Cardiac Electricity

Question 1

Fastest pacemaker in the heart

Answer 1

SA Node ~1000 cells

Question 2

Functional adaptations of pacemaker cells

Answer 2

lack of ion channels that stop spontaneous depolarization; lack of myofibrils

Question 3

Sinoatrial AP curve

Answer 3

shallow upstroke, repolarization to only -65mV

Question 4

Atrial AP curve

Answer 4

Fast upstroke; 100 ms duration

Question 5

Escape mechanism (heart)

Answer 5

Secondary means of creating electrical impulse to start ventricular contraction

Question 6

AV Node

Answer 6

only place for transmission of the SA AP to ventricles

Question 7

Ventricular myocyte polarization waves

Answer 7

endocardial to epicardial depolarization

epicardial to endocardial repolarization

Question 8

Purkinje plateau

Answer 8

at 0 mV for 100-150ms then down to -85

Question 9

Cardiac electrical cycle

Answer 9

0) Depolarization wave (upstroke)
1) Early repolarization wave
2) Plateau
3) Major repolarization wave
4) time between repolarization and next depolarization

Question 10

Conduction velocity of various cardiac cells

Answer 10

AV/SA nodes = 0.05 m/s
Atrial/ventricular muscle = 0.3 m/s
Inter-nodal tracts 1.0 m/s
His/Purkinje fibers 3.0-5.0 m/s

variations in Na channel density responsible for differences

Question 11

Important intervals for ECG

Answer 11

PR interval for inter-nodal conduction and His/Purkinje system
QT interval

Question 12

SA and AV node lack which channels

Answer 12

Nv channels and IRK channels

Question 13

Myocytes repolarization channel (all)

Answer 13

Potassium

Question 14

Myocyte depolarization response (all)

Answer 14

VGCC for Calcium influx

Question 15

Tetrodotoxin

Answer 15

blocks Na channels; useful for study of slow rising (calcium dependent) AP’s

Question 16

Reasons for cardiac myocyte plateau

Answer 16

Calcium influx and slow opening K channels (K channels found in lower concentration on plasmalemma than in other excitable cells)

Question 17

Sodium cardiac myocyte electrical cycle

Answer 17

immediate opening, inactivation in 1-3 ms, inactive until complete repolarization

Question 18

Delayed potassium channel electrical cycle (cardiac myocyte)

Answer 18

open slowly (100-300 ms) and close slowly after repolarization

Question 19

cardiac myocyte ‘the’ IRK channels

Answer 19

raise the resting conductance of K; can be blocked by Mg2+ above -50mV

Question 20

L-type Calcium channels (cardiac electrical cycle)

Answer 20

open around -50mV, open for long duration, usually only 30% recruitment

Question 21

Other types of Calcium channels

Answer 21

T-type (transient-type): in cardiac myocytes, open briefly at the upstroke, then close. N-type (neuronal): in neurons and not found in cardiac myocytes. Neither of these can be affected by dihyrdopyridine or cAMP (catecholamine stimulated cAMP)

Question 22

NCX arrhythmia

Answer 22

when metabolically stressed, cardiac myocytes import too much Ca, this activates NCX which exchanges one Ca for 3 Na. This influx of Na can cause ‘after-depolarization’ and can potentiate a new AP

Question 23

the ‘Ito’

Answer 23

Kv channel “calcium-independent transient outward” these are the cause of the phase 1 early repolarization (cardiac electrical cycle) and are only open briefly

Question 24

the ‘Iks’

Answer 24

delayed K current ‘slow’ version

Question 25

the ‘Ikr’

Answer 25

delayed K current ‘rapid’ version; commonly called HERG; together with Iks are responsible for QT time, ergo malfunctions in these can cause long QT times and arrhthymias

Question 26

K ATP channels

Answer 26

ATP level sensing K channel that opens when ADP levels are too high (ATP too low); shortens AP’s; play a major role in ischemic attacks

Question 27

GIRK (ACh activated K Channel)

Answer 27

respond to parasympathetic ACh release to slow heart rate; only found in atria

Question 28

Long QT pathophys

Answer 28

Ikr and Iks channels are degraded prior to their insertion into the membrane; alternatively prolonged opening of the Na channels can cause late repolarization as well

Question 29

K-ATP channel pathophys

Answer 29

if activated due to a drop in metabolic rate (ischemia); or if Na channels do not deactivate - depolarization; if K-ATP stays open, intracellular K migrates out causing further depolarization

Question 30

ST depression

Answer 30

apparent depression of the ST wave due to higher resting potential - created by too much extracellular K levels (K-ATP open due to ischemia): depression=ischemia

Question 31

ST elevation

Answer 31

conduct of a current through damaged tissue may result in an elevated ST wave; present in MI (STEMI)

Question 32

How do you block ‘the’ IRK (result?)

Answer 32

Barium - result is spontaneous AP generation by all cardiac cells

Question 33

mechanism of nodal pacemaking AP generation

Answer 33

1) non-specific cation channels depolarize to -50 mV
2) Ca channels depolarize to E-Ca
3) delayed K channels open to repolarize
4) slight undershoot, then non-specific channels depolarize again

Question 34

the nonspecific cation channel current

Answer 34

effectively the background positive (depolarizing) current that counters the IRK channels; called “F-type current”; activated by repolarization and by sympathetics to increase HR

Question 35

True pacemakers

Answer 35

healthy pacemakers, SA node

Question 36

latent pacemakers

Answer 36

any cells outside the SA node that can generate a spontaneous AP, most notably the AV node and Purkinje fibers; common during atrial fib.

Question 37

ectopic pacemaking

Answer 37

when cells outside the SA node actually do fire spontaneous AP’s, usually due to NCX arrhythmia