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Cardiology Exam III > Pharm: Anti-Arrhythmics Drugs > Flashcards

Pharm: Anti-Arrhythmics Drugs Flashcards

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1
Q

What are the three mechanisms that can lead to tachyarrhythmias ?

A

Increased automaticity (SA, ectopic pacemaker etc)

Triggered activity

Re-entry (due to unidirectional block)

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2
Q

Increased or altered automaticity and Triggered activity are forms of altered impulse _________.

A

Formation

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3
Q

Re-entry is a form of altered impulse ________.

A

propagation

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4
Q

Bradyarrhytmias are due to __________ impulse formation and exhibit ___________ phase 4 depolarization

A

Decreased

Decreased

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5
Q

What are the mechanisms that lead to impaired conduction ?

A

Ischemic , anatomic or drug induced

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6
Q

To treat bradyarrhythmia with pharm you can give drugs that inhibit vagal tone or drugs that induce chronotropic effects of the heart. Which drug would you give to block vagal effects ?

A

Atropine

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7
Q

Which drugs would you give to induce chronotropic effects in the heart to treat bradyarrhythmia ?

A

B1-receptor agonists
Dopamine
Isoproterenol

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8
Q

How could you treat a bradyarrhythmia long term w/o drugs ?

A

Pacemaker

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9
Q

Altered automaticity leading to tachyarrhythmia results in _______ phase 4 depot on SA node AP.

A

increased

This is known as Sinus tachy.

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10
Q

The pharmacologic goal of treating tachyarrhythmia is

A

to eliminate increased automaticity

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11
Q

How do drugs eliminate automaticity when treating tachyarrhthmia ?

A
  1. Decrease the slope of phase 4 in pacemaker cells. (aka less steep phase 4, slower depolarization)
  2. Make diastolic potential more negative
  3. Make threshold potential less negative
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12
Q

Abnormal automaticity in atrial or ventricular myocytes is due to cells aquiring phase 4 depolarizations. What are two ways this can occur ?

A

Digitalis Toxicity

Increased Sympathetic tone

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13
Q

Triggered activity leads to what kind of non-typical depolarizations ?

A

Early After Depolarizations

Delayed after Depolarization

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14
Q

What is ‘triggered activity’ ?

A

A depolarization that forms after a single or multiple impulses following a preceeding depolarization

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15
Q

Early After Depolarization (EAD’s) occur due to conditions that prolong _______ interval.

A

QT

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16
Q

Due to their mechanism ,EAD predispose patients to what condition ?

A

Torsades De Pointes

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17
Q

What occurs to Phase 2 Ca++ influx in EAD’s ?

A

It is increased (leading to a longer Phase 2 –> Longer QT interval

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18
Q

What occurs to Na+influx in Phase 3 during EAD’s ?

A

It is increased, Longer Phase 3 –> Longer QT interval

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19
Q

DAD’s are theorized to occur due to …

A

Intracellular Ca++ overload

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20
Q

What are the specified goals of treating Triggered activity ?

A

Preventing EAD’s by shortening AP duration

Correct DAD’s by correcting conditions of calcium overload

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21
Q

What is required for Re-entry to occur ?

A 
Unidirectional block
Slowed conduction (retrograde)
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22
Q

What are the overall goals of treating reentry related tacchycardia ?

A

Extinguish the re-entry by impeding propagation in the slow conducting limb

Increase the refractory period of the tissue the re-entry is stimulating. (If it is total refractory it will not be able to fire)

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23
Q

Mechanism of Class I Antiarrhythmics

A

Na+ Channel Blockers

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24
Q

Mechanism of Class IA Antiarrhythmics

A

Block Na+ channels that lead to prolonged depolarization (increased refractory phase)

