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Pharmacology 2 > Antiarrhythmic > Flashcards

Antiarrhythmic Flashcards

1
Q

What are factors that can facilitate cardiac arrhythmias?

A
  • Hypoxemia
  • Electrolyte and acid-base abnormalities
  • Myocardial ischemia
  • Altered Sympathetic Nervous System
  • Bradycardia
  • Administration of Certain Drugs
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2
Q

What are some supraventricular arrhythmias that require treatment?

A

Irregular beats to slow or to fast

  • Bradycardia
  • Tachycardia
  • Atrial fibrillation
  • Atrial flutter (this might need to be a more aggressive treatment if this shows up
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3
Q

What are some ventricular arrhythmias that require treatment?

A

Ventricular Arrhythmias:

  • V-Fib (need to be aggressive with this)
  • V-Tach (this needs to be aggressive with treatment)
  • PVC’s (this depends on the patient, may not need to treat this)
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4
Q

Normal Conduction Pathway

The SA node generates action potential and delivers it to the Blank and the Blank

A

SA node generates action potential and delivers it to the atria and the AV node

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5
Q

Normal Conduction Pathway

The AV node delivers the impulse to the BLANK

A

The AV node delivers the impulse to the purkinji fibers

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6
Q

Normal Conduction Pathway

The purkinje fibers conduct the impulse to the BLANK

A

Purkinje fibers conduct the impulse to the ventricles

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7
Q

What are two types of cardiac action potential cells?

A
  1. Nodal (SA and AV nodes)

2. Cardiac Myocytes

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8
Q

With anti arrhythmic drugs, the CRNA is doing what?

A

RESETTING THE IONS!!!! This is what happens when we give medications..
RESETTING CONCENTRATION GRADIENTS!!!

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9
Q

Where are the Cardiac Myocyte and how many phases do they have?

A

In the atria, purkinje, and ventricles the AP curve consists of 5 phases

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10
Q

Where are the Nodal Myocytes and how many phases do they have?

A

In the SA node and AV node, AP curve consists of 3 phases

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11
Q

In a Nodal Myocyte, what happens during Phase 4?

A

Phase 4: pacemaker potential

Na influx and K efflux and Ca influx until the cell reaches threshold and then turns into phase 0

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12
Q

In a Nodal Myocyte, what happens during Phase 0?

A

Phase 0: upstroke:

Due to Ca++ influx

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13
Q

In a Nodal Myocyte, what happens during Phase 3?

A

Phase 3: repolarization:

Due to K+ efflux

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14
Q

What is the significance of the pacemaker cells having an unstable membrane?

A

Pacemaker cells (automatic cells) have unstable membrane potential so they can generate AP spontaneously

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15
Q

In a Cardiac Myocyte, what happens during Phase 0?

A

Phase 0, Depolarization - Voltage-gated sodium channels open allowing the rapid influx of sodium ions

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16
Q

In a Cardiac Myocyte, what happens during Phase 1?

A

Phase 1, Initial repolarization - Inactivation of voltage-gated sodium channels; voltage-gated potassium channels open allowing efflux of potassium ions

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17
Q

In a Cardiac Myocyte, what happens during Phase 2?

A

Phase 2, Plataeu - Voltage-gated calcium channels open allowing influx of calcium ions this also triggers calcium release from the sarcoplasmic reticulum which leads to increase myocyte contraction

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18
Q

In a Cardiac Myocyte, what happens during Phase 3?

A

Phase 3 Rapid repolarization - More voltage-gated slow potassium channels open allowing major enfflux of potassium ions; voltage-gated calcium channels close

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19
Q

In a Cardiac Myocyte, what happens during Phase 4?

A

Phase 4 Resting potential - Cell is resting, or waiting for next action potential; a few potassium channels remain open, allowing for slow potassium permeability.

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20
Q

What is the Effective refractory period? or absolute refractory period?

A
  • -In this period the cell can’t be excited
  • –Takes place between phase 0 and 3
  • -During a cardiac cycle, once an action potential is initiated, there is a period of time that a new action potential cannot be initiated. This is ERP
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21
Q

What is considered a supraventricular arrhythmia?

A

If the arrhythmia arises from atria, SA node, or AV node it is called supraventricular arrhythmia

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22
Q

What is considered a ventricular arrhythmia?

