Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IC 1.0 > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What is the recommended treatment for asymptomatic or minimally symptomatic arrhythmias?

A

they are not treated because the drugs used to treat arrhythmias can also precipitate lethal arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

PACs/PVCs

A
  • premature atrial/ventricular contractions
  • the most common type of minor/harmless arrhythmia
  • can be due to heart disease, stress, too much exercise, caffeine, or nicotine
  • presents as a feeling of fluttering in the chest or a skipped beat
  • no need for treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are supraventricular arrhythmias? Which specific arrhythmias belong to this group?

A
  • tachycardias that start in the atria or SA node
  • includes atrial fibrillation, atrial flutter, paroxysmal supraaventricular tachycardia, and Wolff-Parkinson White syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Atrial Fibrillation

A
  • the most common type of serious arrhythmia and a supraventricular arrhythmia
  • defined by electrical signals that do not begin in the SA node, but rather other parts of the atria or pulmonary vein
  • the result is an irregular, fast heart beat
  • the primary risk is that blood pools in the atria and can form clots, contributing to stroke, or that it will lead to heart failure
  • primary treatment, then, is a blood thinner
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Atrial Flutter

A
  • a supraventricular arrhythmia defined by a regular, fast heart beat (250-350 bpm) with the atria beating faster than the ventricles
  • if the ventricular rate is less than 120 bpm, it is often asymptomatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Paroxysmal Supraventricular Tachycardia

A
  • a supraventricular arrhythmia defined by a regular heart rate at 150-250 that begins and ends suddenly
  • due to signals beginning in the atria which travel to the ventricles and then re-enter the atria, resulting in extra heart beats
  • more common in young people and can be due to alcohol, nicotine, caffeine, and vigorous activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Wolff-Parkinson White syndrome

A

a syndrome of paroxysmal supraventricular tachycardia, SOA, lightheadedness, and syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the Bundle of Kent?

A

an accessory tract pathway that bypasses the regular conduction pathway through the heart, predisposing patients to tachyarrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which tends to be more serious, an atrial or ventricular arrhythmia?

A

ventricular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ventricular Tachycardia

A
  • an arrhythmia characterized by fast but regular beating of the ventricles
  • short episodes are typically not a problem but longer episodes can be dangerous and turn into more serious arrhythmias, particularly ventricular fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ventricular Fibrillation

A
  • the most serious arrhythmia
  • characterized by uncontrolled, irregular beats up to 300 bpm
  • very chaotic, thus very little blood is pumped out and death can occur in minutes
  • preferred treatment is defibrillation to restore normal rhythm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bradycardia

A
  • a heart rate of less than 60 bpm
  • result because an impulse is not being formed by the SA node or isn’t being conducted properly to the ventricles
  • most often seen in the elderly or those taking anti-hypertensive/anti-arrhythmic drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What factors are known to precipitate arrhythmias?

A
  • ischemia/hypoxia
  • acidosis and alkalosis
  • electrolyte disturbances
  • excessive catecholamine exposure
  • drug toxicities
  • overstitching of muscle fibers, scarred, or diseased tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

All arrhythmias have what in common?

A

they result from disturbances of impulse formation or conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List several factors that all increase the pacemaker rate of the SA node by increasing the slope of phase 4 depolarization.

A
  • beta receptor stimulation
  • hypokalemia
  • positive chronotropic drugs
  • fiber stretch
  • acidosis
  • partial depolarization by currents of injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do EADs compare to DADs?

A
  • EADs are usually at slower heart rates, they interrupt phase 3, and they contribute to long QT-related arrhythmias
  • DADs are usually at faster heart rates and associated with digoxin excess, catecholamines, or myocardial ischemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What three conditions must be met for there to be a re-entry loop?

A
  • conduction has to be blocked by some obstacle, anatomic or physiologic
  • the block must be unidirectional
  • conduction time around the block must exceed refractory period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the difference between therapeutic and toxic doses of anti-arrhythmic drugs?

A
  • therapeutic doses usually affect abnormal tissues more

- toxic disease tend to affect normal tissues as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How might a toxic dose of an anti-arrhythmatic drug induce an arrhythmia?

