Anti- Arrhythmics

Front 1

Anti-arrhythmic drug use continues to ____ b/c of side effects, non pharm interventions (like cardioversions), and AICDs

Back 1

decreasing

Front 2

Cardiac muscle is different from skeletal muscle b/c it can ____ on its own and myocardial cells have a _____ AP due to the _____ phase.

Back 2

1. contract
2. longer(~3-15x)
3. plateau phase

Front 3

Every cell can beat on its own which may lead to _____

Back 3

arrhythmia

Front 4

SA node criss crosses across the ____ and then the impulse meets at the _____ to allow for ventricular filling

Back 4

1. atria
2. AV node

Front 5

TEST Q: The plateau phase allows for longer _____ phase. But this also introduces the likelihood that other cells can get repolarized and other APs can occur.

Back 5

contraction

Front 6

Test Q: The SA node is ______ pacemaker. The SA node has a slow AP but has a more _____ RMP thus will repolarize more quickly making it the primary pacemaker of the heart. What is the threshold potential of the SAN?

Back 6

1. primary
2. positive
3. -30 to -40 compared to -60 to -70 for other cells in the heart

Front 7

ARP occurs at what phases?
RRP occurs at what phases?

Back 7

- from phase 0 through phase 3
- through second half of phase 3

Front 8

The AV node delay allows?

Back 8

Ventricles to fill

Front 9

Arrhythmias can occur b/c of abnormality in impulse _____ or impulse ______.

Back 9

1. generation- enhanced normal automaticity or enhanced abnormal automaticity (from non AV or SA nodal cells)
2. conduction i.e. re-entry or due to conduction block

Front 10

Abnormality in impulse generation includes enhanced normal automaticity which means? Or abnormal automaticity which means? OR triggered abnormal generation.

Back 10

1. enhanced normal-- SAN or AVN cells
2. abnormal automaticity means cells which are not normally automatic

Front 11

Enhanced automaticity in which either the SAN/AVN working more quickly or there is another cell setting the pace can be due to:

Back 11

hypOkalemia

Front 12

Beta blockers work by _______ phase 4 slope.

Back 12

decreasing so it makes it harder to reach threshold once again

Front 13

Potassium channel blockers will ____ AP

Back 13

increase AP -- leading to slower automaticity. delays amt of potassium leaving cell after AP

Front 14

Triggered impulse generation when there is _____ after a normal repolarization. Called ____. This is caused by ______. Tx?

Back 14

1. depolarization
2. DAD-- leads to abnormal secondary beat
3. intracelullar calcium overload-- MI, digoxin intoxication, adrenergic stress, heart failure. Tx is calcium channel blocker

Front 15

EAD (early after depolarization)- another type of triggered abnormal impulse generation results from ___ in phase 3 leading to torsades. This is usually caused by a ____ channel block.
Tx is to shorter AP via isoproterenol.

Back 15

1. depolarization
2. potassium

Front 16

PSVTs-- involve ____ reentry. Will either see no symptoms, syncope, angina, interrupt the AVN loop. If person is hemodynamically UNSTABLE then ____ and if hemodynamically stable then ___

Back 16

1. AVN
2. cardioversion- defib
3. vasovagal maneuvers -- adenosine, verapamil, diltiazem, class 1 AAs, and digoxin

Front 17

A fib is the most common and most dangerous arrhythmia, seen most commonly in old men. Will see very rapid irregular atrial activatn, atrial rate ~ 600 bpm, ventricular capture only about ~ ____. Tx: mechanical ___ w/in ____, chem cardioversion w/ quinidine, procainamide. Control rate with diltiazem, beta blocker. Warfarin also b/c stasis makes blood hypercoaguable.

Back 17

1. 180
2. cardioverison
3. 48 hrs

Front 18

Atrial flutter has both atrial and ventricular rates at _____. Rarer than a fib

Back 18

1.300 bpm

Front 19

V tachycardia -- when ventricles quiver-- is deadly. Should be acutely Txed with ___ and then if that doesnt work ____. Chronically can Tx with _____ and ____

Back 19

1. lidocaine
2. atropine
3. amiodarone
4. pacemaker

Front 20

Class Ia antiarrythmics affect the heart muscle and conductive tissue but ____ the _____

Back 20

1. Class 1 do not affect nodes

Front 21

Class 1a antiarrhytmics MOA

Back 21

- blocks the Na channel that is responsible for the stage 0 upstroke of the cardiac myocyte action potential. Increase ERP – increase QT interval – increase duration of AP
- 1 a (Queen Ann Proclaims Disos Pyramid) equally effective on atrial and ventricular dysrhthimias but 1b (little timmy makes punch) only on ventricular arrhytmias- esp post MI

Front 22

Quinidine: Use, Class, Tox, PK, Drug Intrxns

Back 22

Use: atrial and ventricular arrhythmias
Class: 1a and some Class 3 K+ blockade effects
Tox: GI (really bad) and QT elongation. Can cause bradycardia, asystole, and torsades
PK: narrow Tx window which decreases likelihood of pro-rhythmicity.

