Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CPR exam 2 > Cardiac Anti-Arrhythmic agents > Flashcards

Cardiac Anti-Arrhythmic agents Flashcards

1
Q

what happens when there is increased potassium permeability?

A

Vm close to Ek
strong repolarization
increased threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what happens when there is decreased potassium permeability?

A 
Vm depolarized (toward ENa, ECa) 
decreased threshold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

characteristics of a typical Fast AP

A

conduction velocity determined by phase ) slope
Fast Na channels cause the depolarization
slow ca channels are responsible for the plateau

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

characteristics of a typical slow AP

A

SA and AV nodal tissue
No fast Na channels (phase 0)
More Ca dependent
Spontaneous phase 4 depolarization due to funny Na and Ca channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Action of Na channel blockers

A

decrease conduction velocity (phase 0)

suppress ventricular and atrial muscle firing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Action of K channel blocker

A

increase time for repolarization (phases 2 and 3)
prolongs AP duration , slows down
increases time to “reset” excitability (refractoriness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Action of K channel stimulator

A

increases repolarizing influence (Ek)
decreases slope of phase 4
slows HR (Ach/PNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Action of Ca channel blocker

A

nodal cells: decreases slope of phase 4
decrease excitability of nodal cells
not as effective in Na-dependent cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Spontaneous activity (phase 4) is under …

A

autonomic control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what prevents tetanus in cardiac muscle?

A

Refractory period
Absolute refractory period - another AP cannot fire, Na channels are inactive
Relative refractory period - late phase 3, Na channels are reactivated and another AP could fire

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are inactived Na channels reset?

A

by repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What affinity contributes to Na channel efficacy?

A

blockers have a high affinity for O state (open) or inactive state of the Na channel
faster HR means more time in O or I, so more effective in a heart that is tachycardiac vs normal sinus rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cardiac ATP

A

75% of cardiac ATP is for the Na/K ATP pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does ischemia affect depolarization?

A

lowers ATP and increases intracellular NA so the cells are slightly depolarized because gradient not being closely maintained. There is less “reactivation” of fast Na channels, slower phase 0 upstroke and impulse conduction and may contribute to re-entry of impulses.
Need a negative potential to reactivate Na channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a strategy to decrease arrhythmias?

A

by increasing ERP
makes the cell less sensitive to stimulation
can slow the development/propagation of abnormal rhythms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

K channel blocker

A

slows phase 3 repolarization
increases AP duration
delays “recovery” of Na channels
prolongs Effective repolarizing Potential and R (relative) RP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Na channel blocker

A

binds to and blocks inactive channels
reduces number of “recovered” channels
extends the ERP of atrial/ ventricular myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Ca channel blocker

A

increase ERP and depress phase 4 slope in nodal tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

bradyarrhythmias

A

SA node dysfunction
electronic pacemakers are t.o.c
atropine or isoproterenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

tachyarrhythmias

A

increased impulse generation (automaticity)
increased impulse conduction (propagation)
tx: primarily channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Triggered Activity

A

after depolarizations
occur “after” the normal AP depolarization
can trigger abnormal beat if threshold is reached and sufficient # of Na channels have recovered from inactivation
abnormal beat occurs before optimal diastolic filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Delayed afterdepolarization (DAD)

A

often produced by too much calcium

occurs during phase 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Early afterdepolarization (EAD)

A

can occur with excessive prolongation of AP

occurs during phase 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

3 simultaneous conditions for Premature excitation before next normal impulse

A
  1. area of depressed conduction/block
  2. block must be unidirectional
  3. impulse speed “around the block” must be slow enough to reenter healthy area AFTER the refractory period (sufficient Na channels have recovered and can be opened) this insures abnormal “retrograde” propagation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Circus movement

A

repetitive “circulation” of abnormal impulses can produce a sustained tachyarrhythmia independent of the SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Pharma approach to circus movement issues

