Physio Test 3 - Cardiac Electrophysiology

Front 1

Cardiac conduction system

Back 1

SA node >> internodal tracts >> AV node >> bundle of his >> bundle branches >> purkinje fibers

Front 2

SA node

Back 2

primary pacemaker; spontaneously generates AP's, can be modified by PS and Symp

Front 3

internodal tracts

Back 3

path for rapid spread of AP through muscle

Front 4

atrial myocytes

Back 4

specialized for contraction and rapid conduction. Excitation forces blood into ventricles

Front 5

AV node

Back 5

gateway for propagation of AP into ventricles located on R atrial septum. Specialized for slow conduction

Front 6

Bundle of His, Bundle Branches, Purkinje fibers

Back 6

myocytes specialized for rapid conduction. Purkinje have fastest conduction in heart.

Front 7

Ventricular myocytes

Back 7

specialized for contraction, rapid conduction.

Front 8

contraction within ventricles

Back 8

goes from apex to base and from endocardium to epicardium

Front 9

cardiac cycle

Back 9

AP >> muscular contraction >> pressure in heart chambers increases >> valves open >> blood ejected

Front 10

Ventricular AP phases

Back 10

4: RMP and disastole; 0: rapid depolarization, onset of electrical systole; 1: partial repolarization; 2: plateau; contractile force peaks, mechanical systole; 3: rapid repolarization; end of systole.

Front 11

IRk channels

Back 11

inward rectifying K channels; open when membrane potential is more negative than -70mV and allow K efflux. Blocked by Mg during depolarization and reopen in phase 3.

Front 12

Na channels

Back 12

rapidly activating, voltage dependent; determines threshold in Phase 0. inactivated in phase 1

Front 13

Ito channels

Back 13

transient outward K channels; open during phase 0 and close during phase 2

Front 14

Ca channels

Back 14

voltage-dependent, open during phase 1 and cause plateau in phase 2, inactivated in phase 3

Front 15

DRK

Back 15

delayed rectifying K channels; open during phase 2 to keep membrane potential near 0mV and help return to RMP.

Front 16

Phase 4

Back 16

RMP and diastole; RMP close to -90mV
-IRK channels allow K efflux (condunctance small b/c RMP is near Ek)

Front 17

Phase 0

Back 17

rapid depolarization, onset of electrical systole;
-depolarization triggered by depolarization of neighboring cell; rapidly-activating, voltage-dependent Na channels are opening
-positive feedback loop increases Mp to +55

Front 18

Threshold

Back 18

Voltage at which there are enough Na channels open to produce full-blown AP. critical # of channels needed to overpower hyperpolarizing effects of K efflux through IRK.

Front 19

decreasing # or rate of Na channels

Back 19

higher threshold needed to reach AP

Front 20

Phase 1

Back 20

partial repolarization; 3 steps bring Mp to near 0 mV
-Fast Na channels are inactivated
-Transient outward K channels opened during phase 0 and force MP back toward Ek.
-voltage dependent Ca channels activate

Front 21

phase 2

Back 21

plateau; electrical and mechanical systole. plateau due to slow activation of Ca channels; Ito and DRK channels that keep MP around 0. Ca influx triggers muscle ocntraction

Front 22

Phase 3

Back 22

repolarization, end of systole. Inactivation of Ca channels and persistence of DRK channels elicits return to RMP

Front 23

Return to phase 4

Back 23

Na/Ca/Ito channels recover from inactivation and return to resting, closed state. IRK open and DRk close slowly.

Front 24

Absolute refractory period

Back 24

cannot fire another AP from phase 0 to middle of phase 3. Na channels inactive, Ca active or inactive.

Front 25

Relative refractory

Back 25

slowly propagating/depolarizing AP can occur. Phase 3 to start of phase 4. Na channels still inactive but Ca channels have recovered.

Front 26

MDP for pacemaker cells

Back 26

maximum diastolic polarization, -60 to -70 mV due to lower IRK conductance.

Front 27

Why do pacemaker cells have slow depolarization

Back 27

1. DRk close and IRK are scarce (allow MP to slowly rise) 2. Lh ionic current activated by hyperpolarization allows Na to enter; 3. A few slow Ca channels can be activated above -50mV

Front 28

SA node threshold

Back 28

Ca channels open once MP > -50mV; trigger AP. **Na channels do Not play a role in SA node because RMP is never negative enough to end their inactivation

Front 29

Slow AV node conduction - mechanisms

Back 29

REMP = -55mV, due to fewer IRK channels. Na channels remain inactivated; fewer GJ

Front 30

AV node AP based on

Back 30

calcium

Front 31

AV absolute refractory

Back 31

phase 0 to phase 3; determined by activation of DRK, inactivation of Ca

Front 32

AV RP

Back 32

phase 3- phase 4; larger stimulus needed b/c Ca channels not recovered from inactivation; determined by Ca channel activity

Front 33

Calcium channel blockers and refractory periods

Back 33

reduce ARP but increase RRP

Front 34

How to increase rate of phase 4 depolarization in SA

Back 34

Increase Lh activity, DRK closing, partial activation of calcium channels above -60mV

Front 35

How to change MDP in SA

Back 35

Make more negative to slow rate of depolarization; change IRK, DRK activity

Front 36

How to change threshold potential in SA

Back 36

icreasing activation of Ca channels at -50mV lowers threshold point.

Front 37

Sympathetic innervation of heart

Back 37

pregang from spinal cord releases Ach at sympathetic chain. postgang releases NE at atria, ventricles, nodes. E also delivered from adrenal gland.

Front 38

NE and E innervation of heart

Back 38

stimulate beta adrenergic receptors in cardiac myocytes to increase HR, contractile force

Front 39

Mechanism of positive chronotropy

Back 39

1. increase Ca channel activity; more open at any given voltage increases rate of depol. 2. increased Lh causes increased rate of depol in phase 4. 3. stimulation of DRK - increases rate of repolarization and keeps Ap and refractory period short.

Front 40

Mechanism of positive iontropy

Back 40

increase in contractile force due to 1. increase Ca channel activity; influx leads to more SR Ca release and increase in rate/force of contraction. 2. increase rate of Ca resequestration in SR keeps systole brief

Front 41

PS innervation of heart

Back 41

Branches of vagus release Ach at cardiac plexus, postgang nerves release Ach at SA and AV nodes.

Front 42

mechanisms of negative chronotropy

Back 42

1. inhibition of Ca channels slows phase 4 depolarization and raises threshold for AP. 2. stimulation of K channels causes hyperpolarization. 3. inhibition of lh to slow depolarization.