Antiarrhythmic Drugs Flashcards
1
Q
The ______ node causes slowing of the heart contraction
A
AV
2
Q
Atrial vs ventricular tachyarrythmia
A
- atrial: not as dangerous. The biggest concern is the formation of a clot due to blood stasis in the atria
- ventricular: very dangerous can can be lethal
3
Q
The bundle of Kent/ bypass tract allow impulses to travel more quickly from __________ to ________ than the _____ node
A
Atria to ventricles; AV node
Common cause of arrhythmias
4
Q
The rapid upstroke in phase 0 of the myocardial action potential is due to _____
A
Opening of sodium channels and ends as the sodium channels are inactivated
5
Q
What happens in phase 1 of the myocardial action potential?
A
Phase 1: initial repolarization
- sodium channels inactivate
- K channels rapidly open and close → transient outward current
6
Q
What causes the plateau in phase 2 of the myocardial action potential?
A
Balance of the opening of voltage sensitive calcium channels (depolarization) and slow outward movement of K (repolarization)
7
Q
The repolarization phase (phase 3) is due to:
A
Opening of K and the outward current (polarizing) and calcium channels close
Gain of Na and loss of K (imbalance corrected by Na/K ATPase)
8
Q
What is phase 4 of the myocardial action potential?
A
Resting potential in which there is a small gradual increasing depolarizing to eventually reach threshold of the next AP
9
Q
Where do you see pacemaker action potential?
A
SA and AV nodes
10
Q
The phase 0 upstroke in the pacemaker action potential is due to ________
A
Calcium; (in myocardial AP, the upstroke is due to sodium)
11
Q
Phase 3’s repolarization in the pacemaker action potential is due to ________
A
Inactivation of calicum channels and ↑ activation fo K channels → ↑ efflux fo K
12
Q
___________ channels causes the slow spontaneous depolarization in phase 4 of pacemaker action potential
A
Funny channels (mixed Na/K inward current)
13
Q
Drugs that slow conduction through the _____ node are going to ______ the PR nterval
A
AV node; ↑ PR interval
14
Q
What it’s he QT interval?
A
The time from ventricular depolarization to ventricular repolarization
15
Q
What would affect the QT interval?
A
Extending the acting potential of ventricular myocytes wll extend QT interval
16
Q
Mechanisms of arrhythmias
A
- disturbances in impulse formation
- disturbance in impulse conduction
- mixture of both
17
Q
What are the two classifications for arrhythmias
A
- supraventricular (atrial or AV junctional)
- ventricular
18
Q
What is the leading cause of arrhythmias
A
Drug toxicity, especially from antiarrhythmics
19
Q
What are common causes of arrhythmias
A
Most arise from either abnormal automaticity or from defects in impulse conduction
- abnormal automaticity (generates complete stimuli)
- re-entrant circuits
- afterdepolarizations
- accessory tract pathways
20
Q
_____ node sets the pace of myocardium contraction
A
SA
21
Q
Most antiarrhymtics suppress automaticity by blocking either _______ or ________ and what phase is affected in the action potential?
A
Na and Ca;
- ↓ slope of phase 4 depolarization and/or ↑ threshold of discharge to a less negative voltage
Above two lead to a ↓ frequency of discharge
22
Q
Most antiarrythmics cause a decrease in the slope of phase ____ depolarization
A
Phase 4
23
Q
________ is the most common cause of arrhythmias
A
Re-entry; occurs if there is a unidirectional block. The problem here is that the impulses will travel backwards via the dead/non excitable area and re enter the tissues that have already been stimulated
24
Q
What are mechanisms that antiarrhythmics can prevent re-entry?
