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Pharm2 Mod 1: > Mod 1 Lecture 2: anti-arrhythmic therapies > Flashcards

Mod 1 Lecture 2: anti-arrhythmic therapies Flashcards

1
Q

what node produces an electrical impulse at regular internals that allows for cardiac contractions

A

SA Node

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2
Q

what is an arrhythmia

A

electrical activity that deviates from the previous description as a result of an abnormality in impulse initiation and/or impulse propagation

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3
Q

what are the treatment options for arrhythmias

A

pharmacotherapy, pacemakers, cardioversion, catheter ablation and surgery can be pursued

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4
Q

what are the mechanisms of arrhythmias

A

disturbances in impulse formation
disturbances in impulse conduction

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5
Q

what is depolarization

A

when the cells of the heart are activated

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6
Q

what is repolarization

A

when the cells of the heart are at rest

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7
Q

when should treatment of arrhythmias be avoided in general

A

asymptomatic or minimally symptomatic arrhythmias

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8
Q

How do arrhythmias arise?

A

ischemia ( as well as scarred or diseased tissue)
hypoxia
acidosis or alkalosis
electrolyte disturbances (potassium, calcium and chloride)
excessive catecholamine exposure (illicit drugs or excess adrenaline, cortisol, etc)
autonomic influences
Drug toxicities

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9
Q

what is the P wave

A

atrial depolarization

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10
Q

what is the T wave

A

ventricular repolarization

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11
Q

what is depolarized during the QRS complex

A

ventricular depolarization

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12
Q

what ions are involved during cardiac action potential

A

Na+
K+
Ca+

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13
Q

what is cardiac action potential

A

change in voltage across myocardial cells
involves movement of ions across cell membranes

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14
Q

what occurs at phase zero of the fast AP

A

Influx of Na+ and a spike from negative voltage to positive

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15
Q

what occurs at phase one of the fast AP

A

K+ and Cl- out

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16
Q

what occurs at phase 2 of the fast AP

A

Ca2+ in and K+ out

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17
Q

what occurs at phase 3 of the fast AP

A

K+ outward and decrease in voltage back to negative

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18
Q

what occurs at phase 4 of the fast AP

A

K+ with a net negative change of -96mV

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19
Q

what regulates the pacemaking activity

A

both parasymathetic and sympathetic activity

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20
Q

what are latent pacemaker cells

A

purkinje cells that demonstrate slow phase 4 depolarization
cells that take control of packing of the heart when SA node conduction/impulse generation is impaired - leads to disturbed impulses

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21
Q

when do Early Afterdepolarizations (EADs) occur

A

during phase 3 of action potential

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22
Q

when do delayed afterdepolarizations (DADs) occur

A

during phase 4 of action potential

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23
Q

what usually triggers EADs

A

factors that prolong action potential duration in the ventcile -> leads to QT prolongation -> torsades de pointes, tachycardia and other arrhythmias

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24
Q

what is QT prolongaction

A

caused by a blockage of rapidly activating delayed rectifier potassium channels
can be intrinsic (congenital) or extrinsic (some drugs can cause)
slow HR and hypokalemia can exacerbate states of long QT syndrome which is life threatening

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25
Q

when does DADs occur

A

when there is excess accumulation of intracellular calcium - especially at fast heart rates and can lead to ventricular tachycardia

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26
Q

what are possible triggers of DADs

A

digital toxicity
excess catecholamines
myocardial ischemia

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27
Q

what are disturbances of impulse conduction

A

most common form affecting AV note - results in various degrees of heart block
AV node is under tonic influence of PNS to slow conduction - anti-muscarinic agent like atropine can sometimes relieve heart block

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28
Q

what are the varied responses of impulse conduction disturbances

A

from slowing impulse prolongation to complete heart block (no conduction from atria to ventricles)
in complete heart black - latent purkinje pacemaker cells dictate ventricular rate

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29
Q

what is re-entry of impulse conduction disturbances

A

a serious form of conduction abnormality
one impulse re-enters and excites area of the heart more than once
paths of re-entry can be very small or involve large portions of atria or ventricles
arrhythmia from re-entry can be from a few extra beats to sustained tachycardia

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30
Q

what is Wolff-Parkinson-White Syndrome

A

re-entry circuit of atrial tissue, AV node, ventricular tissue, accessory AV connection

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31
Q

what can generate “daughter impulses”

A

re-enty arrhythmia -> VT or Afib

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32
Q

what is the clinical presentation of enhanced automaticity

A

(impulse formation)
acceleration of AP thru normal or abnormal cardiac tissue (ST, AT)

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33
Q

what is the presentation of triggered activity

A

abnormal AP triggered by preceding AP (early or delayed afterdepolarization)
AF, VT

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34
Q

what is the presentation of re-entry

A

impulse fails to die out after normal activation (usually related to an obstacle and availability of another circuit - bypass to normal conduction)
AVNRT (atrial ventricular nodal re-entry tachy) or Wolff-parkinsons-white (WPW)

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35
Q

what are types of arrhythmias

A

atrial fibrillation
atrial flutter
AV nodal re-entry (SVT)
Ventricular fibrillation
Ventricular tachycardia

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36
Q

What are the classes of anti-arrhythmic agents

A

Class 0
Class 1: action is sodium channel blockade
Class 2: action is sympatholytic
Class 3 : action manifests as prolongation of AP duration.
Class 4: action is blockade of the cardiac calcium current.

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37
Q

what is the action of class 1 anti-arrhythmic agents

A

action is sodium channel blockade. these drugs have effects on the action potential duration

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38
Q

what is the action of class 2 anti-arrhythmic agents

A

action is sympatholytic. drugs with this action reduce beta-adrenergic activity in the heart.

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39
Q

what is the action of class 3 anti-arrhythmic agents

A

action manifests as prolongation of the action potential duration. most drugs with this action block the rapid component of the delayed rectifier potassium current, I Kr

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40
Q

what is the action of class 4 anti-arrhythmic agents

A

action is blockade of the cardiac calcium current. the action slows conduction in regions where the action potential upstroke is calcium dependent, SA and AV nodes

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41
Q

What is class 1a drugs

A

sodium channel blockade, prolonged refractoriness
Quinidine
Disopyramide
Procainamide

42
Q

what is class 1b drugs

A

sodium channel blockade, little effect on refractoriness
Lidocaine
phenytoin
mexilitine

43
Q

what is class 1c drugs

A

sodium channel blockade, slight prolongation of refractoriness
flecainide
proprafenone

44
Q

what are class 0 drugs

A

blocks HCN4 (hyper-polarization - activated cyclic nucleotide - gated) the If (funny channel)
Ivabradine (corlanor)

45
Q

What is ARP

A

absolute refractory period
time during which another stimulus will not lead to another AP

46
Q

what is RRP

A

relative refractory period
interval following ARP in which a 2nd stimulus is inhibited, but not impossible

47
Q

what is ERP

A

Effective refractory period (ERP)
time in which a cell does not produce a new AP (phase 0,1,2,3)

48
Q

What class of drugs are used to treat sinus tachycardia

A

Class II, IV
other underlying causes may need treatment

49
Q

what class of drugs are used to treat afib/flutter

A

Class IA, IC, II, III, IV digitalis
ventricular rate control is important goal; anticoagulation is required

50
Q

what class of drugs are used to treat paroxysmal supraventricular tachycardia

A

class IA, IC, II, IIII, IV adenosine

51
Q

what class of drugs are used to treat AV block

A

Atropine
acture reversal

52
Q

what class of drugs are used to treat ventricular tachycardia

A

Class I, II, III

53
Q

what class of drugs are used to treat premature ventricular complexes (PVC)

A

Class II, IV
magnesium sulfate
PVS are often benign and do not require treatment

54
Q

what class of drugs is used to treat digitalis toxicity

A

class IB
magnesium sulfate

55
Q

What are the two primary class 1A agents

A

Quinidine
Procainamide

56
Q

what is Quinidine

A

class 1A drug
uncommon med
primarily used in Atrial, AV junction and ventricular tachyarrhythmias
Oral

57
Q

what are the adverse effects of Quinidine

A

blurry vision, tinnitus, headache and psychosis

58
Q

what was Quinidine previously used for

A

treatment of malaria

59
Q

what is procainamide

A

class 1A drug
IV ONLY
atrial/ventricular arrhythmias
not in common use
can be used in tx of hemodynamically stable, sustained monomorphic ventricular tachycardia

60
Q

what is the adverse effects of procainamide

A

hypotension

61
Q

what are the affects of class 1A agents

A

sodium channel blockade

62
Q

what are the affects of class 1B agents

A

block activated and inactivated sodium channels with rapid kinetics
additionally shorten phase 3 depolarization and decrease the duration of the action potential
have greater effect on cells with long AP compared to atrial cells

63
Q

what are the two class 1B agents commonly used

A

Lidocaine
mexiletine

64
Q

what is lidocaine

A

class 1B agent
IV only
can be used to terminate ventricular tachycardia/fibrillation and prevention of Vfib after cardioversion in setting of acute ischemia
little to no affect on atrial or AV junction arrhythmias

65
Q

what is mexiletine

A

class 1b agent
used in chronic (preventive) treatment of ventricular arrhythmias (in pts prone to VT)

66
Q

what are the adverse effects of Lidocaine

A

mostly CNS changes (nystagmus, drowsiness, slurred speech)

67
Q

what are the adverse effects of mexiletine

A

N/V; has narrow Therapeutic Index

68
Q

what are the effects of class 1C agents

A

slowly dissociate from resting sodium channel in Purkinje and myocardial fibers causing marked slowing of PHase 0 depolarization
considered contraindicated in pts with structural heart disease

69
Q

what are the two class 1C agents

A

Flecainide
Propafenone

70
Q

what is flecainide

A

class 1C agent
potent blocks of sodium and potassium cahnnels with slow unblocking kinetics
can be effective in suppressing premature ventricular contractions
oral only
“pill-in-pocket” for pts with paroxysmal afib; rarely used as primary prevention against SVT, PVCs given its toxicity

71
Q

what can Flecainide cause

A

severe exacerbation of arrhythmias in pts with pre-existing ventricular tachyarrhythmias and those with previous MI and ventricular ectopy

72
Q

what is propafenone

A

class 1C agent

73
Q

what is propafenone

A

class 1C agent
used primarily to control rhythm in atrial arrhythmia including flutter and afib)
also used to prevent paroxysmal SVT in pts with AV re-entrant tachycardia (AVRT)

74
Q

what are the adverse effects of Propafenone

A

beta-blocking effects, so can cause bronchospasm; beware of use in asthmatics

75
Q

what are the adverse effects of flecainide

A

blurry vision and nausea

76
Q

what are class 2 agents

A

beta-blockers
diminish phase 4 depolarization to prolong AP
decrease impulse automaticity, chronotrophy, dromotropy, and inotropy
useful primarily in treating tachyarrhythmias caused my increase sympathetic activity

77
Q

what are class 2 agents less effective at treating

A

ventricular ectopy than sodium channel blockers (class 1 agents), but can be used to prevent recurrent infarction and sudden death due to ventricular arrhythmias in pts recovering from acute MI

78
Q

what are the different class 2 agents used

A

Metropolol
Propranolol
Esmolol

79
Q

what is metropolol

A

class 2 agent
cardioselective beta-blocker, most widely used in tx of cardiac arrhythmias
Oral, IV preparations available

80
Q

what is propranolol

A

non-selective beta blocker
IV, Oral available

81
Q

what is esmolol

A

very short acting, fast onset beta-blocker used to abort acute arrhythmias
IV only

