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Pharm II Exam 2 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

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1
Q

PSVT

A

paroxysmal supraventricular tachycardia

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2
Q

predominant pacemaker

A

SA node

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3
Q

lethal arrhythmia

A

v. fib

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4
Q

causes of arrhythmia

A

digoxin (25%)
anesthesia (50%)
AMI (80%)

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5
Q

Slow response fibers

A

SA node

AV node

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6
Q

fast response fibers

A

Atria
Ventricles
Bundle of His
Purkinje cells

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7
Q

Highest automaticity

A

SA node (sets HR)

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8
Q

lethal arrhythmias can be causes by

A

antiarrhythmic agents

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9
Q

Channels for slow acting fiber (SA and AV)

A

calcium channels

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10
Q

ERP

A

shortest interval at which a premature stimulus results in a propagated response (phase 0., 1, 2, and most of 3)

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11
Q

ERP length of ADP

A

ERP is ~85% of APD

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12
Q

AP in purkinje cell phases

A

Phase 0: opening of Na channels, rapid depol, inactivaiton of Na channels

Phase 1: rapid partial repol due to inactivation of fast Na channels and increased K+c channel permeability

Phase 2: plateau: Ca (L-type) and some Na (“window” or late current” channels are open)

Phase 3: Repolarization: Ca channels inactivated and K+ channels open, Na channels turning to rest

Phase 4: resting membrane potential

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13
Q

SA node AP phases

A

Phase 4: funny sodium current (spontaneous depol)
Phase 0: T-type Ca open and start to depol, then L-type Ca cause AP
Phase 1: Ca channels close, K+ activated
Phase4: spontaneous regeneration via Na funny channels

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14
Q

Causes of arrhythmia

A

distrbuance in impulse generation
impulse conduction
both

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15
Q

Precipitating factors of arrhythmias

A 
ischemia, hypoxemia
alkalosis, electrolyte abrnomalities
Excess catecholamines
Drug toxicity (digoxin, antiarrhythmic)
Overstretched fiber
scarred/diseased tissue
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16
Q

Factors that decreases rate of pacemaker cells

A

Increase depol potential (more neg)
Increase AP duration
Increase slope of phase 4 depol (K+)
Increase threshold hypotential

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17
Q

Simple blocks

A

AV block

Bundle branch Block

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18
Q

Reentry mechanism

A

obstacle to homogenous conduction; unidirectional block; conduction time long enough to find excitable tissues

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19
Q

Aims of antiarrythmic therapy

A

reduce ectopic pacemaker activity

modify conduction or refractoriness to disable reentry

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20
Q

Mechanism of antiarrhythmic (sodium channel blockade)

A

Sodium channel block
block sympathetic effects (BB)
prolong ERP
Calcium channel blockade

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21
Q

Lengthen ERP

A

Active Na channel blockers (class 1a: quinidine, procainamide)

K+ channel blockers amiodarone, sotalol)

