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Pharm term 2 module 1 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

What does the SA node do

A

Electrical impulse at regular intervals that allow for contraction

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2
Q

What is the frequency of the SA node

A

60-100

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3
Q

What happens when the pulse leaves the SA node

A

spreads through atria
enters the AV node

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4
Q

What is the AV node

A

The conduction pathway between atria and ventricle

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5
Q

What structure propagates the impulse to all parts of the ventricle

A

Purkinje fibers

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6
Q

What does premature ventricular depolarization cause

A

Ventricular fibrillation

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7
Q

What are the two mechanisms of arrhythmias

A

Disturbance in impulse formation

Disturbance in impulse conduction

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8
Q

What occurs in the heart during depolarization

A

heart cells are activated

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9
Q

What occurs in the heart during repolarization

A

Cells of the heart are at rest

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10
Q

What is occurring in the heart during the P wave

A

Atrial depolarization

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11
Q

What is occurring in the heart during the T wave

A

Ventricular repolarization

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12
Q

What electrolytes are involved with cardiac action potential

A

Ca2+
Na+
K+

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13
Q

When are the atria re-polarized

A

During the QRS complex (Ventricular contraction)

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14
Q

How do disturbed impulses present

A

Early afterdepolarization (EAD)

Delayed after depolarization (DAD)

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15
Q

When does EAD occur

A

Phase 3

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16
Q

When does DAD occur

A

Phase 4

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17
Q

What causes EAD

A

Triggered by factors that prolong action potential duration in the ventricle

leads to QT prolongation

which ends up as tachycardia, Torsades de pointe, or other arrhythmias

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18
Q

What causes QT prolongation specifically

A

Blockage of rapidly activation delayed rectifier K+ channels

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19
Q

What is intrinsic QT prolongation

A

Congenital

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20
Q

What is extrinsic QT prolongation

A

Drugs or external factors cause QT prolongation

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21
Q

What issues can exacerbate states of long QT syndrome

A

Slow heart rate and hypokalemia

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22
Q

What causes DADs

A

Excess accumulation of intracellular calcium (esp. at fast heart rates)

Can lead to V-Tach

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23
Q

What are some triggers of DADs

A

Digoxin toxicity
excess catecholamines
MI

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24
Q

What node is commonly effected by disturbances in impulse conduction and what is the end result

