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Block 9 Week 2 > Anti-Arrhythmics Drugs-Harvey > Flashcards

Anti-Arrhythmics Drugs-Harvey Flashcards

1
Q

What are all the anti-arrythmic drugs?

A
  • Procainamide
  • Quinidine
  • Lidocaine
  • flecainide
  • Propranolol
  • Metoprolol
  • Amiodarone
  • Verapamil
  • Adenosine
  • Digoxin
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2
Q 
What is the 0 of the AP?
What is the 1 of the AP?
What is the 2 of the AP?
What is the 3 of the AP?
What is the 4 of the AP?
A 
upstroke 
early fast repolarization
plateau
repolarization
diastole
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3
Q

What happens during phase 0?

A

activation of Na+ channels; deactivation of inward rectifier K+ channel

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4
Q

What is happening during phase 1 in a fast response AP?

A

inactivation of Na+ channels

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5
Q

What is happening during phase 2 in a fast response AP?

A

Activation of Ca+ channels

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6
Q

What is happening during phase 3 in a fast response AP?

A

inactivation of Ca2+ channels; activation of delayed rectifier K+ channels

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7
Q

What is happening during phase 4 in a fast response AP?

A

deactivation of delayed rectifier K+ channels, reactivation of inward rectifier K+ channels

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8
Q

What are the phase 3 K+ channels?

A

Ikr=HERG + MiRP1

Iks=KvLQT1 + minK

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9
Q

What is the slow response AP?

A

Phase 0 – activation of Ca2+ channels

Phase 3 – inactivation of Ca2+ channels; activation of delayed rectifier K+ channels

Phase 4 – deactivation of delayed rectifier K+ channels, activation of pacemaker channels

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10
Q

What is the effective refractory period (ERP)?

A

stimulus cannot generate another AP (b/w 1-3)

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11
Q

What is the relative refractory period (RRP)?

A

stimulus can generate an abnormal AP (part of 3 and all of 4)

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12
Q

AP generated before all Na+ channels recover (RRP) will have (blank) upstroke velocity. Slow upstroke velocity means that the AP conduction velocity will also be (blank)

A

slow

slow

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13
Q

What is a cardiac arrhythmia?

A

a disruption of rate. rhythm, or pattern of electrical activity

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14
Q

What are the dangers of cardiac arrhythmias?

A

vascular stasis

Loss of CO

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15
Q

What is the incidence of Cardiac arrhythmia in patient who suffer a MI?
Who undergo a seizure?
Who are treated with cardiac glycosides?

A

80%
50%
25%

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16
Q

What are the mechanisms behind cardiac arrhythmia?

A
  • disturbance of electrical impulse formation (automaticity)

- Disturbance in conduction of electrical activity

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17
Q

In sinus tachycarcia, what is the atrial rate? ventricular rate? rhythm?

A

> 100
100
regular

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18
Q

In sinus bradycardia, what is the atrial rate? ventricular rate? rhythm?

A

<60

regular

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19
Q

In atrial tachycardia, what is the atrial rate?
What is the ventricular rate?
rhythm?

A

250-350
80-150
Variable

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20
Q

In Atrial fib what is the atrial rate?
ventricular rate?
rhythm?

A

doesnt have one
variable
very irregular

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21
Q

In ventricular tachycardia, what is the atrial rate? the ventricular rate? the rhythm?

A

variable
100-250
variable

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22
Q

In ventricular fibrillation, what is the atrial rate, ventricular rate, rhythm?

A

variable
doesnt have one
doesnt have one

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23
Q

Why does bradycardia occur (less than 60)?

A

excessive parasympathetic tone, sick sinus syndrome

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24
Q

Why does tachycardia occur (greater than 100)?

A

excessive sympathetic tone

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25
Q

What are the disturbances in impulse formation?

A

-problems in the sinus node/ sinus rhythm
(bradycardia/tachycardia)
-problems w/ conducting syndrome (ectopic)
-Atrial or ventricular myocardium (ectopic)

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26
Q

T or F
SA node pacemaker activity varies reflexly with respiration
Why?

A

T

because you get a decrease in vagal/parasympathetic tone upon inspiration

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27
Q

If you have an ectopic conducting system what does this mean?

