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Year 2 CV > Anti arrhythmics, Kinder DSA and LEC > Flashcards

Anti arrhythmics, Kinder DSA and LEC Flashcards

1
Q

What are the Class Ia Na Channel blocker antiarrhythmics

A

Procainamide!!
guinidine
disopyramide

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2
Q

what are the class Ib Na Channel blocker antiarrhythmics

A

Lidocaine (xylocaine)!!
mexiletine
tocainide

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3
Q

what are the class Ic Na Channel Blockers

A

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

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4
Q

What are the class II antiarhythmics

A

Beta blockers
Emolol!!
meotrolol!!
propanolol!!

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5
Q

What are the class III antiarhythmics

A

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

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6
Q

What are the class IV antiarrhythmics

A

Ca channel blockers
Verapamil!!
Diltiazem!!

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7
Q

What are other antiarrhythmic drugs, not in a class

A

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

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8
Q

what is the electrical gradient in heart

A

-90mV inside 0 mV outside

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9
Q

what occurs in phase 0 of depolarization?

A

rapid deoplarization from increase in Na permeability

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10
Q

describe phase 1 depolarization

A

bried repolarization

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

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11
Q

describe phase 2 depolarization

A

plateau phase, Ca influx continues, balance by K efflux

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12
Q

describe phase 3 depolarization

A

repolarization continue K efflus

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13
Q

describe phase 4 cell deplarizaiton

A

gradual depolarization, Na leak balance by K efflux

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14
Q

what ways do antiarrhythmics depress autonomic properties of abnormal pacemaker cell

A

decrease slope of phase 4

elevate threshold potential

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15
Q

hwo can antiarrhythmics alter conduction of reentrant loop

A

facilitate conduction by shortening regractoriness

depress conduction by prolonging refractoriness

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16
Q

what are the effects of class Ia Na ch blocker

A

dec conduction velocity
increase refractoriness
decrease autonomic properties

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17
Q

what are the effects of class Ib Na ch blocker

A

no effect on velocity

may decrease refractoriness

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18
Q

what are the effects of claa Ic Na ch blocker

A

dec conduction velocity

no effect on refractoriness

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19
Q

what are the effects of class II antiarrhythmics

A

beta blockers
dec conduction velocity
increase refractoriness
decrease autonomic properites

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20
Q

what are the effects of class III antiarrhythmics

A

K ch blocker
increase refractoriness
increase AP duration

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21
Q

what are the effects of class IV antiarrhythmics

A

Ca ch blocker
dec conductionv velocity
increase refractoriness
decrease autonomic properties

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22
Q

what are class Ia antiarhyth used for

A

atrial and ventricular arrhythmias

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23
Q

what occurs with class Ia, Procainamide toxicity

A

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

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24
Q

what is lidocaine used for

A

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

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25
Q

what phase in AP does lidocaine shorten

A

phase 3 repolarization

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26
Q

what can toxicity of lidocain cause

A

least cardiotoxic!!

hypotension, neurologic (paresthesias, tremor, nausea, lightheadedness)

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27
Q

Which Na Ch blocker cannot be used in structural heart disease

A

Ic
Flecainide
Moricizine
Propafenone

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28
Q

What are the effects of flecainide on AP

A

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

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29
Q

what is therapeutic use for flecainide

A

supraventricular arrhythmias

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30
Q

wat can occur with toxicity of flecainide

A

severe excaervation of arrhythmias

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31
Q

what is therapeutic use of class II

A

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

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32
Q

what can occur with toxicity of propanolol

A

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

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33
Q

what is benefit of esmolol

A

beta 1 selective and ultra-short acting

34
Q

how does amiodarone change AP

A

prolongs AP duration and QT interval

significantly blocks Na Ch, weak adrenergic and CCB

35
Q

what is therapeutic use of amiodarone

A

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

36
Q

What occurs with amiodarone toxicity

A

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
Q

what are common drug interactions with amiodarone

A

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

38
Q

how does sotalol change AP

A

both beta blocking and AP prolonging

39
Q

what is therapeutic use of sotalol

A

life threatening ventricular arrhythmias, maintenace of sinus rhythm in AF

40
Q

what can toxicity of sotalol cause

A

dose related TdP

depression of LV function in patients with HF

41
Q

which K Ch blocker has interaction withs thiazides and verapamil

A

Dofetilide

42
Q

how do Class IV change AP

A

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

43
Q

how does verapamil work on AP

A

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

44
Q

therapeutic use of verapamil

A

SVT, decrease ventricular rate in AF, angina, HTN

45
Q

what are extracardial effects of verapamil

A

peripheral vasodilation

46
Q

what occurs with toxicity of verapamil

A

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

47
Q

therapeutic use of diltiazem

A

SVT, angina, HTN

48
Q

what occurs with toxicity of diltiazem

A

edema, HA, AV block, bradycardia, hypotension

49
Q

What are the effects of adenosine on AP

A

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

50
Q

therapeutic use of adenosim

A

Drug of Choice conversion of paroxysmal SVT

51
Q

what occurs with toxicity of adenosine

A

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

52
Q

what are drug interactions of adenosine

A

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

53
Q

what are the affects of atropine on AP

A

block actions Ach at PAN sites, increases CO

54
Q

therpeutic use of atropine

A

bradycardia, neuromuscular blockade reversal, cholinergic poisoning

55
Q

what occurs with toxicity of atropine

A

arrhythmia, tachy, dizziness, constipation, urinary retention

56
Q

how does MgSO4 change AP

A

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

57
Q

therapeutic use of MgSO4

A

digitalis induced arrhythmias, TdP

58
Q

how does digoxin change AP

A

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
Q

therapeutic use of digoxin

A

AF SVT, HF

60
Q

toxicity of digoxin

A

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

61
Q

Which antiarrhythmics may cause 2nd or 3rd degree blocks

A

Class II an IV

62
Q

which antiarrhythmics work only on ventricular tissue

A

Class Ib

63
Q

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

A

Class Ic (structural heart disease)

64
Q

which antiarrhythmics increase risk of Torsades de point

A

Class Ia and III

65
Q

what does adenosine feel like when you take it

A

Heart attack, t1/2 is 10 sec

66
Q

What are supraventricular arrhythmias

A 
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
Q

what are ventricular arrhythmias

A

originate below bundle of His
PVC
VT VF

68
Q

what are types of conduction blocks

A

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

69
Q

What do we use to Tx acute AF

A

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

70
Q

what do we use to Tx chronic AF

A

oral BB, CCB

digoxin if intolerable sideeffects to above drugs

71
Q

what is the long term goal with Tx AF

A

rate control more important than rhythm control

72
Q

what is the most effective cardioversion for AF

A

direct current cardioversion rather than chemical

73
Q

How to we Tx acute paroxysmal supraventricular tachy

A

IV adenosine (drgu of choice), verapamil or diltiazem

74
Q

how do we Tx chronic paroxysmal supraventricular tachy

A

radiofrequency catheter ablation

drugs: verapamil, diltiazem, BB or digoxin

75
Q

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

A

Ic, could increase mortality

76
Q

If have PVC after MI what drug is used

A

Beta blockers

77
Q

What do we use in hemodynamic instability with sustained ventricular tachy

A

synchronous cardioversion

78
Q

Tx for stable VT patients

A

procainamide, sotalol, amiodarone

79
Q

for hemodynamically stable torsades patients what drug is given

A

MgSO4 or class Ib agents

80
Q

what is Tx for hemodynamic compromise of torsades de pointes

A

electrical cardioversion

Year 2 CV (31 decks)

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