A

AV node

Various degrees of heart block result

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25
What is occurring during complete heart block
There is no conduction from the atria to the ventricles
26
Why can anti-muscarinic agents sometimes help with heart block
b/c AV node is always under influence of parasympathetic system... allows atropine to sometimes be helpful
27
What is re-entry conduction
Impulse re-enters and excited an area of the heart more than once -can be small or large
28
Which disease is characterized by re-entry circuit of atrial tissue, AV node, ventricular tissue, and accessory AV connection
WPW Wolfe Parkinson White syndrome
29
What is enhanced automaticity
Acceleration of AP thru normal or abnormal cardiac tissue
30
How does triggered activity with impulse conduction present clinically
A fib V tach
31
How do re-entry conductions present clinically
Impulse fails to die out after normal activation AVNRT WPW
32
What are the types of arrhythmias
Atrial fibrillation atrial flutter AV node re-entry (SVT) Ventricular fibrillation Ventricular tachycardia
33
How many classes of anti-arrhythmics are there
4
34
What is the MOA of class 1 anti arrhythmic
Sodium channel blockade - effect action potential
35
What is the MOA of class 2 anti- arrhythmics
Sympatholytic Reduce beta adrenergic activity in the heart
36
What is the MOA of class 3 anti-arrhythmics
Manifests as a prolongation of the action potential duration block the rapid component of the delayed rectifier K+ current
37
What is the MOA of class 4 anti arrhythmics
Blockade of cardiac Ca+ current Slows conduction in regions where the Ap upstroke is Ca+ dependent (SA & AV) node
38
What are the classifications of sodium channel blockers
A (moderate) B (weak) C (strong)
39
What are the beta blockers for class 2
Propranolol esmolol Metoprolol
40
What are the K+ channel blockers in class 3
Amiodarone Ibuttiide Dofetilide Sotalol
41
What are the Ca+ channel blockers for class 4
Verapamil Diltiazem
42
What is the absolute refractory period (ARP)
Time during which another stimulus will not lead to another AP
43
What is the relative refractory period (RRP)
Interval following ARP in which a 2nd stimulus in inhibited, but not impossible
44
What is the effective refractory period (ERP)
Time in which a cell does not produce a new AP (Phase 0,1,2,3)
45
In someone who has sinus tachycardia, what drug class will you use to treat them
Class II and IV
46
If someone has Afib or A flutter, what drug class will you use to treat them
Class 1A, 1C, II, III, IV, digoxin *ventricular rate control is important goal and anticoagulant is required
47
What class of drugs will you use to treat someone with paroxysmal SVT
Class IA, IC, II, III, IV or adenosine
48
How would you treat someone with an AV block
Atropine *break parasympathetic hold on the node
49
How would you treat someone with VTach
Class I, II, III
50
How would you treat someone with PVCs IF they need treatment
Class II, IV, Magnesium
51
And how would you treat someone who is in digoxin toxicity
Class IB Magnesium sulfate
52
What drugs are class IA anti arrhythmics
Quinidine Procainamide Disopyramide
53
What is the MOA of class IA drugs
Blocks cardiac Na+ channels -decrease conduction velocity and delayed depolarization
54
What is the use for Quinidine
Broad spectrum agent against SVT and ventricular dysrhythmias *primary indication is long term suppression of SVT, Aflutter, Afib, and sustained VT
55
When is procainamide used
Acute atrial or ventricular arrhythmia -can tx WPW -largely replaced by amoiderone
56
What are the class IB anti arrhythmics
Lidocaine Mexiletine
57
When is Lidocaine used in the cardiac problems
Used ONLY for short term treatment of ventricular dysrhythmias -particularly prevention of fib after cardioversion
58
When is mexiletine used
Oral analogue of lidocaine used for chronic tx of ventricular dysrhythmias
59
What is the MOA of class IB agents
-Blocks the Na+ channels -decrease conduction(AP) -greater effect on cells with long AP (not atrial cells) -shorten phase 3
60
What are the class IC agents
Flecinide Propafenone
61
What is the MOA of IC cardiac agents
Block Na+ and K+ channels -slowly dissociate from resting sodium channels in purkinje and myocardial fibers -slows phase 0 depolarization *contraindicated in those with heart disease
62
When is flecinide used
Maintenance therapy for supra ventricular dysrhythmia (Afib etc)
63
When is propafenone used
Maintenance therapy of atrial arrhythmias -can prevent paroxysmal SVT in patients with AVRT
64
When is metoprolol used
Most widely used beta blocker in the treatment of cardiac arrhythmias
65
What is the MOA for metoprolol
Selectively antagonizes beta 1 receptors
66
What is the MOA for propranolol
Nonselective beta blocker -decreases the rate at which the SA nose fired -red conduction velocity in AV node
67
When is propranolol used
Very useful for tx of dysrhythmias caused by excessive sympathetic stimulus. -Sinus tachy -Severe recurrent VT -Paroxysmal atrial tachycardia from emotion / exercise
68
