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Emily: Pharm 2 > Quiz 4: Antiarrhythmics > Flashcards

Quiz 4: Antiarrhythmics Flashcards

1
Q

What occurs at phase 0 during cardiac action potential:

A
  • RAPID DEPOLARIZATION

- Action potential is initiated by an increase in Na+ conductance through ion-specific fast channels

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2
Q

What occurs at phase 1 during cardiac action potential:

A
  • EARLY RAPID RE-POLARIZATION
  • Na+ permeability is rapidly inactivated over 1-2 ms
  • The cell starts to repolarize
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3
Q

What occurs at phase 2 during cardiac action potential:

A
  • PLATEAU
  • Repolarization is delayed by an increase in conductance of Ca++ through slow channels
  • Maintains Vm at +10 to -20 mV for over 100ms
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4
Q

What occurs at phase 3 during cardiac action potential:

A
  • RAPID REPOLARIZATION

- Complete repolarization due to inactivation of Ca++2 conductance and an increase in K+ permeability

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5
Q

What occurs at phase 4 during cardiac action potential:

A
  • SPONTANEOUS DEPOLARIZATION
  • Slow depolarization characteristic of all pacemaker cells
  • Results from a complex interaction between inward and outward currents of Ca +2 and K+ during diastole
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6
Q

Ion specific channels that are SLOW channels mediated by _______.

A

-Ca+2

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7
Q

Slow conduction velocity is a _____ mediated and is responsible for phase __ and affects the __ and __ nodes.

A
  • Ca+2
  • 0
  • SA
  • AV
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8
Q

Prolongs refractory period is a ___ mediated and contributes to phase __ in the ______ contractile cells.

A
  • Ca+2
  • 2
  • ventricle
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9
Q

Slow channels in cardiac electrophysiology affects phase __ in spontaneous depolarization.

A

0

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10
Q

T/F: Slow channels in cardiac electrophysiology is facilitated by catecholamines.

A

TRUE

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11
Q

Ion specific channels that are fast channels are mediated by __.

A

Na+

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12
Q

Fast channels that are Na+ mediate in phase 0 are responsible for the rapid (sharp) upstroke in the _________ system and _____ and ______muscles.

A
  • His-Purkinje
  • atrial
  • ventricular
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13
Q

Na+ mediated cardiac channel have a SLOW conduction velocity.

A

FALSE (Na+ mediate cardiac channel have a FAST conduction velocity.)

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14
Q

What is the difference in a comparison of a ventricular cell and the sinoatrial cell when considering the slow channel mediated activity?

A

-In ventricular cells Ca2 accounts for the plateau phase 2, while in S-A cells it is the prime determinant of initial depolarization phase 0.

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15
Q

T/F: Cells that undergo phase 0 depolarization are automatic and capable of impulse generation.

A

FALSE (Cells that undergo phase 4 depolarization…)

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16
Q

Factors that reduce automaticity at the higher pacemaker sites will _______ favor the movement of the pacemaker to lower sites.

A

-passively

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17
Q

What factors will reduce automaticity at the higher pacemaker sites to passively favor the movement of the pacemaker to the lower sites?

A
  • Vagal influences
  • digitalis drugs
  • parasympathomimetic drugs
  • Halothane
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18
Q

Ectopic foci result from enhanced automaticity at a site outside the SA node and are called ____ ___.

A

-Ectopic pacemaker

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19
Q

What factors influence the ectopic pacemaker?

A
  • Sympathomimetic influence
  • Hypercarbia
  • Hypoxia
  • Dig. Toxicity
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20
Q

For a re-entry arrhythmia to occur what must happen?

A
  • Unidirectional block of impulse conduction (area of injury)
  • Slow conduction
  • Impulse finds the unidirectional block repolarized and able to conduct the impulse retrograde
  • Impulse reactivates the alternate pathway and repeats the process
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21
Q

Pharmacologic arrhythmia management relies upon the different ion channels responsible for impulse generation in the __ and __ versus the __ and __ nodes

A
  • atria
  • ventricles
  • SA
  • AV
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22
Q

The Na+ channel drugs effect the ion channel where in the heart?

A
  • Atria

- Ventricle

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23
Q

The Ca++ channel drugs effect the ion channel where in the heart?

A
  • SA node

- AV node

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24
Q

Class I antiarrhythmic drugs mechanism of action:

A
  • inhibits fast Na+ channels
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25
Q

What drugs fit within the antiarrhytmic drug class of I:

A
  • IA: Quinidine, Procainamide, Disopyramide, Moricizine
  • IB: Lidocaine, Mexilitine
  • IC: Flecainide, Propafenone
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26
Q

Class II antiarrhythmic drug’s mechanism of action is:

A

-Decrease rate of depolarization

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27
Q

What type of drugs fit within the antiarrhythmic class of II:

A

-Beta Blockers

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28
Q

Class III antiarrhythmic drug’s mechanism of action is:

A

-Inhibit potassium ion channels

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29
Q

What type of drugs fit within the antiarrhythmic class of III:

A
  • Amiodarone
  • Sotalol
  • Ibutilide
  • Dofetilide
  • Bretylium
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30
Q

Class IV antiarrhytmic drug’s mechanism of action is:

A

Inhibit slow calcium channels

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31
Q

What type of drugs fit within the antiarrhythmic class of IV:

A
  • Diltiazem

- Verapamil

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32
Q

A sodium channel blocker is what class and how does it exactly work?