A

impulse formation is not dominant in SA node, instead is dominant in AV node/bundle of His, or Purkinje fiber

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28
Q

When do you get ectopic conducting system problems with a purkinje fiber dominating?

A

hypokalemia

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29
Q

Put the conducting systems in order of most quick to least quick.

A

SA node> AV node> Purkinje fibers

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30
Q

How can you tell if you have a junctional rhythm?

A

you have inverted P wave that follows the QRS complex

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31
Q

How can atrial or ventricular myocardium cause disturbances in impulse formation?

A

You can have ectopic problems resulting in EADs and DADs

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32
Q

When do DADs occur?

A

during resting membrane potential

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33
Q

When do EADs occur?

A

during repolarization

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34
Q

How are EADs formed? What is it associated with?

What can it lead to?

A
  • by prolonging ventricular AP duration (APD)
  • prolongation of QT interval
  • Torsade de pointes (TdP)-a type of ventricular tachycardia
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35
Q

What are the risk factors for Torsades de pointes (TdP)? Why?

A

-pharmacologic- acquired long QT syndrome
because HERG (potassium channel) is a target for a lot of drugs to attack and thus causes a prolonged QT
-genetic (inherited long QT syndrome)
-electrolyte imbalance
-female gender
-bradycardia (LQT3)
-Sympathetic stimulation (LQT1, LQT5)

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36
Q

There are a lot of drugs that are still prescribed that are known to prolong the QT interval, why do we still give them?

A

Because EADs are caused by multipe events not just one event so the drug itself wont cause EADs without other factors

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37
Q

Most genetic causes for long QT syndrome are (blank) of function except for 2

A

Loss of function (lose potassium channel function)

2 are gain of function and deal with sodium and calcium

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38
Q

What type of LQT is bradycardia?

What type of LQT is sympathetic stimulation?

A

LQT3

LQT1, LQT5

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39
Q

What causes DADs?

A

excess Ca2+ in the SR causes spontaneous release of calcium into the cytoplasm. The calcium/sodium exchanger then kicks into gear putting 3 sodium into the cell for every one calcium creating a more positive charge inside the cell and thus depolarizes it.

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40
Q

What commonly causes DADs?

A 
Digoxin
Catecholamines
Hypercalcemia
Increased Heart rate
Genetic defect
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41
Q

What are 2 genetic causes for DADs?

A

CPVT-1 gain of function: Ryanodine receptor (move calcium out of SER) causing increased calcium
CPVT-2 loss of function: calsequestrin is lost so you cant bind calcium and thus you have increase of calcium

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42
Q

What is this:

slowed conduction w/out reentry

A

AV node dysfunction

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43
Q

What results when you have 1st degree AV node dysfunction?
What results when you have 2nd degree AV node dysfunction?
What results when you have 3rd degree AV node dysfunction?

A
  • prolonged PR interval
  • intermittent failure of AV conduction
  • complete failure of AV impulse conduction
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44
Q

How do you get slowed conduction with reentry?

A

-atrial, AV node, and ventricular

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45
Q

What are the requirements for reentry?

A
  • multiple parallel conduction pathways
  • area of unidirectional block
  • slowed conduction
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46
Q

What happens if you get subendocardial ischemia?

Why do you get increased depolarization in this case?

A
  • slow conduction and unidirectional block

- increased extracellular potassium caused by lack of ATP and thus dysfunction of the NaK ATPase

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47
Q

Ischemia induced change in extracellular K+ causes (blank) of resting membrane potential (RMP)

A

depolarization

48
Q

Ischemia induced changes in RMP are…?

A
  • Slows Na+ channel recovery from inactivation

- Prevents some channels from recovering at all

49
Q

What does inactivation of Na channels do?

A

slow or block conduction

50
Q

What are the three requirements for established reentrant circuit?

A
  • Multiple parallel pathways
  • unidirectional block
  • slowed conduction
51
Q

What is the cellular basis for reentry?

