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MHD1/Pharm1 Exam 4 > (THER) Antiarrhythmic Agents I and II > Flashcards

(THER) Antiarrhythmic Agents I and II Flashcards

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1
Q

What is the difference between pacemaker cells and regular myocytes?

A

They lack fast Na+ channels and as such their refractory period is determined by time, via a slow inward Na+ current (If = funny channels)

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2
Q

ALL arrhythmias result from what (3) things?

A
  1. Disturbed impulse formation
  2. Disturbed impulse conduction
  3. Combination of 1 and 2
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3
Q

General symptoms from cardiac arrhythmias

A

Wide range from asymptomatic to severe hemodynamic consequences with reduced CO and death.

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4
Q

Types of Cardiac Arrhythmias (3)

A
  1. Too slow (bradycardia/bradyarrhythmia)
  2. Too fast (tachycardia/tachyarrhythmia)
  3. Asynchronous
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5
Q

In general, the aim of anti-arrhythmic therapy is to reduce…

A

Ectopic pacemaker activity and/or modify conduction characteristics to restore normal function.

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6
Q

What is one of the most dangerous potential side effects of anti-arrhythmic drugs?

A

The development of lethal arrhythmias because these drugs do not act specifically.

Depends on dosage or physciological conditions, such as faster heart rate, acidosis, electrolytes or presence of ischemia.

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7
Q

Are early afterdepolarizations usually at slow or fast heart rates? DAD’s?

A

EAD: slow

DAD: fast

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8
Q

What are the (3) requirements for reentry?

A
  1. Block (SA/AV block)
  2. Unidirectional conduction
  3. Slowed conduction through block
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9
Q

What are the (4) ways to regulate rate of pacemaker cells with abnormal automaticity?

A
  1. Reduction of phase 4 slope
  2. Increase of max Em
  3. Increase of threshold potential
  4. Increase of action potential duration
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10
Q

How might a drug that affects the recovery time Na+ or Ca2+ channels effect arrhythmias?

A

Tachy-arrhythmias and premature beats (short cycle lengths) depend on the ability of Na+ channels to activate, inactivate and recover from inactivation RAPIDLY.

If a drug prolongs the recovery time of the Na+ channel (or Ca++ channel), then it may prevent re-entry, block tachycardias and prevent premature beats from occurring.

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11
Q

Describe the functioning of use-dependent or state-dependent drug action

A

They selectively block depolarized cells

They suppress channels that are used/inactivated frequently are more suceptible e.g. during fast tachy (when many channels are activated/inactivated) or in ischemic or infarcted tissues (more positive RMP).

Normal cells rapidly lose the drug during the resting phase

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12
Q

What drug is best for treatment of asymptomatic or minimally symptomatic arrhythmias?

A

TREATMENT SHOULD BE AVOIDED!

This is due to the potential of anti-arrhythmics to cause lethal arrhythmias

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13
Q

Name the Vaughan Williams Classification of Anti-Arrhythmic Drug Actions

A

Class I: Na+ channel blockers

Class II: B-adrenoceptor blockers

Class III: prolongation of the AP duration

Class IV: Ca2+ channel blockers

Other

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14
Q

Describe Class I Anti-Arrhythmics

What are they? What does their action depend on?

A

Na+ channel blockers (local anesthetic action)

Block fast Na+ channels. Actions depend on HR, Em and drug specific blocking kinetics

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15
Q

How do Na+ channel Blockers (Class I anti-arrhythmics) influence depolarization? repolarization?

A

Depolarization influence via: reduction of conduction velocity by reducing rate and magnitude of depolarization

Repolarization influence via: effects on K+ channels which may proong the AP duration

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16
Q

What are the (3) subclasses under type I anti-arrhythmics and which drugs full under which categories?

