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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
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

Year 2 CV (31 decks)

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