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Flashcards in arrhythmia mechanism Deck (31):
1

Almost all arrhythmias are

acquired:
1. myocardial infarction (MI)
2. ischemia
3. acidosis
4. alkalosis
5. electrolyte abnormalities.

2

Drug toxicity is a common cause of arrhythmia: including

1. cardiac glycosides
2. some antihistamines (astemizole, terfenadine)
3. antibiotics (sulfamethoxazole)

3

Cardiac Arrhythmia Suppression Trial (1989):

post-MI patients treated with flecainide or encainide had a 2-3x >mortality compared to placebo.

4

Consequence of CAST trial:

catheter ablation of ectopic foci and implantable cardioverter- debrillator devices (ICDs) are very often used in place of drugs.

5

Drugs
(1) remain useful in treating some arrhythmias, like ____
(2) are used with_____
(3) would be more useful if we ____

1. supraventricular
2. ICDs to
3. understood the mechanism of action AND molecular targets better

6

The primary targets of antiarrhythmic drugs are:

1. cardiac Na+ channels
(current = INa)
2. cardiac Ca2+ channels
(current = ICa-L)
3. cardiac K+ channels
(currents = IKs and IKr)
4. B -adrenergic receptors (BAR)

7

direct drug targets

1. Na+ channels
2. Ca2+ channels
3. K+ channels
4. B adrengeric receptors

8

indirect targets of antiarrhythmic drug action.

Via the B adrenergic pathway

9

only ____ have been demonstrated to reduce the incidence of sudden cardiac death

B blockers

10

prolonged ST interval corresponds to

increased AP duration

11

APs in which Ikr channels are partially blocked result in

prolongation of plateau phase

12

at ___% block, ____ are observed.

75%

after-depolarization

13

torsades de pointes

degenerate to ventricular fibrillation

14

Ina is the

cardiac Na+ channel

15

Ica-L is the

cardiac Ca2+ channel

16

INCX is the

electrogenic Na:Ca exchanger

17

Ikr is the

rapidly activated cardiac delayed rectifier K+ channel

18

Iks is the

slowly activated cardiac delayed rectified K+ channel

19

Ik1 is the

hyperpolarization activated K+ channel largely responsible for resting potential in ventricular myocytes

20

Ito is a

very rapidly activated K+ channel that is responsible for phase 1 of the fast response

21

voltage sensor

S4

22

NaV =

voltage- gated Na+ channels

23

familial long QT syndrome results in a

a prolongation of the duration of the cardiac action potential (QT interval) that can lead to ventricular arrhythmia and sudden death

24

In Familial long QT syndrome, prolongation of the plateau phase of the fast response action potential in ventricular myocytes initiates ____

a polymorphic ventricular tachycardia (called torsades de pointes) which can degenerate into ventricular fibrillation followed by syncope and sudden cardiac death.

25

Torsades de pointes is typically triggered by an ____

abrupt increase in sympathetic tone as occurs with emotional excitement, fright, or physical activity.

26

current clinical practice includes treating long QT patients with

β-adrenergic receptor blockers (β-blockers).

27

Thus the autosomal dominant form of long QT syndrome:

Romano-Ward syndrome (RWS), is genetically heterogeneous:

28

In an autosomal recessive form of long QT syndrome,

Jervell-Lange-Nielson syndrome (JLNS),

29

Some of the mutations in cardiac sodium channels and potassium channels that prolong QT interval:

1. a subunit of I-ks
2. a subunit of I-kr
3. a subunit of cardiac sodium channel

30

Long QT mutations in cardiac K+ channel subunits generally

1. reduce the number of K+ channels expressed in the myocyte plasma membrane (loss of function mutations)
2. prolonged plataeu

31

Long QT mutations in the cardiac Na+ channel (INa).

1. prevent Na+ channels from inactivating completely (gain of function mutations)
2. thereby prolonging phase 2 of the fast response.