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MED233 Cardiovascular > PMT - Konorev Antiarrhythmic Drugs > Flashcards

PMT - Konorev Antiarrhythmic Drugs Flashcards

1
Q

Explain function of sodium channel and relationship to concentration gradients.

A
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2
Q

What is the Na concentraiton gradient?

A

140mmol/L outside, 10-15mmol/L inside

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3
Q

What are the 3 sodium channel states?

A
  1. Resting state - channel closed
  2. Activated State - depol to threhold opens m-gates
  3. Inactivated state - h-gates closed, inward sodium iflux inhibited, channel is not available for reactivation - responsible for refractory period
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4
Q

What is the potassium concentration gradient?

A

4mmol/L outside, 140mmol/L inside

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5
Q

Describe the function of K and Na regulation of membrane potential?

A
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6
Q

What is the function of K+ channels?

A
  1. At resting state - Inward rectifying K+ channels open during resting state.
  2. Regulation of action potential - VGKC regualte repolarization of cell.
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7
Q

Cardiac AP - what has fast AP, what has slow AP?

A
  1. Fast AP - Ventricle, artium, Purkinje
  2. Slow (pacemaker) AP - SA node, AV node
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8
Q

Fast action potential in cardiac muscle. Phases

A

Phase 0 - INa(fast)

Phase 1 - IK = repol

Phase 2 - plateau phase, IK and ICa(slow)

Phase 3 - Ca channels close, K exits faster

Phase 4 - Resting membrane potential restored by Na/K-ATPase and Na/Ca-exchanger

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9
Q

Fast action potential in cardiac muscle - deconvolution of cationic fluxes of cardiac AP

A
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10
Q

Pacemaker AP Phases

A

Phase 4 - slow, spontanous depol = ICa(T-type, slow) and If

Phase 0 - Upstroke of AP = Ca influx thorugh ICa(L-type)

Phase 3 - repolarization, inactivation calcium channels with increased IK

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11
Q

What is the mechanism of arrhythmia?

A

Altered automaticity of the SA node due to

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12
Q

The two types of abnormal pulse formations.

A
  • Early afterdepolarizations - in phases 2 or 3 of AP
    • Prolonged repol d/t impaired function of K-channels
    • Abnormal depol d/t Ca or Na channel opening
  1. Delayed afterdepolarizations - in phase 4 of AP
    * increased cytosolic Ca
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13
Q

Torsade de point - what is it?

A
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14
Q

What is a proarrhythmia?

What rarely induces TdP?

A

Drug-induced new arrhythmia or worsening of pre-existing arrhythmia.

Due to: antiarrhythmic drugs (groups 1A and 3), antipsychotics, antihistamines, antibiotics, antidepressants

Amiodarone rarely induces TdP

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15
Q

Do not give TdP-inducing drugs if QTc is less than what?

How is QTc calculated?

A

QTc = less than 450ms

QTB= (QT)/(square root of RR)

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16
Q

What can cause delayed afterdeloparizations?

A

Digitalis toxicity, cat excess, myocardial ischemia

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17
Q

What are digoxin-induced arrhythmias?

A

Spontaenous Ca release fromSR activates 2Na/2Ca exchange, leading to net depolarizing current.

Digoxin induced bigeminy NSR, PVB, and ST

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18
Q

List the 5 classes of drugs

A
  1. Class 1 - Na Channel blocker
  2. Class 2 - Beta Blockers
  3. Class 3 - Potassium Channel Blockers
  4. Class 4 - Calcium Channel Blockers
  5. Unclassified
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19
Q

What is the MOA of Class 1A drugs?

What do they preferentially target?