A

If the arrhythmia arises from the ventricles it is called ventricular arrhythmia

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23
Q

Mechanisms of Arrhythmogenesis

If an abnormal impulse is generated from a Myocyte, what are two possibilities can occur?

A

You can have a Delayed after depolarization, digoxin induced ventricular ectopy

or a Early after depolariztion, torsades, R on T

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24
Q

Mechanisms of Arrhythmogenesis

If an abnormal impulse is generated from a Nodal cell, what two possibilities can occur?

A

An enhanced normal automaticity, which is two fast, that leads to increase AP from the SA node, this will increase the slope of Phase 4

or

Ectopic focus, such as junctional rhythms which the AP arises from sites other than the SA node

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25
Q

In the case of an abnormal generation of an impulse in a nodal myocyte, what two changes can occur in the AP?

A

Decrease of phase 4 slope (in pacemaker cells)

or

Raises the threshold

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26
Q

In the case of an abnormal generation of an impulse in a nodal and cardiac myocyte, what two changes can occur in the AP?

A

decrease in conduction velocity (remember phase 0)

or

Increase in ERP (so the cell wont be reexcited again)

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27
Q

What are some Supraventricular Arrhythmias?

skipped this on lecture

A

Sinus Tachycardia: high sinus rate of 100-180 beats/min, occurs during exercise or other conditions that lead to increased SA nodal firing rate

Atrial Tachycardia: a series of 3 or more consecutive atrial premature beats occurring at a frequency >100/min

Paroxysmal Atrial Tachycardia (PAT): tachycardia which begins and ends in acute manner

Atrial Flutter: sinus rate of 250-350 beats/min.

Atrial Fibrillation: uncoordinated atrial depolarizations.

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28
Q

What is an AV block?

skipped this in lecture

A

A conduction block within the AV node , occasionally in the bundle of His, that impairs impulse conduction from the atria to the ventricles.

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29
Q

What are some Ventricular Arrhythmias?

skipped this in lecture

A

Ventricular Premature Beats (VPBs): caused by ectopic ventricular foci; characterized by widened QRS.

Ventricular Tachycardia (VT): high ventricular rate caused by abnormal ventricular automaticity or by intraventricular reentry; can be sustained or non-sustained (paroxysmal); characterized by widened QRS; rates of 100 to 200 beats/min; life-threatening.

Ventricular Flutter - ventricular depolarizations >200/min.

Ventricular Fibrillation - uncoordinated ventricular depolarizations

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30
Q

What is the ultimate goal of antiarrhythmic drug therapy?

A

Restore normal sinus rhythm and conduction

Prevent more serious and possibly lethal arrhythmias from occurring.

31
Q

What are Antiarrhythmic drugs used for?

A

—Decrease conduction velocity (slow things down)
The speed with which an electrical impulse can be transmitted through excitable tissue, ie, action potential through His Purkinje Fibers of the heart
—Change the duration of the effective refractory period (ERP) (so you don’t go to fast)
Once an AP is initiated, there is a period of time a new AP can’t be initiated.
—Suppress abnormal automaticity (this is on the electrical part, we want to decrease this so we don’t have any arrhytmias)
Cardiac cells ability to spontaneously generate an electrical impulse (depolarize)

32
Q

Class IA Antiarrhythmics, How intense is the sodium channel blockade?

A

Quinidine

Moderate Na Channel blockade

increase ERP

33
Q

Class IB Antiarrhythmics, How intense is the sodium channel blockade?

A

Lidocaine

Weak Na Channel blockade

Decrease ERP

34
Q

Class IC Antiarrhythmics, How intense is the sodium channel blockade?

A

Flecainide

Strong Na Channel Blockade

EPR?

35
Q

What is the MOA of Ia antiarrhytmics?

A

Block fast (Na) channels in the “activated/open state” which leads to a decrease rate and rise of action potential

Block (K) channels which leads to Increased duration of action potential

36
Q

What are the uses of Class Ia Antiarrhythmics?

A

Ventricular tachy arrhythmias

Wolff-Parkinson-White syndrome

Paroxysmal recurrent atrial fibrillation

Supraventricular and ventricular arrhythmias

37
Q

What are some examples of Class Ia Antiarrhythmics?

A

Quinidine

Procainamide

Disopyramide

38
Q

What are some adverse effects of Quinidine?