A
- slowing conduction
- ↑ the refractory period
25
After treatment of re-entrant circuits, a _________ conduction block becomes a __________ conduction block
Unidirectional; bidirectional
26
Early afterdepolarizations occur during phase ________ of the AP and are triggered by conditions that ___________
Phase 2 or 3; conditions that prolong action potential such as drugs that prolong QT interval
27
Drugs that prolong ______ interval can trigger early afterdepolarizations
QT
28
When digoxin causes early afterdepolarizatoins, it is due to ________
Changes in calcium and sodium ions
29
_________ afterdepolarizations arises from the plateau
Early;
30
Delayed afterdepolarizations occur shortly after __________ so it arises from the _______
Completion of depolarization; resting potential
31
________ has been used to treat bradyarrhythmias
Atropine;
cardiac pacemakers are the treatment of choice
32
Class 1-4 antiarrhythmic drugs
Class I: Na channel blockers
Class II: β blockers
Class III: K channel blockers
Class IV: Calcium channel blockers
33
What are the class IV anti-arrhythmic drugs?
- verapamil and diltiazem
34
Class I antiarrhythmic drugs block ________ and thus affects phase ______
Inward Na channels;
Slows the rate of rise of phase 0 depolarization
35
Antiarrhymic drugs possess use/state dependence. What is this?
These drugs bind to channels when they are open or closed NOT very well in their resting state → have more effect when there is arrhythmia (adds to selectivity)
36
What are the class 1A antiarrhythmics
- quinidine
- procainamide
- disopyramide
37
Procainamide and other similar drugs (class ________ antiarrhythmics) affect: __________ and _________ phases
- Slows rate of change of phase 0 by acting on the sodium channels (↑ QRS)
- prolongs phase 3 by inhibiting K channels and thus ↑ the ventricular effective refractory period (inc. QT → early afterdepolarizations causing more Na channels to open)
Class 1A
38
Quinidine can also block K channels and affects _______ and ______ but NOT _______
Atrial and ventricular AP’s BUT NOT the nodal action potential
39
What are the presenting features of cinchonism and what drug is this group of adverse effects associated with?
- blurred vision, tinnitus, headache and pscyhosis
| - associated with quinine and quinidine
40
What are some adverse effects of quinidine?
- SA/AV block
- thrombocytopenic purpura
- ventricular tachycardia in toxic doses
- cinchonism: blurred vision, tinnitus, headache and psychosis
- mixed α adrenergic block and antimuscarinic properties
- can ↑ concentration of digoxin by ↓ renal clearance
41
________ can ↑ concentration of digoxin by _______
Quinidine; ↓ renal clearance of digoxin
42
Quinidine should not be given to patients with _____
Heart block
43
________ and _______ are class 1A antiarrhythmic drugs that have anti-muscarinic properties but _______ has the most severe antimuscarinic effects
Quinidine and procainamide; disopyramide
44
_________ and _______ are drugs that are associated with reversible lupus like syndrome
Hydralazine and procainamide
45
The acetylation of _________ produces NAPA which prolonged the _________ blockade
Procainamide; potassium channel
46
Which class 1A antiarrhythmic is contraindicated in patients with lupus?
Procainamide; this drug also causes reversible lupus like syndrome
47
Which class 1A drug has the strongest negative ionotropic effect?
Disopryamide
48
Dispyramide causes peripheral _________
Vasoconstriction; class 1A antiarrhythmic
49
What are the class 1B antiarrhythmics
Lidocaine and mexiletine
50
What phases do the class 1B antiarrhythmic drugs affect?
Slows phase 0 and ↓ slow of phase 4
Shortens phase 3 repolarization (this is not clinically significant and is actually pro-arrhythmic and has no adverse effects)
51
If you give a person without an arrhythmia lidocaine, would you see any changes on the EKG?
```
NO
(Same with class 1A drugs)
```
52
Class 1B drugs are used specifically for _________ arrhythmias
VENTRICULAR
53
Class ____ drugs are used for both atrial and ventricular arrhythmias
1A
54
Which class 1 antiarrhythmic sub class as a milder sodium channel block?
Class 1B
55
1st treatment for ventricular tachyarrhythmias is _________ and the second line is ________
1st line: amiodarone
| 2nd line: lidocaine
56
What are some symptoms you see in a lidocaine OD?
Convulsions and coma
57
Does lidocaine have any ionotropic effect?
NO
58
________ is the oral version of lidocaine and thus can expect to see more _____ adverse effects
Mexitene; GI
59
Which class 1 drug rapidly associated and disassociated with sodium channels?