A
  • a therapeutic dose of the same drug preferentially affects abnormal tissue
  • at higher, toxic dose, however, normal tissues are also affected
  • this may slow conduction enough in normal pathways to allow for a re-entrant loop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why are anti-arrhythmic drugs so carefully controlled?

A
  • because they have the potential for causing life-threatening arrhythmias themselves
  • furthermore, there is a very narrow margin of safety and therapeutic doses may very well overlap with toxic ones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the major mechanisms anti-arrhythmic drugs use to stop arrhythmias?

A

they either slow down heart rate (rate control) or change abnormal rhythm to normal rhythm (rhythm control)

  • can do so by blocking sodium, potassium, or calcium currents
  • or blocking sympathetic autonomic effects
  • or prolonging the refractory period
22
Q

What role can anti-arrhythmic drugs play in treating bradycardia?

A

they can’t because they aren’t able to reliably speed up the heart, a pacemaker is required instead

23
Q

How can anti-arrhythmic drugs prolong the refractory period of a cell?

A

by binding ion channels that facilitate depolarization and stabilizing the inactive form (closed gate conformation)

24
Q

What are the three major classes of drugs used for rate control of arrhythmias?

A
  • beta blockers
  • calcium channel blockers
  • digoxin
25
Q

What are the two major drug classes used for rhythm control of arrhythmias?

A

potassium and sodium channel blockers

26
Q

How are anti-arrthymic drugs classified?

A
  • Class I: sodium channel blockers
  • Class II: beta blockers
  • Class III: potassium channel blockers
  • Class IV: calcium channel blockers
  • Class V: other
27
Q

How do class I anti-arrthymic drugs work?

A

they decrease heart rate by blocking sodium channels and thereby elevating the threshold for excitation and decreasing the slope of phase 4 depolarization of the SA node

28
Q

Generally speaking, how do Class IA, IB, and IC anti-arrhythmics compare to one another?

A
  • all three slow depolarization (flatten phase 0) but to different degrees based on strength of blocking activity
  • IA have moderate blocking activity, dissociated with intermediate kinetics, and prolong action potential duration
  • IB have mild blocking activity, fast dissociation, and shorten action potential duration
  • IC have strong sodium channel blocking activity, slow dissociation, and minimal effect on APD
29
Q

Which drugs are Class IA, IB, and IC anti-arrhythmcis?

A
  • IA: procainamide, quinidine, disopyramide
  • IB: lidocaine, mexiletine
  • IC: flecainide, propafenone, moricizine
30
Q

Procainamide

A
  • a class IA anti-arrhythmic drug
  • it increases the effective refractory period of the atria and ventricles and can directly depress the SA and AV nodes
  • it prolongs action potential duration by nonspecific blocking of potassium channels (presents with long QT)
  • also has ganglion-blocking activity which reduces peripheral vascular resistance and can lead to hypotension
  • toxicity: may cause excessive action potential prolongation, inducing tornadoes de pointes, arrhythmia, or syncope
  • with long-term use, may see a reversible lupus-like syndrome with rash, arthralgia, arthritis, and pericarditis
  • nausea, diarrhea, hepatitis, and agranulocytosis are also possible
  • it does NOT elevate digoxin levels
  • effective agents most atrial and ventricular arrhythmias
  • less useful for long-term oral treatment because of it’s short half-life and adverse effects
  • drug of second or third choice for sustained ventricular arrhythmias associated with MI
31
Q

What are the drugs of choice for sustained ventricular arrhythmias associated with MI?

A
  • lidocaine
  • amiodarone
  • procainamide
    in that order
32
Q

Quinidine

A
  • a class IA anti-arrhythmic drug
  • it increases the effective refractory period of the atria and ventricles and can directly depress the SA and AV nodes
  • like procainamide, it prolongs action potential duration by nonspecific blocking of potassium channels (presents with long QT)
  • has a modest anti-muscarinic effect and blocks alpha-adrenergic receptors to cause tachycardia and vasodilation
  • side effects include marked hypotension and reflex tachycardia, thrombocytopenia, torsade de pointes, cinchonism (headache, dizziness, tinnitus)
  • it increases plasma digoxin and may precipitate digoxin toxicity
  • rarely used because of the cardiac and extra cardiac adverse effects
33
Q