82
Q

what are the effects of class 3 agents

A

prolong AP primarily by blocking potassium channels in cardiac muscles (results in a prolonged effective refractory period)
need to be used with extreme care; can increase risk of torsades de pointes
most drugs in this class cause QT prologation

83
Q

what are common class 3 agents

A

amiodarone
Dronedarone
Sotalol

84
Q

what is amiodarone

A

class 3 agent
many effects; including prolongation of AP, sodium channel-blockade, adrenergic and calcium channel antagonism
oral or IV
used to treat hemodynamically stable sustained monomorphic ventricular tachy as well as pulseless VT/VF
highly effective for treating or preventing SVT, esp Afib

85
Q

what is amiodarone toxicity

A

symptomatic bradycardia and heart block in pts with known sinus or AV nodal disease
causes peripheral vasodilation - > hypotension
pulmonary fibrosis
thyrotoxicity and hepatotoxicity
often avoided as long-term agent in YOUNGER patients

86
Q

what is dronedarone

A

class 3 agent
oral medciation; only clinical use is to maintain NSR in pts with atrial arrhythmias
less effective than amiodarone

87
Q

what patients is dronedarone contraindicated in

A

patients with symptomatic HF

88
Q

what is sotalol

A

nonselective beta blocker
used to treat life-threatening ventricular arrhythmias (ACLS algorithm)
used for cardioversion to and maintenance of sinus rhythm in patient with Afib

89
Q

what are the effects of class 4 agents

A

non-dihydropyridine calcium cannel blockers
their activity slows phase 4 spontaneous depolarization and slows conduction in tissues dependent on calcium currents (AV and SA nodes)
major effect of these agents is on vascular smooth muscles and heart
useful in treating atrial more than ventricular arrhythmias and reentrant SVT

90
Q

what are the class IV agents

A

verapamil and diltiazem

91
Q

what is verapamil

A

class 4 agent
used to terminate supraventicular tachycardia (IV)
also used for rate control in Afib and flutter (IV, oral forms) but rarely is able to convert from atrial flutter/fibrillation to NSR

92
Q

what is diltiazem

A

class 4 agent
similar in efficacy to verapamil for managing supraventricular arrhythmia
works well to control Afib; similar efficacy for converting AF to NSR
IV and oral forms available

93
Q

what are other non-categorized agents for arrhytmias

A

Digoxin
Adenosine
atropine

94
Q

what is digoxin

A

inhibits sodium/potassium - ATPase pump which shortens refractory period in atrial and ventricular myocardial cells or prolongs the refractory period and diminishes conduction velocity in the AV node
control ventricular response rate in Afib/flutter
narrow therapeutic index
need to be “loaded”, either IV or orally prior to maintenance dosing

95
Q

what is adenosine

A

used to inhibit AV nodal conduction and increase AV nodal refractory period
IV
drug of choice for prompt conversion of paroxysmal SVT to sinus rhythm
Flushing, SOB, chest pain are not uncommon side effects

96
Q

what is atropine

A

anti-muscarinic agent can be used IV form to abort life-threatening bradycardia including: symptomatic bradycardia due to medication toxicity/overdose, second degree heart block, complete heart block)

97
Q

what is the goal of treating Afib

A

relieve patient symptoms and prevent complications of thromboembolism and tachycardia - induced heart failure

98
Q

what are the objectives of treating Afib

A

initial treatment is objective= control of ventricular rate
- first line: CCB alone or in combination with adrenergic blocker
Second objective = restoration and maintenance of normal sinus rhythm

99
Q

in the US what is the first choice therapy for rhythm control

A

DC cardioversion (shock)

100
Q

what is the first line agent for patients with heart failure with low ejection fraction(EF) and/or hypertension

A

amiodarone to maintain NSR

101
Q

what is the first line treatment for a patient with CAD

A

Sotalol

102
Q

what are the mainstay treatments for patients with mild heart disease that do not revert to NSR with cardiac ablation and/or have established persistent Afib

A

Flecainide or Sotalol are mainstay
amiodarone is used if these fail

Pharm2 Mod 1: (3 decks)

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