A
  • Sodium Channel Blockers
  • Use-dependent block - preferentially bind to active/open Na-channels and ectopic pacemaker cells with faster rhythms
  • Block postassium channels
20
Q

Procainamide:

Indications

Effects

Pharmacokinetics

AE

A

Class 1A

  • Indications - sustained vtach, MI-associated arrhythmias
  • Effects - Antimuscarinic activity and ganlgion-blocing properties (PVR=hypoT)
  • Pharmacokinetics - active metabolic N-acetylprocainamide has class3 activty and accumulates in renal dysfunction
  • AE - SLE-like syndrome, hematoxicity (agranulocytosis), CV effects (torsades)
21
Q

Quinidine:

Indications

Effects

AE

A

Class 1A

  • Indications - sustained vent arrhytmia, restores rhythm in aflutter/fib in person with normal heart
  • Effects - antimuscarinic activity enhances AV conductance, bblocking activity, may cause hypotension >> tachy
  • AE
    • Cardiac: QTi prolongation, torsades induction
    • Extracardiac: GI (NVD), thrombocytopenia, hepatitis, fever
22
Q

Disopyramide

Indications

Effects

Pharmacokinetics

AE

A

Class 1A

Indications - recurrent ventricular arrhymias

Effects - antimuscarinic effects

Pharmacokinetics

AE

  • Cardiac - torasdes
  • Extracardiac - anticholinergic effects/atropine-like/sympathetics: urinary retention, dry mouth, blurred vision, constipation, exacerbation of glaucoma
23
Q

Class 1B drugs MOA

A
  • Block inactivated Na channels
    • Preferentially bind to depolarized cells
  • Do not block K channels!
24
Q

Lidocaine

Pharmacodynamics

Indications

Pharmocokinetics

AE

A

Class 1B

  • Block inactivated channels - makes damaged tissue silent
  • Indications - arrhythmias associated with actue MI
  • Pharmacokinetics - extensive first pass, used only by IV
  • AE
    • Cardio - hypoT in HF pts by inhibiting contractility
    • Neuro - paresthesia, tremor, slurred speech, convulsions
25
Q

Mexiletine:

Pharmacodynamics

Indications

Pharmocokinetics

AE

A

Pharmacodynamics - orally active

Indications - ventricular arrhythmias, releive chronic pain (diabetic neuropathy and nerve injury)

Pharmocokinetics - same as lidocaine

AE - tremor, blurred vision, nausea, lethargy

26
Q

MOA of the class this image shows.

A

Class 1C drugs MOA

  • Block sodium channels
  • Block certain potassium channels
27
Q

Flecainide:

Pharmacodynamics

Indications

AE/CI

A

Class 1C

  • Pharmacodynamics - no antimuscarinic effects
  • Indications - in patients with normal hearts, but premature vent. contractions.
    • Treats supraventricular arrhythmias including AF, paroxysmal SVT (AVNRT, AVRT)
    • Treats sustained/long term Vtach
  • AE - May cause severe exacerabation of vent arrhythmias >> FATAL when administered to people with:
    • Preexisting vent tachyarrhythmias
    • Previous MI
    • Ventricular ectopic rhythms
28
Q

Propafenone

Pharmacodynamics

Indications

AE

A
  • Pharmacodynamics - weak Bblocker
  • Indications
    • Prevent paroxysmal AF and SVT in patients without structural disease
    • In ventricular arrhythmias.
  • AE
    • Exacerbation of ventricular arrhythmias
    • Metallic taste
    • Constipation
    • Do not combine with CYP2D6 and CYP3A4 inhibitors >> increased risk of proarrhythmia
29
Q

Whta class does this represent?

A

Class 2 MOA

  • Slow AP - decrease slope of phase 4 (diastolic currents of AP in pacemakers)
    • dec. SAN - dec HR
    • dec. AVN - dec. AV conductance
  • Ventricular myocardium - decrease Ca overload, prevent afterdepolarizations
30
Q

Propranolol

Indications

Effects/Advantages

A

Class 2

Indications

  • Stress relatie darrhythmias
  • Re-entrant arrhythmias that in volve AV node
    • AV nodal reentrant tachy (AVNRT)
    • AV reentrant tachy (AVRT)
  • Afib aflutter
  • Arrhythmias associated with MI
    • Advantage - decrease mortality in pts with acute MI
31
Q

Esmolol

Pharmacodynamics

Indications

A

Class 2

  • Pharmacodynamics - short acting (10min half life), IV continuous infusion needed
  • Indications
    • supraventricular arrhythmias
    • Arrhythmias associatedw ith thyroxicosis
    • MI or acute myocardial infarction with arrhythmias
    • Adjunct with general anesthesia to conrtol arrhythmias perioperatively
32
Q

What does this represent?

