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Pharmacology II > Cardiac antiarrhythmic drugs > Flashcards

Cardiac antiarrhythmic drugs Flashcards

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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
General characteristics of class I antiarrhythmic drugs
- "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)
26
What does Class I antiarrhythmic drug do?
- suppress excitable tissues - decrease conduction velocity through atria, ventricles and HIS purkinje fibers
27
Indications for Class I antiarrhythmic drugs
- ventricular arrhythmia - supraventricular arrhythmia
28
Name some Class I arrhythmic drugs
Lidocaine, Mexiletine, Quinidine, procainamide
29
Features of Lidocaine
- Class I drug - blocks mostly Na+ channels (some Ca2+ channels) - more effective on ventricular cells - rapid association/dissociation rate
30
What is lidocaine used for?
Reverting ventricular arrhythmias ( decrease AP amplitude & automaticity
31
How are Lidocine administered & why?
CRI due to short half-life and high first pass effect
32
Adverse effects of Lidocaine
nausea, vomiting, skeletal fasciculation, CNS excitement/ seizure
33
Drug interaction of lidocaine
- metabolized in liver - affected by drugs that affect hepatic blood flow & metabolism - hepatic enzyme inhibitor/ hepatic enzyme inducer
34
What is Mexiletine
- non-selective blocker of NA+ channels - oral administration - long-term treatment for ventricular arrhythmia
35
What drug is Mexiletine commonly given with?
beta blockers
36
Adverse effects of Mexiletine
tremors, bradycardia, vomiting
37
General features of Quinidine
- class I drug - affect atrial, ventricular & HIS Purkinje fibers - cytochrome P450 inhibitor - can increase HR
38
What are the effects of quinidine?
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
What drug is usually given with quinidine and why
- Negative chronotropic drug - decrease HR to combat vagolytic effect og quinidine
40
Clinical use of quinidine
- mainly horses (due to high vagal tone) - used to convert atrial fibrillation
41
Adverse effects of quinidine
- hypotension due to alpha 1 blockage - AV block - ventricular tachycardia -LA: colic, diarrhea, laminitis...etc
42
How to reverse quinidine toxicity
- rapid alkalinization of blood with sodium bicarbonate (enhance quinidine binding to plasma protein)
43
Drugs that may interact with quinidine
Digoxin: displace Digoxin from tissue binding sites hence increase plasma Digoxin concentration
44
General features of Procainamide
- 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
Adverse effects of Procainamide
dose-related hypotension, worsening arrhythmia, vomiting or diarrhea
46
General characteristics of Class II antiarrhythmic drugs
- decrease sympathetic input - beta blocker: block beta1 receptor and decrease Na+ & Ca2+ influx - block catecholamine enhancement of abnormal cell at normal concentration
47
Class II antiarrhythmic drug actions
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
Adverse effects of Class II antiarrhythmic drugs
- dose-related beta2 blockade (decreased cardiac contractility & bradycardia - bronchoconstriction ( beta2 blockade)
49
Clinical indications of Class II drugs
- arrhythmias due to excess sympathetic stimulation - controlling ventricular rate in supraventricular & ventricular arrhythmia & premature complexes - benefit dogs with dilated cardiomyopathy
50
Name some class II antiarrhythmic drugs
propanalol, atenolol, metoprolol
51
General characteristics of propanolol
- non-specific beta blocker - drug metabolized in liver - negative inotrope & - chronotrope
52
General characteristics of atenolol
- 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
Contraindication of atenolol
renal disease (delay excretion)
54
What is atenolol commonly used to treat?
- hypertrophic cardiomyopathy - decrease HR in hyperthyroid cats - atrial fibrillation
55
General characteristics of metoprolol
- class II drug - beta 1 specific drug - hepatic clearance - high first-pass effect - can cause excessive cardiovascular depression/ AV block
56
What does Class III antiarrhythmic drugs do?
- block K+ channels and antagonize K+ efflux - prolong AP duration, repolarization, & extend refractory period - delay conduction
57
What type of drug is Sotolol?
- non-selective beta blocker at low doses - inhibitor of K+ efflux at high doses
58
General characteristics of Sotolol
- oral drug - has negative inotrope effect - high bioavailability - excreted unchanged through kidney - racemic drug (L-isomer responsible for most of the beta-blocking)
59
What are Sotolol used to treat?
- long-term treatment for ventricular arrhythmia
60
Adverse effects of Sotolol
bradycardia, hypotension or GI irritation
61
Contraindication of Sotolol
- patients prone to dilated cardiomyopathy - patients with renal disease
62
What drug can be used in combination with Sotolol for improvement of heart condition?
- pimobendan: prevent decreased contractility & HR ( when use of Sotolol in patients with heart failure) - mexiletine: provide good suppression of ventricular arrhythmia
63
How do the Class IV drugs treat arrhythmia?
- block slow Ca2+ninflux channels in cardia cells - decrease sinus rate and AV conduction - some may cause vasodilation
64
What do class IV drugs treat?
- supraventricular tachycardia - feline hypertrophic cardiomyopathy - atrial fibrillation
65
Why are Ca2+ channel blockers contraindicated in animals with CHF?
- decrease cardiac contractility
66
What drugs can interact with Ca2+ channel blockers?
any drugs affecting p-glycoprotein & P450 enzymes (Quinidine)
67
Name some class IV drugs
Diltiazem, Verapamil
68
General characteristics of Dilriazem
- Class IV drug - effective in dogs with supraventricular arrhythmia
69
General characteristics of Verapamil
- Class IV drugs - used for supraventricular tachycardia - reduce ventricular rate response in patients with atrial fibrillation - significant first pass effect - negative inotrope & chronotrope
70
What are the adverse effects of Verapamil?
- dose-related hypotension - cardiac depression - bradycardia - AV blockade
71
How can Digoxin treat arrhythmia?
parasympathetic effect
72
How can anticholinergic drugs treat arrhythmia?
- antagonize Ach at muscarinic receptors - resulting in increased sinus rate and AV conduction during the presence of excessive vagal tone
73
What type of arrhythmia can anticholinergic treat?
- sinus bradycardia - AV block during anesthesia (by blocking Ach receptor in AV node)
74
What type of arrhythmia is Atropine most useful in treating?
- bradycardia due to action on SA node - cardiac arrest due to asystole
75
What can happen when giving a low dose of atropine to patients?
decrease HR due to stimulation of vagus nerve
76
Atropine adverse effects
CNS excitation, decreased GI contraction, decreased urinary bladder tone, bronchodilation
77
Glycopyrrolate usage in correcting arrhythmia
- used as pre-anesthetic drug to treat sinus arrhythmia, SA arrest, or incomplete AV block - increase HR without crossing BBB
78
What drugs are used to correct ventricular arrhythmia?
Emergency drug: Lidocaine (class I) Long-term: mexiletine, procainamide, Sotalol (beta-blocker; Class III)
79
What drugs are used to treat atrial tachycardia?
Class IV drugs Beta-blockers Quinidine Digoxin

Pharmacology II (8 decks)

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