA: colic, diarrhea, laminitis…etc
42
Q

How to reverse quinidine toxicity

A
  • rapid alkalinization of blood with sodium bicarbonate (enhance quinidine binding to plasma protein)
43
Q

Drugs that may interact with quinidine

A

Digoxin: displace Digoxin from tissue binding sites hence increase plasma Digoxin concentration

44
Q

General features of Procainamide

A
  • class 1 drug
  • no interaction with Digoxin
  • less vagolytic effect ( can increase impulse through AV node)
  • main indication is for ventricular arrhythmia that is unresponsive to lidocaine
45
Q

Adverse effects of Procainamide

A

dose-related hypotension, worsening arrhythmia, vomiting or diarrhea

46
Q

General characteristics of Class II antiarrhythmic drugs

A
  • decrease sympathetic input
  • beta blocker: block beta1 receptor and decrease Na+ & Ca2+ influx
  • block catecholamine enhancement of abnormal cell at normal concentration
47
Q

Class II antiarrhythmic drug actions

A
  1. Decrease HR by depression of SA node
  2. Decrease ventricular response to atrial stimulation due to slow AV conduction
  3. Prolonging refractory period
  4. Suppression of catecholamine-induced arrhythmia
48
Q

Adverse effects of Class II antiarrhythmic drugs

A
  • dose-related beta2 blockade (decreased cardiac contractility & bradycardia
  • bronchoconstriction ( beta2 blockade)
49
Q

Clinical indications of Class II drugs

A
  • arrhythmias due to excess sympathetic stimulation
  • controlling ventricular rate in supraventricular & ventricular arrhythmia & premature complexes
  • benefit dogs with dilated cardiomyopathy
50
Q

Name some class II antiarrhythmic drugs

A

propanalol, atenolol, metoprolol

51
Q

General characteristics of propanolol

A
  • non-specific beta blocker
  • drug metabolized in liver
  • negative inotrope & - chronotrope
52
Q

General characteristics of atenolol

A
  • class II drug
  • longer duration & more selective (beta1)
  • decrease AV node conduction
  • decrease myocardial O2 consumption
  • excreted unchanged by kidneys
  • only affect beta2 receptors at high doise
53
Q

Contraindication of atenolol

A

renal disease (delay excretion)

54
Q

What is atenolol commonly used to treat?

A
  • hypertrophic cardiomyopathy
  • decrease HR in hyperthyroid cats
  • atrial fibrillation
55
Q

General characteristics of metoprolol

A
  • class II drug
  • beta 1 specific drug
  • hepatic clearance
  • high first-pass effect
  • can cause excessive cardiovascular depression/ AV block
56
Q

What does Class III antiarrhythmic drugs do?

A
  • block K+ channels and antagonize K+ efflux
  • prolong AP duration, repolarization, & extend refractory period
  • delay conduction
57
Q

What type of drug is Sotolol?

A
  • non-selective beta blocker at low doses
  • inhibitor of K+ efflux at high doses
58
Q

General characteristics of Sotolol

A
  • oral drug
  • has negative inotrope effect
  • high bioavailability
  • excreted unchanged through kidney
  • racemic drug (L-isomer responsible for most of the beta-blocking)
59
Q

What are Sotolol used to treat?

A
  • long-term treatment for ventricular arrhythmia
60
Q

Adverse effects of Sotolol

A

bradycardia, hypotension or GI irritation

61
Q

Contraindication of Sotolol

A
  • patients prone to dilated cardiomyopathy
  • patients with renal disease
62
Q

What drug can be used in combination with Sotolol for improvement of heart condition?

A
  • pimobendan: prevent decreased contractility & HR ( when use of Sotolol in patients with heart failure)
  • mexiletine: provide good suppression of ventricular arrhythmia
63
Q

How do the Class IV drugs treat arrhythmia?

A
  • block slow Ca2+ninflux channels in cardia cells
  • decrease sinus rate and AV conduction
  • some may cause vasodilation
64
Q

What do class IV drugs treat?

A
  • supraventricular tachycardia
  • feline hypertrophic cardiomyopathy
  • atrial fibrillation
65
Q

Why are Ca2+ channel blockers contraindicated in animals with CHF?

A
  • decrease cardiac contractility
66
Q

What drugs can interact with Ca2+ channel blockers?

A

any drugs affecting p-glycoprotein & P450 enzymes (Quinidine)

67
Q

Name some class IV drugs

A

Diltiazem, Verapamil

68
Q

General characteristics of Dilriazem

A
  • Class IV drug
  • effective in dogs with supraventricular arrhythmia
69
Q

General characteristics of Verapamil

A
  • Class IV drugs
  • used for supraventricular tachycardia
  • reduce ventricular rate response in patients with atrial fibrillation
  • significant first pass effect
  • negative inotrope & chronotrope
70
Q

What are the adverse effects of Verapamil?

A
  • dose-related hypotension
  • cardiac depression
  • bradycardia
  • AV blockade
71
Q

How can Digoxin treat arrhythmia?

A

parasympathetic effect

72
Q

How can anticholinergic drugs treat arrhythmia?

A
  • antagonize Ach at muscarinic receptors
  • resulting in increased sinus rate and AV conduction during the presence of excessive vagal tone
73
Q

What type of arrhythmia can anticholinergic treat?

A
  • sinus bradycardia
  • AV block during anesthesia (by blocking Ach receptor in AV node)
74
Q

What type of arrhythmia is Atropine most useful in treating?

A
  • bradycardia due to action on SA node
  • cardiac arrest due to asystole
75
Q

What can happen when giving a low dose of atropine to patients?

A

decrease HR due to stimulation of vagus nerve

76
Q

Atropine adverse effects

A

CNS excitation, decreased GI contraction, decreased urinary bladder tone, bronchodilation

77
Q

Glycopyrrolate usage in correcting arrhythmia

A
  • used as pre-anesthetic drug to treat sinus arrhythmia, SA arrest, or incomplete AV block
  • increase HR without crossing BBB
78
Q

What drugs are used to correct ventricular arrhythmia?

A

Emergency drug: Lidocaine (class I)
Long-term: mexiletine, procainamide,
Sotalol (beta-blocker; Class III)

79
Q

What drugs are used to treat atrial tachycardia?

A

Class IV drugs
Beta-blockers
Quinidine
Digoxin

Pharmacology II (8 decks)

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