A

Class IA: intermediate kinetics, increases action potential duration (APD)

Drugs: Procainamide, Quinidine and Disopyramide

Class IB: Fast kinetics, decreases APD

Drugs: Lidocaine, mexiletine

Class IC: slow kinetics, no effect on APD

Drugs: Flecainide, Propafenone

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17
Q

Procainamide MOA and Effects

(what does it block? via what type of action? what is the electrical effect of its action? how does this effect rate?)

A

Blocks Na+ and K+ channels via use/state dependent action

This slows upstroke of AP and conduction, prolonging the QRS.

This has direct depressant actions on SA/AV nodes

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18
Q

Procainamide Indications

(also, what choice drug is it?)

A

Atrial and ventricular arrhythmias

2nd choice for vent. arrhythmias after acute MI

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19
Q

Procainamide route/half-life/ elimination

A

Route: PO/IV

t1/2: 3-4 hrs

elim: renal

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20
Q

Procainamide AEs (4)

A
  1. Torsades des pointes
  2. Hypotension
  3. Anticholinergic effects
  4. Lupus syndrome (long term use)
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21
Q

Quinidine is similar to what drug?

A

Procainamide

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22
Q

How does quinidine differ from procainamide?

A
  1. stronger anticholinergic effects
  2. cinchonism (headache, dizzines, tinnitus)
  3. it is rarely used because of cardiac/extra-cardiac AEs
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23
Q

Disopyramide is similar to what other drug?

A

Procainamide

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24
Q

How is disopyramide different from procainamide? (2)

A
  1. Much greater anticholinergic effects than procainamide and quinidine
  2. Negative inotropic effects which may induce heart failure
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25
Because of the anti-cholinergic effects of disopyramide, it requires co-administration of drugs that...
slow AV conduction
26
What is the only inducation that disopyramide is approved for?
It is a 1st or 2nd choice drug for _ventricular arrhythmias_
27
Lidocaine MOA/effects (What does it do? What kind of drug action?)
Na+ channel blockade. Use/state-dependent drug action
28
Lidocaine Indications What is it _not_ recommended for?
1. Ventricular arrhythmias after MI 2. 1st choice for V. tach/V. fib after cardioversion in setting of ischemia/infarction Not recommended for prophylactic treatment (may increase mortality)
29
Lidocaine route/ metabolization/ t 1/2
**Route:** IV only **Metabolism**: Extensive 1st pass metabolism **t1/2**: 1-2 hours
30
Lidocaine AEs
Least cardiotoxic drug among Class I drugs Neurological side ffects due to local anesthetic properties.
31
What is Mexiletine?
An oral lidocaine analogue. Actions/AEs are similar to lidocaine.
32
How is Mexiletine different from lidocaine? (half-life? Other uses?)
**t 1/2**: 8-20 hours **Off-label use**: chronic pain (diabetic neuropathy/nerve injury)
33
Flecainamide MOA
Na+ and K+ blockade
34
How does flecainamide affect AP duration and cholinergic effects?
Although K+ channel blocker, _no effects on AP duration or anticholinergic effects_
35
Flecainamide indications
**Indication**: supraventricular arrhythmias in patients with otherwise normal hearts
36
Flecainamide AEs
Increases mortality in patients with v. tach, MI, and ventricular ectopy (**ALL CONTRAINDICATED)**
37
Flecainamide 1/2 life and elimination
**t 1/2**: 20 hours **elmination**: liver/kidney
38
Propafenone MOA What is it structurally similar to?
Potent blocker of Na+ channels; may also block K+ channels Structurally similar to _propanolol_ with weak B-blocking activity
39
Indications for Propafenone
Used for supraventricular arrhythmias in patients with otherwise normal hearts.
40
Propafenone AEs (4)
1. Arrhythmogenic 2. Sinus bradycardia/bronchospasm (B-blockade) 3. Metallic taste 4. Constipation
41
Name the key non-selective B-blockers
**PROPRANOLOL**, sotalol and timolol
42
Name the (relatively) "cardioselective" B-blockers
**ESMOLOL** and acebutolol
43
Propranolol indications
1. Prevention of recurrent infarction and sudden death after MI 2. Atrial fibrillation 3. Atrial flutter 4. AV nodal reentry
44
Propranolol AEs
1. Bradycardia 2. Reduced excercise capacity 3. heart failure 4. hypotension 5. AV block Contraindicated in patients with sinuse bradycardia and partial AV block
45
What is the warning for propanolol for patients with asthma/COPD? Diabetics?
* Bronchospasm caution in patients with asthma/COPD * May mask tachycardia associated with hypoglycemia in diabetic patients
46
Key indication for esmolol
Supraventricular tachycardia (acute only)
47
Esmolol half-life and route
**t 1/2**: 9 mins **route**: IV _only_
48
Amiodarone mechanism
Blocks K+ channels, as well as Na+ and Ca2+ channels and B-receptors. Causes prolongation of AP duration, prolongs refractoriness and slows conduction, thereby **suppressing abnormal automaticity**.
49
Amiodarone Indication (oral route? IV route?)
**Oral:** 1. Recurrent v. tach or v. fib which is resistant to other drugs 2. A. fib. **IV:** 1. 1st choice drug for out-of-hospital cardiac arrest 2. termination of v. tach or v.fib
50
Amiodarone half-life and route
3-10 days Oral and IV
51
Toxicities of Amiodarone (6) Which is most important to watch out for?
1. Accumulation in several organs (due to high lipophilicity) 2. Bradycardia and heart block in patients with SA/AV node disease 3. Pulmonary/hepatic toxicity 4. Photodermatitis 5. Cornea microdeposits 6. Blocks T4 conversion so can cause thyroid issues ## Footnote **PULMONARY TOXICITY IS MOST IMPORTANT**
52
Dronedarone is a structural analogue of what? How is it different?
Amiodarone It lacks the iodine atoms, thereby avoiding thyroxine metabolism
53
Dronedarone Indications? Contraindications? 1/2 life?
_Indications_: A. fib/flutter _Contraindications_: severe or recently decompensated symptomatic heart failure _t 1/2_: 24 hrs
54
Sotalol MOA
non-selective B-blcoker that inhibits delayed rectifyer and posisbly other K+ currents.
55
Sotalol Indications
1. Ventricular/ Supraventricular arrhythmias 2. Maintenance of sinus rhythm in patients in patients with atrial fibrillation
56
Verapamil MOA
Blocks activated and inactivated Ca2+ channels (L-type) primarily in the heart.
57
Verapamil Effect
Use/state-dependent action 1. Directly slows AV node conduction and increases AV node refractoriness 2. Slows SA node automaticity **Lowers HR and increases PR interval**
58
Verapamil Indications (3)
1. Supraventricular arrhythmias (**1st choice**) 2. Re-entry arrhythmias/tachycardias involving the AV node 3. Slows ventricular rate in atrial flutter/fibrillation
59
Verapamil metabolization? Route? t1/2?
Extensive metabolism in the liver Oral/IV t1/2 = 7hrs
60
General Adverse Effects associated with Verapamil (After IV injection? Effects on inotropy? General effects to be wary of?)
Vasodilation after IV injection Negative inotropic effects: hypotension and fibrillation Generally must be carefully of arrhythmias/blocks in susceptible patients
61
What can happen to patients on B-blockers if they take verapamil?
They have a high risk for heart block
62
What drug is Diltiazem similar to? How is it different from this drug? (3)
Similar to Verapamil 1. Lower cardioselectivity Also used for 2. hypertension and 3. angina pectoris
63
Adenosine MOA
Increases K+ conductance (hyperpolarization) and inhibits Ca2+ currents via purinergic receptors
64
Effects of Adenosine (3) | (and where does it primarily work?)
**Primarily acts on atrial tissues** 1. Slows AV node conduction 2. Increases AV node refractoriness 3. Produces transient cardiac arrest
65
Adenosine indications
Conversion of paroxysmal (acute attack of) SVT to sinus rhythm
66
Adenosine route/ t 1/2
Rapid IV bolus _t 1/2_: seconds
67
Adenosine interactions (2)/ AEs (2)
_Interactions_: 1. Less effective with theophylline/ caffine 2. Potentiated by dipyridamole _AEs_: 1. Flushing 2. SOB
68
Magnesium MOA
Mechanism unknown (infuences Na/K+ and Ca channels/pumps to alter surface charge)
69
Magnesium effect
1. Anti-arrhythmic effects in some patients with normal Mg2+ levels. 2. May inhibit afterdepolarizations
70
Magnesium indications
1. Digitalis induced arrhythmias with hypomagnesemia 2. May be effective against torsades des points
71
Magnesium Route of Admin
IV
72
K+ MOA (in hyperkalemia? in hypokalemia?)
In _hyperkalemia_ it depolarizes RMP In _hypokalemia_ it decreases K+ permeability
73
K+ effects (in hyperkalemia? In hypokalemia?)
In _hyperkalemia_: slows conduction In _hypokalemia_: enhances ectopic automaticity; lengthens AP duration
74
K+ Indications
Maintains normal plasma K+
75
K+ adverse effects
1. May lead to reentry/Av block in _hyperkalemia_ 2. May lead to EADs (torsades de pointes) in _hypokalemia_
76
K+ route
IV/PO
77
Digitalis is what type of drug?
Cardiac Glycoside
78
Digitalis MOA
Inhibit Na+/K+-ATPase, thereby increasing Na+Ca++ exchange, increase intracellular Ca++
79
Digitalis effects (2)
1. Positive inotropic actions (used widely in heart failure) 2. Parasympathomimetic effects: (increase AV nodal refractoriness and slow AV node conduction.)
80
Digitalis Indications
1. Atrial arrhythmias (slow AV nodal conduction, thereby slowing excessively high ventricular rates) 2. Heart Failure
81
Digitalis t 1/2 and elimination
**t 1/2**: 40-160 hours Renal elimination
82
Digitalis AEs/toxicities
1. Narrow therapeutic window may lead to DADs 2. Visual disturbances (yellow-green) 3. Drowsiness/depression 4. GI issues 5. Many drug interactions
83
What physiological states may enhance the toxic effects of digitalis?
Hypokalemia/Magnesemia
84
Severe digitalis toxicity can be reversed by...
Digoxin antibodies
85
What patients are strictly contraindicated from use of verapamil?
Patients in V. Tach (due to the drugs negative inotropic effects)
86
Name the non-pharmacologic anti-arrhythmic therapies (4)
1. Vagal maneuvers 2. Radiofrequency ablation/Cryoablation 3. Electrical cardioversion 4. Implantable Cardioverter-Defibrillator (ICD)
87
**Name the 1st and 2nd line drugs that should be used for:** Conversion to sinus rhythm
1. Adenosine/ Amiodarone 2. Flecainide
88
**Name the 1st and 2nd line drugs that should be used for:** Maintenance of sinus rhythm
1. Amiodarone/Dronedarone 2. Flecainide/Propafenone
89
**Name the 1st and 2nd line drugs that should be used for:** Ventricular rate control
1. Diltiazem/verapamil 2. Propanolol/Esmolol
90
**Name the drugs that should be used for:** V. tach/ V. fib in patients without heart disease
1. Amiodarone 2. Lidocaine
91
**Name the 1st and 2nd line drugs that should be used for:** A. fib
1. Diltiazem/ Verapamil 2. Propanolol
92
**Name the 1st and 2nd line drugs that should be used for:** Paroxysmal SVT
1. Adenosine/Amiodarone 2. Verapamil/Diltiazem/Propranolol

MHD1/Pharm1 Exam 4 (26 decks)

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