Anti arrhythmics, Kinder DSA and LEC Flashcards Preview

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Flashcards in Anti arrhythmics, Kinder DSA and LEC Deck (80):
1

What are the Class Ia Na Channel blocker antiarrhythmics

Procainamide!!
guinidine
disopyramide

2

what are the class Ib Na Channel blocker antiarrhythmics

Lidocaine (xylocaine)!!
mexiletine
tocainide

3

what are the class Ic Na Channel Blockers

Flecainide (tambocor)!!!
moricizine
propafenone(rythmol)

4

What are the class II antiarhythmics

Beta blockers
Emolol!!
meotrolol!!
propanolol!!

5

What are the class III antiarhythmics

K channel blockers
amiodarone!!
sotalol!!!
bretylium, dofetilide, ibutilide

6

What are the class IV antiarrhythmics

Ca channel blockers
Verapamil!!
Diltiazem!!

7

What are other antiarrhythmic drugs, not in a class

Adenosine!!
Atropine!!
MgSO4!!
anticoagulants, digoxin, Naloxone, vasopressors: epi, norepi, vasopressin and dopamine

8

what is the electrical gradient in heart

-90mV inside 0 mV outside

9

what occurs in phase 0 of depolarization?

rapid deoplarization from increase in Na permeability

10

describe phase 1 depolarization

bried repolarization
transient K efflux, Ca begins to move in, causing slow depolarization

11

describe phase 2 depolarization

plateau phase, Ca influx continues, balance by K efflux

12

describe phase 3 depolarization

repolarization continue K efflus

13

describe phase 4 cell deplarizaiton

gradual depolarization, Na leak balance by K efflux

14

what ways do antiarrhythmics depress autonomic properties of abnormal pacemaker cell

decrease slope of phase 4
elevate threshold potential

15

hwo can antiarrhythmics alter conduction of reentrant loop

facilitate conduction by shortening regractoriness
depress conduction by prolonging refractoriness

16

what are the effects of class Ia Na ch blocker

dec conduction velocity
increase refractoriness
decrease autonomic properties

17

what are the effects of class Ib Na ch blocker

no effect on velocity
may decrease refractoriness

18

what are the effects of claa Ic Na ch blocker

dec conduction velocity
no effect on refractoriness

19

what are the effects of class II antiarrhythmics

beta blockers
dec conduction velocity
increase refractoriness
decrease autonomic properites

20

what are the effects of class III antiarrhythmics

K ch blocker
increase refractoriness
increase AP duration

21

what are the effects of class IV antiarrhythmics

Ca ch blocker
dec conductionv velocity
increase refractoriness
decrease autonomic properties

22

what are class Ia antiarhyth used for

atrial and ventricular arrhythmias

23

what occurs with class Ia, Procainamide toxicity

excessive AP prolongation, QT prolongation, hypotension, reversible lupus erythematosus, nasuea and diarrhea, rash, fever, hepatitis, agranulocytosis

24

what is lidocaine used for

Drug of choice for temination of VT and prevension of VF after cardioversion in setting of acute ischemia

25

what phase in AP does lidocaine shorten

phase 3 repolarization

26

what can toxicity of lidocain cause

least cardiotoxic!!
hypotension, neurologic (paresthesias, tremor, nausea, lightheadedness)

27

Which Na Ch blocker cannot be used in structural heart disease

Ic
Flecainide
Moricizine
Propafenone

28

What are the effects of flecainide on AP

block Na and K
does not prolon AP or QT
depress rate of rise of membrane AP, slows depolarization

29

what is therapeutic use for flecainide

supraventricular arrhythmias

30

wat can occur with toxicity of flecainide

severe excaervation of arrhythmias

31

what is therapeutic use of class II

tachyarrhythmias, AF, AV nodal re-entrant tachy, HTN, HF, ischemic heart disease

32

what can occur with toxicity of propanolol

bradycardia, heart blokc, worsening asthma or COPD, cold extremities, fatigue, cardiac decompensation(if relying on sympathetic)

33

what is benefit of esmolol

beta 1 selective and ultra-short acting

34

how does amiodarone change AP

prolongs AP duration and QT interval
significantly blocks Na Ch, weak adrenergic and CCB

35

what is therapeutic use of amiodarone

AF, recurrent VT, adjucnt to ICD to reduce uncomfortable discharges

36

What occurs with amiodarone toxicity

symptomatic bradycardia, heart block
accumulates in heart, lungs, liver, skin,tears
pulmonary toxicity and fatal pulm fibrosis
abnormal LFTs, skin deposits, gray-blude ski discoloration
hypo or hyperthyroidism

37

what are common drug interactions with amiodarone

CYP3A4 blockers like cimetidine increase amiodarone levels
CYP3A4 inducers like rifampin decrease amiodarone levels
amiodarone increases drug levels of statins, digoxin, warfarin