When is esmolol used
Immediate treatment of ventricular rates in patients with Supraventricular arrhythmias only
69
What is the MOA of Esmolol
Cardioselective beta-1 blocker -decrease rate at which SA node fires
70
What is the MOA of Amiodarone
K+ blocker -delayes depolarization of fast potentials -Na+ and Ca+ channel blockade as well
71
What is the MOA of Sotalol
Nonselective beta blocker and K+ channel blocker
72
When is Sotalol used
Life threatening ventricular dysrhythmias cardioversion and maintenance of NSR in patients with afib *not commonly used because a loading dose while inpatient is required
73
When is amiodarone used
Highly effective against both atrial and ventricular dysrhythmias
74
What is the MOA of Dronederone and Dofetilide
K+ channel blocker -delays depolarization of fast potentials
75
When is Dronedarone used
Maintain NSR in patients with aflutter and afib
76
When is Dofetilide used
Highly symptomatic atrial dysrhythmias
77
What is the MOA of class 4 agents
Ca2+ channel blocker -slows SA nodal automaticity -delays AV nodal conduction -reduces myocardial contractility
78
When is verapamil used
Slow ventricular rate afib/flutter -terminate SVT caused by an AV nodal reentrant circuit *Rate controlling drug
79
When is diltiazem used
Slow ventricular rate afib/flutter -terminate SVT caused by an AV nodal reentrant circuit *IV form often given in ER for afib with RVR
80
When is Digoxin used
Primary indication is HF -also used in the tx of supra ventricular tachydysrhythmias
81
When is Adenosine used
DOC for termination Paroxysmal SVT -WPW syndrome
82
When is atropine used
Aborts life threatening second degree/complete heart block
83
What is the MOA of atropine
Competitive blockade at muscarinic receptors
84
What is the MOA of adenosine
Decrease automaticity in SA node and greatly slows conduction through AV node Inhibits cAMP-induced calcium influx
85
What is the MOA of Digoxin
Inhibits Na+/K+/ ATPase pump -shortens refractory period in atria and ventricles and prolongs refractory period in AV node
86
What are the adverse effects of Quinidine
Cinchonism (Tinnitus, HA, Nause, vertigo, psychosis) -hypotension -widen QRS complex & prolonged QT interval -Drug interactions w/ digoxin & class 3 agents
87
What are some adverse effects of procainamide
SLE-like effects -hypotension -widen QRS complex and prolonged QT interval
88
What are the adverse effects of lidocaine
Drowsiness -confusion -paresthesias -toxic dose can cause seizures and respiratory arrest
89
What are the adverse effects of Mexiletine
N/V and neurologic side effects
90
What are some of the adverse side effects of Flecainide
Widen QRS Prolonged PR Contraindicated in those with structural heart damage
91
What are the pharmacokinetics of Mexiletine
Hepatic narrow TI
92
What are the pharmacokinetics of Lidocaine
IVV only Rapid hepatic metabolism plasma levels easily controlled
93
What are the adverse effects of Propafenone
N/V bronchospasm widen QRS prolonged PR can cause HF
94
What are the adverse effects of Metoprolol
Bradycardia reduced cardiac output AV heart block Prolonged PR
95
What are the adverse effects of propranolol
Heart failure AV heart block Sinus arrest Hypotension bronchospasm prolonged PR
96
What are the adverse effects of esmolol
Prolonged PR Hypotension bradycardia heart block HF
97
What are the pharmacokinetics of esmolol
IV infusion only very short half life (9min)
98
What are the adverse effects of sotalol
Bradycardia AV block prolonged QT and PR CAN TRIGGER TORSADES
99
What are the adverse effects of amioderone
Lung fibrosis visual impairment thyroid toxicity hypotension hepatotoxicity avoid in younger patients Widen QRS
100
What are the pharmacokinetics of amioderone
Metabolized by liver very long half life (20-100 days) oral or IV
101
What are the adverse reactions of dronedarone
Diarrhea skin reactions weakness hepatotoxicity can trigger torsade Contraindicated and those with HF
102
What are the pharmacokinetics of dronedarone
Shorter half life than amioderone (24 hours)
103
What are the adverse reactions of dofetilide
Prolonged QT can trigger Torsades
104
What are the adverse effects of verapamil
Bradycardia AV block heart failure hypotension peripheral edema constipation *adjust for renal impairment
105
What are the adverse effects of Diltiazem
Bradycardia AV block HF peripheral edema
106
What are the adverse effects of Digoxin
Cardiotoxicity N/V visual disturbances
107
What are the adverse effects of adenosine
Prolonged PR interval Sinus Brady Dyspnea Facial flushing chest discomfort / pain
108
What are the adverse effects of atropine
Xerostomia blurred vision photophobia incr. intraocular pressure Urinary retention anhidrosis tachycardia asthma
109
What are the pharmacokinetics of Atropine
Parenteral admin
110
What are the pharmacokinetics of Adenosine
IV bolus as close to the heart as possible Very short half life (1-10 seconds)
111
What is the pharmacokinetics of Digoxin
Oral / IV Narrow TI Need loading dose

Pharm term 2 module 1 (3 decks)

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