Cardiology: Vt And Antiarrythmics

Front 1

1) VT occurs in ___1___ hearts
2) SVTs occur in ___2___ hearts
2) VT leads to...

Back 1

1) diseased hearts
2) healthy hearts
3) cardiac arrest

Front 2

1) VT is much more common than, but can be confused with
2) Easiest way to discriminate the two

Back 2

1) Wide complex SVT ( SVT with abberent ventricular conduction)

2) Extreme right axis deviation is seen in VT, not in SVT.

Front 3

What histological feature encourages VT?

Back 3

MI scar in the ventricle

Front 4

Channels during phase 0

Back 4

Na+ influx

Front 5

Channels during phase 1

Back 5

Na+ channels close,
K+ efflux

Front 6

Channels during phase 2

Back 6

K+ efflux
Ca++ influx

Front 7

Channels during phase 3

Back 7

K+ and Ca++ efflux

Front 8

Channels during phase 4

Back 8

K+ efflux (RMP_
Na+ influx slow (Ifunny)

Front 9

Early after depolarizations:
1) Associated with what cause?
2) What is usually lengthened in these
3) Can induce what really bad rhythm
4) occurs during which phase(s)

Back 9

1) Ischemia
2) Long QT
3) TDP
4) 2 or 3- before repolarization is done

Front 10

Delayed after depolarizations:
1) Associated with what cause?
2) occur during what phase?

Back 10

1) Digoxin Toxicity
2) 4- after full repolarization

Front 11

1-3) three parameters than can influence automaticity of a focus
4) If automatcity is obtained in a ventricular focus, we get...
5) ____5____ triggers ventricular automaticity foci.

Back 11

1) Change of phase 4 slope
2) Change of dep. threshold
3) Change of Resting MP
4) Vt
5) Ischemia

Front 12

1) Blockade of Na+ channels influences which phase of depolarization
2) Blockade of K+ channels influences which phase of depolarization

Back 12

1) 0
2) 2-3

Front 13

The normal relationship that ___1____ RMP yields a faster phase 0 upstroke. Na+ blockade shifts this curve to the ____2___ such that this a given RMP will cause a ___3___ upstroke. This is seen on the EKG as the widening of the ___4___. All Class ___5____ agents have this property to some degree.

Back 13

1) more negative
2) RIght
3) Slower
4) QRS.
5) Class I (A,B,C)

Front 14

Class:
Quinidine

Back 14

1A

Front 15

Class:
Procainamide

Back 15

1A

Front 16

Class:
Disopyramide

Back 16

1A

Front 17

Class: Lidocaine

Back 17

1B

Front 18

Class: Mexiletine

Back 18

1B

Front 19

Class: Flecainide

Back 19

1C

Front 20

Class: Propafenone

Back 20

1C

Front 21

Class: Propranolol (B-blocker)

Back 21

2

Front 22

Class: Amiodarone

Back 22

3

Front 23

Class: Ibutalide

Back 23

3

Front 24

Class: Sotalol

Back 24

3

Front 25

Class:
Ca++ Channel blockers
(Verapamil, Diltiazem, -ipine)

Back 25

4

Front 26

What class of antiarrhythmic puts you at risk for Ventricular arryhtmia in the presence of an MI scar

Back 26

1C

Front 27

1) Which two classes block Na+ influx (phase 0) only?
2) What is the difference between the two?

Back 27

1) 1B and 1C

2) 1B has rapid dissociation constant and is therefore not active during normal speed HR, only during tachycardia.
1C has slow dissociation constant, so it has true blocking effect even at normal HR.

Front 28

What channel(s) does class 1 block?

Back 28

Na+ Primarily
K+ secondarily

Front 29

What is the primary channel blocked by Class III?

Back 29

K+

Front 30

Propafenone is a class ___1___ agent that also blocks ____2____

Back 30

1) 1C
2) Beta adrenergic receptor.

Front 31

1) Which class of drugs specifically predisposed to TDP?

2) Which drug in this class is less dangerous in this respect?

Back 31

1) III
2) Amiodarone

Front 32

Which clas of drugs is used spcifically for Vent. arrythmia secondary to MI or ischemia?

Back 32

1B

Front 33

Disopyramide is a class ___1___ agent which also has a ___2____ effect.

Back 33

1) 1A
2) Negative inotropic

Front 34

Which class III agent blocks K+ channels in the most pure manner?