A
  • Class I

- Slow conduction and prolong the QRS complexes in the atria and ventricles

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33
Q

A calcium channel blocker is what class and how does it exactly work?

A
  • Class IV

- Slow the atrial rate (SA node effect) and slow conduction through the AV node (Prolonging the PR interval)

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34
Q

A potassium channel blocker is what class and how does it exactly work?

A
  • Class III
  • Interrupts reentry by slowing conduction or increasing the refractory period
  • Prolongs the QT interval and induces triggered activity in the ventricle causing polymorphic VT (Torsades de Pointes)
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35
Q

How does class Ia effect the action potential:

A
  • slows phase 0 (Na channel blockade)

- Prolongs phase 3 (K channel blockade)

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36
Q

How does class Ib effect the action potential:

A
  • Slows phase 0 (Na channel blockade)

- Shortens phase 3 (K channel promoter)

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37
Q

How does class Ic effect the action potential:

A
  • Very slow phase 1

- NO effect phase 3

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38
Q

How does class II effect the action potential:

A

-Reduces slope of 4

Decreases heart rate

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39
Q

How does class III effect the action potential:

A

-Prolongs phase 3

Blocks K+ ion Channel

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40
Q

How does class IV effect the action potential:

A

-Reduces slope of 4

Calcium channel blocker

41
Q

Which class has a less powerful sodium channel blocker? Class Ia or Class Ib

A

-Class Ib

42
Q

What class of antiarrhythmic is associate with more of a prodysrhythmic effect?

A

-Class Ic
(Flecainide and Propafenone)

-Could consider Class III

43
Q

What does Amiodarone and Sotalol block:

A
  • Sodium channels (Class I )
  • Beta Blockade (Class II)
  • Calcium channel blockade (Class IV)
44
Q

What are the two unclassified antiarrhythmic drugs?

A
  • Adenosine

- digoxin

45
Q

What is prodysrhytmic effect?

A

-Brady/tachydysirhythmias that represent new cardiac dysrhytmias associated with chronic antidysrhytmic drug treatment.

46
Q

What are the types of prodysrhytmic effects?

A
  • Torsades de pointes
  • Increased ventricualr tachycardias
  • Wide Complex ventricular rhythm
47
Q

What causes Torsades de Pointes?

A

-K channel blockade may prolong the QT interval and induce triggered activity in the ventricle causing polymorphic VT or ventricular fibrillation

48
Q

What class block K+ and prolongs QTc interval?

A
  • Class Ic

- Class III

49
Q

What are the predisposing factors for torsades:

A

DECREASE

  • K+
  • Mg++
  • slow heart rate
  • Pre-existing long QT interval
50
Q

What is the treatment of Torsades??

A
  • D/C the offending agent
  • Correction of electrolyte
  • Administer Mg++ 2 grams
  • Increase HR with pacing or isoproterenol
  • Cardiovert only if hemodynamically compromised
51
Q

Incessant Ventricular Tachycardia is usually brought on by what class(es) of antiarrhythmics used:

A
  • Ia

- Ic

52
Q

Wide complex ventricular rhythm are associated with what class?

A

-Ic

53
Q

What are the goals of using antirrhytmic drugs:

A
  • restore NSR
  • Abolish ectopic beats
  • control the heart rate
54
Q

What would be some easily reversible conditions for the treatment of arrhythmias:

A
  • Hypoxia
  • Acidosis
  • Hypercarbia
  • Electrolyte imbalances
  • Alkalosis
  • Temperature
55
Q

What does Halothane do to the heart?

A

-Makes it sensitive to catecholamine

56
Q

What do inhalational agents do to the heart?

A

-affect conduction and cause junctional rhythms

57
Q

What muscle relaxants are vagolytic:

A
  • pancuronium

- gallamine

58
Q

What does succinylcholine do after repeated doses do to the heart:

A
  • Cause SB
  • Junctonal rhythms,
  • ventricular arrhythmias
  • asystole
59
Q

What may be the first signs of ischemia with the heart?

A
  • PVC

- conduction changes

60
Q

Yes/No: To increase the heart rate to an anesthetized patient you could give Pancuronium or gallamine.

A

YES

61
Q

T/F: Intra-op bradycardia can be handled using a beta antagonist or a cholinergic agent.

A

FALSE (… Handled using a beta agonist or a anticholinergic agent.)

62
Q

Intra-Op SVT cardioversion is needed if SBP < __ .

A

80

63
Q

What type of drug would be avoided if patient has a AV reciprocating SVTs arise from reentrant circuits that involve accessory pathways (WPW or Pre-excitation).

A

-Class II
(Beta blockers)
-Class IV
(Diltiazem and verapamil)

64
Q

What drugs would work for a patient that has a AV reciprocating SVTs arise from reentrant circuits that involve accessory pathways?

