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pharmacology > Drugs used in Cardiac Arrhythmias > Flashcards

Drugs used in Cardiac Arrhythmias Flashcards

1
Q

What causes arrhythmias

A

Abnormal pacemaker activity or abnormal impulse propagation

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2
Q

What is the goal of therapy of arrhythmias

the actual arrhythmia

A

to reduce ectopic pacemaker activity and modify conduction/refractoriness to disable circus movements

This modifying happens in the reentry circuits

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3
Q

What are the major pharmacologic mechanisms available to accomplish what arrhythmias do?

4 total

A
  1. sodium channel block
  2. bloackade of sympathetic autonomic effects in the heart
  3. prolongation of the effective refactory period
  4. calcium channel block
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4
Q

What are antiarrhythmic drugs classified by?

A

Their effect on the myocardium

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5
Q

Are antiarrhythmic drugs used in pts with non-life threatening arrhythmias?

A

No, this can increase mortality

especially in pts with structural heart disease

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6
Q

what do antiarrhythmic drugs do at the SA node

specifically the pacemaker cells

A

decreases automaticity of ectopic pacemakers

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7
Q

what do antiarrhythmic drugs do to the refractory period

A
  • reduce conduction and excitability
  • increase the refractory period
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8
Q

How do antiarrhythmic drugs work?

A

selectively blocking sodium or calcium channels of depolarized cells

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9
Q

What is automaticity?

A

ability to produce its own

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10
Q

What phase do channel-blocking drugs readily bind to activated channels?

A

Phase 0

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11
Q

MOA of channel blocking drops

What phase do channel-blocking drugs readily bind to in-activated channels?

A

phase 2

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12
Q

MOA channel blocking drugs

How do channel blocking drugs bind to rested channels?

A

Poorly or not at all

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13
Q

What type of MOA are channel-blocking drugs described as?

A

use-dependent or state-dependent

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14
Q

what happens when there is a more active a channel

For MOA of channel blocking drugs

A

more blocking

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15
Q

MOA of channel-blocking drugs

What phase do channel blocking drugs reduce?

A

Phase 4

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16
Q

MOA of channel blocking drugs

What channels do channel blocking drugs block?

A

Sodium or calcium channels

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17
Q

MOA of channel blocking drugs

The more the heart acts up the ___ the drug will work?

A

better

because as activity increases = blocking can increase

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18
Q

What do channel blocking drugs do to the ratio of sodium/calcium permeability to potassium permeability

A

reduces the ratio between Na+/Ca2+ perm to K+ perm

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19
Q

MOA of channel blocking drugs

what do beta-adrenoceptor blocking drugs do to phase 4? What is the process?

A

indirectly reduces phase 4
-by blocking the positive chronotropic action of norepipherine in the heart

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20
Q

Phase 4 of the AP of the heart

A

Resting potential
K+ moves out of the cell to repolarize

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21
Q

Phase 0 of the AP of the heart

A

Na influx to depolarize to threshold
then RAPIDLY depolarizes beyond 0mV

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22
Q

Phase 1 of the AP of the heart

A

Partial repolarization
-brief influx of chloride and efflux of K+
-membrane potential decreases slightly

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23
Q

Phase 2 of the AP of the heart

A

Plateau phase
opens L-type Ca2+ channels and there is an influx of Ca2+
~0mV

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24
Q

Phase 3 of the AP of the heart

A

Rapid repolarization
K+ moves out of the cell
-back to -90mV

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25
Q

When do we use sodium channel blockers

A

the sodium channels let in too much sodium (more than the cycle allows) ???????????

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26
Q

What is happening in the heart during the P-wave? What phase does this correlate to

A

SA node signals and there is Atrial contraction
-phase 0

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27
Q

What is happening in the heart during the QRS complex? What phase does this correlate to?

A

Depolarization of the ventricles
-phase 0
Repolarization of the ventricles
-start of phase 1

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28
Q

What is happening in the heart during the T-wave? What phase does this correlate to?