A

make unidirectional block Bidirectional
further decrease conductance through injured region (block retrograde impulse)
Na channel blocker or Ca channel blocker (nodal tissue)
Increase ERP in tissues so impulse cannot be conducted -(k channel blockers can lengthen ERP, makes healthy tissue refractory to retrograde impulse, abnormal excitation dies out)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Class I drugs

A 
Na channel blockers - decrease velocity of phase 0 
Class 1A - (quinidine, procainamide, disopyramide) prolong AP duration, dissociate with intermediate kinetics 
class 1B -(lidocaine, mexiletine) shorten AP duration, rapid dissociation 
Class 1C - (Flecaindine, propafenone) - High affinity, minimal effect on AP duration, slow dissociation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what type of block will not work on Nodal tissue?

A

Na block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Class 2 drugs

A

Beta adrenergic blockers -> decrease in nodal automaticity and conduction
propranolol, non selective beta blocker (sotalol), metoprolol, esmolol, beta 1 blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Agents that prolong AP duration: K channel blockers

A

amiodarone - k channel blocker weak non selective beta blocker (Dronedarone - non iodinated amiodarone)
sotalol - K channel block and non selective beta blocker
dofetilide & ibultilide - k channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Ca channel blockers (hits SA and AV, non DHP)

A

verapamil, diltiazem- inhibit slow, inward calcium current

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

MOA of class 1 drugs

A

slower rate of phase 0 depolarization and decreased conduction velocity (primarily in non nodal tissue)
Threshold Vm for activation is also increased
greater depolarization is required to elicit a response

Use-dependent: bind to open or inactivated Na channels only. Reduce tachyarrhythmia, but little effect on normal sinus rhythm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Class 1A

A

intermediate binding, dissociation kinetics intermediate depression of phase 0
block K channels (increase ERP, APD)
increases the slope of phase 0
ex: quinidine
-moderate Na channel blockade, increase ERP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Class 1B

A

weaker binding, rapid dissociation
little depression of phase 0 (less than 1A)
pure Na channel blockers (no K channels)
ex: Lidocaine
-Weak Na channel blockade, decrease ERP

35
Q

Class 1C

A

strong binding, slower dissociation
strong depression of conductance (phase 0)
little effect on ERP
ex: flecainide
-strong Na+ channel blockade, shift to right ERP

36
Q

Quinidine class?

A

Class 1A

37
Q

Quinidine

A

anti malarial drug - “opium of the heart”
Na and K blockade
tx: atrial and ventricular arrhythmia

38
Q

Side effects of Quinidine

A

Cinchonism: tinnitus, blurred vision, HA
ventriculr arrhythmias/torsades de pointes (prolonged APD)
GI problems (N/V)
Anticholinergic/vagolytic
contaminant of online herbal preparations of cinchona bark

39
Q

Procainamide class??

A

Class 1A

40
Q

Procainamide

A

derived from procaine (local anesthetic)
Na and K channel blockade
Metabolic: N-acetylprocainamide (class III action, prolong APD) ~50% of americans are “rapid acetylators” and in these individuals [NAPA]>[procainamide]
Tx: atrial and ventricular arrhythmias

41
Q

Procainamide side effects

A

lupus like autoimmune syndrome

ventricular arrhythmias and prolonged QT: torsades de pointes

42
Q

Disopyramide class?

A

Class 1A

43
Q

Disopyramide

A

similar to quinidine and procainamide in use but fewer side effects
Na and K chnnel blockade
Tx: atrial and ventricular arrhythmias

44
Q

Disopyramide side effects

A

Anticholinergic effects (dry mouth, constipation, urinary retention)

45
Q

Class 1A

A

Quinidine
Procainamide
Disopyramide

46
Q

Lidocaine class?

A

class 1B

47
Q

Lidocaine

A

local anesthetic with fast binding/dissociation kinetics
inactive orally
Mech: blockade of open or inactive Na channels, more effective for tachyarrhythmia or depolarized tissues
little effect on SA or AV node
Tx: hyper excitability, Life threatening ventricular arrhythmias, PVCs inhibited due to blocked Na channel

48
Q

Lidocaine side effect

A

CNS effects: drowsiness, dizziness, confusion, High doses can produce seizures and convulsions

49
Q

Epi helps what stay locally?