A
  • Adenosine
  • Procainamide (Class Ia (WPW))
  • Flecainide??
65
Q

What are nonsustained VT:

A
  • 3 or more PVC
  • Rate exceeding 100 beats/min
  • Last 30 seconds or less
  • without hemodynamic compromise
  • Preserved ventricular function, not predivitve of serious VT, no Tx. needed
  • Evaluate and treat potential etiologies
  • Poor LV function or severe LVH, prophylaxis with lidocaine
66
Q

What drug would be given in Polymorphic VT:

A
  • Class Ib (Lidocaine)

- phenytoin

67
Q

What drug would be give in sustained VT or VF:

A
  • Class Ib (lidocaine)
  • Class Ia (procainamide)
  • Class III (Amiodarone)
68
Q

What is the mechanism of action of procainamide:

A
  • Class Ia
  • Na+ and K+ channel blocker
  • PREVENT reenty by converting unidirectional to bidirectional block
  • Depresses automaticity by decresing the slope of phase 4 depolarization, increases refractoriness
69
Q

What would be the indication for procainamide:

A
  • ventricular tachydysrhythmias and atrial tachycardia in the presence of accessory pathways
  • SVT
  • A. Fib
  • PVC
  • VT
70
Q

What drug toxicity results in the systemic lupus erythematosus like syndrome possible with chronic administration.

A

-Procainamide

71
Q

Lidocaine is a __ channel blocker.

A

Na

72
Q

T/F: Lidocaine is the first choice for supraventricular arrhythmias.

A

FALSE (..first choice for ventricular arrhythmias.)

73
Q

Lidocaine is _____ against Supraventricular arrhythmias.

A

ineffective

74
Q

What phase does lidocaine work in and where at can the effects be seen?

A
  • Decrease phase 4

- Purkinje fibers

75
Q

What does lidocaine toxicity do to the CNS and CV system?

A

-CNS: depression to stimulation
-CV: depress LV function in preexisting LV dysfunction
CV:RARELY cause further slowing in patients with sinus bradycardia

76
Q

Phenytoin is a __ channel blocker.

A

Na

77
Q

Phenytoin _____activity triggered by digitalis induced after depolarization in purkinje fibers.

A

-abolishes

78
Q

What drug would you use for ventricular dysrhythmias assoociated with digitalis toxicity.

A

Phenytoin

79
Q

What is the problem with phenytoin when administered through a peripheral IV?

A

-Highly alkaline and can cause phlebitis

80
Q

Phenytoin administered rapidly will cause:

A
  • respiratory arrest
  • severe hypotension
  • Ventricular ectopy
  • DEATH
81
Q

What will phenytoin toxicity do to the CNS?

A

-Drowsiness, nystagmus, nausea, vertigo

82
Q

T/F: Flecainide is used to treat WPW.

A

TRUE

83
Q

What are the side effects of Flecainide?

A
  • Moderate negative inotropic effect
  • Vertigo
  • Difficulty in visual accommdation
84
Q

Propranolol toxicity includes:

A
  • Profound bradycardia or asystole
  • LV failure
  • Acute bronchospasm
85
Q

Amiodarone may ______ beta blockers and Ca++ channel blocker.

A

potentiate

86
Q

T/F: Amiodarone would work in suppression of tachydysrhythmias associated with WPW.

A

TRUE

87
Q

Where does amiodarone accumulate in the body?

A

Thyroid

88
Q

Is Amiodarone lipid soluble or not?

A

Soluble

89
Q

What is the half life of Amiodarone?

A

-Weeks to months

90
Q

What are the toxicity of amiodarone?

A
  • RESP: ARDS, pulmonary fibrosis
  • CV : bradycardia, hypotension, dysrhythmias, heart failure, heart block, sinus arrest
  • HEME: coagulation abnormalities
  • Hepatic: increase in LFT and liver failure
  • ENDO: hypo/hyperthyroidism
91
Q

Dronedarone (MULTAQ) is just like ___ and is used for ____ and is ONLY administered __.

A
  • amiodarone
  • A. FIB
  • PO
92
Q

T/F: Verapamil has NO effeccct on accessory tracts.

A

TRUE

93
Q

Digoxin slows the ventricular response rate in ____ but, enhances conduction through _______ pathways which can lead to increase ventricular response in __.

A
  • A. Fib.
  • accessory
  • WPW
94
Q

Digoxin inhibits what:

A

-Na+/K+ ATPase pump

95
Q

Adenosine has what type of receptor?

A

-adenosine (A1 receptor)

96
Q

What will methylxanthine do to adenosine?

A

-inhibits adenosine by binding to the A1 receptor

97
Q

Dipyridamole will do what to adenosine?

A

-Potentiate adenosine effects by being an adenosine uptake inhibitor.

98
Q

What will be seen with adenosine toxicity?

A
  • Facial flushing
  • dyspnea
  • chest pressure most common but subsides in < 60 seconds
  • May exacerbate bronchoconstriction in asthmatic.

Emily: Pharm 2 (11 decks)

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