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Elam Anti-arrhythmic agents Flashcards

1
Q

Diltiazem and Verapamil belong to the class of…

A

Non-Dihydropyridine Calcium Channel Blockers

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2
Q

Diltiazem and verapamil inhibit

A

L-Type–>voltage gated calcium channels

  • raises the threshold for cell of the SA and Av nodes
  • ->slows phase 0 depolarization
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3
Q

Diltiazem and verapamil cause increases in (lengthens)…

A

R-R interval (slow the HR)

P-R interval–> slow conduction through the AV node–>this also slows heart rate

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4
Q

Flecanide and other Sodium channel blockers work via

A

inhibition of voltage gated sodium channels

  • -> slow phase 0 depolarization
  • ->slow conduction speed through the atria, His-Purkinji system, and ventricles
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5
Q

EKG changes brought about by sodium channel blockers

A

Widened QRS

Lengthened R-R Interval

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6
Q

Potassium channel blocker work via..

A

slow repolarization of Atrial and ventricular myocytes

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7
Q

Potassium channels blockers will show what EKG changes…

A

prolonged QT interval

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8
Q

Adenosine is used to treat which cardiac condition

A

Supraventricular tachyarryhtmias

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9
Q

Adenosine works to

A

slow conduction through the sinus node and to slow conduction through the AV node

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10
Q

EKG changes brought about by bolus of adenosine

A
  • ->slows heart rate (lengthened R-R)

- ->increase in PR interval

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11
Q

Beta blockers work via

A

simulate the effects of activating the sympathetic nervous system

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12
Q

Beta agonists are used to treat

A

bradycardia

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13
Q

Beta agonists cause which EKG change

A

> increase HR–(shortened R-R)
Shorten P-R interval
narrow the QRS

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14
Q

name two beta agonists

A

isoproterenol

epinephrine

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15
Q

beta agonists work via

A

> increase diastolic polarization of sinus node
increase rate of AV conduction
increase the rate of re-polarization

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16
Q

re-entrant imupulses can become what..

A

self-sustained ectopic pacemaker

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17
Q

pharmacologic treatment of re-entrant circuits are trying to…

A

alter the elctrophysiologic properties of the tissue by:

  • ->increasing the refractory period
  • ->or slowing conduction through the tissue
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18
Q

drugs used to treat re-entrant circuitry clinically

A

–>Potassium channel blockers (AMIODARONE)
SOTATLOL, IBUTALIDE DOFETALIDE–>increase refractory period
*impulses re-entering are less likley to trigger the fast channels and the re-entrant impulse will die out
–>NA channel blockers–> LIDOCAINE AND FLECAINIDE
–> drugs that inhibit sodium and potassium channels (PROCAINAMIDE, QUINIDINE)

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19
Q

MOST COMMON CAUSE OF DEATH IN PT.’S WITH MI OR TERMINAL HEART FAILURE

A

ARRHYTHMIAS

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20
Q

a normal AP is dependent on

A

sodium, potassium AND calcium

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21
Q

2 major mechanisms for arrhythmias

A
  • ->re-entry

- -> automaticity

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22
Q

ventricular arrhytmia often induced by anti-arrhythmic drugs

A

torsades de pointes

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23
Q

which phase is the most important determinant for conduction velocity for most of the heart

