Topic 11 Flashcards
1
Q
Arrhythmia Definition
A
Abnormalities in the electrical impulse generation or conduction through the heart. ...too slow, too fast, irregular, wrong direction, wrong origin, etc
2
Q
___% of anesthetized patients have arrhythmias
A
> 50%
3
Q
___% of patients with MIs have arrhythmias
A
80%
4
Q
___% of patients on CPB will be affected with arrhythmias!
A
100%
5
Q
Virtually all antiarrhythmics work by altering the
A
ionic transmembrane balance (Na⁺,Ca⁺⁺, K⁺) or the sympathetic tone to the heart. …which alters the shape of this graph!
6
Q
4 Classes of antiarrhythmics
The Vaughan Williams Classification
A
Na+ channel blocker
B-Adrenoreceptor blocker
K+ channel blocker
Ca++ channel blocker
7
Q
Class I : Na⁺ Channel Blockers: Preferentially bind to
A
open Na⁺ channels rather than to fully repolarized Na⁺ channels.
8
Q
Class I (Na+ Channel Blockers) drugs preferentially block
A
conduction in tissues that are depolarizing more frequently. This is called “use-dependence” blockade.
9
Q
Class I : Na⁺ Channel Blockers: Ia=
A
Shorten the action potential and affect QRS complexes
10
Q
Class I : Na⁺ Channel Blockers: Ib=
A
Shorten the action potential without affecting QRS
11
Q
Class I : Na⁺ Channel Blockers: Ic=
A
Do not shorten the action potential
12
Q
Class Ia: Na⁺ Channel Blockers: Shift the action potential (AP) to the
A
right by slowing Phase 0 depolarization (hence their
nickname, “membrane stabilizers”).
13
Q
Class Ia: Na⁺ Channel Blockers: inhibit some
A
K⁺ channels (Class III activity) which widens the AP causing prolonged QT intervals.
14
Q
Class Ia: Na⁺ Channel Blockers: Drug names
“Double Quarter Pounder”
A
Disopyramide (Norpace)
Quinidine (Quinidex)
Procainamide (Pronestyl, Procan)
15
Q
Disopyramide
A
(Norpace)
16
Q
Quinidine
A
(Quinidex)
17
Q
Procainamide
A
(Pronestyl, Procan)
18
Q
Quinidine is given ____ and used for_____
A
Orally
various tachyarrhythmias
19
Q
Quinidine: Rarely used because of
A
toxic side effects
- Cinchonism
- Torsades de pointes
20
Q
Torsades de pointes=
A
“Polymorphic Ventricular Tachycardia”
•Usually resolves spontaneously
•May devolve into V-fib
21
Q
Disopyramide: Like Quinidine, but more
A
negative inotropic effects and increased SVR
-Dont use on a sick heart- might precipitate HF!
22
Q
Most widely used Ia
A
Procainamide
23
Q
Procainamide is derived from
A
procaine (a local anesthetic)
24
Q
Procainamide is given
A
orally, IV, IM
25
Procainamide Adverse effects similar to
Quinidine (although less severe) but may cause reversible lupus erythematosus
26
Class Ib: Na⁺ Channel Blockers: Shift the action potential (AP) to the
left by shortening Phase 3 repolarization.
27
Class Ib: Na⁺ Channel Blockers: have their greatest effect on heart cells with
long action potentials like Purkinje fibers and ventricular myocytes
28
Class Ib: Na⁺ Channel Blockers: Drug names
| Lettuce Mayo Tomato
Lidocaine (Xylocaine)
Mexiletine (Mextil)
Tocainide (Tonocard)
29
Lidocaine
(Xylocaine)
30
Mexiletine
(Mextil)
31
Tocainide
(Tonocard)
32
Lidocaine is a
Local anesthetic
33
Lidocaine is given ONLY
parenterally
34
Lidocaine therapeutic index is
Wide
35
Lidocaine Major toxic side effect (at high doses) is
cardiac depression
36
Lidocaine Extends refractory period further into
diastole in depressed cardiomyocytes than in healthy ones.
37
Lidocaine ***D.O.C. for
ventricular arrhythmias (PVCs), particularly those associated with “sick hearts” with arrhythmias like post-MI.
38
Lidocaine is Frequently used as a component of
cardioplegia
39
Mexiletine is Like an oral
lidocaine
40
Mexiletine is used in what treatment
? look it up
41
Tocainide is given
Orally
42
Tocainide Used in patients resistant to &/or sensitive
| to
lidocaine/mexiletine
43
Tocainide Pulmonary toxicity fairly common— can cause
pulmonary fibrosis rendering Tonocard a 2nd or 3rd line treatment
44
Class Ic: Na⁺ Channel Blockers: does what to the action potential
Nothing- it does NOT shift
45
Class Ic: Na⁺ Channel Blockers: have profound effects on
normal hearts.
| --Recent studies indicate some are very dangerous and are not used when better/safer alternatives exist.
46
Class Ic: Na⁺ Channel Blockers: drug names
| Fries Please
Flecainide (Tambocor)
| Propafenone (Rhythmol)
47
Flecainide
(Tambocor)
48
Propafenone
(Rhythmol)
49
Flecainide is given
Orally
50
Flecainide Suppresses Phase...
ZERO upstroke in Purkinje fibers and cardiomyocytes
51
Flecainide Dramatically slows
conduction and automaticity is decreased via an increase in the threshold pote ntial
52
Flecainide used for what type of arrhythmia
refractory ventricular arrhythmias
| particularly PVCs
53
Flecainide has what effects
Negative inotropic effects worsen CHF
54
Recent studies suggest Flecainide is more likely to
harm than help in the long-run
55
Propafenone has similar uses as
quinidine
56
Propafenone is given
Orally
57
Propafenone Considered to be a “broad spectrum”
| antiarrhythmic but used mostly for
supraventricular tachyarrhythmias
58
β₁-blockers are cardioselective but
many/most have other adrenergic blocker activity. Some have partial adrenergic agonist activity.
59
Class II : β-Adrenoceptor Blockers: work by
```
diminishing Phase 4 depolarization =
decreased automaticity
prolonged AV conduction
negative chronotrope
negative inotrope
```
60
Class II : β-Adrenoceptor Blockers: what arrhythmias are they used for?
1. Atrial tachyarrhythmias...including AV nodal re-entrant tachyarrythmias (the most common type, particularly in women.)
2. extensively used post-MI for ventricular arrhythmias
61
Class II : β-Adrenoceptor Blockers: drug names
Propranolol (Inderal)
Metoprolol (Lopressor, Toprol-XL)
Esmolol (Brevibloc)
62
Propranolol
(Inderal)
63
Metoprolol
(Lopressor, Toprol-XL)
64
Esmolol
(Brevibloc)
65
Propranolol (Inderal): Extensively used for decades.
| *Has been proven to
decrease incidence of mortality within the first year of an MI
66
The most commonly used β-blocker for treating cardiac arrhythmias
Metoprolol (Lopressor, Toprol-XL)
67
Very short-acting IV β-blocker commonly used during surgery and during emergencies
Esmolol (Brevibloc)
68
Class III: K⁺ Channel Blockers: Block K⁺ channels with little effect on
Na⁺ channels
69
Class III: K⁺ Channel Blockers: By blocking the outward flow of K⁺ during REpolarization they
prolong the action potential without affecting Phase 0 (depolarization).
70
Class III: K⁺ Channel Blockers: have what effect
refractory period and “refractoriness”
71
Class III: K⁺ Channel Blockers: have a prolonged action potential with
“normal” conduction velocity block re-entrant arrhythmias.
72
Class III: K⁺ Channel Blockers: Exhibit the negative side effect of
“reverse use-dependence blockade” which can contribute to arrhythmias.
73
Class III: K⁺ Channel Blockers: Generally prolong the
QT
74
Class III: K⁺ Channel Blockers: drug names
```
Amiodarone (Cordarone)
Drondarone (Multaq)
Dofetilide (Tikosyn)
Sotalol (Betapace, Sorine)
Ibutilide (Corvert)
```
75
Amiodarone
(Cordarone)
76
Drondarone
(Multaq)
77
Dofetilide
(Tikosyn)
78
Sotalol
(Betapace, Sorine)
79
Ibutilide
(Corvert)
80
Amiodarone is an
“iodinated benzofuran” which means it looks a little like thyroxine
81
Amiodarone Effects all cardiac tissues, so it has a
broad-spectrum of antiarrhythmic activity.
82
Amiodarone Often the D.O.C. for
A-Fib
83
Amiodarone Used as a 2nd-line Rx for lots of
refractory arrhythmias
84
Amiodarone has a Very long half-life of
(20-100 days!) combined with high ability to interact with other drugs and a lot of side-effects (particularly with long-term use) limit its use
85
Amiodarone has LESS toxicity at lower dosages of _____ but it takes weeks to months to get to therapeutic levels (because of long half-life). So you have to give high loading doses of ______
(100-200 mg/day)
| 800-1600 mg/day
86
Amiodarone Potential for side effects...
increases with both high doses and long-term use
87
Amiodarone side effects
Sinus Bradycardia
Hypotension
ARDS & Pulmonary Fibrosis
88
Dronedarone: Like amiodarone without the
iodine (whew, no thyroid dysfunction or blue skin!)
89
Dronedarone Much shorter half-life of ____ than ____
(24 hours) than amiodarone
90
Dronedarone Less effective than amiodarone for
a-fib but has fewer of those side effects except death
91
Sotalol is a
a non-selective β-blocker
92
Sotalol Not only does it reduce post-MI mortality (as do most β-blockers) but it also has
Class III activity
| lengthening of refractory period
93
Sotalol has what effects
reduces myocardial O2 consumption
| acts as a powerful antiarrhythmic
94
Sotalol Helps prevent
fibrillation and makes defibrillating patients easier
| so it’s ideal for post-MI patients
95
Dofetilide: Often the D.O.C. for
a-fib in patients with HF or decreasing EF’s
96
Ibutilide has both
Class III and IA antiarrhythmic properties
97
Ibutilide: DOC for
? look it up
98
All antiarrhythmics can cause
arrhythmias.
99
Class III are more prone than others, particularly in causing
Torsade de Pointes
100
Class IV: Ca⁺⁺ Channel Blockers: Decrease the rate of
Phase 4 spontaneous depolarization
101
Class IV: Ca⁺⁺ Channel Blockers: preferentially
| slow the rate of conduction in
issues dependent on calcium currents for depolarization
102
Class IV: Ca⁺⁺ Channel Blockers: drug names
Verapamail
Cardizem
Nifedipine
103
nifedipine can cause more
arrhythmias
104
Verapamil & Cardizem: Used almost ______ for arrhythmias
interchangeably
105
Verapamil & Cardizem: preferentially block the
voltage-sensitive channels
106
Verapamil & Cardizem: are “use-dependent”=
preferring to block channels on tissues depolarizing too fast and block Ca⁺⁺ channels most effectively on the AV and SA nodes
107
Verapamil & Cardizem: also treat what arrhythmia
Atrial flutter
108
Verapamil & Cardizem: are both
negative inotropes
109
Classless Antiarrhythmics include
Digoxin
Adenosine (Adenocard)
Magnesium sulfate
110
Digoxin shortens the refractory period in
atrial and ventricular tissue while slowing conduction through the AV node
111
Digoxin Used to control
ventricular response rates in a-fib and a-flutter
112
Adenosine
(Adenocard)
113
Adenosine (Adenocard) is the D.O.C. for abolishing
SVT
114
Adenosine (Adenocard) When given fast IV push on bypass (a rarity) ...it
decreases AV node automaticity and cardiac conduction velocity and automaticity
115
Adenosine (Adenocard) Has a very short half-life of_____ and causes _____
(~10-15 seconds!) and causes transient hypotension
116
Adenosine doses
First dose is 6 mg fast IV push
| *If that doesn’t convert the SVT give 12 mg fast IV push
117
Magnesium Sulfate: it slows the rate of
A node impulse formation and the rate at which the impulse travels through myocardium
118
Magnesium Sulfate: DOC for
digoxin-induced arrhythmias
119
Magnesium Sulfate: Must be given
IV to be effective as an antiarrhythmic