A

ischemia/hypoxia reduces cellular ATP which reduces activity of Na/K pump and activates ATP sensitive (inhibited) K+ channels

  • Get an increase in extracellular K levels
  • depolarizes membrane potential
52
Q

Explain why ischemia causes slow action potentials and slow sodium conduction

A

Ischemia-> lose ATP
ATP Na/K wont work and you get potassium outside cell + K ATPase channels activate in the absence of ATP which depolarizes membrane thus your RMP is more positive. Then you sodium channels cant recover with this abnormally positive RMP thus you only have a few remaining sodium channels to push all the sodium through so it will take a while and thus you will have a slow AP and slow conduction velocity.

53
Q

Are premature contractions (PVC, PAC) clinically significant?

A

no

54
Q

What is the mechanism responsible for the majority of clinically significant arrhythmias?

A

slows conduction with reentry

55
Q

What causes atrial or ventricular tachycardia?

A

one sustained reentrant circuit

56
Q

What causes paroxysmal supraventricular tachycardia (PSVT)?

A

AV node reentry

57
Q

What causes nonsustained ventricular tachycardia (NSVT)?

A

one transient circuit

58
Q

What causes atrial flutter?

A

one large reentrant circuit i.e impulses travel in circular course in atria

59
Q

What causes atrial or ventricular fibrillation?

A

large number of reentrant circuits (i.e impulses have chaotic, random pathways in atria)

60
Q

When do you treat cardiac arrhythmias?

A
  • If the arrythmia decreases CO (severe bradycardia, ventricular tachycardia, ventricular fibrillation)
  • if the arrhythmia is likely to precipitate a more serious arrhythmia (e.g a fib may lead to sustained v tach, v tach may lead to v fib)
  • if arrhythmia is likely to precipitate an embolism (e.g. chronic atrial fibrillation)
61
Q

Therapeutic modalities for treating arrhythmias?

A
  • drug therapy
  • correct electrolyte imbalances
  • DC cardioversion (extrenally or by implantable device (ICD))
  • pacemaker
  • carotid sinus massage, Vasalva aneuver (increase vagal tone) (both increase pressure so your response is to increase vagal tone and slow HR)
  • surgical or catheter mediated ablation of ectopic foci
  • life style modification
62
Q

Most antiarrhythmic drugs act by directly blocking or altering the kinetics of (blank). Many of these agents interact w/ ion channels in a (blank) manner.

A

-cardiac ion channels

- state-dependent
i. e they like inactivated or open channels better than resting channels

63
Q

How come some antiarrhythmic agents may be proarrhythmic?

A

because they may affect the electrical activity of normal tissue

64
Q

What is the mechanism of action of 1a class drugs? Why are 2 important drugs in this class? What do they do to the QRS complex? QT complex? upstroke velocity?

A

Na+ channel blockers that increase action potential duration

  • procainamide, quinidine
  • widen QRS complex
  • elongates QT
  • decrease upstroke velocity
65
Q

What is the mechanism of action of 1b class drugs? Why are 2 important drugs in this class? What do they do to the QRS complex? QT complex? upstroke velocity?

A
  • Na+ channel blockers that slightly decrease APD
  • Lidocaine
  • decrease QT
  • no change
66
Q

What is the mechanism of action of 1c class drugs? Why are 2 important drugs in this class? What do they do to the QRS complex? QT complex? upstroke velocity?

A

Na+ channel blockers that don’t change APD

  • flecainide
  • hella increase QRS and slow upstroke
67
Q 
What class are beta blockers?
What are 2 important anti-arrhythmic agents?
A

Class II
-metoprolol, propranolol

(B is second letter in alphabet)

68
Q 
What class are K+ channel blockers?
What do they do to the action potential? What is an important anti-arrhythmic one?
A

Class III
amiodarone
Increase AP duration

69
Q 
What is the mechanism of action of class IV drugs?
What is an important antiarrhythmic belonging to this class?
A

L-type Ca2+ channel bockers

Verapamil

70
Q

What kind of drug is adenosine?

Digoxin?

A
  • adenosine receptor agonists

- Parasympathomimetics

71
Q

What is this:

reduce excitability of ectopic pacemakers, especially purkinje fibers

A

Class I Na+ channel blockers

72
Q 
How do class 1 agents block re-entry?
What do they do to the unidirectional block?
A
  • increasing effective refractory period

- turn unidirectional block into bidirectional block

73
Q

What are the clinical inidactions for class Ia drugs (quinidine and procainamide)?

A
  • atrial and ventricular arrhythmias in pnts w/out a history of ischemic heart disease
  • drug of 2nd or 3rd choice for tx of sustained ventricular arrhythmias following MI
74
Q

What are the first line drugs for sustained ventricular arrhythmias following MI?

A

Amiodarone and lidocaine

75
Q

What is the clinical indication for lidocaine?

A

drug of 2nd choice for terminating ventricular tachycardia and preventing ventricular fibrillation after DV cardioversion (amiodarone first choice)
-Ineffective against atrial arrhythmias

76
Q

What is the clinical use of flecainide?

A

supraventricular arrhythmias in pnts without a history of ischemic heart disease

77
Q

T or F

Class 1 drugs have no role in prevention of cardiac arrhythmias and sudden cardiac death in post-MI patients

A

T

78
Q

How can Na+ channel blockers show proarrhythmic behavior?

A
  • reduced Na current-> induces unidirectional conduction block
    (i. e converts slowed conduction to unidirectional block)
79
Q

What are the three extra cardiac effects of Quinidine?

A
  • adverse GI (nausea, vomiting, diarrhea)
  • CINCHONISM (headache, dizziness, tinnitus)
  • anticholinergic effects (anti muscarinic and anti-nicotinic)
80
Q

Your patient comes in complaining of dry mouth, blurred vision and has hypotension… he is taking quinidine.. whats happening?

A

he is having anticholinergic effects

  • anti-muscarinic: dry mouth, blurred vision
  • anti-nicotinic: ganglionic block-Hypotension
81
Q

What are the adverse effects of procainamide?

A 
anticholinergic effects (less prominent than quinidine) 
reversible lupus-like syndrome with long-term therapy in ~33% patients
82
Q

What are the extra-cardiac effects of Lidocaine?

A

local anesthetic effects at high doses (paresthesias, tremor, nausea, lightheadedness, hearing disturbances, slurred speech, convulsions)

83
Q

What is the adverse effect of flecainide?

A

torsade de pointes

84
Q

What is the only class of antiarrhythmics documented to reduce mortality in MI survivors?

A

Class 2 agents (beta-adrenergic receptor blockers)

85
Q

What are the clinical indications for class 2 agents?

A
  • prevent arrhythmias and sudden death in pnts with history of CHF and MI
  • control ventricular rate in pnts with supraventricular tachyarrhythmias (i.e a fib)
  • catecholaminergic polymorphic V tach (CPVT)
86
Q

What do class II agents do to sympathetic tone? To catecholamines? Pacemaker automaticity?
DADs?
Conduction, what will this cause?

A 
decrease
decrease
decrease
decrease
decrease, prevent supraventricular tachyarrhythmias from becoming ventricular tachyarrhythmias
87
Q 
In regards to class II agents:
(blank) blocks both beta-1 and beta-2 adrenergic receptors

(blank) and (blank) are more selective for beta-1 receptors
(blank) has a very short duration of action (10 minutes) – used for emergency treatment of atrial flutter or atrial fibrillation
(blank) is a non-selective beta blocker that also blocks alpha receptors

A
  • Propranolol
  • Metoprolol and Esmolol
  • Esmolol
  • Carvedilol
88
Q

What are possible side effects of class II?

A 
bradycardia
hypotension
left ventricular failure
AV node block
bronchospasms (propranolol)
89
Q

What drug do you use for acute suppression of post-MI ventricular arrhythmias?

A

amiodarone

90
Q

What are the clinical indications for amiodarone?

A
  • post mi ventri arrhythmia
  • prevention of recurrent V tach in post MI (doesnt increase mortalitiy like class I)
  • adjuvant to reduce shock in post-MI pnts with ICD
  • conversion of A fib to normal sinus rhythm
  • maintain normal sinus rhythm in a fib
91
Q

So which drug can you give for prevention of V tach?

A

amiodarone

92
Q

What is the mechanism of action of K channel blockers?

A
  • blocks re-entry by increasing ERP duration

- converting unidirectional block to bidirectional block

93
Q

(blank) reduces effectiveness of class 3 agents

A

hyperkalemia

94
Q

Amiodarone is the most non-selective antiarrhythmic agent and its effectiveness is also due to the block of…?

A

Na+ channels
Ca2+ channels
alpha-adrenergic receptors
beta-adrenergic receptors

95
Q

What are some potentially serious extra-cardiac effects of K+ channel blockers?

A

hypothyroidism
hyperthyroidism
pulmonary fibrosis

96
Q

What are the clinical indications for class IV agents (Ca2+ channel blockers)?

A
  • control of ventricular rate in patients with chronic atrial fibrillation/flutter (rate control)
  • convert paroxysmal supraventricular tachycardia (PSVT) to sinus rhythm
  • alternative to beta-blockers (class 2 agents) for treating catecholaminergic polymorphic ventricular tachycardia (CPVT)
97
Q

What is the MOA of class IV?

A

slows AV node conduction and increases AV node refractory period duration (blocks AV node reentry)

98
Q

(blank) are not effective in treating ventricular arrhythmias

A

Ca2+ channel blockers

99
Q

Ca2+ channel blockers are contraindicated in pnts with (blank) because of negative inotropic effects

A

heart failure

100
Q

(blank) is primarily used for positive inotropic effects in treatment of heart failure

A

Digoxin

101
Q

What does digoxin do to the PR interval and ST segment?

A

prolongs PR interval

alters ST segment

102
Q

Why is digoxin sort of a sketchy drug?

A

low therapeutic index- can cause life threatening arrhythmias by triggering DADs

103
Q

What is adenosine?

A

a naturally occurring nucleoside that is an agonist at A1 receptors

104
Q

What is the MOA of adenosine?

A

A1 receptor activates Gi protein signaling pathways, produces same effects as M2 muscarinic receptors (slows SA nodal firing rates, slows AV node conduction)

105
Q

Adenosine inhibits (blank) reentry

A

AV node

106
Q

What is the drug of choice for treating paroxysmal supraventricular tachycardia (PSVT) if carotid sinus massage or valsalva maneuver doesnt work?

A

Adenosine

107
Q

How come adenosine doesnt have that horrible of side effects?

A

it has a short half life (seconds) that minimizes side effects (hypotension, bronchospasms, asystole)

108
Q

When can adenosine trigger A fib?

A

in v tach patients so dont use on them

109
Q

What is the most common cardiac arrhythmia?

A

A fib
~0.5% of individuals < 65 years of age
~10% of individuals > 80 years of age

110
Q

Is A fib typically a one time event?

A

no -> patients who develop it once are predisposed to developing it again (AF begets AF) due to electrical remodeling of the atria

111
Q

What are the symptoms of a fib?

A

palpitations, dyspnea, fatigue, decreased exercise tolerance, chest pain

112
Q

What are the risk factors of a fib?

A

hyperthyroidism, hypertension, age, congestive heart failure, previous AF

113
Q

What are the complications of a fib?

A

thromboembolism (stroke), ventricular tachycardia, tachycardia-induced heart failure, ventricular bradycardia

114
Q

What is the tx goal for a fib?

A
  • rate control (allow AF to persist but control ventricular rate)
  • rhythm control (eliminate atrial arrhythmia; convert to normal sinus rhythm (cardioversion)
  • anticoag therapy
115
Q

Which is better to achieve, rate control or rhythm control in a fib?

A

neither, showed no difference in mortality

116
Q

How do you achieve rate control in a fib?

A
  • class 2 agent, class 4 agent, and/or digoxin
  • pacemaker (for pnts with slow ventricular response
  • AV node ablation with a pacemaker (for pnts with fast ventricular response)
117
Q

How do you achieve rhythm control in a fib?

A 
Cardioversion
-direct current
-class 1c agent (flecainide)
-class 3 agent (amiodarone)
Maintenance of normal sinus rhythm
-class 3 agent (amiodarone)
-class 1c agent (flecainide)
Catheter ablation

Block 9 Week 2 (7 decks)

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