9. Emod Flashcards

(36 cards)

1
Q

wt does the PR interval represent?
normal value?
wt does larger than normal indicate?

A

Conduction delay/atrial depolarization (time for stimulus to spread through atria and pass AV junction)
normal = <0.2 sec
>0.2 sec –> first degree heart block

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2
Q

wt does QRS represent?

wt phase of action potential?

A

ventricular depolarization

phase 0

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3
Q

wt is brugada syndrome?

A

defective Na channels in cardiac myocytes

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4
Q

wt pump is responsible for repolarization?

A

Na-K ATPase

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5
Q

function of Na/Ca exchanger?

A

bring in Ca during systole

remove Ca during diastole

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6
Q

role of L-type Ca channels?

T -type?

A
L = phase 2
T = phase 0
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7
Q

wt is responsible for refractory period of conduction?

A

inactivated Na channels

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8
Q

is sympathetic or parasympathetic more predominant in regulating resting HR?

A

para

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9
Q

wt happens with a myocyte is overleaded w Ca?

A

Ca is removed via NCX and results in premature depolarizations

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10
Q

wt is Mobitz type 1 conduction block?

A

progressive lengthening of PR interval resulting in dropped beat

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11
Q

wt is Mobitz type 2 conduction block?

A

dropped beats not preceded by increased PR interval

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12
Q

2 short term txs for AV block?

permanant solution?

A

Vagolytic agent (atropine) or catecholamine (isoproterenol

pacemaker

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13
Q

wt is PSVT?
3 acute tx?
2 chronic tx?
DOC?

A

paroxysmal supraventricular tachy
- rapid onset and termination tachy

acute - adenosine, CCB, digoxin

Chronic - 1a (quinidine) 3 (amiodarone)

DOC - amiodarone

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14
Q

wt causes delayed after-depolarizations?

tx?

A

Ca overload

Ca blockers (verapamil)

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15
Q

wt causes a fib?

2 components?

A

block w multiple reentry

reduced conduction velocity
reduced refractory period

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16
Q

most important predisposing factor to EAD?

tx?

A

polonged APD

isoproterenol

17
Q

wt channel abnormalities causes long-QT syndrome?

A

K mutations

Na mutations

18
Q

wt is the principal of the conduction velocity approach to tx reentry?

A

block fast Na channels –> makes it a bidirectional block

19
Q

2 ways to increase tissue refractoriness to tx reentry?

A

block Na channels from reactivating (no QT)

block outwar rectifier K channels (long QT)

20
Q

2 factors affecting # of availability of Na channels?

A

membrane potential

recovery time constant

21
Q

MOA of class 1A anti-arrhythmics?

ECG effects?

3 drugs?

A

Na blockers –> dec automaticity/CV
K blockers –> prolong APD

widen QRS and QT

Quinidine
procainamide
disopyramide

22
Q

MOA of class 1B AA?

effect on QT?

name 2?

A

binds inactive Na channels –> prolongs refractory

no effects on QT or QRS

lidocaine mexilitine

23
Q

MOA of class 1C AAs?

effect on ECG?

AE?

name 2

A

long acting Na channel blockers –> decrease CV

widen QRS

unidirectional block

flecainide propafenone

24
Q

MOA of beta blockers/class II?

effect of ECG?

name 2

A

dec node conduction –> prevent shortening of APD and refractory period

prolong QT

propranolol, esmolol

25
MOA of class III drugs? effect on ECG? AE? name 3
inhibit K channels --> prolong APD prolong QT and PR and QRS torsade de pointe amiodarone, sotolol, bretylium
26
2 side effects of amiodarone?
corneal microdeposits | pulmonary fibrosis
27
MOA of class IV drugs? use?
B blockers control rate involving AV node
28
Tx for sinus bradycardia?
pacemaker
29
2 tx for sinus tachycardia?
beta blockers or CCB
30
tx for a fib/flutter if pt is hemodynamically unstable?
transthoracic cardioversion
31
should you tx a fib/flutter w rhythm or rate control? 4 rate drugs? DOC for rhythm?
rate is better digoxin b blockers CCB amiodarone amiodarone
32
2 drugs to tx monomorphic V tach and flutter?
1a | III
33
another name for polymorphic VT? cause? DOC?
torsade de pointes long QT and Ca currents (EADs) magnesium
34
tx for V fib?
cardioversion
35
contraindication for amiodarone?
lung disease
36
tx of choice for arrhythmias?
DC cardioversion pacemaker defibrillator