A

phase 0

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24
Q

phase zero )upstroke determines what

A

conduction velocity

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25
phase zero in non SA-AV cells in controlled by...
I-Na channels
26
therefore which ion regulates conduction velocity
I-Na
27
for SA and AV node which ion determines conduction velocity
Ca-->this is still set by the rate of Phase 0
28
phase 2 in most of the heart is determines by which ion
>calcium--> LTYPE--> >and one or more Potassium currents *responsible for plateau phase
29
Afib or Vfib is fatal
V fib if not corrected within minutes
30
define Afib and Vfib
arrhythmias involving rapid reentry and chaotic movement of impulses through the tissues of the atria of ventricles
31
define SVT
a reentrant arrhythmia that travels through the AV node, it may also be conducted through atrial tissue as part of reentrant circuit
32
Ventricular tachycardia
often associated with MI, abnormal automaticity or abnormal conduction-->impairs CO and may turn into Vfib-->requires PROMPT MANAGEMENT
33
time that must pass after and upstroke before a new AP will be conducted in that cell or tissue
Effective refractory period
34
which ion channel allows for rapid repolarization of non-pacemaker cells
inward rectifying Potassium channel (Ik)
35
the Refractory period of sodium-dependent cardiac cells is a function of
how rapidly sodum channels recover (repolarize) from inactivation *depends on repolarization time and extracellular potassium
36
in the AV node-->rate of recovery is dependent upon
recovery from inactivation of calcium channels
37
group 1 drugs belong to which class
sodium channel blockers
38
1A
procainamide (MAJOR) quinidine amiodarone (some class 3 activity)
39
1B
LIDOCAINE
40
1C
FLECAINIDE
41
effect on AP for procainamide
prolonged AP
42
effect on AP duration for lidocaine
shorten AP
43
effect of AP for Flecainide
no change on AP
44
All group 1 drugs work to
slow conduction in ischemic and depolarized cells and slow or abolish abnormal pacemakers (whenever they are dependent on Na channels)
45
most selective of the Na channel blockers (group 1) for ISCHEMIC TISSUE
IB-->lidocaine *LITTLE EFFECT ON OTHERS 1A AND 1C BLOCKERS-->REDUCE SODIUM IN EVEN NORMAL CELS
46
NA CHANNEL BLOCKERS are all_____ which means_____.
USE DEPENDENT/STATE DEPENDENT: THEY ALL BIND MORE READILY IN THE OPEN OR INACTIVATED STATE-->than when fully repolarized (therfore are selective for abnormal tissue)
47
USE DEPENDENT NA CHANNEL BLOCKERS WILL INHIBIT CHANNELS...
UNDERGOING RAPID DEPOLARIZATION >TACHYCARDIA > HYPOXIA
48
Antiarrhythmic drug with group 1A and group 3 actions
amiodarone
49
Na channel blockers are useful in both ____ and ___ arrhytmias.
Atrial and ventricular
50
Blocking I-Na will bring about
-->slower conduction velocity in the atria, PF's, and Ventricles
51
high doses of Na channel blockers might
slow AV conduction
52
drugs with 1B action
Lidocaine-->major mexilitine sometimes phenytoin
53
1B drugs are selective for
ischemic OR DEPOLARIZED PF's or ventricles | little to no effects on the atria
54
1B drugs work via
reduce AP duration | prolong effective refractory period
55
because !b agents have little to no effect on normal cardiac cells
little to no EKG changes
56
Group 1C drugs
flecainide
57
flecainide (1C) works via
slowing conduction velocity in atria and ventricles increase QRS on EKG >no effect on ventricular AP duration or Qt interval
58
Indications for procainamide...
any type of arrhythmia and during the acute phase of MI
59
quinidine reduces clearance of
digoxin
60
all group 1 drugs prolong
ERP by slowing recovey of sodium channels from inactivation
61
Group 1 drug useful in acute ischemic ventricular arrhythmias
lidocaine
62
lidocaine nver given orally because
first pass degration | metabolites are cardiotoxic
63
group 1 drug toxicities are aggrevated by
hyperkalemia | *counteract by sodium lactate
64
all drugs that prolong AP duration can case
torsades de pointes
65
Group 2 Antiarrhythmics=
beta blockers
66
protypical drugs in group 2
Propranolol | Esmolol
67
MOA for beta blockers
beta receptor blockade and reduction in cAMP-->reduces both SODIUM AND CALCIUM currents -->supresses abnormal pacemakers
68
Cardiac are particularly sensitive to beta blockers
AV node
69
group 3 drugs with some group 2 activity
amiodarone (also 1a) and sotalol (2)
70
Beta blocker with shortest half life
esmolol
71
side effects of beta blockers
AV block, heart failure, decrease CO, and bronchospasm
72
beta blockers with beta and alpha antagonistic properties
labetolol | carvedilol
73
beta blocker with partial beta 2 agonist activity
labetolol
74
do group 2 drugs affect phase 0
NO
75
Name the group 3 drugs
Dofetilide Ibutilide Sotalol (group 2 and 3) Amiodarone (1a, 2, and 3)
76
hallmark of group 3 drugs
prolongation of the AP duration by blockage of Potassium channel (cheifly I-Kr) responsible for phase 2 *very drawn out repolarization
77
prolongation of AP-->
lengthened ERP | *reduces the ability of the heart to respond to rapid tachycardias
78
Group 1A and Group 3 drugs all prolong
QT interval | -->inhibit rate of depolarization-->therefore prolong AP and increase ERP
79
do group 3 drugs affect upstroke
no-->only rate or repolarization
80
most eficacious of all antiarrhythmic drugs
amiodarone
81
amiodarone blocks...
calcium, sodium, potassium, and beta receptors
82
greatest effect of blockade by amiodarone is....
potassium receptors-->therefore it is a group 3 drug
83
Group 4 antiarrhythmic agents
CCB's
84
name the protype CCB and the less effective on
verapamil (phenylalkylamine) and the diltiazem (benzothiazepine) these drugs cannot be given with a Beta Blocker because that would cause heart block
85
are DHP drugs useful in tx of arrhythmias
NO--.they are selective and only work in the vasculature
86
CCB's are most effective against
AV nodal arrhythmias-->these tissues are calcium dependent
87
Verapamil and Diltiazem in AV nodal tissues cause
state and use dependent selective depression of Calcium conductivity-->this slow AV nodal condution velocity and causes prolonged PR interval and ERP
88
which drug can conver AV nodal tachycardia back into normal sinus rhythm
CCB's
89
drug that works via increasing Ik1 conduction and hyperpolarizing AV nodal cells in high doses
adenosine bolus--> AV block in high doses
90
Misc. DOC for AV nodal arrhythmia
adenosine-->15 second half life
91
Misc. drug for supression of ectopic pacemakers inclduing those caused by digitalis toxicity
potassium ion
92
hypokalemia leads to
arrhythmias (especically in pt.'s with digoxin tx.)
93
hyperkalemia leads to
reentrant arrhythmias

Cardiovascular (6 decks)

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