Back 34

Sotalol

Front 35

Ibutilide is a class ___1___ agent used specifically for ____2____.

Back 35

1) III
2) Breaking acute arrythmias, because it has a very short half life.

Front 36

1) Which agent that we talked about has the most notably long half-life?
2) Which one has the most notably short half life?

Back 36

1) Amiodarone
2) Ibutalide- ised to break arrythmias acutely.

Front 37

Three places AMmio has side effects?

Back 37

Liver
Thyroid
Lungs

Front 38

1) How do class II agents prevent arrythmias?
2) Hows does this predispose to arrythmias too?

Back 38

1) Lengthens refractoriness
2) Elongates QT, predisposing to TDP

Front 39

Class 1B works most on ____1_____ Na+ receptors

Back 39

Ventricular

Front 40

Four determinants of drug Plasma concentration

Back 40

Bioavailibility
Distribution
Biotransformation
Elimination

Front 41

Three determinants of drug bioavailibility

Back 41

Preparation
Absorption
First pass metabolism

Front 42

Name the two medium bioavailibility agents which compete for protein binding, and thus can cause toxicity if used together?

Back 42

Amiodarone, Digoxin

Dig gets displaces and becomes toxic

Front 43

Why do we use such caution when using Amiodarone and Digoxin together?

Back 43

They compete for protein binding and can cause Digoxin displacement and toxicity.

Front 44

What is the only antiarrythmic agent broken down at the cellular level?

Back 44

Adenosine

Front 45

Things I would want to know about a drug before giving it

Back 45

Elimination
active metabolites
protein binding
Half life
Bioavailibility

Front 46

____1___ is a hepatic enyme in charge of breaking down many antiarrythmics in class 1C and III. People with deficits in this enzyme (poor-metabolizers) are moset at risk of toxicity from ____2____, a class ___3___ agent.
This enzyme is inhibited by ____4____, and hence coadminstraction of this drug with ____2_____ could result in toxicity.

Back 46

1) P450D6
2) Propafenone
3) 1C
4) Quninide

Front 47

What is important to remember about quinidine?

Back 47

Inhibits P450D6, and hence should not be mixed with many drugs like propafenone

Front 48

Things I would want to know about a drug before giving it

Back 48

Elimination
active metabolites
protein binding
Half life
Bioavailibility

Front 49

____1___ is a hepatic enyme in charge of breaking down many antiarrythmics in class 1C and III. People with deficits in this enzyme (poor-metabolizers) are moset at risk of toxicity from ____2____, a class ___3___ agent.
This enzyme is inhibited by ____4____, and hence coadminstraction of this drug with ____2_____ could result in toxicity.

Back 49

1) P450D6
2) Propafenone
3) 1C
4) Quninide

Front 50

What is important to remember about quinidine?

Back 50

Inhibits P450D6, and hence should not be mixed with many drugs like propafenone

Front 51

Describe Three reasons that CHF alters pharmcokinetics in drugs like antiarrythmics, causing a narrow toxic/therapeutic window.

Back 51

1) Decreased Vd caused by diuresis increases plasma drug concentrations
2) Decreases Hepatic and renal blood flow increases half life
3) Passive hepatic congestion results in longer half life.

Front 52

Name the 5 drugs that cause Increased Digoxin levels!

Back 52

Verapamil
Quinidine
Amiodarone (protein binding comp)
Flecainide
Propafenone

Front 53

What is the only system that Amiodarone has NO toxic effect on?

Back 53

Kidney

Front 54

___1___, a class ___2____ drug has the highest rate of pro-arrythmia of all agents that we studied.

Back 54

1) Quinidine
2) 1A

Front 55

1) ____1____ predisposes to TDP
2) Can you see this on a TDP ECG?

Back 55

1) Long QT
2) Nope, need to have seen a prior ECG

Front 56

1) What drug is the most important one which INCREASES Defibrillation threshold?
2) What does it do to pacing threshold?

Back 56

1)Amiodarone
(necessitates bigger shocks)

2) Increase

Front 57

What parameters of artificial electrical input to the heart can be changed by antiarrythmics?

Back 57

Defibrillation threshold (DFTS)
Pacing threshold

Front 58

How to we interrogate a pacer/defibrillator

Back 58

give it a bad rhythm, and see if it kicks in a shock.

Front 59

What antiarrythmic is helpful in the highest % of patients?

Back 59

Amiodarone