Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
Circus movement
repetitive "circulation" of abnormal impulses can produce a sustained tachyarrhythmia independent of the SA node
26
Pharma approach to circus movement issues
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)
27
Class I drugs
``` 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 ```
28
what type of block will not work on Nodal tissue?
Na block
29
Class 2 drugs
Beta adrenergic blockers -> decrease in nodal automaticity and conduction propranolol, non selective beta blocker (sotalol), metoprolol, esmolol, beta 1 blockers
30
Agents that prolong AP duration: K channel blockers
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
31
Ca channel blockers (hits SA and AV, non DHP)
verapamil, diltiazem- inhibit slow, inward calcium current
32
MOA of class 1 drugs
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.
33
Class 1A
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
34
Class 1B
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
Class 1C
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
Quinidine class?
Class 1A
37
Quinidine
anti malarial drug - "opium of the heart" Na and K blockade tx: atrial and ventricular arrhythmia
38
Side effects of Quinidine
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
Procainamide class??
Class 1A
40
Procainamide
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
Procainamide side effects
lupus like autoimmune syndrome | ventricular arrhythmias and prolonged QT: torsades de pointes
42
Disopyramide class?
Class 1A
43
Disopyramide
similar to quinidine and procainamide in use but fewer side effects Na and K chnnel blockade Tx: atrial and ventricular arrhythmias
44
Disopyramide side effects
Anticholinergic effects (dry mouth, constipation, urinary retention)
45
Class 1A
Quinidine Procainamide Disopyramide
46
Lidocaine class?
class 1B
47
Lidocaine
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
Lidocaine side effect
CNS effects: drowsiness, dizziness, confusion, High doses can produce seizures and convulsions
49
Epi helps what stay locally?
Lidocaine
50
Mexiletine class?
Class 1B
51
Mexiletine
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
Mexiletine side effects
CNS effects: tremor, blurred vision | GI: nausea (lessened by food intake)
53
Class 1B drugs
Lidocaine | Mexiletine
54
Flecainide class?
Class 1C
55
Flecainide
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
Flecainide side effects
Proarrhythmic effect: potentially lethal ventricular tacyarrhythmia when given after MI, blurred vision, depression of LV performance
57
Propafenone class?
class 1C
58
Propafenone
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
Propafenone side effects
weak beta adrenergic blocking action (bronchospasm)
60
Class II agents
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
Propranolol
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
Propranolol side effects
beta adrenergic blocking action
63
Metoprolol and Esmolol
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
Metoprolol and Esmolol side effects
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
Class III agents
``` 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
Amiodarone
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
Amiodarone side effects
``` 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
Dronedarone
class III Newer, non iodinated form of amiodarone Mech: similar to amiodrone but slightly less effective
69
Dronedarone side effects
fewer compared to amiodarone less thyroid, pulmonary and hepatic tox. can increase mortality due to heart failure
70
Sotalol
``` 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
Sotalol side effects
risk of torsades de pointes necessitates inpatient monitoring effect typically associated with beta adrenergic blockers
72
Dofetilide
``` 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
Dofetilide side effects
life threatening ventricular arrhythmias can occur | restricted to physicians who have undergone manufacturers training
74
Ibutilide
``` 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
Class IV agents
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
Verapamil
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
Verapamil side effects
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
Diltiazem
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
Diltiazem side effects
negative inotropic effet - limited use in pts with LV dysfunction hypotension - due to vasodilatory effect bradycardia and AV block
80
Adenosine
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
Adenosine side effects
limited because of very short duration of action vasodilation - flushing, HA bronchoconstriction
82
Digoxin
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
Digoxin side effects
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.
© 2025 Bold Learning Solutions. Terms and Conditions