A

Ventricular repolarization
phase 3

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29
Q

What type of channels does Calcium come through in phase 2

A

voltage gate L-Type

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30
Q

action potential phase 0

A

upstroke

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31
Q

what is a Reentry Arrhythmias

A

continuous repetitve propagation of an excitatory wave returning to its site of origin

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32
Q

What arrhythmias can reentry cause?

6 total

A

sinus note reentry
atrial flutter
atrial fibrillation
av noda reentry
av reentry using a bypass (AVRT)
ventricular tachyarrhythmias

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33
Q

what types of conduction do reentry arrhythmias rely on

A

critically depressed conduction

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34
Q

reentry arrhythmia

What does steady-state reduction do?

A

reduces the excitatory currents to a level below that required for propagation

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35
Q

reentry arrhythmia

What does prolongation do?

A

prolongs the recovery time of the channels that still reach rested/available state
-increases the effectiveness of the refractory period

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36
Q

what 2 mechanisms of antiarrhythmic agents slow conduction

A
  1. Steady-state reduction in available unblocked channels
  2. Prolongation (refactory period)
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37
Q

What do antiarrhytmic drugs suppress?

A

ectopic automaticity and abnormal conduction

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38
Q

What can happen as antiarrhythmia drug dosage is increased? what does this result in?

A

can depress conduction in normal tissue
result: drug-induced arrhythmias

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39
Q

What can antiarrhytmia drugs become and when?

A

Proarrhythmic
during fast heart rates

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40
Q

What does antiarrhythmic drugs turned proarrhythmic lead to?

A

Acidosis
Hyperkalemia
ischemia within myocardial tissue

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41
Q

What does acidosis do in terms of pharmacological function

A

slows recovery from the block for most drugs

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42
Q

What is Singh-Vaughan Williams classifications

A

method for classifying drug action
4 classes

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43
Q

Singh-Vaughan Williams class 1

A

Action is a sodium channel blockade

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44
Q

singh-vaughn williams classification class 1a MOA

A

prolongs the APD and has intermediate dissociation kinetics

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44
Q

Lidocaine is _____ use in what?

A

Second Use
serious ventricular arrhythmias

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45
Q

What level of toxicity and effectiveness does Lidocaine have in arrhythmias

A

Low incidence of toxicity
high degree of effectiveness

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46
Q

How is Lidocaine administered for arrhythmias

A

IV

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47
Q

What is the MOA of Lidocaine

A

blocks activated and inactivated sodium channelss with rapid kinetics

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48
Q

for Lidocaine

what does the inactivated state block ensure?

A

a greater effect on cells with long action potentials (purkinje fibers or ventricular cells)

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49
Q

What does Lidocaine do to depolarized cells?

A

increases activation and slows unbinding kineticss
results: selective depression of conduction

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50
Q

Why does Lidocaine have to be admisitered patenterally (IV)?

A

extensive first pass hepatic metabolism if given orally

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51
Q

what is the half life of lidocaine

A

1-2 hours

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52
Q

What is the loading dose of lidocaine in adults? How long is it administered over?

A

150-200mg over 15 minutes

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53
Q

What is the maintenance infusion of lidocaine following the loading dose?

A

2-4mg/min

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54
Q

What is the therapeutic plasma level goal of lidocaine once on a maintenance dose?

A

2-6 mcg/mL

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55
Q

What is the loading dose of Lidocaine for adults with ventricular arrhythmias (associated with MI)

A

IV 1.0-1.5 mg/kg

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56
Q

if required, what is the second bolus dose of Lidocaine for ventricular arrhythmias? when can it be administerd

A

0.75-1.5mg/kg
1.5

5-10 minutes after first dose

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57
Q

If the loading doses and first dose don’t work, what bolus dose of lidocain can be administered for ventricular arrhythmias?
what is the timing and max dose?

A

0.5-0.75 mg/kg
every 5-10 minutes
max dose: 3mg/kg

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58
Q

What is the plasma clearance in pts with liver disease? what is the volume of distribution?

A

markedly reduces and volume of distribution is increased

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59
Q

How do you adjust lidocaine dose given to patients with liver disease?

A

maintenance dose is decreased
loading dose is normal

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60
Q

what drugs decrease lidocaine clearance? what impact does this have?

A

Drugs that decrease liver blood flow (propranolol, cimedtidine)
increases toxicity risk

61
Q

Lidocaine is one the ____ cardiotoxic of the current sodium channel blockers

A

least

62
Q

What are symptoms of cardiotoxicity?

A

proarrhythmic effects
SA node arrest
impaired conduction
ventricular arrhythmia

63
Q

What can Lidocaine cause in patients with preexisting heart failure

A

hypotension

64
Q

What type of adverse effects are most common for lidocaine

A

neurological in nature

65
Q

What neurological symptoms occur with lidocaine

A

paresthesia, tremor, nausea, lightheadedness, hearing disturbances, slurred speech, convulsions

66
Q

For lidocaine, what population experiences the adverse neurological effects the most?

A

elderly or vulnerable patiens

67
Q

Two types of more effective B-blocking drugs class two?

A

propranolol and nadolol

68
Q

what type of drug is esmolol

A

short acting b-blocker as an antiarrhytshmic drug for intraoperative and acute arrhythmias

69
Q

MOA of flecainide and the effects (

A

slows conductsion in the cardiac tissue by altering ions
-causes: slight prolongation of refractory periods, decreases rate of rise of AP, increases electrical stimulation threshold, local anesthetic and moderate negative inotropic effects

70
Q

What type of drug class is flecainide

A

class 1c

71
Q

what is the dosage of Flecainide

A

50mg, 100mg, 150mg PO

72
Q

What are indications for Flecainide?

A
  1. paroxysmal A-fib/flutter and paroxysmal SVT
  2. Prevention of ^^ in patients without structural heart disease
  3. prevention of documented life threatening ventricular arrhythmias in pts without structural heart disease
73
Q

for what type of patients is flecainide not reccommended for?

A

less severe ventricular arrhythmias

Why: proarrhytmic effects (the risk doesn’t outweigh the benefit)

74
Q

CI of use of Flecainide (4)

A
  1. hypersensitivity to the drug
  2. pre-existing 2nd or 3rd degree AV block with RBB when associated with L hemiblock
  3. cardiogenic shocck
  4. concurrent use of ritonavir
75
Q

Most common adverse reactions of flecainide?

list 5 general topics

A
  1. dizziness (mc)
  2. visual dis
  3. dyspnea
  4. Cardiovascular (palpation, chest pain, edema, tachycardia, proarrhythmic, sinus node dysfunction)
  5. CNS (headache, fatigue, nervousness, fever, mailaise, hypoesthesia, paresis, ataxia, vertigo etc)
76
Q

what do class three drugs do?

A

prolong the effective refractory period by prolonging the AP

77
Q

what is the MOA of Class three drugs

A
  • blocks potassium channels in cardio muscle or enhances inward sodium channels
  • this prolongs the AP
  • can POSSIBLY cause prolonged Q-T intervals
78
Q

what is the risk of QT interval prlongation

A

ventricular arrhythmias

b/c long QT is an irregularity of the electival activity

79
Q

Are QT interval prolongation complications common or rare?

A

rare

80
Q

How is amiodarone administered

A

IV or Oral

81
Q

What is amiodarone mainly used for?

A

treating serious ventricular arrhythmias

82
Q

What can Amiodarone also be used to treat?

A

Supraventricular arrythmias (like A-fib)

83
Q

What class type is amiodarone? what does this mean the MOA is?

A

Class 3
prolongs the AP duration by blocking IKr

84
Q

what can be blocked secondarly by amiodarone

A

IKs (chronic use)
Inactivated sodium channels

85
Q

What does amiodarone not do?

A

adrenergic action and calcium channel blocking action

86
Q

what is the bioavailability of amiodarone

A

35-65%

87
Q

what is the half life of amiodarone

A

rapid- 3-10 days 50% of drug
this slows down to become several week half lifes

88
Q

After discontinuation, how long does amiodarone stay in the body

A

1-3 months

89
Q

what is the total loading dose of amiodarone? What steps are taken?

A

10g
0.8-1.2g daily dose

90
Q

what is the maintenance dose of amiodarone

A

200-400mg daily

91
Q

What is amiodarone a substrate for?