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22
Q

K+ channel blockers

A

amiodarone

sotalol

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23
Q

1a drugs

A

block activated Na channels; lenghten AP, inc. ERP

Quinidine, Procainamide

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24
Q

1b drugs

A

block inactivated Na channels
dec AP, dec ERP

Lidocaine

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25
1c drugs
block all Na channels no effect on AP, or ERP Flecainide
26
Quinidine MOA
slows rate of rise (Vmax) in normal cells by blocking active Na+ channels No depolarization in damaged cells 2ndary: Inhibits K+ channels (prolong AP and ERP)
27
When is quinidine used
"BROAD SPECTRUM" acute and chronic supra and ventricular arrhythmias rarely used due to effects
28
SE of quinidie
Cardiotoxic: SA, AV block, ventricular arrhythmia Low therapeutic index Cinchonism DIARRHEA, n/v block alpha rec: hypotension and reflex tach paradoxical tach: "anticholinergic like effect" Quinidine syncope - prolonged QRS and QT TORSADES (inc. AP)
29
Torsades due to
increasing AP
30
Cinchonism
``` loss of hearing angioedema vertigo visual distrubance thrombocytopenic purpura tinnitus vascular collapse ```
31
Procainamide
hepatic metabolism -- slow, fast acetylators | less alpha block - less atropine like effects
32
SE of procainamide
LUPUS: slow acetylators (NAT2 gene)
33
Class 1B drug
lidocaine
34
MOA of Lidocaine
inhibits inactive Na channels preferentially effects damaged cells (more inactive Na channels) -- blocks the slow Na "window" current dec. APD and ERP - via window current block fast binding and dissociation
35
Use of Lidocaine
acute ventricular arrhythmia
36
why is lidocaine only used for ventricular arrhythmias
blocks Na window current -- only present in purkinje and ventricular wall cells
37
Why is lidocaine good
preferential for damaged cells (inactive Na channels) | least negative inotropic antiarrhythmic
38
SE of lidocaine
bradycardia paresthesia, convulsions (lightheaded, tinnitus, mm. twitch, blurred vision, euphoria, hypotension)
39
How often is lidocaine used?
ACUTE ONLY -- prophylactice use can increase mortality
40
Contra for lidocaine
caution in hepatic failure and HF (metabolized in liver)
41
Worst drug for inducing arrhythmias
Flecainide
42
Drugs for PSVT
1. Adenosine 2. Esmolol (IV) 3. Verapimil
43
Blocks K+ channels
Amiloride (main action) Quinidine, Procainamide (2ndary action) both thus increase APD
44
All jobs of amiodarone
``` K+ channel blocker (mainly) Na+ channel blocker (class I) BB (class II) Some Ca channel blocking (IV) Alpha blocker ```
45
Alpha blockers
Amiodarone | Quinidine, procainamide
46
DOC for ventricular arrhythmias
Amiodarone
47
Amiodarone Use
supra and ventricular arrhythmias | DOC: Ventricular arrhythmias
48
SE of amiodarone
dec sinus rate and conduction -- prolonged QT w/o TORSADES**** Bradycardia, heart block HF Deposits in tissue: brown/yello cornea, blue/gray skin, photodermatitis Thyroid dysfunction PULMONARY FIBROSIS
49
Prolong QRS drugs
Quinidine, procainamide | Amiodarone
50
sotalol MOA
class III - K+ channel blocker, BB (non-specific)
51
Contraindications for sotalol
``` BB contras: Asthma DM end-stage HF Bradycardic Heart Block ```
52
SE of sotalol
prolong QT - TORSADES!
53
Cause Torsades
Quinine, procainamide | sotalol
54
Class IV Drugs
Verapamil, Diltiazem
55
MOA of verapamil
block L-type calcium channels; slows AV conduction (dec. HR)
56
Use of verapamil
suptraventricular arrhythmias: a. flutter, a. fib | PVST (3rd line)
57
SE of verapamil
negative inotrope constipation avoid combo w/ BB (bradycardia)
58
Cause constipation
Verapamil, Diltiazam | Bile-acid sequesterants
59
Adenosine MOA
increases K conductance and decreases cAMP-induce Ca influx -- HYPERPOLARIZES and RESETS heart only used in reentry arrhtythmias
60
Adenosine is DOC for
PSVT | WPW Syndrome
61
SE for adenoside
``` SOB chest burning flush hypotension H/a, nausea ```
62
Magnesium use
DOC: torsades Seizures, HTN -- eclampsia Digital induced arrhythmias
63
Potassium levels and arrhythmia
Both hypokalemia and hyperkalemia are arrhythmogenic
64
MOA of potassium
makes resting potential more positive (depolarizes) increases K+ has membrane stabilizing action by increasing K+ permeability, and this action predominates (HYPERPOLARIZES) -- decreased APD
65
Not effective for both supra and ventricular
``` Class IV (Supra - CCB) Class Ib (ventricular - inactive) ```
66
Safest for prophylactic therapy
BB and CCB
67
IV only drugs
lidocaine adenosine Mg
68
Broadest drug w/ most effefcts
Flecainide

Pharm II Exam 2 (4 decks)

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