A

Lidocaine

50
Q

Mexiletine class?

A

Class 1B

51
Q

Mexiletine

A

analog of lidocaine (orally active version) , fast kinetics
Mech: similar to lidocaine
Orally effective - avoids first pass hepatic metabolism

Tx: life threatening ventricular arrhythmias, PVCs inhibited due to blocked Na channels
Treat chronicc pain -diabetic neuropathy

52
Q

Mexiletine side effects

A

CNS effects: tremor, blurred vision

GI: nausea (lessened by food intake)

53
Q

Class 1B drugs

A

Lidocaine

Mexiletine

54
Q

Flecainide class?

A

Class 1C

55
Q

Flecainide

A

derivation of procainamide with slow kinetics
Mech: strong inhibition of phase 0 and general cardiac excitability, weaker ability to block K channels can prolong APD slightly
slight ability to block Ca channels
Tx: supraventricular and ventricular tachy, PVCs, can slow nodal conduction (use in atrial fib)

56
Q

Flecainide side effects

A

Proarrhythmic effect: potentially lethal ventricular tacyarrhythmia when given after MI, blurred vision, depression of LV performance

57
Q

Propafenone class?

A

class 1C

58
Q

Propafenone

A

structurally similar to propranolol
mech: strong inhibition of phase 0 and general cardiac excitability, weaker ability to block K channels can prolong APD slightly, slight ability to block Ca channels
Tx: supraventricular and ventricular tachy, PVC’s, can slow nodal conduction (use in atrial fibrillation)

59
Q

Propafenone side effects

A

weak beta adrenergic blocking action (bronchospasm)

60
Q

Class II agents

A

Anti-arrhythmic - beta blockers
Antagonize sympathetic stimulation of beta 1 adrenoceptors in the heart = decreases HR, contractility, and conduction
side effects: typical for beta blockers

61
Q

Propranolol

A

Class II
non selective beta adrenergic antagonist
mech: inhibition of sympathetic stimulation of heart, inhibit NE activity, block Na channels at high doses
Tx: decreased AV conduction: suraventriculr arrhythmias, slow HR, Post-MI therapy: reduces mortality 2-3 years after MI by decreasing risk of ventricular arrhythmias

62
Q

Propranolol side effects

A

beta adrenergic blocking action

63
Q

Metoprolol and Esmolol

A

Class II
cardio-selective beta adrenergic antagonist
Mech: inhibition of sympathetic stimulation of the heart, preference for the beta 1 adrenoceptor
Tx: (similar to propranolol) decreased AV conduction: supraventricular arrhythmia, slow HR, post MI therapy

64
Q

Metoprolol and Esmolol side effects

A

fewer side effects compared to propranolol
Peripheral beta 2 receptors left intact
Esmolol is very rapidly metabolized iv so is used for acute management of ventricular rate in atrial flutter/fibrillation

65
Q

Class III agents

A 
Anti-arrhythmic agents that Prolong APD 
AP duration and ERP are prolonged 
most class III drugs are K channel blockers 
phase 0 is not affected 
prolongation of AP can increase risk of torsades de pointes (polymorphic ventricular tachy)
66
Q

Amiodarone

A

Class III
iodinated thyroxine derivative, exhibits class I, II, III and IV action.
Often the most prescribed anti-arrhythmic agent
DIRTY!!!!
Mech: K channel block to increase repolarization time (increase ERP), weak alpha and beta adrenergic receptor blocking effect and Ca channel antagnoism reduces automaticity, decreases phase 4 slope in pacemaker cells, decreases AV node conduction (can tx atrial fibrillation)
Tx: recurrent tachy or fibrillation resistant to other drugs, first line treatment for acute V tachy/fib

67
Q

Amiodarone side effects

A 
Thyroid: hyper or hypothyroidism 
blue skin discoloration (blue) 
pulmonary tox/ fibrosis 
corneal microdeposits 
peripheral neuropathy/ weakness 
hepatic dysfunction 
hypotension, esp. with IV administration 
QT prolongation, but risk for torsades de pointes is lower compared to other class III agents