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25
Mechanism of Class IB Antiarrhythmics
Shorten repolarization by blocking Na+ Channels
26
Mechanism of Class IC Antiarrhythmics
Blocks Na+ Channles (no real effect of AP)
27
Mechanism Class II Antiarrhythmics
Beta Receptor Blockers
28
MechanismClass III Antiarrhythmics
K+ Channel blockers, prolong the AP duration by not allowing depolarization
29
Mechanism Class IV Antiarrhythmics
Block Ca++ channels leading to decreased AP duration
30
List the Class IA drugs
Disopyramide(Minor), Quinidine , Procainamide | Pneumonic :Double Quarter Pounder
31
List the Class IB drugs
Lidocaine, Phenytoin, Mexelitine, Tocainide (Pneumonic|: Lettuce, Pickle, Mayo, Tomato
32
List Class IC drugs
Flecainide, Propafone (Minor Pneumonic: Fries Please
33
List Class II Drugs
Propanolol, Metoprolol and Esmolol Propanolol is not Beta1 selective while the other two are.
34
List Class III drugs
Amiodarone, Sotalol, Bretylium, Ibutitide (minor) and Dofetitide (minor) Note: One of the metabolites of Procainamide (1A) is N-Acetylprocainamide and has Class III actions.
35
List Class IV drugs
Verapamil Diltiazem (notice how these are non-DHP CCB's. These have more effect on the heart)
36
List the miscellaneous drugs used for Arrhythmia
Adenosine, digoxin, magnesium
37
What are the overall effects of Class I drugs (Na Channel Blockers)
Decreased automaticity decreased conduction velocity can prevent reentry arrhythmias
38
Indication for class IA drugs
wide variety of reentrant & ectopic supraventricular & ventricular tachycardias
39
Where do class IA drugs mainly have their effects in treating automaticity?
Purkinje Fibers and Ectopic pacemakers (actually have little effect of SA node automaticity)
40
Is it possible for Class IA drugs to convert a-flutter and A-fib to normal sinus rhythm ?
YES !
41
How do Class IA drugs treat reentrant arrhythmias ?
Produce bidirectinal blocks (decreases conduction) increase refractory period ! (UNIQUE TO 1A !!!) (Note:Later on he says that Class III drug affect the refractory quality of the perkinje and ventricular muscle fibers, so maybe Class IA only affect atrial ?)
42
What may Class IA drugs predispose a patient to ?
Torsades De pointes
43
What is the protoype Class IA drug ?
Quinidine
44
Quinidine (IA) has strong anti-muscarinic effects. How will this alter SA node automaticity and AV node conduction ?
Increase both SA and AV node automaticity
45
What can you pre-treat with prior to giving quinidine to ensure minial vasolytic effects ?
Digoxin, BB's or Verapamil (a CCB)
46
Quinidine Side Effects
Diarrhea (most common, 1/3 of all patients) Torsades de pointes Cinchonism
47
What is cinchonism ?
Side effect caused by quinidine resulting in : tinnitus, headache, vertigo, disturbed vision (is usually dose related)
48
What are the drug interactions related to Quinidine
Increases digoxin levels by decreasing it's clearance
49
Procainamide (IA) is like quinidine except..
it is not as anti-muscarinic, meaning that it will not increase the ventricular rate as much as quinidine us would It also has marked decrease in ability to prolong the QT interval, thus less likelyhood of Torsade de Pointes
50
Adverse effects of Procainamide
Lupus Like Syndrome :arthralgias, rash, fever, connective tiss. inflammatio (is reversible with discontinuation) Active metabolite N-Acteylprocainamide works like a Class III drug which may lead to QT prolongation and TdP.
51
When is disopyramide contraindicated ?
Patients w/ heart failure due to negative inotropic effects Not really used much anymore
52
Class IB drugs are most commonly used to ...
Supress Ventricular Arrhythmia (esp if associated w/ ischemia or digitalis)
53
Class IB drugs act to inhibit re-entrant arrhythmias by ..
Decreasing conduction velocity
54
How do IB drugs decrease automaticity of ectopic pacemakers ?
Raising the threshold potential so that depolarization is more difficult.
55
Class IB side effects
Seizures Confusion dizziness
56
Which of the IB drugs are an oral anolog of lidocaine (IB) ?
Mexiletine
57
Adverse effects of Mexiletine
Tremor, nausea and seizure
58
When is Phenytoin going to be used exclusively ?
Digitalis induced arrhythmia (delayed afterdepolarizations)
59
Class IC drugs are indicated for ...
Atrial fib, supraventricular arrhythmia in patients with otherwise healthy hearts
60
Class IC drugs can be proarrhythmic by increasing what ?
QRS comples
61
Indications for Class II
Suppressing arrhythmias induced by excessive catecholamines (stress: exercise, emotional), including triggered arrhythmias A.fib/Flutters Re-entrant rhythms involving the AV node
62
Class II drugs are the only to show
decreased mortality by preventing recurrent infarction and sudden death in patients recovering form acute MI !
63
Which Beta Blocker has Class III interactions ?
Sotalol
64
Which of the beta-blockers have a less complete BB effects ?
Acebutolol, Pindolol HAVE Intrinsic Sympathomimetic Activity (ISA)
65
What is an adverse effect of Class II drugs ?
