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Cardiovascular Block > Antiarrythmics > Flashcards

Antiarrythmics Flashcards

1
Q

Drugs that decrease phase 4 slope

A

Beta Blockers (Class2)

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2
Q

Drugs that increase threshold potential

A

Na+ Channel blockers (Class 1) - Procaineamide (1a) and Flecanie (1c)

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3
Q

Drugs that increase diastolic potential (hyper polarization)

A

Na+ channel blockers - Lidocaine (ventricular cells only)

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4
Q

Drugs that increase action potential duration

A

K+ channel blocker (class 3) - Sotalol (3,2) and Amidarone (3,2,4)

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5
Q

Na+ channel blocker binding

A

bind only to activated and inactivated phases, cannot bind to resting channel because binding site is within channel.

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6
Q

MOA for Class 1

A

decrease rate of rise of phase 0 depolarization resulting in slower conduction of impulses through reentrant circuits; increase effective refractory period (ERP)

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7
Q

Class 1A

A

intermediate dissociation rate; prolongs action potential duration due to K+ Channel blocking properties - Procaineamide, Quinidine, Disopyramide.

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8
Q

Class 1B

A

Rapid dissociation, effective anti-tachycardia drug, narrows AP duration - Lidocaine

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9
Q

Procainamide

A

suppresses ectopic pacemaker activity in partially depolarized cells, reduces conduction velocity (reduced phase 0), prolongs AP duration

Used for Atrial and Ventricular arrhythmias; primarily acute atrial arrhythmias

Side effects: drug induced lupus, Torsades de Pointes

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10
Q

Quinidine

A

Class 1A MOA; dose dependent QT prolongation/Torsades de Pointes and V. Tach/Fib

S.E. diarrhea, autoimmune thrombocytopenia

Rarely used due to pro arrhythmia likelihood

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11
Q

Disopyramide

A

prominent vagolytic effect

Leads to urinary retention, dry mouth, blurred vision, negative inotropic effect leading to HF

Rarely used due to SE

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12
Q

Lidocaine

A

Class 1B - rapid kinetics; preferentially binds to Na+ channels in partially depolarized cells to suppress abnormal automaticity; no effect on conduction with normal heat rate

Highly effective for suppressing Ventricular arrhythmias

Extensive first pass metabolism so must be given IV (rapidly goes to fat tissues so must be given in two phases)

Tox: CNS, agitation, confusion, seizures

Mexilitine can be used orally, but GI distress limits use

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13
Q

Flecainide

A

Class 1C - long lasting Na channel blocker that suppresses automaticity and increases ERP in atria and ventricles

Increased mortality in post MI patients - do not use in patients with structural heart disease

Used for Supraventricular arrhythmias with no structural issues

Only used for life-threatening issues due to high risk of pro-arrhythmic effects

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14
Q

Propafenone

A

Class 1C MOA with Beta adrenoreceptor blocking properties; only used in Afib and Aflutter without structural heart disease

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15
Q

Treatments for V. Tach/Fib

A

Class 1 (not Flecanide) and 3 - treatment is aimed at interrupting reentry

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16
Q

MOA of Class 3 Potassium channel blockers

A

increase AP duration and ERP by blocking K+ channels, prolonging phase 3 of the AP thus prolonging ERP - shown on EKG as prolongation of QT

Prolonging ERP in the slow conducting limb of a reentrant circuit interrupts reentry

17
Q

Amiodarone

A

MOA: K+ channel blockade, Na/Ca channel blockades and Beta adrenergic blocking properties as well; prolongs AP, inhibits abnormal automaticity, decreases conduction velocity, prolongs ERP

EKG: prolongation of PR, QRS, QT and sinus bradycardia

Uses: atrial and ventricular arrhythmias; IV for V. Tach/Fib

Drug of choice for cardiac resuscitation

slow elimination, highly lipophilic; metabolized by CYP3A4 (inhibits)

S.E.: pulmonary fibrosis, photo dermatitis, corneal microdeposits, optic neuritis, hypo/hyper thyroidism, hepatitis, prox. muscle weaknes

Interacts with digoxin and warfarin

18
Q

Dronedarone

A

non-iodinated form of Amiodarone (no thyroid issues) used for paroxysmal AFib or maintenance of sinus rhythm

Contraindicated: patients with decompensated congestive heart failure due to increased risk of death, stroke, and worsened heart failure

19
Q

Sotalol

A

nonselective beta blocker with AP prolonging characteristics

MOA: K+ channel blocker with 1/3 beta blocking effect of propranolol

Uses: atrial, ventricular, AV nodeal reentrant arrythmias including V tach

Effective (not as much as Amiodarone) with less toxicity

Metabolism: kidneys

Contra: extended QT interval, renal issues, asthma/COPD, CHF, brady, acute MI

SE: Torsade de Pointes

20
Q

Dofetilide

A

pure class 3 drug; used for Afib

Rhythm control

SE: Torsades de Pointes

Contra: patients with long QT

initial therapy inpatient with EKG

21
Q

Ibutilide

A

IV only; used for acute termination of A Fib/Flutter

Rhythm control

SE: Transient asystole and Torsades de Pointes

22
Q

Drugs that cause Torsade de Pointes

A

Class 3, Class 1 (Quinidine, Procaineamide), non-sedating antihistamines

23
Q

Optimal treatment for V Tach

A

Implantable Cardiac Defibrillator (ICD); followed by Amiodarone

24
Q

Optimal treatment strategy for A Fib

A

Rate control: digoxin, B-blocker, Diltiazem, Verapamil and Warfarin

25
Q

Propranolol

A

Effect: reduces enhanced automaticity related to catecholamines and ischemia - decreased A or V arrythmias post-MI and increased survival

MOA: slows AV node conduction by blocking positive influence of E&NE particularly in exercise induced AFib

Uses: PVCs in patients w/ or w/o structural heart issues; especially PVC associated w/ hyperadrenergic states including mitral valve prolapse

26
Q

Metoprolol

A

B1 selective; non-FDA use for atrial and ventricular arrythmias

27
Q

Acebutolol

A

B1 selective, ISA; FDA used for ventricular arrhythmias

28
Q

Esmolol

A

B1 selective, ultra short acting; used for acute treatment of supra ventricular arrhythmias; IV infusion only

29
Q

Verapamil/Diltiazem

A

Reduce SA node automaticity and AV node conduction; little effect in normal conditions

SE: SA/AV block, impairing myocardial contractility, hypotension

Great for patients with normal LV function and those who cannot tolerate Beta-blockers due to diabetes or pulmonary disease

Contra: CHF, LV dysfunction, sinus brady, AV block (prolonged PR)

30
Q

Digoxin

A

Slows ventricular response in atrial fibrillation via enhanced vagal efferents to the AV node

Acts by blocking Na/K ATPase leading to intracellular accumulations of Ca2+.

Reduces SA automaticity, AV conduction rate

Tox: delayed afterdepolarizations (triggered automaticity) from intracellular Ca2+ overload - worsened by E&NE and Hypokalemia; antidote - Digibind

31
Q

Treatment for Paroxysmal Supraventricular Tachycardia (PSVT)

A

Adenosine

32
Q

Adenosine

A

used to terminate acute PSVT by blocking AV node; administered rapidly IV

Diagnostic for PSVT - if reverts on admin then PSVT, if sustained something else (Atrial flutter etc)

33
Q

WPW Contraindications

A

Do not use Digoxin in WPW patients due to increased transmission of atrial impulses to ventricles by accessory path leading to V Fib.

Cardiovascular Block (11 decks)

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