Disopyramide

A
  • a class IA anti-arrhythmic drug
  • it increases the effective refractory period of the atria and ventricles and can directly depress the SA and AV nodes
  • like procainamide, it prolongs action potential duration by nonspecific blocking of potassium channels (presents with long QT)
  • has a strong anti-muscarinic effect and can contribute to tachycardia
  • it’s adverse effects are related to this atropine-like activity: urinary retention, dry mouth, blurred vision, constipation, worsening of pre-existing glaucoma
  • contraindicated in those with BPH as it can cause urinary retention as an anticholinergic
  • only approved for ventricular arrhythmias but not used very often because of its antimuscarinic effects and its negative inotropic action, which may induce CHF
34
Q

Compare and contrast the Class IA anti-arrhythmias.

A
  • all block sodium and potassium channels
  • all can prolong action potential duration and induce torsade de pointes
  • disopyramide > quinidine > procainamide antimuscarinic activity
  • procainamide is unique in that it can induce a lupus-like syndrome
  • quinidine is the only one that can induce thrombocytopenia or digoxin toxicity and is the only one with alpha-adrenergic blocking activity
35
Q

Lidocaine

A
  • a class IB anti-arrhythmic drug
  • it blocks activated and inactivated sodium channels with rapid kinetics in the Purkinje fibers and ventricular cells
  • the result is elevated threshold for excitation, reduced automaticity, and suppressed electrical activity of diseased tissue
  • it does not affect atrial tissue or normal ventricular tissue and does not block potassium channels (no torsade de pointes)
  • it is the least cardiotoxic of all currently available sodium blockers and a high degree of effectiveness in ventricular arrhythmias associated with depolarization as in post-MI or digoxin toxicity
  • the agent of choice for termination of V tach and to prevent V fib after cardioversion
  • it must be given IV because of high first-pass metabolism
  • most common side effects are neurologic (paresthesia, tremor, hearing disturbances, slurred speech) but in patients with CHF, high doses can contribute to hypotension
  • seizures are most common after rapid IV administration in elderly patients
36
Q

Mexiletine

A
  • a class IB anti-arrhythmic
  • a lidocaine analog resistant to first-pass metabolism and therefore is effective orally
  • electrophysiology and anti-arrhythmic actions resemble lidocaine
  • can also be used off-label for relief of chronic pain especially for diabetic neuropathy and nerve injury
37
Q

What is the major contraindication for class IC anti-arrhythmias?

A

they increase mortality from cardiac arrest or arrhythmic sudden death in patients with recent MI

38
Q

Flecainide

A
  • a class IC anti-arrhythmic
  • it blocks sodium and potassium channels without QT prolongation, and it has no anti-muscarinic effects
  • it is used to treat supraventricular arrhythmias and is very effective in suppressing premature ventricular contractions
  • increases mortality from cardiac arrest or arrhythmic sudden death in patients with recent MI
39
Q

Propafenone

A
  • a class IC anti-arrhythmic
  • blocks sodium channels and has weak beta-blocking activity
  • it is used to treat supraventricular arrhythmias and is very effective in suppressing premature ventricular contractions
  • it has a metallic taste, can exacerbate arrhythmias, and can cause constipation
  • increases mortality from cardiac arrest or arrhythmic sudden death in patients with recent MI
40
Q

Class II Anti-Arrythmics

A
  • a group of beta-adrenergic blockers
  • beneficial effects are due to diminished sympathetic activation of heart and vasculature as well as diminished cardiac workload and O2 demand
  • propranolol (nonselective) and acebutolol (B1 selectivity) are most frequent used to prevent ventricular fibrillation or to treat arrhythmias caused by sympathetic stimulation
  • esmolol (B1 selective) is a short acting drug that can be used for acute arrhythmias during surgery
  • they have potential to induce or worsen CHF in patients with MI or decompensated heart failure because of their negative inotropic effects
  • CNS penetration may lead to insomnia and depression
41
Q

Which beta blockers are most commonly used as Class II anti-arrhythmics?

