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Pharm > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

Cardiac cell membrane electrical activity is determined by which ions?

A

sodium
potassium
calcium
(chloride)

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2
Q

What path does a cardiac electrical impulse follow?

A

SA node
internodal tracts
AV node
Bundle of His
L and R bundle branches
Purkinje fibers

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3
Q

Stellate ganglion blocks knock out what important cardiac feature? What level?

A

cardiac accelerators
T4

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4
Q

Describe “arrhythmia”

A

electrical impulses/cardiac depolarization that deviates from the normal pathway in site of origin, rate or regularity, or conduction pathway

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5
Q

Which ion regulates resting potential?

A

K+

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6
Q

When are cells most permeable to Na+?

A

at the start of an action potential
(most cells are impermeable to Na+ at rest)

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7
Q

During which period of repolarization is an action potential least likely to fire?

A

absolute refractory period

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8
Q

Summarize what happens during Phase 0 of a ventricular action potential:

A
  • threshold potential is reached
  • gates open, Na+ enters the cell
  • permeability to K+ decreases
  • fast depolarization
  • very brief
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9
Q

Summarize what happens during Phase 1-2 of a ventricular action potential:

A
  • depolarization peaks (+30mV)
  • repolarization slowly starts
  • Na+ influx stops
  • Ca2+ influx starts
  • K+ moves OUT
  • Cl- moves IN
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10
Q

Summarize what happens during Phase 3 of a ventricular action potential:

A
  • fast repolarization
  • K+ moves OUT faster than Na+ and Ca2+ move in
  • @ end of phase 3: cardiac cells will respond to a stimulus greater than normal intensity
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11
Q

Summarize what happens during Phase 4 a ventricular action potential:

A
  • resting potential reaches repolarized state (-90mV)
  • Na+ constantly leaking out
  • diastole occurs
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12
Q

Describe the ion changes during each phase of the ventricular action potential:

A

Phase 0: Na+ in
Phase 1: Cl- in, K+ out
Phase 2: Ca2+ in
Phase 3: K+ out faster than Na+ and Ca2+ in
Phase 4: Na+ leaking out constantly

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13
Q

Is the concentration of Na+ inside cardiac cells higher or lower than the concentration outside the cells?

A

lower inside (Na+ wants to move in)

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14
Q

Is the concentration of K+ inside cardiac cells higher or lower than the concentration outside the cells?

A

higher inside (K+ wants to move out)

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15
Q

Is the concentration of Ca2+ inside cardiac cells higher or lower than the concentration outside the cells?

A

lower inside (Ca2+ wants to move in)

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16
Q

What is the resting membrane potential of a pacemaker/nodal cell?

A

-60mV

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17
Q

Which ion is not involved in nodal APs?

A

chloride

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18
Q

Describe ion movement during Phase 0 of the nodal action potential?

A
  • Ca2+ moves in (L-type channels)
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19
Q

Describe ion movement during Phase 1 of the nodal action potential?

A

trick question - there is no Phase 1

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20
Q

Describe ion movement during Phase 2 of the nodal action potential?

A

trick question - there is no phase 2

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21
Q

Describe ion movement during Phase 3 of the nodal action potential?

A
  • K+ moves out
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22
Q

Describe ion movement during Phase 4 of the nodal action potential?

A
  • K+ moves out
  • Na+ moves in (funny channels)
  • Ca2+ moves in (T-type in late stage)
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23
Q

What are the 2 (general) causes of arrhythmias?

A

1) abnormal pacemaker activity
2) abnormal impulse propagation

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24
Q

List the 4 major mechanisms for antiarrhythmics:

A
  • sodium channel blockade
  • sympathetic autonomic blockade
  • calcium channel blockade
  • prolongation of effective refractory period
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25
Q

What are two causes of bradycardia?

A
  • intra-op hypoxia
  • improper ventilation
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26
Q

What are some causes of sinus tachycardia?

A
  • CHF
  • hypovolemia
  • hypoxemia
  • sepsis
  • anxiety
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27
Q

Atrial ectopy is often due to:

A

poor oxygenation

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28
Q

What drug can lead to PSVT?

A

digitalis toxicity

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29
Q

What are some anesthesia-based causes of arrhythmias?

A
  • mechanical stimulation (intubation)
  • abnormal ventilation leading to hypercapnia, hypoxia
  • anesthetic agents
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30
Q

What are the 3 ways heart rate can be manipulated?

A
  1. rate of spontaneous phase 4 depolarization
  2. threshold potential
  3. resting membrane potential
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31
Q

What effect does sympathetic stimulation have on the nodal action potential?

A

faster diastolic depolarization

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32
Q

What effect does parasympathetic stimulation have on nodal action potential?

A
  • lower maximum diastolic potential
  • slower diastolic depolarization
  • longer action potential duration
    (slide 20)
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33
Q

What does the mnemonic No Body Kisses Cats mean?

A

No - Na+ channel blockers - class 1
Body - beta-blockers - class 2
Kisses - K+ blockers - class 3
Cats - Ca2+ blockers - class 4

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34
Q

What phase of the nodal action potential do sodium channel blockers affect?

A

phase 0

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35
Q

Drugs with higher affinity for Na+ channels produce (more/less) QT prolongation

A

more
C > A > B

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36
Q

Describe Class 1A antiarrhythmics:

A
  • lengthen the duration of the AP
  • interact, bind, and unbind with Na+ channels
  • intermediate affinity for Na+ channels
  • produce moderate QT prolongation
  • used for WPW
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37
Q

Describe Class 1B antiarrhythmics:

A
  • shorten the duration of the nodal AP
  • rapidly interact with Na+ channels
  • lowest affinity for Na+ channels
  • minimal QT prolongation
38
Q

Describe Class 1C antiarrhythmics:

A
  • little to no effect on nodal AP
  • slowly interact with Na+ channels
  • highest affinity for Na+ channels
  • significant QT prolongation
39
Q

What effect do Class 2 antiarrhythmics have on the heart?

A

reduce adrenergic activity

40
Q

What effect do Class 3 antiarrhythmics have on the heart?

A
  • prolong the effective refractory period by a mechanism other than or in addition to Na+ channel blockade
  • K+ channel blockers
41
Q

What effect do Class 4 antiarrhythmics have on the heart?

A
  • slow conduction
  • increase refractory period
  • CCBs
42
Q

What class does Quinidine belong to and what is its MOA?

A
  • class 1
  • binds and blocks activated sodium channels
43
Q

What effect does Quinidine produce?

A
  • depresses pacemaker rate
  • depresses conduction and excitability
  • lengthens AP duration (prolongs QT)
    *proarrhythmic, dirty drug
44
Q

What class does Procainamide belong to?

A

Class 1A

45
Q

What arrhythmias is Quinidine used to treat?

A
  • paroxysmal AFib/flutter
  • PVCs
46
Q

Which patient populations may experience a prolonged effect of Quinidine?

A
  • hepatic dz
  • CHF
47
Q

What is the metabolite of Procainamide and why is it relevant?

A

N-acetyl procainamide (NAPA)

relevant because both Procainamide and NAPA are eliminated by the kidneys and renal pts need reduced doses

48
Q

What is the most important difference between Quinidine and Procainamide?

A

Procainamide has less prominent antimuscarinic action

this makes it more difficult to counteract the increased ventricular rate response

49
Q

Procainamide has ganglionic blocking properties. What effect does this have on the body?

A
  • reduced peripheral vascular resistance
  • hypotension
50
Q

What is the most problematic side effect of Procainamide?

A

lupus-like syndrome characterized by arthralgia and arthritis

51
Q

What is the dose/onset/duration/half-life of Procainamide?

A
  • dose: 100mg q5min, max 1000mg
  • onset: immediate
  • duration: 2.5 hrs
  • half-life: 3-4 hours (frequent dosing)
52
Q

What class does Lidocaine belong to and what is its MOA?

A
  • Class 1B (less potent)
  • exclusively on inactivated Na channels
53
Q

What is the agent of choice for suppression of intraoperative VT and VF after cardioversion if the pt has good cardiac function?

A

Lidocaine

54
Q

Lidocaine toxicity risk increases with which drugs?

A

(drugs that decrease liver BF)
- propranolol
- cimetidine

55
Q

If a large dose of Lidocaine is given to a patient with preexisting HF, what side effect can occur?

A

hypotension d/t depressed contractility

56
Q

List the most common side effects of Lidocaine:

A
  • parasthesias
  • tremor
  • nausea
  • lightheadedness
  • hearing disturbances
  • slurred speech
  • convulsions
57
Q

What class does Flecainide belong to and what is its MOA?

A
  • Class 1C
  • potent Na+ channel blocker (ventricular arrhythmias)
  • potent K+ channel blocker (atrial arrhythmias)
58
Q

What medication is known as the “pill in the pocket”?

A

Flecainide

59
Q

What class does Propafenone belong to?

A

Class 1C

60
Q

This drug has some structural similarities to Propranolol but has only weak B-blocking activity:

A

Propafenone

61
Q

Through which route is Propafenone given and what are 2 resulting side effects?

A
  • oral route

SE: metallic taste and constipation

62
Q

What is another name for Class 2 antiarrhythmics? What is their primary effect?

A

beta blockers

decrease the rate of spontaneous phase 4 depolarization (rate control)

63
Q

Which class 2 antiarrhythmics is most commonly administered in the OR? What dose?

A

Esmolol

dose: 10mg (30?) IVP q5-10min

64
Q

Hypovolemic patients in the OR should not receive this drug class because it can cause hypotension:

A

beta blockers

65
Q

List 3 class 2 antiarrhythmics used in anesthesia:

A

Esmolol
Metoprolol
Propranolol

66
Q

Carvedilol belongs to which drug class? What does it do?

A

technically in Class 2

  • alpha and beta blocker
  • blocks: K+, Ca2+, Na+
  • prolongs AP depolarization
67
Q

What benefit can prolonged use of Carvedilol have on the heart?

A

upregulation of Na, K, and Ca channels (beneficial for diseased hearts)

68
Q

What arrhythmia is Digoxin used to treat?

A

supraventricular arrhythmias

69
Q

Describe the effects of Digoxin:

A
  • decreased activity of SA node
  • prolonged conduction through AV node
  • increased contractility
  • decreased myocardial O2 consumption
70
Q

Synchronized cardioversion performed on a patient with Dig toxicity can result in what? Why?

A

VFib

releases Ca2+ from the sarcoplasmic reticulum and increases r/f arrhythmias

71
Q

What class does Sotalol belong to? What is its MOA?

A
  • Class 3
  • nonselective B-blocker
  • prolongs AP duration
72
Q

What arrhythmias is Sotalol used to treat?

A

SVT & ventricular arrhythmias

73
Q

Which Class 3 antiarrhythmic can result in Torsades de Point? Why?

A
  • Sotalol
  • toxicity associated with beta blockade and AP prolongation
74
Q

Ibutilide is a (Class 1/2/3/4) drug used to treat ______.

A
  • Class 3
  • acute onset of AFib or AFlutter
75
Q

Verapamil belongs to which class? What is its MOA?

A
  • Class 4
  • blocks activated and inactivated Ca2+ channels
76
Q

What are some effects of Verapamil?

A
  • peripheral vasodilation (good)
  • AV block (treated with Atropine, B-receptor stimulants, or Ca2+)
  • constipation
  • nervousness
  • peripheral edema
77
Q

Verapamil is extensively metabolized by which system?

A

liver

78
Q

Which drug is used to treat reentry SVT?

A

Verapamil

79
Q

Diltiazem is a (Class 1/2/3/4) drug used to produce which effect?

A
  • Class 4
  • arterial vasodilation
80
Q

Amiodarone is used to treat which arrhythmias?

A

supraventricular and ventricular arrhythmias

81
Q

What is the MOA of Amiodarone?

A
  • very effective Na+ channel blocker (low affinity for activated channels; prefers inactivated)
  • blocks K+ channels (lengthens AP duration)
  • weak CCB
  • noncompetitive inhibitor of B-receptors
82
Q

List the intended effects of Amiodarone:

A
  • slows sinus rate and AV conduction
  • prolongs QT
  • prolongs QRS duration
  • increases atrial, AV nodal, ventricular refractory periods
  • antianginal effects
83
Q

Describe how Amiodarone produces antianginal effects:

A
  • noncompetitive alpha and beta blocking effects
  • Ca+ blocking in coronary arterial smooth muscle
84
Q

What are the side effects of Amiodarone?

A
  • peripheral vascular dilation
  • symptomatic bradycardia in pts with sinus or AV node dz
  • concentrated in every tissue & organ
  • pulmonary fibrosis/inflammation
  • reduced drug clearance
85
Q

Amiodarone can reduce the clearance of which drugs?

A
  • Flecainide
  • Procainamide
  • Quinidine
  • Theophylline
  • Warfarin
86
Q

What is the MOA of Adenosine?

A
  • enhanced K+ conductance
  • inhibition of cAMP-induced Ca2+ influx
87
Q

How does Adenosine reduce HR?

A
  • marked hyperpolarization and suppression of Ca2+-dependent APs
  • inhibition of AV nodal conduction
  • increased AV nodal refractory period
88
Q

What are some side effects of Adenosine?

A
  • flushing
  • SOB, CP (bronchospasm?)
  • HA
  • hypotension
  • nausea
  • parasthesias
89
Q

Which arrhythmia is Adenosine used to treat?

A

ONLY confirmed PSVT

90
Q

What ion channels does Mg influence?

A
  • Na/K ATPase
  • Na+ channels
  • certain K+ channels
  • Ca2+ channels
91
Q

IV potassium influences both the inside and outside of the cardiac cell membrane. What effects does it have?

A
  • resting potential depolarizing action
  • membrane potential stabilizing action

Pharm (19 decks)

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