Class 1B: lidocaine and mexiletine
60
What can you expect to see on the AP graph of a class 1C drug?
MARKED depression of phase 0 action potential AND NO EFFECT ON PHASE 3 because no effect on K channels
Class 1C drugs: flecainide and propafenone
61
Class ____ drugs associates and reassociates slowly with Na channels
1C: flecainide and propafenone
62
A large ↑ in QRS is seen with _______
Class 1C drugs: flecainide and propafenone
63
What are some clinical applications of flecainide
Class 1C drug;
- severe symptomatic ventricular arrhythmias
- premature ventricular contraction
- ventricular tachycardia resistant to other therapy
- supraventricular arrhythmias
64
Flecainide has _______ inotropic effects
NEGATIVE
65
Which drug is useful to treat arrhythmias in people with CHF and why?
Lidocaine because it does not have any negative inotropic effects
66
Which class 1 drug is associated with β booking activity and thus can cause bronchospasm or aggravate underlying heart failure?
- propafenone (class 1C)
67
Lidocaine and mexiletine _____ QRS and ______ QT
Slight ↑ in QRS and slight ↓ in QT (QT ↓ is clinically insignificant)
68
Class 1 drugs that ↑ both QRS and QT:
Quinidine, procainamide, and disopyramide (1A)
69
Class II drugs are _____ blockers
β1 (↓ HR and contractility)
70
Class ___ affects the SA and AV node
Class II (β blockers)
71
Class II has its main effects on the ____ tissues
Nodal; little effect on the action potential in most myocardial cells
Mainly AV node
72
An ↑ in _____ interval is seen on EKG when given β blockers
PR
73
What drug is given to reduce the incidence of sudden arrhythmic death following an MI?
β blocker
74
_______ drugs are used to CONTROL supraventricular tachycardias (prevent the atrial tachycardia from developing into a ventricular one)
Class 2 drugs (β blocker)
75
What is the β blocker of choice to be given during surgery for a true arrhythmias and given via IV and has short acting β1 selective antagonist?
Esmolol
76
Beta blockers are used to threat ______ but are contraindicated in _____
Chronic heart failure; contraindicated in acute decompensated HF
77
Class III antiarrythmics extend ______ interval because they ______
QT; block repolarizing K channels
78
The arrhythmias caused by amiodarone are the ____________ due to the class ____ activity
Early afterdepolarizations; class 3 activity (blockade of K channels)
79
Which drug extends QT but DOES NOT ↑ risk for ventricular arrhythmias?
Amiodarone
80
Dominant effect of amiodarone
```
K channel blockade;
Has class 1,2 and 3 activity
```
81
Amiodarone blocks mostly ______ sodium channels
Inactivated
82
MOA of amiodarone
- blocks inactivated sodium channels
- blocks K channels (dominant effect)
- weak calcium channel blocker
- inhibits α and β receptors
- anti-anginal
- anti-arrhythmic
83
The DOC for acute ventricular tachyarrhythmia is _______
Amiodarone
2nd line: lidocaine
84
Interstitial pulmonary fibrosis is an AE of __________
Amiodarone
85
What are some adverse effects of amiodarone?
- Hyper or hypothyroidism (thyroxine)
- INTERSTITIAL PULMONARY FIBROSIS
- blue skin discoloration (iodine accumulation)
86
Amiodarone is contraindicated in patients taking:
- digoxin
- theophylline
- warfarin
- quinidine
87
What conditions are amiodarone contraindicated in?
- bradycardia
- SA/AV block
- severe hypotension
- severe respiratory failure
88
Sotalol is a class ____ drug that also acts as a _______
Class 3 (potassium blcoker) that is also a potent NON selective β blocker
89
Sotalol affects what phase of the AP?
- extends QT (K channel blocker)
| - extends PR (β blocker)
90
Which drug is used to maintain sinus rhythm in patients with atrial fibrillation and flutter?
Sotalol (class 3 with also β blocker activity); given as prophylactic to prevent moving out of sinus rhythm
91
Which anti-arrhythmic drug has the lowest rate of acute/long term adverse effects?