Beta blockers cause AV block and thus sinus bradycardia
66
Class III drugs block K+ currents. This leads to
Prolonged AP and refractory period. | Prolonged QT interval
67
Due to their effect on the QT interval, Class III drugs predispose patients to
TdP
68
amiodarone is effective when used for
A.fib/flutter Bypass tract mediated parosysmal SVT V. Tach,
69
Amiodarone is First line drug for ..
Tx. of vent. arr. during cardiac resuscitation
70
Amiodarone is go for treating arrhythmias in patients with vent. sys. dysfunction because
less pro-arrhythmic complications than with many other agents
71
Mechanism of Amiodarone action
Prolong AP duration & refractoriness of all cardiac fibers: blocks K+ rectifier current
72
Amiodarone has effects in all classes. Explain Class I, II and IV effects
Significant Na+ channel blocker effect as well (Class I). Weakly blocks Beta-rec.’s & Ca++ channels (Class 2 & 4) Prolong PR, QRS & QT intervals Additional firing suppression provided by these effects likely account for the absence of Torsades typically seen with agents that produce long QT intervals
73
What are the extracardiac effects of amiodarone ?
peripheral vasodilation (noncompetitive alpha-blocker & blocks Ca++ influx in vascular smooth muscle) perhaps beneficial, rarely requires discontinuation
74
Why will amiodarone accumulate in most organs ?
Highly lipophilic | in plasma, highly bound to proteins
75
Where is amiodarone inactivated ?
In the liver
76
Why is amiodarone difficult to discontinue ?
VERY SLOW ELIMINATION... prolonged effects event after it has been stopped
77
Drug interactions of amiodarone
Increased action of Dig. & warfarin, avoid other drugs with negative chronotropic/inotropic effects (Beta-blockers, verapamil, diltiazem)
78
What occurs with prolonged high dose treatmet with amiodarone ?
Toxicities with the most serious being PULMONARY FIBROSIS Others include : Corneal micro-deposits Hypo and hyperthroid problems
79
Sotalol (III) is used for
supraventricular & ventricular arrhythmias
80
what are the major side effects associated with sotolol >
bradycardia, AV block, CHF, bronchospasm (these are those associated with BB's as well)
81
When is Bretylium tosylate indicated ?
for life-threatening v. tach or v. fib when all other resuscitation attempts fail
82
How does Bretylium tosylate work ?
initially increased release of NE at nerve terminals followed by decreased release. Overall there is a decrease in catecholamines .R aises threshold for vent. fibrillation
83
Side effect of Bretylium tosylate ?
Orthostatic hypotension
84
Dofetilitide is a new AA drug and is unique in that it is a ...
PURE K+ channel blocker --> Delays depolarization
85
When is Dofetilide used ?
Conversion of A-fib & A-flutter  sinus rhythm, maintenance of rhythm after conversion
86
Adverse effect of Dofetilide
TdP
87
When are the Class IV drugs used
reentrant arrhythmias whose circuit involves AV node. Also decreased ventricular rate in A-flutter, A-fib
88
Side effects of Class IV drugs
Similar effects as Betablockers (can cause bradycardia, HF, AV block) May cause hypotension
89
Adenosine is the DOC for ...
termination of PSVT with reentrant circuits involving the AV node, including WPW syndrome
90
How does Adenosine achieve its therapeutic action ?
Activates K+ rectifier current in SA & AV nodes decreases Ca++ influx Leads to hyperpolarization and inhibition of Ca++ dependent depolarization (decreases SA automaticity and AV conduction)
91
What is Adenosines affect of cAMP levels and what will this cause ?
inhibits intracellular adenylate cyclase-->cAMP-mediated effects which occur with sympathetic stimulation This leads to decreased inward pacemaker current (If channels) and decreases Ca influx
92
Why must Adenosine be given as an IV bolus as close to the heart as possible ?
Extremely short plasma t1/2 (< 10 seconds) Rapidly cleared from the blood and thus has minimal adverse effects
93
What are the side effects related to Adenosine
Transient asystole: common but lasts < 5 sec & is, in fact, the therapeutic goal Rarely precipitates A-fib
94
Drug interactions of Adenosine
Methylxanthines block adenosine receptors Caffeine and Theophyline
95
When is digoxin used ?
Commonly used for CHF complicated by A. Fib Not really used much anymore due to narrow therapeutic range and side effects.
96
Digoxin MOA
Decreases AV nodal conduction by direct depressant effect on AV node and by acting in the CNS to increase vagal impulses to the AV node. Leads to prolonged PR interval Decreases SA node automaticity by increasing’ing vagal activity and decreasing sympathetic activity at the node
97
Digoxin has a propensity to cause arrythmias. How do you treat these ?
Treat dig.-induced arrhythmias with digoxin-immune F-ab (digoxin antibody fragments), lidocaine or phenytoin
98
When is MgSO4 indicated ?
IV admin. prevents recurrent episodes of torsades de pointes

Cardiology Exam III (12 decks)

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