A
  • -Nausea, vomiting, diarrhea.
  • -Large doses may produce cinchonism( tinnitus, ocular dysfunction, CNS excitation). hypotension,
  • —Prolongation of QRS and increase in QT interval associated with syncope( which is due to ventricular arrhythmia induced by quinidine)**,
  • -Torsade de pointes.
  • –Thrombocytopenia that disappear on drug withdrawal.
  • -Enhances digoxin toxicity
  • –Due to it’s side effect profile and low therapeutic index and the availability of newer agents, quinidine is rarely used!!!
39
Q

What is the MOA of class Ib Antiarrhythmics?

A

Block (Na) channels in the “activated & Inactivated states” which leads to decrease rate and rise of action potential

Decrease residual (Na) plateau influx which leads to decrease length of Phase 2

40
Q

What are some examples of class Ib Antiarrhythmics drugs?

A

Mexiletine

Lidocaine

Phenytoin

41
Q

What are the class Ib Antiarrhythmics used to treat?

A

Ventricular tachycarias

42
Q

What is the MOA of class Ic Antiarrhythmics?

A

Block (Na) channels in the “activated state” which leads to the largest decrease of rate and rise of action potential

43
Q

What are some examples of class Ic Antiarrhythmics?

A

Flecainide

Moriczine

Propafenone

44
Q

What are class Ic Antiarrhythmics used for??

A

Paroxysmal atrial fibrillation

45
Q

Which class 1 antiarrhythmic drug is noted to have an increase in mortality when used after chronically after an MI?

A

Notice: Class 1C drugs are particularly of low safety and have shown even increase mortality when used chronically after MI****

46
Q

What is the MoA of Class II ANTIARRHYTHMIC DRUGS (β-adrenergic blockers)?

A

Mechanism of action

  • -Negative inotropic and chronotropic action.
  • -Prolong AV conduction (delay)
  • –Diminish phase 4 depolarization which leads to suppressing automaticity(of ectopic focus)
47
Q

How does Class III ANTIARRHYTHMIC DRUGSK+ blockers work?

A
  • –Prolongation of phase 3 repolarization without altering phase 0 upstroke or the resting membrane potential
  • –They prolong both the duration of the action potential and ERP
  • –Their mechanism of action is still not clear but it is thought that they block potassium channels
48
Q

What are some examples of Class III antiarrhytmics?

A

Sotalol

Amiodarone

Ibutilide

49
Q

What other properties dose sotalol have besides beta receptor blocker?

A

It is a non-selective competitive β-adrenergic receptor blocker that also exhibits Class III antiarrhythmic properties by its inhibition of potassium channels.

Because of this dual action, Sotalol prolongs both the PR interval and the QT interval.

50
Q

What is the MOA for amiodarone?

A

Amiodarone is categorized as a class III antiarrhythmic agent, and prolongs phase 3 of the cardiac action potential, the repolarization phase where there is normally decreased calcium permeability and increased potassium permeability.

51
Q

What is amiodarone used for?

A

Amiodarone is an antiarrhythmic agent used for various types of cardiac dysrhythmias, both ventricular and atrial.

It is similar to those of antiarrhythmic classes I a, II, and IV

Amiodarone antiarrhythmic effect  is complex comprising class I, II, III, and IV actions!!!!
Dominant effect: Prolongation of action potential duration and refractoriness
It slows cardiac conduction, works as Ca2+ channel blocker, and as a weak β-adrenergic blocker
52
Q

What does Amiodarone inhibit?

A

Potent P450 inhibitor** this isn’t instant, the happens over time (if someone is on this PO, we have to watch out with the meds we give)

Amiodarone antiarrhythmic effect  is complex comprising class I, II, III, and IV actions!!!!
Dominant effect: Prolongation of action potential duration and refractoriness
It slows cardiac conduction, works as Ca2+ channel blocker, and as a weak β-adrenergic blocker
53
Q

Short summary of Amiodarone?

A

Amiodarone shows beta blocker-like and potassium channel blocker-like actions on the SA and AV nodes, increases the refractory period via sodium- and potassium-channel effects, and slows intra-cardiac conduction of the cardiac action potential, via sodium-channel effects

Amiodarone antiarrhythmic effect is complex comprising class I, II, III, and IV actions!!!!

Dominant effect: Prolongation of action potential duration and refractoriness
It slows cardiac conduction, works as Ca2+ channel blocker, and as a weak β-adrenergic blocker

54
Q

What are some Major side effects of Amiodarone?

A

Toxicity
Most common include GI intolerance, tremors, ataxia, dizziness, hyper-or hypothyrodism***

Corneal microdeposits*** may be accompanied with disturbed night vision

Other SE’s: liver toxicity, photosensitivity, gray facial discoloration**, neuropathy, muscle weakness, weight loss, neurological toxicity shown as peripheral neuropathy, tremors, sleep disturbance, headache or proximal skeletal muscle weakness.

The most dangerous side effect is pulmonary alveolitis (pneumonitis) which occurs in 5-15% of the patients and reported mortality of 5-10%!!!!!!*****

55
Q

Why does pulmonary alveolitis occur with Amiodarone?

A
  • -Etiology unkown
  • -May produce free oxygen radicals in the lungs
  • –Suggested that high-inspired oxygen concentrations may accelerate these reactions
  • –Prudent to restrict the inspired concentration of oxygen** in patients receiving amiodarone and undergoing GETA to the lowest level capable of maintaining adequate systemic oxygenation (may want to give as little oxygen to maintain adequate saturation)
  • -Postoperative pulmonary edema has been reported
  • -Patients with pre-existing amiodarone-induced pulmonary toxicity are at increased risk for developing ARDS which requires cardiopulmonary bypass.***
56
Q

What is Ibutilide?

A

Class III antiarrythmics

  • –Used in recent atrial fibrillation or flutter to normal sinus rhythm.
  • –Hepatic metabolism is extensive
  • –Polymorphic ventricular tachycardia may occur especially in patients with predisposing factors (impaired left ventricular function, preexisting prolonged QT intervals**, hypokalemia and hypomagnesemia)
  • -IV administration
  • -May lead to torsade de pointes
  • -Only drug in class three that possess pure K+ blockade***
57
Q

What is the MOA of the Class IV ANTIARRHYTHMIC DRUGS?

A

Calcium channel blockers decrease inward Ca2+ currents resulting in a decrease of phase 4 spontaneous depolarization (SA node)

They slow conductance in Ca2+ current-dependent tissues like AV node

The effects on slow response structures (SA and AV nodes; class IV)

  • -Conduction is based on Ca++
  • –Depresses spontaneous depolarization of SA node
  • -Decreases AV node conduction
  • Decreases ventricular response in AF and flutter
  • Suppresses AV nodal re-entry tachyarrhythmia
  • –NO major impact on ventricular tachyarrhythmias!!!!!
58
Q

What is Verapamil used for?

A
  • -Class IV (calcium channel blocker)
  • -Prolongs conduction and refractoriness in AV node, slows rate of conduction of SA node
  • -Acute Rx /prophylaxis
  • -Used IV/oral
  • –SUPRAVENTRICULAR NOT VENTRICULAR ARRHYTHMIAS ***(cardiovascular collapse)
  • –Do not use IV verapamil with ß- blocker (heart block)
  • –T1/2 6-8 hours
59
Q

What are the contraindications for Verapamil?

A

Contraindicated in patients with pre-existing depressed heart function because of their negative inotropic activity

60
Q

What are the adverse effects of Verapamil?

A

Cause bradycardia, and asystole especially when given in combination with β-adrenergic blockers

61
Q

How is Verapamil metabolized?

A
  • -70% eliminated by the kidneys
  • -15% in bile
  • -Metabolite, norverapamil may contribute to the parent drugs antiarrhythmic effects.
  • -The need for a large po dose is related to the extensive hepatic first-pass effect that occurs with the oral routs of administration.
62
Q

What is the MOA for Diltiazem?

A
  • –Diltiazem is a potentvasodilator, increasing blood flow and variably decreasing the heart rate via strong depression of AV node conduction. Its pharmacological activity is somewhat similar toverapamil.
  • –It is a potent vasodilator of coronary and peripheral vessels, which reduces peripheral resistance and afterload.
  • –Because of its negative inotropiceffect, diltiazem causes a modest decrease in heart muscle contractility and reduces myocardium oxygen consumption.
  • -Its negativechronotropiceffect results in a modest lowering of heart rate, due to slowing of the sinoatrial node. It results in reduced myocardium oxygen consumption.
  • –Because of its negativedromotropiceffect, conduction through the AV (atrioventricular) node is slowed, which increases the time needed for each beat. This results in reduced myocardium oxygen consumption.
63
Q

What is an indication for Diltiazem?

A

Hypertension
Angina pectoris
Arrhythmia

64
Q

What are some Adverse effects of Diltiazem?

A

Hypotension
Bradycardia
Dizziness
Flushing

65
Q

What are some contraindications for Diltiazem?

A
  • -CHF
  • -AV or SA node disturbances
  • -Low blood pressure (b/c it will drop bp)
  • -Bradycardia
  • -Impairedleft ventriclefunction
  • -Peripheral artery occlusive disease
  • -Chronic obstructive pulmonary disease
66
Q

What are some drug interactions with Diltiazem?

A
  • -Beta blockers**
  • -Quinidine
  • -Diltiazem inhibits hepatic cytochromesCYP3A4,CYP2C9andCYP2D6, possibly resulting in drug interactions.
67
Q

What is the MOA for Digoxin?

A

Inhibition of the Na/K ATPase in the myocardium which leads to

Decrease membrane sodium gradient

Decrease Sodium-calcium exhange

Increase intracellular Ca

  • -Inhibits cell membrane sodium/potassium ATPase which leasds to reversal of the usual sodium calcium exchange. An increased intracellular calcium level enhances the strenght of contraction (Positive Inotropism).
  • –Act on Na/K-ATPase of cell membrane (inhibits Na+/K+ pump, increases intracellular Na+ and calcium)/ increases vagal activity
  • –Digoxin shortens the refractory period in atrial & ventricular myocardial cells while prolonging the ERF & diminishing conduction velocity in the AV node.
68
Q

What is Digoxin used for?

A

–It is used to control the ventricular response rate in atrial fibrillation & flutter.

Increase cardiac contraction and slows AV conduction by increasing AV node refractory period

69
Q

What is Digoxin indicated for?

A

CHF
Atrial arrhythmia
Heart failure

-Atrial fibrillation or flutter (controls ventricular rate)
-Acute Rx/prophylaxis
Oral/IV
-Loading and maintenance doses
-T1/2 36 hours
-Excreted by kidneys
-Narrow therapeutic index***
–Therapeutic drug monitoring
–Reduce dose in elderly/renal impairment

70
Q

What are some adverse effects of Digoxin?

A
  • -Arrhythmias
  • -heart block (3rd degree)
  • –anorexia, nausea, diarrhea
  • Xanthopsia
  • Gynaecomastia
  • Confusion
  • Agitation
  • AE potentiated by hypokalaemia and hypomagnesaemia
  • Overdose – Give Digibind (digoxin binding antibody fragments)*****, phenytoin for ventricular arrhythmias, pacing, atropine
71
Q

What is the MOA for Adenosine?

A

Acts on the Adenosine receptors (GPCR), leads to decrease Adenylyl cyclase, which leads to Decrease cAMP, which leads to Increase K efflux

This leads to cell hyperpolarization, that leads to transient heart block in the AV node

72
Q

What is Adenosine?

A
  • -Not in Vaughan Williams class
  • –Purine nucleotide (activates adenosine receptors)***
  • –Slows AV nodal conduction***
  • -Acute Rx
  • -Termination of SVT/ diagnosis of VT**
  • -Given IV only (rapid bolus)
  • -T1/2 < 2seconds***
73
Q

Adenosine, activates which receptors?

A
  • –Adenosine activates A1-purinergic receptors decreasing the SA nodal firing and automaticity, reducing conduction velocity, prolonging effective refractory period, and depressing AV nodal conductivity**
  • –Stimulates cardiac adenosine1 receptors to increase potassium ion currents, shorten the action potential duration and hyperpolarize cardiac cell membrane. (Acts similar to Ca+ Channel blockers).
  • –It is the drug of choice in the treatment of paroxysmal supra-ventricular tachycardia
  • —It is used only by intravenous bolus, 6mg IV followed by 6 to 12mg, 3 minutes later.
  • –It only has a low-profile toxicity (lead to bronchospasm)** being extremely short acting for 15 seconds only
74
Q

What are some adverse effects of Adenosine?

A
  • –Feeling of impending doom!
  • -Facial flushing, dyspnea, chest pain, transient arrhythmias, headache
  • -Contraindicated in asthma, heart block**
  • –Bronchospasm can occur by activation of adenosine receptors on the bronchial smooth muscle, mast cell degranulation, and stimulation of prostaglandin formation.
  • –Antagonized by theophylline and caffeine.

Pharmacology 2 (11 decks)

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