A
  • propanolol
  • acebutolol
  • esmolol
42
Q

Amiodarone

A
  • a class III anti-arrhythmic
  • prolongs AP duration by blocking potassium channels, decreases the rate of firing in pacemaker cells by blocking inactivated sodium channels, and blocks alpha-and beta-adrenergic receptors and calcium channels to inhibit AV node conduction to produce bradycardia
  • also cause peripheral vasodilation
  • oral and IV formulations available to maintain normal sinus rhythm in patients with atrial fibrillation or to prevent recurrent ventricular tachycardia
  • long half life: rapid component for 3-10 days followed by the slower component acting for several weeks
  • metabolized by CYP3A4 and inhibits other liver cytochromes to elevate levels of digoxin and warfarin
  • has a unique set of toxicities
  • long half life contributes to toxicity long after the drug is discontinued
  • these include asymptomatic bradycardia and AV block in patients with SA or AV node disease, respiratory difficulties leading to fatal pulmonary fibrosis, abnormal liver function and hepatitis, skin deposits resulting in photo dermatitis and grayish-blue skin discoloration in sun-exposed areas
  • nearly all patients develop corneal micro deposits which reduce visual acuity, contribute to optic neuritis, and can progress to blindness
  • need to evaluate thyroid function before treatment, because the drug blocks peripheral conversion of T3 to T4 (may result in hypo- or hyperthyroidism)
  • contraindicated in patients with advanced lung disease
43
Q

Dronedarone

A
  • a derivative of amiodarone (class III anti-arrhythmic) without iodine atoms
  • it blocks several potassium and sodium channels to prolong AP duration, suppress pacemaker rate, and inhibit AV node conduction
  • lack of iodine means that it generates no thyroid dysfunction or pulmonary toxicity
  • however, there is liver toxicity and a black box warning for increased risk of death, stroke, and heart failure in those with decompensated heart failure or permanent atrial fibrillation
44
Q

Sotalol

A
  • a class III anti-arrhythmic drug
  • it is a non-selective beta blocker activity which also blocks potassium channels to prolong action potential duration and the refractory period
  • used for treatment of ventricular arrhythmias, maintaining sinus rhythm in atrial fibrillation, and treatment of supraventricular and ventricular arrhythmias in pediatrics
  • may cause torsade de pointes
45
Q

Dofetilide and Ibutilide

A
  • class III anti-arrhythmias which block the rapid component of the delayed rectifier potassium current to slow cardiac repolarization
  • effective in restoring normal sinus rhythm in atrial fibrillation and flutter
  • prolonged QT and torsade de pointes are common
46
Q

Class IV anti-arrhythmics

A
  • verapamil and diltiazem
  • block L-type calcium channel in myocardium and vascular smooth muscles
  • thereby, decreasing contractility, reduce SA node automaticity, and slow AV node conduction
  • oral CCBs are used for treatment of supraventricular arrhythmias and for rate control of atrial fibrillation
  • nifedipine is not used as an anti-arrhythmic as it is likely to cause reflex tachycardia, due to more pronounced vasodilation
47
Q

Adenosine

A
  • a potential anti-arrhythmic
  • opens rectifier potassium channels to cause hyper polarization, inhibits L-type calcium channels to reduce conduction velocity in the AV node, and inhibits pacemaker current (less SA effect than AV)
  • given IV to convert paroxysmal supraventricular tachycardia to sinus rhythm
  • half life of less than 10 seconds
  • adverse effects: flushing, SOA, chest burning, headache, hypotension, paresthesia
48
Q

Digoxin

A
  • a potent and selective inhibitor of Na/K-ATPase which competes for the K binding site and indirectly increases intracellular calcium
  • it stimulates the vagus nerve and decreases heart rate
  • used in atrial fibrillation
  • narrow therapeutic window and enhanced toxicity with quinidine, amiodarone, captopril, verapamil, diltiazem, and cyclosporine
  • furthermore, drugs that produce a hypokalemia enhance toxicity
  • many antibiotics increase absorption and contribute to toxicity
  • toxicity presents first with GI effects (n/v, diarrhea, abdominal discomfort) and then cardiac toxicity (arrhythmias)
49
Q

Of what benefit is magnesium as an anti-arrhythmic?

A

it has an unknown mechanism of action but has been used to prevent torsade de pointes and treat digoxin-induced arrhythmias

50
Q

How is chronic atrial fibrillation treated?

A
  • rate or rhythm control

- plus warfarin

IC 1.0 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions