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MBBS I CPRS > L52 – Anti-arrhythmic Drugs > Flashcards

L52 – Anti-arrhythmic Drugs Flashcards

(126 cards)

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1
Q

Assign the following ECG landmark with the cardiac cycle: P wave

A

depolarization of atria in response to SA node triggering

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2
Q

Assign the following ECG landmark with the cardiac cycle: PR interval

A

delay of AV node (time lapse between atrial, ventricular contraction)

allow filling of ventricles

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3
Q

Assign the following ECG landmark with the cardiac cycle: QRS complex

A

depolarization of ventricles&raquo_space; triggers main pumping contractions

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4
Q

Assign the following ECG landmark with the cardiac cycle: ST segment

A

beginning of ventricle repolarization

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5
Q

Assign the following ECG landmark with the cardiac cycle: T wave

A

ventricular repolarization

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6
Q

Assign the following ECG landmark with the cardiac cycle:QT interval

A

duration of action potential in ventricle

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7
Q

Explain the action of sympathetic activation causing a change in pacemaker potential/ depolarization.

A

Sympathetic activation increases slope of pacemaker depolarization

(right) Sympathetic activation > hyperpolarization-activated L type funny channels OPEN EARLIER > Increase Na+ influx > steeper slope

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8
Q

Explain the action of parasympathetic activation causing a change in pacemaker potential/ depolarization.

A

Parasympathetic activation (vagus nerve) > increase K+ permeability in pacemaker phase (IKAch open) > DECREASE slope of phase 4 pacemaker potential

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9
Q

What are 3 ways to regulate pacemaker activity?

A

Change any of:

1) Threshold potential
2) Maximum diastolic potential
3) Slope of phase 4/ pacemaker depolarization

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10
Q

Compare the effects of parasympathetic and sympathetic activation on phase 4 depolarization?

A

Sympathetic = increase slope

Parasympathetic = decrease slope

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11
Q

Compare the speed of transmission between Non-nodal tissue and nodal tissu.

A
  • Non-nodal tissue: usually Na+ current&raquo_space; faster transmission
  • Slow-response tissue (e.g. AV node): Ca2+
    current&raquo_space; slower transmission
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12
Q

What 2 factors are important in the regulation of impulse propagation?

A

Magnitude of depolarizing current

Geometry of cell-cell electrical connections

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13
Q

Explain how Geometry of cell-cell electrical connections can influence impulse propagation?

A

more gap junction proteins (governs direction of propagation) at ends than side of cardiac cells

impulse spread along cells 2-3 times faster than across cells

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14
Q

What 2 abnormalities can lead to arrhythmia?

A

Abnormal automaticity

Abnormalities in impulse conduction

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15
Q

Classification of arrhythmia?

A

1) Supraventricular: divided into atrial / nodal

2) Ventricular

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16
Q

Name some causes of arrhythmia?

DIE HAI

A

Drug toxicity
Infection
Electrolyte abnormalities

Hypoxia
Autonomic influences
Ischaemia

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17
Q

Where are the sites of Abnormalities in impulse conduction?

A

atrial (A) / ventricular (V) / junctional (AV)

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18
Q

How does a decrease in rate of impulse conduction lead to uncoordinated cardiac contraction?

A

Decrease rate of conduction&raquo_space; impulse conduction easy to be blocked&raquo_space; atria and ventricles have different impulses&raquo_space; no longer coordinated

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19
Q

What are the 2 types of impulse conduction block?

A

Simple block

Transient block

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20
Q

What is simple impulse conductance block due to? Where does the simple block usually occur?

A

 Myocardial infarction» dead muscle
 Altered ionic balance

Most commonly in atrioventricular (AV) node

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21
Q

What is Transient impulse conductance block due to?

A

Hypoxia > Insufficient O2

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22
Q

What is the result of a transient block?

A

Weaker force of contraction

Initially same rhythm

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23
Q

How does a transient block of impulse lead to unidirectional block and fibrillation?

A

Transient block > impulses not synchronized > when tissue recovers conduction, impulse can be transmitted BACKWARDS causing unidirectional block

This triggers RE-ENTRY (circus movement) in different parts of the heart > Fibrillation

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24
Q

Abnormal automaticity is observed when the resting potential is…?

A

reduced resting membrane potential (decreased membrane K+ conductance
» Vm more positive / less negative)

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25
What 2 things can enhance abnormal automaticity?
 Enhanced by sympathetic nerve activity >> tachycardia  Enhanced by hypokalemia >> activate less Na+ channel causing bradycardia
26
Extra heart beats are triggered by ___?
afterdepolarizations
27
Why is long QT indicative of Early Afterdepolarization (EAD)?
prolonged repolarization phase >> Long QT
28
What are the 2 types of afterdepolarization?
EAD - early afterdepolarization | DAD - Delayed afterdepolarization
29
Compare the electrolyte abnormalities that cause EAD and DAD?
EAD = Reduction of repolarizing K+ currents DAD = increased intracellular Ca2+ level
30
What is early afterdepolarization?
Another depolarization occurs BEFORE repolarization is complete
31
What is DAD?
another depolarization occurs AFTER repolarization but | sooner than normal
32
Compare the abnormal automaticity in EAD and DAD?
EAD = depolarize BEFORE complete repolarization DAD = depolarize AFTER complete repolarization but sooner than normal
33
In which phases of non-nodal cardiac cycle does EAD occur?
phase 2 (plateau) phase 3 (rapid repolarization)
34
What is polymorphic ventricular tachycardia/ Torsades de Pointes?
uncoordinated impulses generated in all parts of heart
35
What causes polymorphic ventricular tachycardia?
Caused by EAD triggers functional re-entry and circus movement because of the heterogeneity of AP durations across the ventricular wall **many AP each with different timing**
36
2 Therapeutic goals of Anti-arrhythmic drugs?
 Terminate ongoing arrhythmia  Prevent arrhythmia
37
What are some acute therapies for arrhythmia?
intravenous administration, defibrillation device
38
What is the Vaughan-Williams Classification for Antiarrhythmic drugs? Natalie Borrows Kelvins Car
Class I - Sodium channel blockers Class II- B-adrenergic receptor blockers Class III - Potassium channel blockers Class IV - Calcium channel blockers
39
Describe the m (outer) and h (inner) gates of sodium channel during resting potential?
Resting (closed): m gates closed, h gates opened
40
Describe the m (outer) and h (inner) gates of sodium channel during threshold to activation?
m gates open, h gates | remain open
41
Describe the m (outer) and h (inner) gates of sodium channel during Inactivation?
m gates remain open, h gates close >> then recover to resting
42
Na+ channel blockers preferentially bind to during which phases?
Bind preferentially to pore area when channel is: 1) activated (open) 2) inactivated (i.e. when m gates are open)
43
What is the effect of Class I antiarrhythmic drug on tachycardia?
Block Na channel during activated or inactivated state > Decrease Na+ conduction velocity > Decrease slope of depolarization > Block Tachycardia
44
What is the relationship between the frequency of Na channel activation and the degree of channel block by Class I drug?
more frequently the channels are activated, the greater is the degree of block
45
What are the 3 subtypes of Class I drugs?
Class Ia Class Ib: rapid kinetics Class Ic: Slow kinetics
46
Name some Class Ia sodium channel blockers?
Procainamide Quinidine Disopyramide
47
Name some Class Ib sodium channel blockers?
Lidocaine | Mexiletine
48
Name some Class Ic sodium channel blockers?
Flecainide Encainide Propafenone
49
Compare the rate of dissociation from Na channels between Class I a,b,c drugs?
``` Ia = intermediate rate Ib = rapid Ic = slow ```
50
What period of cardiac cycle does Class Ia drug increase?
effective refractory period
51
Explain the action of Class Ia drug given it is non-selective?
Also block K+ channels > decrease rate of repolarization > increase duration of AP to prevent extra beat
52
What is the adverse effect of Class Ia drug? (think K+)
Risk of EAD due to Reduction of repolarizing K+ currents + Anticholinergic effect = risk of inducing torsades de pointes arrhythmia/polymorphic ventricular tachycardia
53
What is the gross effect of Class Ia drug?
- Inhibit increase in automaticity - Moderate decrease in conduction - Decrease rate of repolarization = increase duration of AP/ ERP
54
Adverse effect from long term use of procainamide?
lupus-related symptoms, e.g. arthralgia, arthritis
55
Adverse effect of procainamid and quinidine (less with disopyramide)?
Gastrointestinal disturbances, e.g. diarrhea / constipation, nausea, vomiting
56
Rank each of the class Ia drugs on their effects on lowering force of contraction?
disopyramide > quinidine > | procainamide
57
What does Class Ib drugs block?
preferentially block premature beats
58
What is the action of Class Ib on sodium channels? (which state, when...)
Selective for inactivated (refractory) Na+ channels > suppress depolarized cells Dissociate RAPIDLY within the time frame of normal heartbeat (before next impulse from SA node)
59
Explain why Class Ib drugs can cause CNS disturbances?
Affect faster-acting Na+ channels in central nervous system for impulse conduction
60
What are some adverse effect symptoms of Class Ib drug?
``` CNS disturbances e.g. tremor, nausea, drowsiness, disorientation, convulsions ```
61
What is the gross effect of class Ic drugs?
Decrease conduction even at normal HR
62
What is the interaction between Class Ic drug and Na channels?
dissociate slowly from Na+ channels (still blocked when next impulse comes)
63
What are some adverse effects of Class Ic drugs (flecainide, propafenone)
Proarrhythmia Worsen Heart failure
64
How does class Ic drug cause pro-arrhythmia as adverse rxn?
Decrease in HR = decrease cardiac output Increase incidence of sudden death especially in presence of severe heart failure
65
What is the adverse reaction caused by propafenone (class Ic)? (think heart failure and chemical structure)
structurally similar to propranolol can act as weak B -adrenergic receptor blocker > -ve inotropic effect > worsens heart failure
66
What are the gross effects of Class II drugs?
B blockers oppose B-adrenergic stimulation  SA : lower heart rate  AV: Increase nodal conduction time (slow down)  Ventricle: lower intracellular Ca2+ overload
67
Can Class II drugs prevent DAD?
Yes
68
2 types of B-blockers?
Selective B1-adrenergic receptor blockers, e.g.:  Metoprolol  Esmolol Non-selective β-adrenergic receptor blockers, e.g. propranolol
69
Why does esmolol have a short half life?
Rapidly metabolized by erythrocyte esterases
70
When are selective B1-adrenergic receptor blockers used?
primarily used for intraoperative, acute arrhythmias >> need IV admin.
71
When are Non-selective B-adrenergic receptor blockers used?
arrhythmia induced by adrenaline-induced hypokalemia **associated with severe stress e.g. acute MI, resuscitation from cardiac arrest
72
What is the action of Non-selective B-adrenergic receptor blockers?
Antagonize both B1- and B2-adrenergic receptors
73
Which groups of patients cannot use Class II drugs?
Heart failure Asthma or COPD Diabetes
74
Why cant class II drugs be used in patients with HF?
B blocker decreases both force and rate of contraction
75
Why cant class II drugs be used in patients with asthma or COPD?
B blocker can cause bronchospasm
76
Why cant class II drugs be used in patients with diabetes?
B blocker can cause hypoglycaemia by inhibiting glycogenolysis in liver
77
What are the gross effects of Class III drugs?
Decrease rate of repolarisation + Decrease normal automticity and disable re-entry > increase AP duration/ ERP
78
What does Dodetilide block?
Potent, “pure” blocker for the rapid delayed | rectifier potassium channel
79
Adverse effect of Dodetilide?
Reduced rate of repolarization > risk of EAD and torsades de pointes
80
Dodetilide is avoided in which patients?
hypokalemia advanced renal failure Taking inhibitors of renal cation transport
81
What are the gross effects of Amiodarone?
Broad spectrum: - K+ channel blockade - Block inactivated Na+ channel - Weak adrenergic block - weak calcium channel block
82
What is the commonly used drug for most kinds of arrythmia?
Amiodarone
83
What are some adverse effects of Amiodarone on the heart?
Low incidence of torsades de pointes May cause bradycardia and heart block >> chance of arrhythmia
84
What are some adverse effects of Amiodarone on organs other than the heart? Why ?
Due to Iodine: ``` Skin >> photosensitivity Eye - corneal deposits >> visual problems Thyroid >> hypo- / hyper-thyroidism Lung >> pulmonary fibrosis Liver >> hypersensitivity hepatitis ```
85
What are the symptoms of photosensitivity?
skin rashes, grey-blue skin discoloration following sun exposure
86
What are some drug interactions of Amiodarone?
Metabolized by cytochrome P450 (CYP3A4): Plasma level of amiodarone can be increased or decreased by drugs interacting with CYP3A4
87
What is the interaction between Amiodarone and cimetidine?
Cimetidine inhibits CYP3A4 >> increase Amiodarone plasma level
88
What is the interaction between Amiodarone and Rifampin?
Rifampin induces CYP3A4 >> Decrease amiodarone plasma | level
89
What is the interaction between Amiodarone and drugs that depend on CYP 3A4 for metabolism?
Amiodarone increases the plasma levels of drugs that depends on CYP3A4 for metabolism (e.g. statins, warfarin, digoxin)
90
What influence does Amiodarone have on cardiac devices?
Need to increase pacing and defibrillation threshold
91
What is the action of Dronedarone?
Same mechanisms of actions as amiodarone > broad spectrum
92
Why is Dronedarone taken after eating?
Absorption increases 2- to 3-fold when taken with food
93
What are some adverse effects of Dronedarone?
Pro-arrhythmia (bradycardia and heart block) Low incidence of iodine adverse effects Low incidence of torsades de pointes
94
What is the action of Sotalol?
``` class III antiarrhythmic drug with class II action ```
95
What is he mixture in Sotalol?
Racemic mixture of:  d-sotalol  l-sotalol (contains B -adrenergic receptor blocking activity)
96
What patient group is Sotalol used for?
Treat supraventricular and ventricular | arrhythmias in the pediatric age group
97
Adverse Effect of Sotalol?
1 ) Pro-arrhythmia (risk of torsades de pointes) 2) Block β >> depress left ventricular function caution in patients with heart failure
98
Effect of Sotalol on cardiac devices?
decrease threshold for cardiac defibrillation
99
Gross action of Class IV drugs? (CCB)
Decrease in : HR AV nodal conduction velocity Calcium overload (thus effective against DAD)
100
How could Class IV/ CCBs cause heart failure?
AV block Hypotension Decrease force of heart contraction >> all can lead to HF
101
Does CCBs cause peripheral edema?
Yes
102
Class IV drugs are avoided in which patient groups?
hepatic dysfunction ventricular tachycardia
103
Explain how CCBs can cause centricular tachycardia?
Cause Hypotension >. reflex tachycardia >> cardiac arrest
104
Which anti-arrhythmic drugs are rate control?
Class Ic, II
105
Which anti-arrhythmic drugs are Rhythm control?
Class Ia/b, III, IV
106
Explain how adenosine can decrease normal automaticity?
Activate presynaptic purinergic receptors on sympathetic nerve terminals > decrease release of noradrenaline
107
Explain how adenosine can decrease calcium overload?
Activate A1 receptors on SA and AV nodes > inhibit adenylyl cyclase > decrease intracellular cAMP production > decrease calcium overload
108
Explain how adenosine can decrease conduction velocity?
Activate K channels in SA and AV nodes > increase maximal diastolic potential (more hyperpolarized) > prolong phase 4/ pacemaker depolarization > decrease conduction velocity
109
Adenosine is potentiated and inhibited by what?
Potentiate ( drug A boosts the effects of drug B ) by dipyridamole Inhibited by Caffeine
110
Why do adverse effects of Adenosine rapidly resolve?
Rapid uptake into cells for metabolism > short half life in blood
111
Why does Adenosine cause flushing, hypotension + chest pain and shortness of breathe?
activate A2 receptors in vascular smooth muscle >> decrease calcium release >> VASODILATION > Flush > Hypotension >> reflex hyperventilation
112
Gross effect of Cardiac | glycosides: e.g. digoxin?
Parasympathomimetic effects: Decrease in both - heart rate - conduction velocity (especially at AV node)
113
Which two electrolytes can be taken to treat arrhythmia?
K | Mg
114
How could cardiac glycosides cause DAD?
Inhibit Na+-K+ ATPase activity > increase ntracellular Na+ level >> less Ca2+ expulsion by Na+/Ca2+ exchanger >> increase intracellular Ca2+ > DAD/ ectopic beats
115
Adverse effects of cardiac glycosides?
GI disturbances, e.g. diarrhea, nausea, vomiting CNS disturbances, e.g. drowsiness, disorientation
116
Risk of DAD is increased by which electrolyte imbalances?
 Hypokalemia  Hypercalcemia  Hypomagnesmia
117
Name one muscarinic receptor antagonist>
Atropine
118
How does Atropine manage bradycardia?
Block muscarinic receptor = decrease vagal influence Increase HR and conduction veolcity (esp. at AV node)
119
Name some side effects of Atropine after OD or repeated dosing?
 Tachycardia  Dry mouth  Dilation of pupils  Constipation
120
List some non-pharmacological therapy of cardiac arrhythmia?
Pacemaker Electrical cardioversion Implantable cardioverter-defibrillator Heart surgery (Maze procedure) Catheter Ablation
121
Route of administration of drug for emergency arrhythmia?
IV
122
Why is combo therapy given for arrhythmia?
prevent adverse effects
123
What are 3 signature symptoms of Arrhythmia?
Palpitations Syncope (dizzy) Cardiac arrest
124
If patient has arrhythmia and syncope, which antiarrhythmic drug should you NOT use?
hypotension: do not give IV (CCB)
125
If patient has arrhythmia and cardiac arrest, which antiarrhythmic drug should you NOT use?
Ic (Na channel blocker, slow response) II (B-adrenergic) III (Potassium channel blocker) IV (CCB)
126
For decreasing long-term mortality in asymptotic patients, which antiarrhythmic drug should be used?
``` Avoid pro-arrhythmic ones e.g. Class III, class Ic ```

MBBS I CPRS (78 decks)

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