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Pharmacology Unit 4 > Antiarrhythmics I and II > Flashcards

Antiarrhythmics I and II Flashcards

1
Q

Describe the conduction thru the heart

A

SA node -> Atrium -> AV node -> Bundle of His -> Bundle branches of Purkinje fibers -> Ventricle

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2
Q

Describe the four phases of the typical myocardial action potential and the ions primarily responsible for each phase (not SA or AV nodes)

A
  • Phase 0: Na+ influx
  • Phase 1: K+ efflux
  • Phase 2: Ca2+/Na+ influx
  • Phase 3: K+ efflux
  • Phase 4: High conductace of K+ predominates
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4
Q

What channel is responsible for the slow upstroke in the SA and AV node? What ion is responsible for the AP once the SA/AV nodes reach threshold?

A

The funny current (If); Calcium

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6
Q

What are 2 general mechanisms of arrhythmias?

A
  • Disturbance of Impulse Formation - Inappropriate automaticity (Rhythm initiated in place other than the SA node)
  • Disturbance of Impulse Conduction
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8
Q

What are the two general classes of arrhythmias? (Give me some subtypes too!)

A
  1. Bradyarrhythmia - Sinus bradycardia, sinus arrest, heart block (I, II, III)
  2. Tachyarrhythmia - Supraventricular Tach, Ventricular Tach
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10
Q

What bradyarrhythmias are cause by a problem with impulse initiation? Impulse conduction?

A
  • Impulse Initiation - Sinus arrest, sinus bradycardia, sinoatrial exit block
  • Impulse conduction - Heart block
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12
Q

Diagnosis?

A

Sinus Arrest

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14
Q

Diagnosis? Why?

A

First Degree Heart Block; PR interval > .2 s

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16
Q

Diagnosis?

A

Second Degree Heart Block (Mobitz I aka WENCKBACH)

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18
Q

Diagnosis? Treatment?

A

Second Degree Heart Block, Mobitz II; Pacemaker

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20
Q

Diagnosis? Treatment?

A

Third Degree Heart Block; Pacemaker

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22
Q

What are the three general classes of tachyarrhythmia? Which is most common? Least common?

A
  1. Impulse Initiation (Increased automaticity)
  2. Triggered Automaticity - Early and Delayed Afterdepolarizations (Least Common)
  3. Impulse Conduction: Reentry (Most Common)
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24
Q

What are three tachyarrhythmias that fall under increased automaticity? Causes?

A
  1. Atrial tach - Impulse from atrial tissue other than SA
  2. Junctional tach - abnormal impulse from AV junction
  3. Ventricular tach - Abnormal impulse coming from ventricle
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26
Q

What is multifocal tachycardia?

A

Three or more P-waves of variable morphology with rate > 100 bpm. Multiple foci fire at the same time

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28
Q

What is ventricular arrhythmia?

A

3 or more consecutive ventricular beats at > 100 bpm, usually wide and regular

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30
Q
  1. When in the action potential do EADs occur?
  2. What condition is thought to arise from EADs?
  3. When in the AP do DADs occur?
  4. What is an example of DAD?
  5. What type of tachyarrhythmi are EADs and DADs examples of?
A
  1. Phase 3
  2. Long QT Syndrome
  3. Phase 4
  4. Digoxin toxicities
  5. Triggered Automaticity
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32
Q

What is the top arrow pointing to? The bottom arrow?

A
  • Top arrow: Early After Depolarization
  • Bottom Arrow: Delayed After Depolarization
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34
Q

What are the three components necessary to have a reentry arrhythmia?

A
  1. Parallel fast and slow conduction pathway
  2. Unidirectional block
  3. Final common pathway
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36
Q

Describe the mechanism of reentry arrhythmia

A
  1. An extrasystole may occur when the fast pathway is still refractory, sending a signal down the slow pathway
  2. The slow signal reaches the His and may find the fast pathway and return to the atria
  3. The signal is propagated up the fast path to the slow pathway where steps 1-3 can happen over and over and over and over and over….
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38
Q

A patient has an EKG tracing showing the following. What is the arrow pointing to? What is the diagnosis? What is the mechanism?

A
  1. DELTA Wave
  2. Wolff-Parkinson-White
  3. An abnormal accessory conduction pathway betwixt the atria and ventricles conducts signal faster than the AV node and can result in tachyarrhythmias
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40
Q

Shown below are schematics of the AV node an aberrant connection betwixt the atrium and the ventricle. The arrow indicates the direction of the signal flow. What is the diagnosis for 1? 2?

A
  1. Orthodromic Atrioventricular Reentrant Tachycardia
  2. Antidromic Atrioventricular Reentrant Tachycardia
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42
Q

Diagnosis? Rhythm?

A

Atrial fibrillation; Irregularly Irregular

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43
Q

How do you treat a bradyarrhythmia?

A

Withhold inciting agents and use a pacemaker if needed.

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45
Q

What are 3 broad strategies used to treat tachyarrhythmias?

A

Ablation therapy, antiarrhythmic agents, and implantable defibrillators.

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47
Q

How does ablation work?

A

Radio frequency is used to permanently disable culprit tissue (areas of reentry or accessory pathways).

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49
Q

Which of the great vessels may be isolated from the heart in attempt to fix atrial fibrilation?

A

The pulmonary veins (isolated from the left atrium).

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51
Q

What is another name for membrane active agents?

A

Antiarrhythmics.

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53
Q

What are the pros and cons of ablation?

A

Pro: if the mechanism of arrhythmia is identified and targeted appropriately, ablation is likely to be successful in curing the arrhythmia. Con: ablation is invasive with procedural risks (ex. create a heart block).

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55
Q

What are the pros and cons of antiarrhythmic use?

A

Pro: It is non-invasive and can be stopped at any time. Con: these drugs are not specific in vivo and carry substantial pro-arrhythmic risks as well as other side effects.

57
Q

Describe the ideal antiarrhythmic.

A
  • Has specific activities against arrhythmia mechanism. - Specifically targets the site of arrhythmia. - Clear mechanism of action in vivo. - Safe (not pro-arrhythmic). - Effective (terminates and prevents recurrence). - No negative inotropic effect. - Does not interfere with other drugs. - No end organ toxicity.
59
Q

Are the characteristics of the idea antiarrhythmic agent found in todays drugs?

A

No. We have a limited understanding of in vivo action, and mechanisms are postulated based on in vitro effects. Most work on both the atria and the ventricles.

61
Q

What are the genera mechanisms of action of antiarrhythmics?

A
  • Decrease automaticity. - Prevent reentry and triggered activities. - Prolong the refractory period. - Inhibit conduction (negative dromotropy).
63
Q

Which parts of the heart have a calcium dependent upstroke (phase 0)?

A

The SA and A/V nodes.

65
Q

What channel’s recovery determines the refractory period of the His-Purkinje system and the ventricular myocytes?

A

Fast sodium channels.

67
Q

What should be done before initiating any antiarrhythmic?

A

A precise diagnosis of the arrhythmia should be made with identification of the substrate, trigger, and mechanism of the arrhythmia. Risks and benefits in light of the patient should be considered for any drug.

69
Q

How are the Vaughan Williams classes organized?

A

Based on in vitro channel blocking properties. This does not have any real clinical value and important agents (Adenosine, Digoxin) are left out.

71
Q

Name the four classes and their drugs.

A

Ia: Quinidine, procainamide, disopyramide. Ib: Lidocaine, mexiletine, tocainide. Ic: Flecainamide, propafenone, moricizine. II: Beta blockers. III: Amiodarone, dronedarone, sotalol, ibutilide, dofetilide, bretylium. IV: Verapamil, diltiazem (Non-dihydropyridine calcium channel blockers).

73
Q

What is the difference between use dependence and reverse use dependence?

A

Use dependent drugs bind activated channels are work better in tachycardia. Reverse use dependence drugs work on resting membranes and are less effective in tachycardia.

75
Q

What channel(s) do the Ia agents block? How does this change the action potential?

A

They block sodium (at high dose and fast heart rate) and potassium (IKr) (at low dose and slow heart rate) channels. The action potential duration and the refractory period are increased.

77
Q

What is quinidine used for?

A

Atrial fribrillation (though secondary to other drugs), Brugada’s syndrome, and short QT syndrome.

79
Q

Where is quinidine metabolized and what are its side effects?

A

Hepatic metabolism. - Cinchonism. - Nausea and diarrhea. - Torsades de pointes (enhanced by hypokalemia (such as from thiazide and loop diuretics). - Displaces digoxin from protein binding. - Quinidine syncope.

81
Q

What is procainamide used to treat and how is it metabolized?

A

Pre-excited atrial fibrillation. Procainamide prolongs the QRS, slows conduction, slows the SA and A/V nodes. Metabolized in the liver via acetylation to NAPA (N-acetyl procainamide which is an active class III antiarrhythmic).

83
Q

What are the side effects of procainamide?

A
  • Hypotension (due to ganglion block). - Drug induced lupus in 1/3 of cases.
85
Q

What is disopyramide used for and how does it act?

A

Vagally-mediated atrial fibrillation. Disopyramide is a vagolytic drug as well as a sodium channel blocker. It is also used for ventricular tachycardia.

87
Q

What are the side effects of disopyramide?

A

It can worsen ejection fraction in those with prior morbidity due to negative inotropic actions. It also causes anticholinergic side effects (urinary retention, blurred vision, worsening glaucoma).

89
Q

How do the class Ib drugs work?

A

They bind to and block inactivated sodium channels in ischemic or damaged tissues, thereby preventing ventricular tachycardia by blocking slow pathways. This shortens the action potential duration (shorter QT) and therefore may be given with drugs that prolong the QT. Ib drugs do not work in atrial tissue.

91
Q

Which Ib drug is given via IV and which one is given orally? Why can’t the former be given orally?

A

Lidocaine is given by IV and mexiletine is given orally because oral lidocaine is almost entirely metabolized on first pass of the liver.

93
Q

What are the side effects of lidocaine?

A

Although it is the least proarrhythmic of any of the antiarrhythmics, lidocaine may cause SA node arrest and impaired conduction. It also causes neurologic side effects including tremor, slurred speech, convulsion, and confusion after 3 days of use.

95
Q

What is the side effect of mexilietine?

A

GI toxicity.

97
Q

When are the class Ic drugs used and not used?

A

As the most potent class I drugs, the Ic drugs are used to eliminate potent PVCs but are not used during ischemia (due to proarrhythmic effect) or LV dysfunction (due to negative inotropic effect).

99
Q

Do class Ic drugs affect the action potential duration?

A

No. They are sodium channel blockers only which slow the phase 0 upstroke without affecting the QT. However, they do prolong the atrial refractory period.

101
Q

Which Ic drug has an active metabolite?

A

Propafenone has 5-hydroxypropafenone.

103
Q

How are beta blockers antiarrhythmogenic? What conditions are they used for?

A

They increase the refractory period of the A/V node. They may be used in atrial tachycardias and ventricular tachycardias (although the mechanism is unclear), supraventricular tachycardias, sinus tachycardias, and premature ventricular complexes.

105
Q

What are the side effects of beta blockers and when are they contraindicated?

A

Side effects include (among others) bradycardia, bronchospasm, worsening claudication, impotence, fatigue. Contraindications include severe bradycardia, sick sinus syndrome, heart block, unstable LV dysfunction. Relative contraindications are asthma, severe peripheral vascular disease, and severe depression.

107
Q

How do class III antiarrhythmics work? Do they work better at slow or fast heart rates? How do they affect the action potential? What is the major risk of class III drugs?

A

Class III drugs are potassium channel (IKr) blockers. They work best in slow hearts. They increase the action potential duration and the refractory period (QT prolongation). Thus, they cause a risk of Torsades de pointes.

109
Q

Which of the class III drugs are excreted renally?

A

Sotalol and dofetilide.

111
Q

What is special about sotalol? What tests need to be performed while a patient is on sotalol?

A

Sotalol is also a non-specific beta blocker. Serum K, Mg, and renal function should be closely followed.

113
Q

When is amiodarone used? How does its potency compare to other class III drugs?

A

It is used for atrial and ventricular tachyarrhythmias. It is more potent than sotalol.

115
Q

What are the side effects of amiodarone?

A
  • Hypo- or hyperthyroidism. - Pulmonary fibrosis. - Corneal deposits. - Liver toxicity. - Blue skin. - Photosensitivity. - GI distress. - Ataxia. - Torsades de pointes (although not very common). - Inhibition of CytP450 with increased activity of many drugs. Must evaluate LFTs, PFTs, thyroid hormone levels, opthalmologic examination, ECG, CXR, and renal function tests.
117
Q

What is dronedarone and how does it differ from amiodarone?

A

It is a milder version of amiodarone that does not contain iodine. It is less effect and less toxic (non-toxic to the lungs and thyroid). However, it is contraindicated in heart failure.

119
Q

What is a concern when starting a patient on ibutalide or dofetilide?

A

Both have a chance of creating an arrhythmia (Torsades de pointes) with onset of medication. Therefore, patients need to be kept in the hospital for 4 hours after initiating ibutalide and 3 to 5 days after initiating dofetilide (with subsequent EKG monitoring every few months).

121
Q

Describe the channel affects of ibutalide and dofetilide and their respective uses.

A

Ibutalide is a potassium channel (IKr) blocker and an initiator of slow inward Na current. It is used for atrial flutter more than atrial fibrillation. Dofetilide is a pure IKr channel blocker that is used for atrial fibrillation. Dofetilide is the most widely studied antiarrhythmic agent including trials in patients with MI and HF.

123
Q

Which two drugs belong in class IV and how do they work against arrhythmias?

A

Diltiazem and verapamil are the two drugs. They inhibit L-type calcium channels to slow the impulse of the SA and A/V nodes, increasing conduction time and refractoriness. They are both used for supraventricular tachycardia.

125
Q

What are the side effects and contraindications for class IV agents?

A

They are negative chronotropic and inotropic agents which can decrease cardiac output. They can also cause leg edema and constipation. They are contraindicated in sick sinus syndrome, severe bradycardia, heart block, and decompensated heart failure

127
Q

How does Adenosine work? Which class does it belong to?

A

Adenosine activates potassium currents and inhibits calcium currrents (via Gi receptors) to hyperpolarize heart tissue. This shortens the action potential while slowing automaticity and decreasing A/V conduction. Adenosine only works in atrial tissue. It does not belong to any of the classes.

129
Q

What are the side effects of adenosine?

A

Flushing, sedation, dyspnea, chest tightness, and nausea.

131
Q

When is adenosine used?

A

It is the drug of choice for supraventricular tachycardia. It causes a brief (half life is 10 seconds) blockade of the A/V node in attempt to reset for sinus conduction.

133
Q

What is Torsades de pointes? What may be used to treat it? How?

A

Torsades de pointes is a ventricular tachycardia caused by a lengthening QT. It may be treated with Mg ions which outcompete calcium ions. Mg ion salts may also be used to treat digitalis toxicity.

135
Q

What is the most troubling complication of atrial fibrillation?

A

Stroke from coagulation in static left atrium.

137
Q

What is the difference between the upstream and downstream approaches of arrhythmia treatment?

A

Upstream prevents the evolution of disease processes that are arrhythmogenic (such as ischemic hypertrophy). Drugs include ACEIs, ARBs, and Statins. Downstream therapy treats arrhythmias once they have occurred.

Pharmacology Unit 4 (9 decks)

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