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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
Mexiletine: ## Footnote Pharmacodynamics Indications Pharmocokinetics AE
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
MOA of the class this image shows.
Class 1C drugs MOA * Block sodium channels * Block certain potassium channels
27
Flecainide: Pharmacodynamics Indications AE/CI
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
Propafenone Pharmacodynamics Indications AE
* 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
Whta class does this represent?
**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
Propranolol Indications Effects/Advantages
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
Esmolol Pharmacodynamics Indications
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
What does this represent?
**Class 3 MOA** * **Block potassium channels** - *slow repol (phase 3) of AP* * **Prolong refactory period,** AP duration, and QTi
33
Amiodarone Pharmacodynamics Indications Pharmakokinetics
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
AE of Amiodarone
* Cardiac - brady, AV block, torsades * Extracardiac * *Pulmonary fibrosis* * *Heaptitis* * *Photodermatitis/**blue skin color*** * *rneal deposits/opitcal euritis, hyper/hypothyroidism*
35
Dronedarone Pharmacodynamics Indications AE **CI**
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
Sotalol Pharmacodynamics Indications AE
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
Dofetilide ## Footnote Pharmacodynamics Indications AE
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
What class (and MOA/results) is this?
**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
Verpamil and Diltiazem Pharmacodynamics Indications Effects AE
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
Misc Agents - Adenosine MOA
* 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
Adenosine: Indications/Use AE
Indications - **conversion to sinus rhythm in *paroxysmal SVT*.** AE * **SOB** * **bronchoconstriction** * **Chest bruning** * **AV block** * **Hypotension**
42
Misc Agent - Magnesium Indications
**Digitalis induced arrhythmias** ***Torsades***
43
Factors that determine pacemaker AP - (firing rate/automaticity)
Rate of spontaneous depol in phase 4 (slope) Threshold potential Resting potential
44
Mechanism of abnormal impulse formation/altered automaticity of sinus node. SNS
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
Mechanism of abnormal impulse formation/altered automaticity of sinus node. PNS
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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