Sotalol
92
_______ is a potent and PURE K channel blocker
Dofetilide
93
________ is a classs 3 drug given to convert atrial fibrillation/flutter to normal sinus rhythm
Dofetilide
94
Class IV antiarrhythmics block ______ channels leading to ↓ rate of phase _____
Calcium; phase 0 depolarization in nodal tissues (similar to class 2 drugs by slowing conduction in SA and AV nodes)
95
With class IV drugs, there is a ↑ in _____ interval
PR
96
What are the two class IV drugs ?
- verapamil
| - diltiazem
97
Major effects of diltiazem and verapamil
These two drugs are class IV antiarrhythmic drugs that are calcium channel blockers
- ↓ contractility
- ↓ HR
- ↓ conduction velocity
98
Verapamil and diltiazem bind to _____ calcium channels
Open, depolarized; (prevents repolarization before the drug dissociates)
99
Class IV is more effective in ______ arrhythmias
Atrial
Class IV drugs: verapamil and diltiazem
100
High risk of constipation is an AE of what drug?
Verapamil (class IV)
101
Doses of _______ must be altered when giving what class IV drug?
Doses of: digoxin, dofetilide, simvastatin, and lovastatin
When giving verapamil
102
What drug SHORTENS the refractory period in atrial and ventricular myocardial cells?
Digoxin
103
Digoxin ________ the refractory period in _______
PROLONGS in the AV node
104
Digoxin _______ refractory period in the atrial and myocardial cells
SHORTENS
105
What is the pro-arrhythmic effect of digoxin?
Shortening the refractory period in the atrial and ventricular myocardial cells
106
Clinical application of digoxin?
- control of ventricular resisters rate in atrial fibrillation with impaired left ventricular function or HF
107
What drug is best to give to treat atrial fibrillation when they patient also has left ventricular dysfunction or HF
Digoxin
108
Which drugs slow the concussion through the AV node and ↑ PR interval?
- β blockers
- calcium channel blockers
- digoxin
109
Digoxin treats atrial fibrillation by controlling ________
Ventricular rate; (β blockers and calcium channel blockers do the same)
110
What is used to treat the ventricular arrhythmias caused by digoxin?
- lidocaine OR magnesium
111
DOC for acute supraventricular tachycardia?
ADENOSINE
112
What is the effect of high doses of adenosine?
- ↓ conduction velocity
- prolongs refractor period
- ↓ automaticity in AV node
113
Adenosine leads to ___________ of the AV node via:
Hyperpolarization of the AV node; enhancing K conduction and inhibits cAMP mediated calcium influx
114
DOC for acute ventricular tachycardia
Amiodarone
115
Magnesium is a _______ antagonist
Calcium
116
Magnesium is used for the treatment of: (3)
- trades de pointes
- digitalis induced arrhythmias
- prophylaxis of arrhythmia in acute MI
117
Which classes of anitarrhythmics act on the SA node?
- Class 2 (β blockers)
- class IV (calcium channel blockers)
- digoxin
118
What class of drugs affects the AV node?
- Class IV (calcium channel blockers)
- Class II (β blockers)
- digoxin
119
Which anti arrhythmic drugs affect the atrial myocytes?
- Class 1A and 1C
| - Class III (K channel blockers)
120
Which classes of antiarrhythmics affects the ventricular myocytes?
- class I (Na channel blockers, includes 1B because 1B only works on ventricles while 1A and 1C works on both atria and ventricles)
- Class III (K channel blockers)
121
Which antiarrythmics affect the accessory pathways?
- Class 1A
| - Class III (K channel blockers)
122
_______ channel blockade seems to have an affect on the accessory pathway
Potassium
123
What drugs are used to treat ventricular and supraventricular arrhythmia ?
Class 1A and 1C, and Class III (K channel blockers)
124
What drugs are used to treat mainly ventricular arrhythmias?:
Class 1B: lidocaine and mexiletene
125
What drugs are used to treat mainly supraventricular arrhythmias
```
- class IV drugs (calcium channel blockers)
Class II drugs (β blockers)
```