DI: P450 2D6-- inhibitor-- can double serum levels of digoxin

Front 23

Procainamide: Use, Class, Tox, PK, DI

Back 23

Use: prevention and Tx of atrial and v. dysrhythimas, and PVCs
Class: 1a
Tox:- drug induced lupus, Rash, GI, QT prolongation, hypotension
DI: lots
PK: Active metabolite (NAPA) is renaly cleared -> affects K+, not Na+- if this is not cleared new drug is created

Front 24

Disopyramide: Use, Class Tox, PK, DI

Back 24

Use: Supraventricular and ventricular arrhytmias but only in pts with good ventricular Fn b/c of negative ionotropic effects-- strong anticholinergic effects (Which limits use)
Class: 1a

Front 25

Lidocaine- Use, CLass, PK, Tox

Back 25

Use: SHORT term ventricular arrhthmia
Class: 1b-- used post MI, and only with ventricular arrhythmia
PK: short, repeat dosing required
Tox: Sedation, confusion, asystole, seizures, coma

Front 26

Class 1 B: MOA, little timmy makes punch

Back 26

- Na (block INACTIVATED sodium channels)
o Hypoxic tissue is depolarized because the Na/K transporter quits working as well; since it is depolarized, the channels become inactivated; hence, Ib drugs concentrate in hypoxic tissue
o Good for use post-MI
- MO: reduces action potential duration, little effect on healthy tissue.
o Mechanism by which it reduces action potential duration: besides the “fast” Na channels that are normally discussed, there are also “SLOW” Na channels that are active during the action potential. Since this leak current causes the cell to stay depolarized, blocking it causes the cells to repolarize more quickly, hence a shorter action potential duration

Front 27

Class 1c: MOA, drug names

Back 27

- Na (affects activated, inactivated, and resting sodium channels)
- MO: profoundly slows conduction velocity. No change on action potential duration.
- For: ventricular arrythmias. Last resort because of high incidence of sudden cardiac death
- encainide, flecainide, propafenone

Front 28

Class 2: MOA

Back 28

- Strongest effect is on nodal tissue
- β-blocker works on Ca (indirectly)
- MO: you guys know all about these! Block β1 receptors in the SA/AV to decrease the slope of phase 4 in nodal tissue via decreased sodium influx; basically makes the nodal cells take longer to hit the threshold potential

Front 29

Class 2: Use

Back 29

Tx of A fib and PROPHYLAXIS OF A FIB AFTER MI-- ß-blockers (the ONLY AA’s class) decrease sudden cardiac death after AMI, presumably due to arrhythmia. Effects NODAL tissue most

Front 30

Class 2 : Tox

Back 30

Low compliance b/c bad side effects, Bronchospasm, masks symptoms of hypoglycemia. Fatigue, decreased libido

Front 31

Class 3: MOA

Back 31

Blocks the outward K+ current
markedly prolongs the action potential duration. Prolongs repolarization by prolonging refractory period

Front 32

Class 3: Tox, Use, MOA

Back 32

MOA: potassium channel blocker
Use: A fib
Tox: torsades

Front 33

Sotalol, Bretylium, Amiodarone, Ibutilide, Dofetilide- Class

Back 33

Class 3
- sotolol has both 2 and 3

Front 34

Sotalol: Class, Use, CI, PK

Back 34

Class: BOth class 3 and Class 2
Use: Life threatening VT, A fib or flutter
CI: asthmatics, heart block, CHF, abrupt withdrawal. Should only be given in hospital with constant monitering
PK: VERY short acting, can have intense rebound effects, 100% bioavailability

Front 35

Amiodarone- Class, Use

Back 35

Class: all 4 classes, predominant effect is to prolong repolarization (i.e. class 3).
Use: recurrent V fib/tach and atrial fib

Front 36

What antiarhythmic has been shown to consistently decrease mortality in most clinical trials-- TEST Q

Back 36

Amiodarone

Front 37

Amiodarone: Class, TOX (TEST Q), PK

Back 37

Class-- all 4, but most imp is Class 3-- longer repolarization time
Tox: shown to be least pro rrhythmic but has LOTS of other side effects-- PULM FIBROSIS, pneumonitis, AV block, cataracts, hypotension, cirrhosis, bradycardia, hypo/hyperthyroidism, abnormal LFTs, blue gray syndrome (20-45%)
PK: half life is 30-100 DAYS, takes about 300 days to get theraputic, so if have bad effects takes a while to clear system

Front 38

Dofetilide: Class, MOA, Use, Tox

Back 38

Class: PURELY potassium channel blocker- pure class 3
Use: a fib maintenance NOT conversion
Tox: high incidence of torsades, intricate dosing for pts with renal dysfunction

Front 39

Ibutilide: Class, PK, Use, CI!

Back 39

Class: III
Pk: IV
Use: conversion of a. fib / a. flutter, hospital, assess renal fxn
CI:- Hx of Torsades
- QTc > 440
- K< 4.0 mEq/L
- Concomitant Type 1 or III drug
- HR <60
- Severe LV dysfunction (EF < 30%)- important

Front 40

Class 4: MOA

Back 40

- Ca channel blockers
- depresses slow Ca current (phase 0 of nodal tissue) to increase ERP and decrease conduction velocity. Affects nodal tissue. Increases refractory period

Front 41

Diltiazem: Class, Use, Tox

Back 41

Class: 4- calcium channel blockers
Use: DOC for A fib and flutter- decreases ventricular capture
Tox: hypotension but rel well tolerated

Front 42

Adenosine- Important- DOC for what?
Tox

Back 42

DOC: in diagnosing, treating AV nodal arrhythmia- Paroxysmal Supraventricular Tachycardia
MOA: binds to Gi-linked adenosine receptors in heart, which decrease cAMP essentially shutting off the AV node for 10 seconds
Tox: flushing b/c strong vasodilation and bronchospasm

Front 43

K+ depresses ectopic pacemakers especially in ___ toxicity

Back 43

digoxin

Front 44

Mg+2 acts like false caclium and is effective in ____ and ____ toxciity.

Back 44

1. torsades
2. digoxin