A

Class 3 MOA

  • Block potassium channels - slow repol (phase 3) of AP
    • Prolong refactory period, AP duration, and QTi
33
Q

Amiodarone

Pharmacodynamics

Indications

Pharmakokinetics

A

Class 3

Pharmacodynamics - Increased APD and ERP in all cardiac tissues…

Indications - any ventricular arrhythmia, afib (but not PDA approved)

Pharmacokinetics - metabolized by CYP3A4 (half life increased by drugs that inhibits (cimetidine) or induce (rifampin), LONG half life (weeks-months; 1-3 months duration), inhibits may CYP enzymes, review other meds in pts taking this

34
Q

AE of Amiodarone

A
  • Cardiac - brady, AV block, torsades
  • Extracardiac
    • Pulmonary fibrosis
    • Heaptitis
    • Photodermatitis/blue skin color
    • rneal deposits/opitcal euritis, hyper/hypothyroidism
35
Q

Dronedarone

Pharmacodynamics

Indications

AE

CI

A

Class 3

Pharmacodynamics

  • Blocks multiple K channels, Na current, L-type Ca current
  • Stronger adrenergic effects than amiodarone

Indications - afib/flutter, not as effective as amiodarone in maintaining sinus rhythm

AE- worsening HF, GI (NVD), less SE than amiodarone

CI - increase mortality in people with decompensated HF

36
Q

Sotalol

Pharmacodynamics

Indications

AE

A

Class 3

Pharmacodynamics

  • Class 2 (NS BB) and Class 3 agent (prolongs APD)

Indications - tx life-threatening vent arrhythmias, maintenance of sinus rhythm in pts with afib

AE - depression of cardiac function, provokes torsades

37
Q

Dofetilide

Pharmacodynamics

Indications

AE

A

Pharmacodynamics - narrow therapeutic window eliminated by kidneys.

Indications - converts AF to sinus rhythm and maintians after cardioversion

AE - QTi prolongation and increased risk of ven arrhythmias.

38
Q

What class (and MOA/results) is this?

A

Class 4 Drugs

  • Block activated and inactivated L-type Ca-channels
  • Active in slow response cells - decrease slope of phase 4 depol.
  • Result:
    • Dec. phase 0 and phase 4
    • Dec. SAN and AVN activity
39
Q

Verpamil and Diltiazem

Pharmacodynamics

Indications

Effects

AE

A

Class 4 Drugs

Pharmacodynamics - prolong AP duration and refractory

Indications

  • Prevention of paroxysmal SVT
  • Rate control in AFib and atrial flutter

AE

  • Cardiac - negative inotropy, AV block, hypotension, bradyarrhythmias
  • Extracardiac - constipation (verapamil)
40
Q

Misc Agents - Adenosine MOA

A
  • INCREASES K EFFLUX - Activates K current and inhibits Ca and funny currents >> hyperpolarization and suppression of AP in slow cells
  • Inhibits AV conduction and increases nodal refractory period.
41
Q

Adenosine:

Indications/Use

AE

A

Indications - conversion to sinus rhythm in paroxysmal SVT.

AE

  • SOB
  • bronchoconstriction
  • Chest bruning
  • AV block
  • Hypotension
42
Q

Misc Agent - Magnesium

Indications

A

Digitalis induced arrhythmias

Torsades

43
Q

Factors that determine pacemaker AP - (firing rate/automaticity)

A

Rate of spontaneous depol in phase 4 (slope)

Threshold potential

Resting potential

44
Q

Mechanism of abnormal impulse formation/altered automaticity of sinus node.

SNS

A
  1. SNS = (T/L Ca-ch, If , B1 receptor)
    1. cAMP
    2. If = increased slope
    3. T-type Calcium channels = increased slope (rate of spontaneous depol)
    4. L-type Calcium channels have lowered threshold
45
Q

Mechanism of abnormal impulse formation/altered automaticity of sinus node.

PNS

A
  1. PNS = (M2 and K-ch)
    1. cAMP
    2. K-channels affected = hyperpol
    3. Decreased slop due to If and T-type channels
    4. Increased threhold due ot L-Ca channels

MED233 Cardiovascular (18 decks)

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