A

liver cytochrome CYP3A4

92
Q

What impact does inhibatory liver enzyme drugs have on amiodarone

A

increased levels since liver enzyme is decreased

93
Q

In drugs that increase CYP3A4, what happens to amiodarone

A

decreased concentration when coadministered

94
Q

What can amiodarone do to other drugs in the system

A

Increase levels because it blocks liver enzymes which results in drugs staying in the system longer
(statins, digoxin, warfarin)

95
Q

Following the initiation of amiodarone, what should happen to warfarin dose?

A

reduce the warfarin does by 1/3 -1/2
monitor prothrombin times closely

96
Q

In patients with A-fib, what is the dose and result of amiodarone?

A

low dose of 100-200mg/d
maintains normal sinus rhythms

97
Q

what is amiodarone most effective for?

A

PRevention of recurrent ventricular tachycardia

98
Q

what is the first dose of amiodarone for ventricular fib or pulseless VT

A

300s mg IV/IO push

99
Q

what is the second dose of amiodarone for ventricular fibrillation or pulseless VT

A

150 mg IV/IO push

100
Q

For pts with A-fib, heart failure or rapid ventricular response what is amiodarone useful for?

A

controlling the ventricular response

101
Q

What is the adverse side effects of amiodarone on the heart?

A

bradycardia and heart block (in pts with prexisting SA or AV disese)

102
Q

where does amiodarone accumulate in the body?

5 things

A

Heart (MOST COMMON)
lung
liver
skin
tears

103
Q

wha is the most important adverse effect of amiodarone

A

Pulmonary toxicity even in low doses (<200mg)
(may lead to pulmonary fibrosis)

104
Q

What is the adverse effect of amiodarone on the liver?

A

hypersensitivity hepatitis
abnormal liver function tests

105
Q

What is ammiodarone’s impact on thyroid hormones?

A

Blocks T4 and T3 from eachother

106
Q

What class are calcium channel blocking drugs?

A

class 4

107
Q

what drug is the prototype of Class 4 drugs?

A

verapamil

108
Q

What channels does verapamil block?

A

activated and inactivated L-type calcium channels

109
Q

What does verapamil cause in the PV systme?

A

peripheral vasodilation
-beneficial for hypotension and vasospastic disorder

110
Q

what is the MOA of class 4 verapamil

A

-AV nodal conduction and refractory period are prolonged
-slowed SA node (hypotensive action can result in small increase of SA rate)

111
Q

what is the main indication for use of verapamil?

A

Supraventricular tachycardia

112
Q

What is verapamil and adenosine preferred over?

A

older treatments
-propranolol, digoxin, edrophonium, vasoconstriction and cardioversion)

113
Q

what is the agent of first choice for patients in SVT without heart failure or AV/SA nodal disease

A

adenosine

114
Q

what is the agent of second choice for patients in SVT without heart failure or AV/SA nodal disease

A

parenteral verapamil

115
Q

what is the Verapamil dosage (initial and time) and second dose?

A

5mg over 2-5minutes
2nd: 5mg bolus if needed

116
Q

4 drugs that are miscellaneous antiarrhythmic agents?

A

digitalis
adenosine
magnesium
potassium

117
Q

What drug is a nucleoside that occurs naturally in the body?

A

adenosine

118
Q

singh-vaughn williams classification class 1B MOA

A

no effect on APD
-may shorten it
fast dissociation kinetics

119
Q

singh-vaughn williams classification class 1c MOA

A

drugs have no effect on APD and have slow dissociation

120
Q

singh-vaughn williams classification class 2 MOA

A

Sympatholytic
-reduce B-adernergic activity in the heart

121
Q

singh-vaughn williams classification class 3 MOA

A

Manifests as prolongation of the APD
-block the rapid component of the delayed rectifier potassium current IKr

122
Q

singh-vaughn williams classification class 4 MOA

A

Blockade of the cardiac calcium channel
-slows conduction in regions where action potential upstroke is calcium dependent (SA and AV nodes)

123
Q

What drug shares all four classes of action

A

amiodarone

124
Q

Sodium channel blocking drugs (class 1)

A

Procainamide (1a)
Quinidine (1a)
Lidocaine (1b)

Disopyramide (1a)
Flecainide (1c)

125
Q

What is the half life of adenosine in the blood?

A

less than 10 seconds

126
Q

MOA of adenosine

A

activation of inward rectifier K= current and inhibition of calcium current

127
Q

What is the result of Adenosine MOA

A

marked hyperpolarization and suppression of calcium dependent action potentials

128
Q

what is the result of adenosine when administered as a Bolus dose? What does it have less of an effect on?

A

direct inhibitian of AV nodal conduction
-increase in AV nodal refractory period
Less effect: SA Node

129
Q

what condition/situation is adenosine the drug of choice for?

A

conversion of Paroxysmal superventricular tachycardia

130
Q

Why is adenosine the top choice for Paroxysmal SVT conversion?

A

-high efficacy (90-95%)
-short duration of action

131
Q

What is the bolus dose of adenosine administered?

What dose is it followed by?

A

6mg bolus initial dose
followed by a dose of 12mg (1-2 minutes later)

132
Q

How is adenosine administered?

A

Rapid IVP with a 20mL saline flush in a line that is a central line or CLOSE peripheral IV line

133
Q

The presence of what makes adenosine less effective?

A

The presence of adenosine receptor blockers
ex. theophylline, caffeine

134
Q

clinical side effects of adenosine

A
  1. flushing
  2. SOB/bronchospasm
  3. Chest burning
  4. sense of impending doom
    Less: headache, HTN, nausea, paresthesisa
135
Q

Toxicity of adenosine in the body?

A

1.** induction of high grade AV block (short lived). **
2. A-fibb
3. asystole

136
Q

What was magnesium originally used for?

A

Patients with digitsalis-induced arrhythmias who were hypomagnesemic

137
Q

MOA of Magnesium

A

influences the Na+/K+ ATPase, sodium channels, calcium channels, certain potassium channels

138
Q

What is conditions/situations is magnesium indicated for?

A
  1. digitalis induced arrhythmias if hypomagnesemia is present
  2. some patients with torsades de points (serum mag. can be normal)
139
Q

What is the dosage of Magnesium? How is it administered?

A

1g (magnesium sulfate)
administered: IV over 20 minutes
repeated as necessary

139
Q

what are the 2 effects of increasing serum potassium?

A
  1. resting potential depolarizing action
  2. membrane potential stabilizing action (latter caused by increased potassium permeability)
140
Q

What does hypokalemia result in? (in the heart)

A

increased risk of early and delayed after depolarizations and ectopic pacemaker activity (in the presence of digitalis)

141
Q

what is the result of Hyperkalemia

A

Depresses ectopic pacemakers and slows conduction

142
Q

What is required to suppress the SA node?

A

Hyperkalemia

143
Q

8 steps

what is the indepth MOA of Adenosine (adenocard)

A
  1. activates Gi protein
  2. inhibition of adenylate cyclase
  3. decrease cAMP
  4. Deactivation of L-type Ca2+ channels and activation of K+ channels
  5. Lowers Ca2+ and increases K+ efflux
  6. hyperpolarization
  7. transient AV node block (short acting <15 seconds)
  8. acute termination of SVT
144
Q

When should the initial dose of adenosine be reduced? what should it be reduced to?

A

if pt is currently receiving carbamazepine or dipyridamole, has a transplanted heart, or if administered via central line
-3mg bolus followed by saline flush

145
Q

Can potassium effect nerve conduction?

A

Yes

146
Q

When should adenosine be AVOIDED completely? why?

A

-Pts with suspected pre-excitation tachycardia
-it may exacerbate the tachycardia via accessory pathway routes.

147
Q

4 contraindications to adenosine

A
  1. pre-excitation syndrome (antidromic AVRT, WPW)
  2. AV block
  3. Asthma
  4. Theophylline or caffeine usage
148
Q

WPW

A

wolff-parkinson-white syndrome
-congenital heart defect causes arrhythmias

149
Q
A

pharmacology (32 decks)

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