Anti-arrhythmic

Question 1

Sodium channel open
inward sodium depolarization
class 1 drugs affect this phase

Answer 1

phase 0 - fast response

Question 2

sodium channel inactivated

outward K+ & inward chloride current contribute to notch & overshoot

Answer 2

phase 1 - fast response

Question 3

inward L type Calcium and outward K+ current from plateau

Answer 3

phase 2 - fast response

Question 4

repolarization by outward K+ current, note that a slow inward Na+ current (window current) prolonging APD
class 3 drugs affect this phase

Answer 4

phase 3 - fast response

Question 5

returning to resting potential by Na+/K+ ATPase

Answer 5

phase 4 - fast response

Question 6

absolute no response to any stimuli

Answer 6

effective refractory period

Question 7

strong stimulus can elicit a response, but not sync with rest of heart

Answer 7

relative refractory period

Question 8

1) bradycardia, occurs with AV block

2) tachycardia, occurs when a reentrant circuit develops

Answer 8

mechanisms for arrhythmia

Question 9

V max decrease

decrease conduction velocity

Answer 9

rate of phase 0 depolarization

Question 10

less negative

slower conduction velocity

Answer 10

threshold potential

Question 11

more negative the RP

faster conduction velocity

Answer 11

resting potential

Question 12

pacemaker phase

inward Na+ funny & Ca2+ (T type) and inward K+ current

Answer 12

phase 4 - slow response

Question 13

inward Ca2+ (L type)
class 4 affect this phase

Answer 13

phase 0 - slow response

Question 14

outward K+ current

classes 2 & 3 affect this phase

Answer 14

phase 3 - slow response

Question 15

is innervated by PANS & SANS activated by M2 & B1 receptors

Answer 15

SA Node

Question 16

In what phase is slope increased by increase in cAMP resulting from B1 activation and slowed by decrease in cAMP resulting from M2 activation

Answer 16

phase 4 of slow response

Question 17

1) Increase upstroke velocity in pacemakers by increase calcium L type
2) shorten APD by increase K+
3) Increase HR by increase of funny Na thus increase slope of phase 4

Answer 17

Results of Increase cAMP

Question 18

1) does opposite of increase cAMP
2) also produces K+ current, which slows the rate of diastolic depolarization and decrease HR
3) B Blockers prevent cAMP formation, with primary effects on SA and AV node tissues

Answer 18

Results of decrease cAMP

Question 19

treats sinus bradycardia
makes slope steeped
blocks M2 causing increase cAMP, PKA & HR

Answer 19

Atropine

Question 20

causes bradycardia

treats sinus tachycardia

Answer 20

Ivabradine

Question 21

decrease slope of phase 0 upstroke (slows conduction of cardiac AP) AP will almost look tipped over with decrease slope by blocking sodium channels

Answer 21

Class 1

Question 22

bind to open or inactivated sodium channels

Answer 22

class 1

Question 23

use dependence - have greater effect on rapidly depolarizing tissues (increase heart rate causes slower phase 0 upstroke)

Answer 23

class 1

Question 24

affect the sodium dependent cardiac AP (no action at the SA and AV nodes)

Answer 24

class 1

Question 25

widen QRS complex (decrease AP conduction velocity) this will happen when the HR increases b/c that will increase effect of the drug

Answer 25

class 1

Question 26

1) intermediate binding to Na channel 2) increase APD (dec phase 0) 3) block K+ ch prolonging phase 2 & 3 of AP = prolonged refractory period 4) treat SVT and ventricular arrhythmias

Answer 26

class 1A

Question 27

1) use to treat atrial, AV juntion and ventricular tachycardia 2) block M receptor - increase HR & AV cond 3) block alpha 1 - postural hypotension and reflex tachycardia 4) effect dec by P450 inducers and enhance by P450 inhibitors

Answer 27

quinidine

Question 28

1) cinchonism 2) severe headache 3) hypotension 4) prolong QT interval

Answer 28

ADR of quinidine

Question 29

no anti M and anti alpha effect | metabolized by acetyltransferase

Answer 29

procainamide

Question 30

reversible lupus erythematous like synd. | prolong QT - torsades de point

Answer 30

procainamide ADR

Question 31

used to treat ventricular arrhythmias | contraindicated in HF

Answer 31

Disopyramide

Question 32

anticholinergic | negative inotropic effect (dec contractility)

Answer 32

Disopyramide ADR

Question 33

have low binding affinity to Na ch (dec APD) | shorten phase 2 & 3 of AP - shorten refractory period = no chance of tornadoes de point

Answer 33

class 1B

Question 34

treat ventricular arrhythmias (ischemic tissues) in Na ch. spending more time in open and resting state b/c of longer AP

Answer 34

class 1B

Question 35

greater tendency to work with ischemic heart problems

Answer 35

class 1B

Question 36

treats ventricular arrhythmias by IV not useful in atrial arrhythmias decreases APD SE: CNS toxicity

Answer 36

lidocaine

Question 37

similar to lidocaine in action but given orally

Answer 37

Mexiletine

Question 38

other drugs in class 1B

Answer 38

phenytoin and tocainide

Question 39

strong binding affinity for Na ch (drastic slowing go phase 0) effects QRS, prolongs ERP in Av node, no change in APD

Answer 39

class 1C

Question 40

treats supraventricular (a fib) and ventricular arrhythmias; can restore and maintain normal sinus rhythm in a fib and flutter

Answer 40

class 1C

Question 41

Class 1C drugs

Answer 41

Flecainide | Propafenone

Question 42

Class 1B drugs

Answer 42

Lidocaine Mexiletine Phenytoin Tocainide

Question 43

Class 1A drugs

Answer 43

Quinidine Procainamide Disopyramide

Question 44

decrease cAMP - leads to closure of membrane Ca2+ ch preventing upstroke of AV node AP

Answer 44

Class 2

Question 45

prolong phase 4 of nodal AP decrease pacemaker activity prolong conduction time and refractory period

Answer 45

class 2

Question 46

can cause heart block

Answer 46

class 2

Question 47

treats arrhythmias blocking SANS inout to SA and AV node | supra ventricular arrhythmias (A fib/ flutter

Answer 47

class 2

Question 48

prevents rapid ventricular response in atrial fib/ flutter "rate control" but does not fix the atrial fib

Answer 48

class 2

Question 49

class 2 drugs

Answer 49

beta blockers

Question 50

Class 3 drugs

Answer 50

Amiodarone | Sotalol

Question 51

block K+ ch prolonging phase 2 and 3 of AP - prolong refractory period widen QT interval induce torsades

Answer 51

Class 3

Question 52

treats both SVT and ventricular arrhythmias and A fib / flutter

Answer 52

Class 3

Question 53

can restore and maintain normal sinus rhythm in a fib and flutter

Answer 53

Class 3 (class 1C can also)

Question 54

``` neurological SE grey corneal deposits hyperthyroidism hypothyroidism pulmonary fibrosis - restrictive lung dz induces HF hyposensitivity hepatitis grey blue skin discoloration photodermatitis inhibits cytochrome P450 inhibition ```

Answer 54

ADR of Amiodarone

Question 55

Class 4 drugs

Answer 55

Diltiazem | Verapamil

Question 56

``` blocks L type calcium channels blocks phases 4 and 0 prolong conduction prolong PR interval prevents RVR in A fib and flutter ```

Answer 56

Class 4

Question 57

exert a greater effect on tissues that fire more freq. that use calcium current

Answer 57

class 4

Question 58

treats SVT | use as IV to treat PSVT

Answer 58

Class 4

Question 59

can cause heart block if used with a drug like digoxin

Answer 59

class 4

Question 60

constipation AV block HF

Answer 60

class 4 ADR

Question 61

Class 5 drugs

Answer 61

digoxin magnesium adenosine

Question 62

exerts direct PANS effect by stimulating vagus nerve - AV nodal inhibition; useful in A fib (not 1st line); prevents RVR in A fib "rate control"

Answer 62

digoxin

Question 63

treats torsades

Answer 63

magnesium

Question 64

causes peak T waves and shortens QT interval

Answer 64

hyperkalemia

Question 65

induces U waves at end of T waves on EKG severe muscle weakness abnorm glucose

Answer 65

hypokalemia

Question 66

inhibitory A1 receptor on myocardium @ SA & AV nodes (outward increase K+ current(hyper polarize) and suppresses Ca2+ inward current) prolongs AV refractory period

Answer 66

Adenosine

Question 67

causes transient high grade heart block (direct AV node inhibition for about 10s)

Answer 67

Adenosine

Question 68

1st line agent for acute treatment for PVST

Answer 68

Adenosine

Question 69

causes coronary dilation (mediated by A2 receptor)

Answer 69

Adenosine

Question 70

cutaneous flushing SOB, chest pain and impending sense of doom fainting, headache and hypotension

Answer 70

Adenosine ADR

Question 71

inhibited by caffeine and theophylline

Answer 71

Adenosine