Very lipophilic, requires high loading dose

68
Q

Dronedarone

A

class III
Newer, non iodinated form of amiodarone
Mech: similar to amiodrone but slightly less effective

69
Q

Dronedarone side effects

A

fewer compared to amiodarone
less thyroid, pulmonary and hepatic tox.
can increase mortality due to heart failure

70
Q

Sotalol

A 
class III 
non selective beta blocker that also blocks K channels 
Mech: blocks K channels to increase APD and ERP
automaticity can also be decreased due to beta blockade, slows SA and AV node conduction

Tx: supraventricular and ventricular tachy, approved for PEDs

71
Q

Sotalol side effects

A

risk of torsades de pointes necessitates inpatient monitoring
effect typically associated with beta adrenergic blockers

72
Q

Dofetilide

A 
class III 
pure K channel blocker (at clinical doses) 
Mech: blocks K channels to increase APD and ERP 
Tx: anti-fibrillatory effect in atria
73
Q

Dofetilide side effects

A

life threatening ventricular arrhythmias can occur

restricted to physicians who have undergone manufacturers training

74
Q

Ibutilide

A 
class III
pure K channel blocker (at clinical doses) 
Mech: blocks K channels to increase APD and ERP 
Tx: terminate atrial flutter/fib, iv admin required

side effects : QT prolongation/torsades de pointes

75
Q

Class IV agents

A

Anti arrhythmic - Ca channel blockers
Block the “slow” inward Ca current
non-DHP (on T tubules) - more cardio-selective, DHPs are greater affinity for vascular ca channels
Target Ca-dependent cells: SA/AV nodes - slows conduction
decrease slope of phase 4 depolarization

76
Q

Verapamil

A

Class IV
blocks voltage-sensitive Ca channels
Mech: decreases automaticity (depresses phase 4 slope) and afterdepolarization formation, slows conduction in SA and AV nodes and ventricular contractility can be decreased (phase 2)

Tx: primarily atrial tachyarrhytmias (protects ventriculars from this misfiring)

77
Q

Verapamil side effects

A

Negative inotropic effect - limited use in patients with LV dysfunction
Hypotension - due to vasodilatory effect (reflex tachy)
bradycardia and AV block - lengthens PR interval
constipation - blocks SM ca channels

78
Q

Diltiazem

A

Class IV
blocks voltage sensitive Ca channels
Mech: decreases automaticity (depresses slope of phase 4) and afterdepolarization, slows conduction in SA and Av nodes, ventricular contractility can be decreased (phase 2)

Tx: primarily atrial tachyarrhythmia

79
Q

Diltiazem side effects

A

negative inotropic effet - limited use in pts with LV dysfunction
hypotension - due to vasodilatory effect
bradycardia and AV block

80
Q

Adenosine

A

Non classified
endogenous nucleoside, rapid and transient depression “stops and resets the heart”
Mech: stimulates the ACh sensitive K current to decrease phase 4 slope and antagonizes the effects of cAMP to reduce calcium currents )increase nodal refractoriness and inhibit DADs) and rapid uptake and metabolism (deamination)

Tx: primarily for acute treatment of supraventricular tachy and produces transient ASYSTOLE (~5 seconds)

81
Q

Adenosine side effects

A

limited because of very short duration of action
vasodilation - flushing, HA
bronchoconstriction

82
Q

Digoxin

A

non classified
cardiac glycoside
Primary use: Positive inotropic effect
Mech: inhibit Na/K ATPase activity, vagotonic action - (inhibit ca current, increase ACh stimulated K current), increased AV node refractoriness/ lower conductance and increased calcium: higher tendency for DADs

Tx: control ventricular rate in atrial flutter/ fib, slow conduction in AV node

83
Q

Digoxin side effects

A

low therapeutic index
ventricular arrhythmias (VT, PVC)
hypokalemia increases risk of arrhythmia

CPR exam 2 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions