AntiDysrhythmics Flashcards

1
Q

What are the 4 classes of Antidysrhythmics?

A
  1. Sodium Channel Blockers
  2. Beta Blockers
  3. Potassium Channel Blockers
  4. Calcium Channel Blockers
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2
Q

What are the subclasses and medications within the Class I - Sodium Channel Blockers?

A

1A: Quinidine, Procainamide, Disopyramide
1B: Lidocaine, Phenytoin, Mexiletine
1C: Flecainide, Propafenone

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3
Q

What are some drugs in the class three – potassium channel blockers?

A

Amiodarone
Sotalol
Dofetilide

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4
Q

What are two Class 4 - CCB used for arrhythmias

A

Verapamil and Diltiazem

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5
Q

Should drugs administered for the chronic suppression of cardiac arrhythmias be continued up to the time of induction of anesthesia?

A

Yes, these drugs pose little threat to the uneventful course of anesthesia and should be continued up to time of induction

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6
Q

Catheter ablation techniques are preferred treatments for?

A

Many supraventricular, arrhythmias, including atrial and certain types of atrial fibrillation

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7
Q

Magnesium is involved in many enzymatic reactions and produces:

A

systemic and coronary vasodilation,
inhibits platelet aggregation, and
decreases myocardial reperfusion injury.

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8
Q

Atrial fibrillation after heart surgery is a c ommon
complication that has been associated with prolonged hospitalization and cardiovascular morbidity. Prophylactic therapy with _______, _______, _______, and ______ has been effective in reducing the occurrence of atrial fibrillation, length of hospital stay, and cost of hospital treatment and may be effective in reducing the risk of stroke.

A

amiodarone, b blockers, sotalol, and magnesium

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9
Q

The two major physiological mechanisms that cause ectopic cardiac arrhythmias are:

A

Reentry and enhanced automaticity

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10
Q

factors encountered in the perioperative period that facilitate cardiac arrhythmias due to both mechanisms (reentry and enhanced automaticity) include:

A

Hypoxemia
Electrolyte and acid base abnormalities
Myocardial ischemia
Altered sympathetic, nervous system activity
Bradycardia
Administration of certain drugs

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11
Q

antiarrhythmic drugs produce pharmacological effects by blocking passage of ions across which ion channels present in the heart?

A

Sodium ion, potassium ion and calcium ion channels

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12
Q

what determines the clinical effect of anti-arrhythmic drugs

A

The effect these drugs have on the action potential and refractory of the cardiac action potential.

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13
Q

Cardiac arrhythmic drugs are most commonly classified into four groups based primarily on the ability of the drug to:

A
  1. Control arrhythmias by blocking specific ion channels.
  2. Disrupt currents during the cardiac action potential.
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14
Q

Class 1 antiarrhythmics are sodium channel blockers, they inhibit what kind of sodium am ion channels?

A

Inhibit, fast sodium ion channels

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15
Q

Class 2 - Antiarrythmics (Beta Blockers) have what MOA

A

Decrease rate of depolarization

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16
Q

Class 4 - antiarrhythmics (CCBs) inhibit what kind of calcium channels?

A

inhibit SLOW calcium channels

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17
Q

Which antiarrhythmics have no effect on ventricular tachycardia?

A

-Calcium Channel Blockers (Verapamil & Dilt)
-Digitalis
-Adenosine

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18
Q

Which class of antiarrhythmics have no effect on paroxysmal super ventricular tachycardia?

A

Class 1B: Lidocaine, Mexiletine, Tocainide

Moricizine (a 1A drug)

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19
Q

Although used in the past, __________ is no longer recommended as prophylactic treatment for patients in the early stages of acute MI and without malignant ventricular ectopy

A

Lidocaine

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20
Q

Supraventricular Tachyarrhythmias associated with Wolff-Parkinson-White syndrome are effectively suppressed by which antidysrhythmic

A

Quinidine - Class 1A
(fast sodium channel blocker)

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21
Q

Quinidine is a class 1A drug that is effective in the treatment of acute and chronic super ventricular arrhythmias however it is rarely used because?

A

Of its side effects. Low therapeutic ratio with SEs including
-Heart Block
-Hypotension
-Proarrythmia effects

22
Q

MOA of Class 1A AntiArrythmics

A

Fast Sodium Channel Blockers in the Ventricular Myocyte. (but some potassium too lol)

Increased AP duration and prolongation of repolarization phase.

Slows/decreases the slope of the phase 4 upstroke of the action potential, slowing conduction.

Prolongs the Effect/Absolute Refractory Period, which prolongs the QRS and QT with some potassium channel blockade.

23
Q

Despite being in the same class and sub class, how do Procainamide and Quinidine differ in their treatments of arrhythmias?

A

They are equally effective for ventricular tacky arrhythmias, but procainamide is less effective at terminating atrial tacky arrhythmias.

IV admin of procainamide is usually better tolerated than IV Quinidine, but still may cause hypotension.

24
Q

True or False: Procainamide undergoes hepatic metabolism and its half-life is dependent on if a patient is a rapid or slow acetylator.

A

True.

Patients who are rapid acetylators, the
elimination half-time of procainamide is 2.5 hours compared with 5 hours in slow acetylators

25
Chronic administration of procainamide may be associated with a syndrome that resembles?
Systemic lupus erythmatosus (same with Hydalazine)
26
Hypotension from procainamide is more likely caused by _________ than peripheral vasodilation
Direct myocardial depression
27
What is lidocaine principle used for when relating to anti-arrhythmias?
Suppression of ventricular arrhythmia is having minimal if any effect on supraventricular tachyarrhythmias
28
Advantages of lidocaine over quinidine or procainamide:
- rapid onset in prompt disappearance of effects when continuous infusion is stopped - greater therapeutic index - reduced side effect profile
29
MOA of Lidocaine (and Class 1B)
Shorten the action potential duration via decreasing rate of spontaneous phase 4 depolarization and shortening the refractory period in cardiac ventricular muscle cells.
30
When does the "Effective" or "Absolute" Refractory period in the ventricular myocyte occur?
From Phase 0 to the middle of Phase 3.
31
Does lidocaine have active hepatic metabolites?
Metabolites may possess cardiac antiarrhythmic activity
32
Phenytoin (Class 1B) is particularly effective in the suppression of ventricular arrhythmia's associated with?
Digitals toxicity in may be useful in the treatment of paradoxical ventricular tachycardia or torsades de pointes
33
IV dose of Phenytoin when using for cardiac arrythmias
100mg (1.5mg/kg) every 5min until rate is controlled
34
Phenytoin exerts a greater effect on the EKG ______interval than does lidocaine and shortens the _____ interval more than any of the other antiarrhythmic drugs.
QTc
35
Phenytoin toxicity most commonly manifests as:
CNS disturbances, especially cerebellar disturbances. Symptoms include ataxia, nystagmus, vertigo, slurred speech, sedation, and mental confusion
36
What are Phenytoins effects on blood sugar?
Phenytoin partially inhibits insulin secretion and may lead to increased blood glucose levels in patients who are hyperglycemic.
37
Warfarin, phenylbutazone, and isoniazid may inhibit metabolism and increase _______ blood levels
phenytoin
38
Wide complex Ventricular rhythm is usually associated with what class of antiarrythmics?
Class 1C (Flecainide, Propenone)
39
The ability of some volatile anesthetics to depress the sinoatrial node is a consideration to acknowledge during the administration of phenytoin. Why?
With Phenytoin, conduction of cardiac impulses through the atrioventricular node is improved, but activity of the sinus node may be depressed. So volatiles can double the SA depression.
40
Leukopenia, granulocytopenia, and thrombocytopenia may occur as a manifestation of drug-induced bone marrow depression by which drug?
Phenytoin
41
Which Beta-Blockers are approved for prevention of sudden death following myocardial infarction?
Acebutolol, propranolol, and metoprolol
42
Multifocal atrial tachycardia may respond to esmolol or metoprolol but is best treated with:
Amiodarone
43
Dose of Amiodarone in ACLS
150mg and if not effective 300mg IV for VT or VF resistant to defib
44
What drug can enhance conduction of cardiac impulses through accessory bypass tracts and can dangerously increase the ventricular response rate in patients with Wolff-Parkinson-White syndrome?
Digitalis
45
If you have Wolff-Parkinson-White syndrome, what antiarrythmics would and wouldnt you want to use ?
Do not want to use any drug that depresses the AV node, this would encourage alternate conduction pathways. Avoid CCB, BetaBlockers, Digoxin. Sodium Channel Blockers Potassium Channel Blockers good
46
Digitalis toxicity is a risk and may manifest as virtually any cardiac arrhythmia, Most commonly?
atrial tachycardia with block
47
Can you use Adenosine in WPW?
Apparently, yes according to Stoelting. Ninja says NO lol
48
MOA of Adenosine
Adenosine stimulates cardiac adenosine1 receptors to increase potassium ion currents, shorten the action potential duration, and hyperpolarize cardiac cell membranes.
49
Why is Adenosine so short lived?
elimination half-time 10 seconds) are due to carrier-mediated cellular uptake and metabolism to inosine by adenosine deaminase
50
Side Effects of Adenosine
may produce transient atrioventricular heart block – Bronchospasm has been observed after the IV administration of adenosine