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Spring '20/ L. Pharm Exam 3 - sympatholytics/mimetics, LAs, antiarrhythmics, vaso > ANTIARRHYTHMIC DRUGS (from PPT) > Flashcards

ANTIARRHYTHMIC DRUGS (from PPT) Flashcards

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1
Q

How do Antiarrhythmic drugs produce their pharmacologic effects?

A

by blocking passage of ions across sodium, potassium, and calcium ion channels present in the heart

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2
Q

How many phases does the heart have (according to Hammon’s notes)?

A

Five phases

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3
Q

The cardiac action potential results from?

A

the interplay of multiple inward and outward currents via specific ion channels responsible for each of the five phases.

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4
Q

The duration of each phase of the action potential, does that differ from atrial to ventricular?

A

yes, it differs in atrial compared with ventricular myocardium.

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5
Q

Is their a difference in ion channel density based on what part of the heart you are dealing with? (SA, AV, Bundle of HIS, etc…)

A

Yes! Specialized systems for conduction of cardiac impulses differ in ion channel density.

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6
Q

What are Ion channels?

A

large membrane-bound glycoproteins that provide a pathway across cell membranes for the passage of ions

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7
Q

What are Ion channels?

A

large membrane-bound glycoproteins that provide a pathway across cell membranes for the passage of ions

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8
Q

The resting state of the hearts conduction cycle is more prevalent when?

A

during diastole

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9
Q

The active state occurs during?

A

the upstroke of the action potential.

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10
Q

The inactive state occurs during?

A

the plateau phase of repolarization.

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11
Q

Cardiac arrhythmic drugs are most commonly classified into how many groups?

A

four groups

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12
Q

Cardiac arrhythmic drugs are grouped based on what?

A

the ability of the drug to control arrhythmias by blocking specific ion channels and currents during the cardiac action potential.

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13
Q

Other characteristics of cardiac arrhythmic drugs that may be more important clinically would be what? (2 things)

A

the impact of the drug on autonomic nervous system activity and myocardial contractility.

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14
Q

Based on table 21-3 of the book, protein binding % from greatest to least. (The drugs in all Caps are more important or commonly used drugs)

A 
AMIODARONE - 96%
Propafenone - > 95%
PROPRANOLOL - 90-95%
VERAPAMIL - 90%
QUINIDINE - 80-90%
Mexiletine - 60-75%
LIDOCAINE - 55%
Flecainide - 30-45%

Procainamide and Disopryramide both are 15%
Tocainide is 10-30%

SOTALOL has no protein binding percentage listed in table?

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15
Q

What triggers Torsades de pointes?

A

triggered by early afterdepolarizations in a setting of delayed repolarization and increased duration of refractoriness manifesting as prolongation of the QTc interval on the ECG.

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16
Q

Drug-induced Torsades de pointes is often associated with what heart rhythm?

A

bradycardia because the QTc interval is longer at slower heart rates.

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17
Q

What are some exacerbating factors that may cause Torsades? (Important predisposing factors that help in the development of Torsades)

A

hypokalemia, hypomagnesemia, poor left ventricular function, and concomitant administration of other QT-prolonging drugs are important predisposing factors in the development of this life-threatening rhythm..

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18
Q

Incessant ventricular tachycardia may be precipitated by drugs that do what?

A

drugs that slow conduction of cardiac impulses (class IA and class IC drugs) sufficiently to create a continuous ventricular tachycardia circuit (reentry).

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19
Q

Incessant ventricular tachycardia is more likely to occur with high doses of what drug class? (1)

A

Class IC drugs

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20
Q

Incessant ventricular tachycardia is more likely to occur in patients with a history of what two things?

A

prior history of sustained ventricular tachycardia and poor left ventricular function

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21
Q

Incessant Ventricular Tachycardia is rarely associated with which antiarrhythmic drug class? Why?

A

class IB drugs, which have a weaker blocking effect of sodium channels.

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22
Q

Wide complex ventricular rhythm is usually associated with which class of drugs, and what heart dz does the patient also have to have?

A

IC drugs in the setting of structural heart disease.

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23
Q

Excessive plasma concentrations of class IC drugs or abrupt change in the dose makes Wide complex ventricular rhythm more or less likely to occur?

A

more likely to occur.

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24
Q

Wide complex ventricular rhythm is thought to reflect what kind of tachycardia?

A

a reentrant tachycardia

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25
Wide complex ventricular rhythm easily degenerate to what heart rhythm?
Ventricular fibrillation
26
Although commonly used in the past, WHAT DRUG is no longer recommended as prophylactic treatment for patients in the early stages of acute myocardial infarction and without malignant ventricular ectopy?
LIDOCAINE
27
lidocaine does not decrease and may increase mortality because of an increase in the occurrence of what?
fatal brady arrhythmias and asystole.
28
WHAT DRUG type is not recommended as routine treatment of patients with acute myocardial infarction because mortality is not decreased by these drugs?
Calcium Channel Antagonists!
29
In patients with heart failure, WHAT DRUG reduces the risk of sudden cardiac death by 29% and therefore represents a viable alternative in patients who are not eligible for or who do not have access to implanted cardiac defibrillator (ICD) therapy for the prevention of sudden cardiac death from arrhythmias?
AMIODARONE
30
WHAT DRUG can be considered as an adjuvant therapy to ICD in preventing recurrent shocks?
AMIODARONE
31
Amiodarone is used with ICD's to prevent what?
to prevent recurrent shocks
32
Does amiodarone therapy increase, decrease, or is neutral with respect to all-cause mortality?
Neutral
33
Amiodarone therapy is associated with a two- and fivefold incrased risk of what two types of toxicity respectively? (what organ)
pulmonary and thyroid toxicity.
34
there is little role for prophylactic antiarrhythmic medications for the primary prevention of sudden cardiac death in patients with heart failure with the exception of WHAT DRUG?
AMIODARONE
35
Class I antiarrhythimc drugs do what?
inhibit fast sodium ion channels (sodium channel blockers)
36
What drugs fall under Class 1A
Quinidine Procainamide Disopyramide
37
What drugs fall under Class 1B
Lidocaine Mexiletine Tocainide
38
What drugs fall under Class 1C
Flecainide | Propafenone
39
Class II antiarrhythmic drugs do what?
decrease rate of depolarization (B blockers)
40
What drugs fall under class II
Esmolol Metoprolol Propranolol
41
Class III antiarrhythmic drugs do what?
inhibit potassium ion channels (K+ channel blockers)
42
What drugs fall under class III
Amiodarone Bretylium Sotalol
43
Class IV antiarrhythmic drugs do what?
inhibit slow calcium channels (Ca++ channel blockers)
44
What drugs fall under class IV
Diltiazem | Verapamil
45
What two drugs are listed in the PPT that do NOT fall under any other class but are considered antiarrhythmic drugs?
Adenosine | Digoxin
46
There are five phases of the cardiac action potential, how are they numbered?
phase 0-4
47
Phase 0 can also be called what?
fast upstroke (ppt) or rapid depolarization (book)
48
Tell me what happens in phase 0?
Na+ channels open (fast channels) resulting in a fast inward current. (potassium channels are closed at this time) Upstroke ends as Na+ channels are rapidly inactivated.
49
Phase 1 can also be called?
``` partial repolarization (ppt) or initial repolarization (book) ```
50
What happens in phase 1?
1) inactivation (closure) of sodium channels. 2) Potassium channels that rapidly open and close, causing a transient outward current. (simply stated, sodium channels close and potassium channels open)
51
what drug class blocks sodium current in phase 0? (slow phase 0 depolarization)
Class IA ex. would be quinidine.
52
Phase 2 is also known as?
Plateau
53
what occurs during phase 2?
Voltage-sensitive calcium channels open, resulting in a slow inward (depolarizing) current that balances the slow outward (polarizing) leak of K+
54
Phase 3 is also known as?
Repolarization
55
What happens in phase 3?
1) calcium channels close. 2) K+ channels open, resulting in an outward current that leads to membrane repolarization. (extra info) The net result of the action to this point is a net gain of sodium and loss of potassium. This imbalance is corrected by the sodium potassium pump.
56
Phase 4 is also known as?
Forward current
57
what happens in phase 4?
Increasing depolarization results from gradual increase in sodium permeability. The spontaneous depolarization automatically brings the cell to the threshold of the next action potential. (simply stated: phase 4 is the resting potential during which time K+ channels are open and sodium and calcium channels are closed)
58
What is the effective refractory period?
the time during which the cell can not be depolarized again.
59
Class IA drugs do what to the cardiac action potential?
They slow phase 0 depolarization in ventricular muscle fibers.
60
Class IB drugs do what to the cardiac action potential?
They shorten phase 3 repolarization in ventricular muscle fibers, and decrease the duration of the action potential.
61
Class IC drugs do what to the cardiac action potential?
Markedly slows Phase 0 depolarization in the ventricular muscle fibers.
62
Class II drugs do what to the cardiac action potential?
Inhibit phase 4 depolarization in SA and AV nodes.
63
Class III drugs do what to the cardiac action potential?
Prolongs Phase 3 repolarization without altering phase 0 in ventricular muscle fibers.
64
Class IV drugs do what to the cardiac action potential?
Inhibits action potential in SA and AV nodes.
65
We know that Class IA drugs slow phase 0 depolarization. In addition, because of their Class III activity, these drugs also do what?
prolong the action potential. (see slide 17 for a good visual that explains this)
66
According to slide 21, whats another way to say what class IV drugs do?
slow phase 4 spontaneous depolarization and slow conduction in tissues dependent on calcium currents, such as the AV node.
67
Class 1A is responsible for what two of the following? - increase AP - decrease AP duration and refractory period - slow or block conduction - No effect on AP - increase QT interval
increase AP | increase QT interval
68
Which two of the following drugs fall under Class 1A? - Lidocaine - Quinidine - procainamide - esmolol
quinidine | procainamide
69
Class IA drugs are responsible for all of the following in relation to the cardiac AP cycle except (select two) - decrease phase 0 depolarization - increased QT interval - shorten phase 3 repolarization - increase effective refractory period - increase AP - increase PR interval
shorten phase 3 repolarization increase PR interval
70
What does Quinidine toxicity look like?
cinchonism- headache, tinnitus, thrombocytopenia, torsades de pointes due to increased QT interval.
71
What does procainamide toxicity look like?
lupus like syndrome
72
True or False, Class IA drugs do NOT effect both atrial and ventricular arrhythmia?
False, Class IA drugs effects both atrial and ventricular arrhythmia
73
Can you tell me the four parts of the cardiac action potential cycle that class IA drugs change?
decreased phase 0 depolarization increased Action Potential (AP) increased effective refractory period increased QT interval
74
What do Class IB drugs do to phase 3 repolarization?
SHORTEN phase 3 repolarization
75
Do Class IB drugs increase or decrease AP duration and refractory period?
Decrease
76
Are class IB drugs capable of slowing or blocking conduction?
yes, part of their action is to slow or block conduction.
77
When would you use a Class II antiarrhythmic?
They are B blockers, used for V-tach, SVT, A fib, and atrial flutter.
78
What do B blockers end in?
olol
79
Toxicity with B blockers would show what symptoms?
impotence, bronchospasm, bradycardia, AV block, mask the hypoglycemic symptoms
80
Do B blockers increase or decrease cAMP, Ca++ current, slope of phase 4, myocardial O2 consumption?
Decrease
81
Do B blockers increase or decrease PR interval?
Increase the PR interval
82
Class III antiarrhythmics (K+ channel blockers) increase or decrease AP duration and the effective refractory period?
Increase
83
What class of drug is known to prolong phase 3 repolarization without altering phase 0?
K+ channel blockers
84
What class of antiarrhythmic drugs are used when other antiarrhythimcs have failed?
Class III (K+ channel blockers)
85
Toxicity with Amiodarone would show as what possibly?
pulmonary fibrosis, hepatotoxicity, hypo or hyperthyroidism , corneal deposit, skin deposit.
86
Class IV (Ca++ channel blockers) increase or decrease ERP and PR interval?
increase
87
Can diltiazem or Verapamil decrease conduction velocity?
Yes, they are calcium channel blockers and thus decrease conduction velocity.
88
What class of drug is used for prevention of nodal arrhythmias?
Class IV which are Calcium channel blockers
89
Toxicity with Calcium channel blockers would look like what (S/S)
Constipation, Vertigo, HA, Fatigue, Hypotension.
90
What class of drugs are used for V-tach, SVT, A fib, and atrial flutter?
Class II which are B blockers
91
How does Adenosine work in the heart to slow HR and conduction?
In the heart, adenosine binds with A1 receptor (Gi protein) leads to opening of K+ channels leads to hyperpolarization Also decreases cAMP in cardiac cells which leads to decrease entry of Ca++ leading to slow HR and conduction.
92
What is the drug of choice for SVT?
Adenosine
93
How does Adenosine cause vasolilation?
In vascular smooth muscles binds with A2 receptor (Gs protein) causing increased cAMP leading to vasodilation.
94
Adenosine is very short acting, what is the approx. time?
~ 15 sec
95
What are adenosine receptor antagonists? What foods are they found in?
Xanthines found in Caffeine and Theophylline (found in tea in traces)
96
What compound is an adenosine uptake inhibitor? What does it do?
Dipyridamole“Persantine” Potentiates adenosines effects.
97
Do Class IC Antiarrhythmic drugs increase or decrease AP?
No effect on AP
98
What class of antiarrhythmics decrease phase zero depolarization and conduction?
Class IC, sodium channel blockers.
99
Digoxin is considered what type of drug?
cardiac glycoside
100
What two things does digoxin do to the heart?
decreases AV node conduction Depression of SA node
101
What will you notice in a person with Digoxin toxicity?
NVD, yellow vision, increased PR, decreased QT, T wave inversion, arrhythmia
102
What does hypokalemia do to someone having digoxin toxicity?
Toxicity is WORSENED by hypokalemia (pump inhibition is potentiated)
103
What do you give to someone with digoxin toxicity?
Give anti-dig Fab fragment
104
Tell me the three steps of how Digoxin works.
1. digoxin inhibits sodium potassium exchange by the sodium potassium pump (also known as Na+/K+ ATPase) 2. The concentration of intracellular sodium increases, and the concentration gradient across the membrane decreases. 3. Increased sodium decreases the driving force for the sodium/calcium exchanger, so there is decreased extrusion of calcium into the extracellular space. (see slide 28 for a visual)
105
Basically, how does lidocaine work?
Lidocaine works in injured or ischemic myocardial cells to retard sodium influx and restore cardiac rhythm.
106
How do arrhythmias develop at the cellular level? (ischemic myocardial cell)
Normal myocardial cells permit a limited amount of sodium ions to enter, which leads to controlled depolarization. Ischemic myocardial cells allow a rapid infusion of sodium ions. This causes the cells to depolarize much more quickly than normal and then begin firing spontaneously. The result is a ventricular arrhythmia.
107
How does lidocaine suppress arrhythmias?
By slowing sodium's influx, lidocaine raises the cells' electrical stimulation threshold (EST). The increased EST prolongs depolarization in the ischemic cells and returns control to the SA node, the heart's main pacemaker.

Spring '20/ L. Pharm Exam 3 - sympatholytics/mimetics, LAs, antiarrhythmics, vaso (17 decks)

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