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Yr 2 Sem 2 CPT > 3.1 Cardiac Arrhythmia Drugs > Flashcards

3.1 Cardiac Arrhythmia Drugs Flashcards

(90 cards)

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1
Q

Arrhythmias can be due to disturbances in..

A

Pacemaker impulse formation
Contraction impulse conduction
Combination

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2
Q

What is the consequence of arrhythmia?

A

Rate or timing of contraction of heart muscle that is insufficient to maintain normal cardiac output

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3
Q

What is the effect of drugs that block Na channels? Fast

A

Slowing of conduction in tissue (phase 0)
Upslope of AP offset to the right
Minor effects on duration of AP

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4
Q

What effect do beta blockers have in the AP? Fast

A

Diminish phase 4 depolarisation and automaticity
Affects the plateau
Increases duration slightly

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5
Q

What is the effect of potassium blocking drugs on AP? Fast

A

Increase duration

Because increases refractory period

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6
Q

What effect can calcium blockers have on AP? Fast

A

Decrease calcium inward currents
Results in decrease of phase 4 spontaneous depolarisation
Effects plateau phase

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7
Q

What effect can calcium channel blockers have on slow cardiac AP?

A

Decreased slope of phase 0

Prolonged refractory period

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8
Q

Name some drugs that effect automaticity

A

Beta agonists increase slope

Muscarinic agonists and adenosine decrease slope

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9
Q

Where can fast action potentials be found?

A

Cardiac tissue

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10
Q

Where can slow action potentials be found?

A

SAN or AVN

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11
Q

What two types of rhythms can be generated by abnormal impulse generation?

A

Automatic and triggered

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12
Q

What can automatic rhythms lead to?

A

Enhanced normal automaticity and ectopic focus

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13
Q

What can triggered rhythms lead to?

A

Delayed after depolarisation and early after depolarisation

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14
Q

Name two types of abnormal conduction

A

Conduction clock

Reentry

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15
Q

What is conduction block and how is it treated?

A

When impulse isn’t conducted from atria to ventricles

Treated by pacemakers

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16
Q

Name a location in the heart where there could be an accessory pathway in WPW

A

Bundle of Kent

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17
Q

What is a condition caused by abnormal anatomical conduction?

A

Wolf Parkinson white syndrome

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18
Q

What is the affect of scarred heart tissue on depolarisation?

A

Causes a functional block of depolarisation

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19
Q

What do you want to do to the slop of the AP in abnormal generation of rhythms ? Which class of drugs?

A

Decrease of phase 4 slope
Raises the threshold
Give calcium channel blocker
Harder to generate rhythm

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20
Q

What three things can antiarrhythmic Drugs be used to do?

A

Decrease conduction velocity
Change the duration of ERP
Suppress abnormal automaticity

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21
Q

Name some class 1a agents?

A

Procainamide, quinidine, disopyramide

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22
Q

How can class 1a agents be given?

A

Oral or IV

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23
Q

What effects do class 1a agents have in cardiac activity?

A

Decreased conduction (decrease phase 0)
Increase refractory period
Decreased automaticity
Increase Na threshold

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24
Q

What effects may class 1a agents produce on ECG?

A

Increased QRS,

increased QT

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25
What channel do class 1a agents block?
Sodium
26
Two uses of quinidine
Maintain sinus rhythm in AF and flutter and prevent reoccurrence Brugada syndrome
27
Use of procainamide
Acute IV treatment of supraventricular and ventricular arrhythmias
28
Side effects of class 1a agents
``` Hypotension - duento recpduced CO Proarrhythmia Dizzy, confused, insomnia, seizure GI effects Lupus like syndrome especially procainamide ```
29
Name some class 1b agents and the route of administration
Lidocaine - IV | Mexiletine - oral
30
Effects of class 1b agents on cardiac activity
``` Fast binding offset kinetics No change in phase 0 in normal tissue APD slightly decreases in normal tissue Increased Na threshold Decreased phase 0 conduction in fast beating or ischaemic Tissue ```
31
Effects on ecg of class 1b agents
None in normal tissue | Increased QRS in fast beating or ischaemic
32
Uses of 1b agents
Ventricular tachycardia | Not used in atrial arrhythmias or av junctions arrhythmias
33
Advantage of class 1b agents over class 1a
Less pro arrhythmic as less QT effect
34
Side effects of class 1b agents
Dizzy, drowsy | Abdominal upset
35
Name some class 1c agents and their route of administration
Flecainide and propafenone | Oral or IV
36
Effect of class 1c agents on cardiac activity
Very slow binding offset kinetics Substantial decrease in phase 0 Na Decrease automaticity so increased threshold Increased apd (k) and increased refractory period
37
Effect of class 1c agents on ecg
Increased PR, QRS and QT
38
What are some uses for class 1C agents?
Supraventricular arrhythmias (fibrillation and flutter) Premature ventricular contractions Wolff-Parkinson-White Syndrome
39
What are some side effects of class 1c agents?
Proarrhythmia and sudden death Increases the ventricular response to supreventricular rhythms (flutter) CNS and GI effects
40
Why should you avoid using a class 1C agent in flutter?
They increase the ventricular response to the flutter so need to block the AVN with another drug if using these drugs
41
Name some class II agents?
Propranolol, bisoprolol, metoprolol, esmolol
42
How can propanolol be administered?
IV and oral
43
Which class II agent can be given IV only?
Esmolol
44
What are the cardiac effects of Class II agents?
Increased APD and refractory period in AV node to slow AV conduction velocity Decrease phase 4 depolarisation - catecholamine dependent
45
What effects can be seen on the ECG due to class II agents?
Increase PR | Decrease HR
46
Uses of Class II agents
Treat sinus and catecholamine dependent tachycardia Converting re-entrant arrhythmias at AVN Protect ventricles from high atrial rates due to slowing of conduction at AVN
47
Side effects of class II agents
Bronchospasm | Hypotension
48
When should Class II agents not be used? Why?
In partial AV block or ventricular heart failure | As it will further increase the AV block
49
Name some class III agents
Amiodarone, sotalol
50
Why is amiodarone very effective?
Because it effects all phases of action potential
51
What are the cardiac effects of amiodarone?
``` Increase refractory period and ADP (K+) Decrease phase 0 and conduction (Na+) Increase threshold Decrease phase 4 (B block and Ca block) Decrease speed of AV conduction ```
52
Effects on ECG of amiodarone
Increase PR, QRS, QT | Decrease HR
53
Why is amiodarone useful for very wide spectrum?
Very fat soluble
54
Which drug has side effects which increase with time?
Amiodarone
55
Name some side effects of amiodarone
``` Pulmonary fibrosis- breathess Hepatic injury Increase LDL cholesterol Thyroid disease (hypo or hyper) Photosensitivity Optic neuritis - transient blindness ```
56
Which drugs may need to be reduced or monitored more if taking amiodarone?
digoxin and warfarin
57
How is sotalol administered?
Oral
58
Cardiac effects of sotalol
Increased APD and refractory period in atrial and ventricular tissue Slow pahse 4 (B blocker) Slow AV conduction
59
ECG effects of sotalol
Increase QT - effects K channels | Decrease HR
60
Uses of sotalol
Wide spectrum | Supracentricular and ventricular tachycardia
61
Side effects of sotalol
Pro-arrhythmia, fatigue, insomnia
62
Why is sotalol pro-arrhythmic?
It effects QT interval
63
Name some class IV agents
Verapamil, dilltiazem
64
Cardiac effects of class IV agents
Slow conduction through AV (Ca++) Increase refractory period in AVN Increase slope of phase 4 in SA to slow HR
65
Effects of class IV agents on ECG
``` Increase PR (dec conduction through AVN) Increase or decrease HR depending on bloop pressure response and baroreflex ```
66
Uses of Class IV
Control ventricles during supra ventricular tachycardia | Convert supraventricular tachycardia (reentry around AVN)
67
When should caution be used in prescribing class IV agents?
Partial AV block | Hypotension, decreased CO or sick sinus
68
What is the relevance of the type of administration of adenosine?
Rapid IV bolus Very short half life - seconds Stops conduction at AVN for 20 seconds whilst drugs gets metabolised
69
What is the mechanism of action of adenosine?
Binds A1 receptors and activates K currents in AVN and SAN Decreases APD, hyperpolarisation causing decreased HR Decrease Ca current = Increased refractory period at AVN
70
What are the effects of adenosine on the heart?
Slows AVN conduction
71
Uses of adenosine
Convert re-entrant supravenricular arrhythmias Hypotension during surgery Diagnosis of coronary artery disease by looking for perfusion defects
72
How is vernakalant administered?
IV bolus over 10mins
73
Mechanism of action of vernakalant
Blocks ATRIAL specific K channels
74
What are the cardiac effects of vernakalant?
Slows atrial conduction | Increased potency with higher heart rates
75
Side effects of vernakalant
Hypotension, AV block | Sneezing and taste disturbances
76
Uses of vernakalant
Convert RECENT onset AF to normal sinus rhythm
77
What is the mechanism of action of Ivabradine?
Blocks If ion current which is highly expressed in sinus node
78
What are the cardiac effects of ivabradine?
Slows the sinus node | Doesn't effect BP
79
Uses of ivabradine
Reduce inappropriate sinus tachycardia | Reduce HR in angina and HF
80
What group of drugs does digoxin belong to?
Cardiac glycosides
81
What is the mechanism of action of digoxin?
Enhances vagal activity | Slows AV conduction and slows HR
82
How does digoxin enhance vagal activity?
Increase K current Decrease Ca current Increases refractory period
83
Uses of digoxin
Reduce ventricular rate in AF and flutter
84
How should digoxin be added to a treatment programme?
As an adjunct
85
What is the mechanism of action of atropine?
Selective muscarinic antagonist
86
What are the cardiac effects of atropine?
Block vagal activity to speed AV conduction and increase HR
87
Uses of atropine
Treat vagal bradycardia
88
Which drugs can be used in AF?
Rate control - Bisoprolol, verapamil, diltiazem +/- digoxin Rhythm control - Sotalol, flecainide with isoprolol, amiodarone
89
Should flecainide be used alone in AF?
No | Give AV nodal blocking drugs to reduce ventricular rates in flutter
90
Best drug for treatment of WPW?
Flecainide | Amiodarone

Yr 2 Sem 2 CPT (9 decks)

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