38

how does sotalol change AP

both beta blocking and AP prolonging

39

what is therapeutic use of sotalol

life threatening ventricular arrhythmias, maintenace of sinus rhythm in AF

40

what can toxicity of sotalol cause

dose related TdP
depression of LV function in patients with HF

41

which K Ch blocker has interaction withs thiazides and verapamil

Dofetilide

42

how do Class IV change AP

decrease inward Ca
decrease phase 4 spont depol
slo conduction in tissues dependent on Ca (AV node)

43

how does verapamil work on AP

blocks activated and inactivated L type Ca Ch, slow SA node and suppres early and after delayed depolarization

44

therapeutic use of verapamil

SVT, decrease ventricular rate in AF, angina, HTN

45

what are extracardial effects of verapamil

peripheral vasodilation

46

what occurs with toxicity of verapamil

hypotension and VF if given to patient with VT and misdiagnosed SVT
can induce AV block
constipation, lassitude, nervousness, Peripheral edema

47

therapeutic use of diltiazem

SVT, angina, HTN

48

what occurs with toxicity of diltiazem

edema, HA, AV block, bradycardia, hypotension

49

What are the effects of adenosine on AP

activates inward rectifier K current and inhibits Ca current resulting in marked hyperpolarization and increased refractory period

50

therapeutic use of adenosim

Drug of Choice conversion of paroxysmal SVT

51

what occurs with toxicity of adenosine

flushing, SOB, chest burning, high grade AV block, AF, HA, hypotension, nausea, paresthesias

52

what are drug interactions of adenosine

less effective in presence of adenosine R blockers, potentiated by adenosine uptake inhibitors

53

what are the affects of atropine on AP

block actions Ach at PAN sites, increases CO

54

therpeutic use of atropine

bradycardia, neuromuscular blockade reversal, cholinergic poisoning

55

what occurs with toxicity of atropine

arrhythmia, tachy, dizziness, constipation, urinary retention

56

how does MgSO4 change AP

influence Na/K ATPase, Na Ch, K Ch, Ca Ch

57

therapeutic use of MgSO4

digitalis induced arrhythmias, TdP

58

how does digoxin change AP

inhibits Na/K ATPase, results in + inotropy, increased intracell Na, decreased Ca expilsion, increased free Ca, decreased HR, decreased refractory period, decreased conduction velocity

59

therapeutic use of digoxin

AF SVT, HF

60

toxicity of digoxin

nausea, vomiting, diarrhea, disorientation, visual distrubances, abberation of color perception, delayed afterdepolarization

61

Which antiarrhythmics may cause 2nd or 3rd degree blocks

Class II an IV

62

which antiarrhythmics work only on ventricular tissue

Class Ib

63

Which antiarrhythmic should never be used after MI or with CHF or severe LV hypertrophy

Class Ic (structural heart disease)

64

which antiarrhythmics increase risk of Torsades de point

Class Ia and III

65

what does adenosine feel like when you take it

Heart attack, t1/2 is 10 sec

66

What are supraventricular arrhythmias

originate above bundle od HIS and characterized by normal QRS
sinue brady, sinus tachy
paroxysmal supraventricular tachy
atrial flutter
atrial fib
wolff parkingson white
premature atrial conductions

67

what are ventricular arrhythmias

originate below bundle of His
PVC
VT VF

68

what are types of conduction blocks

supraventricular: 1, 2, 3 degree AV blocks
Ventricular: R or L BBB

69

What do we use to Tx acute AF

Beta blockers are 1st choice- not if systolic heart failure
nonDHP CCBs IV
digoxin (slower)

70

what do we use to Tx chronic AF

oral BB, CCB
digoxin if intolerable sideeffects to above drugs

71

what is the long term goal with Tx AF

rate control more important than rhythm control

72

what is the most effective cardioversion for AF

direct current cardioversion rather than chemical

73

How to we Tx acute paroxysmal supraventricular tachy

IV adenosine (drgu of choice), verapamil or diltiazem

74

how do we Tx chronic paroxysmal supraventricular tachy

radiofrequency catheter ablation
drugs: verapamil, diltiazem, BB or digoxin

75

If patient has PVCs but asymptomatic, what class of drug should you never use

Ic, could increase mortality

76

If have PVC after MI what drug is used

Beta blockers

77

What do we use in hemodynamic instability with sustained ventricular tachy

synchronous cardioversion

78

Tx for stable VT patients

procainamide, sotalol, amiodarone

79

for hemodynamically stable torsades patients what drug is given

MgSO4 or class Ib agents

80

what is Tx for hemodynamic compromise of torsades de pointes

electrical cardioversion