Cardiac Cell Electrophys

Front 1

Cardiac cells have multiphasic action potentials; e.g., _______ myocardial cells:

Back 1

ventricular

Front 2

Phase 0:

Back 2

rapid upstroke

Front 3

Phase 1

Back 3

early partial repolarization

Front 4

Phase 2

Back 4

plateau; prolonged depolarization

Front 5

Phase 3

Back 5

final repolarization

Front 6

Phase 4

Back 6

interval between depolarizations (resting potential in cells which do not spontaneously depolarize)

Front 7

There are two major types of action potentials the ________ & ________

Back 7

fast response & slow response

Front 8

in “Fast response” APs the resting potential is approx. ______

Back 8

- 90 mV

Front 9

in “Fast response” APs Phase 0 is ________

Back 9

steep (fast).

Front 10

“Fast response” APs occurrence in ________, ______, & ________.

Back 10

Normal ventricular and atrial myocardial cells.
& Normal Purkinje fibers.

Front 11

In "Slow response” cells the
Resting potential is approx. ________

Back 11

-60 mV.

Front 12

In "Slow response” cells Phase __ is slower; phase __ is absent & the plateau is less distinct, not as flat.

Back 12

0
1

Front 13

In "Slow response” cells amplitude is _________

Back 13

diminished

Front 14

In "Slow response” cells ccurr in normal ___ node and ___ node cells & other myocardial cells under abnormal conditions.

Back 14

SA
AV

Front 15

Resting potential (in cardiac cells which do not spontaneously depolarize)is largely determined by distribution of ____ and ____ ions across the sarcolemma, and the permeabilities to these ions

Back 15

K+
Na+

Front 16

Vm =
membrane potential
* don't memorize

Back 16

-61.5 log [K+]i+[Na/K] [Na+]i
_____________________________
[K+]o+[Na/K] [Na+]o

Pk=permeability of K
Pna=permeability of Na

Front 17

Since the ratio (PNa/PK) is only about 0.01 during phase 4, the equation becomes essentially the Nernst equation for the potassium equilibrium potential (EK).

Vm~Ek=

Back 17

-61.5 log [K+]i/[K+]o

Front 18

PNa is not zero, so Vm will always be a bit ________ than EK.

Back 18

less negative

Front 19

Since PK is relatively high, resting potential is very dependent upon ____.

Back 19

[K+]o

Front 20

Progressive increases in ____ result in progressive depolarization of resting cardiac cell membranes toward 0 mV.

Back 20

[K+]o

Front 21

Abnormal plasma _____ levels can have clinically significant effects on myocardial resting potentials.

Back 21

[K+]

Front 22

Since PNa is very low, _______ potential is relatively independent of [Na+]o.

Back 22

resting

Front 23

The normal concentration gradients would gradually decrease if the slight Na+ ______ and slight K+ _____ were uncompensated.

Back 23

influx
efflux

Front 24

Na+ and K+ transport is mediated by a membrane-bound, Na+, K+-activated _____.

Back 24

ATPase

Front 25

The pump is electrogenic: the ratio of Na+ to K+ pumped is about _:_ .

Back 25

3:2

Front 26

Inhibition of the pump (e.g., by cardiac glycosides) results in partial _______ of the sarcolemma.

Back 26

depolarization

Front 27

_________ is opening of “fast” channels for Na+ and increase in gNa (Na+ conductance).

Back 27

Phase 0

Front 28

Opening of fast channels is __________: the degree of opening increases as membrane potential approaches threshold voltage.

Back 28

voltage dependent

Front 29

When resting potential is normal, fast channels open rapidly and completely after _______. Action potential is large and rapidly rising.

Back 29

stimulus

Front 30

Partial depolarization _______ some fast channels. Action potential is smaller and more slowly rising.

Back 30

inactivates

Front 31

______ depolarization to threshold produces normal action potential whereas, ______ depolarization to threshold inactivates some fast channels. Action potential is smaller and slower rising, similar to the result when the resting potential becomes less negative.

Back 31

Rapid
slow

Front 32

Since depolarization is due to Na+ influx, [Na+]o affects the ______ of the action potential.

Back 32

amplitude

Front 33

[Na+]o does not affect the ______ potential significantly, due to low membrane permeability to Na+ in the resting cell.

Back 33

resting

Front 34

The recovery of the ability of fast channels to open is delayed until ______ of the fast response.

Back 34

phase 3

Front 35

In order for fast channels to open, Vm must approach ____(recovery is voltage dependent).

Back 35

-90 mV

Front 36

Full recovery requires several msec after return to resting potential (recovery is _____ dependent).

Back 36

time

Front 37

Fast channels begin to close as Vm approaches _____ during phase 0.

Back 37

0mV

Front 38

______ in gK begins near the end of Phase 0 (K+ current (IK1) diminishes, but doesn’t stop or reverse).

Back 38

Decrease

Front 39

______ in gCa begins during the upstroke (ICa).

Back 39

Increase

Front 40

______ is initiated when the closure of fast channels is complete.

Back 40

Phase 1

Front 41

During phase I, a transient, small efflux of __ ions contributes (Ito). Small influx of ___ ions may contribute.

Back 41

K+
Cl-

Front 42

"Slow” channels carry primarily ___ ions.

Back 42

Ca2+

Front 43

"Slow” Ca2+ channels (L-type, ICa) ____ to open during Phase 0.

Back 43

begin

Front 44

Calcium conductance, gCa increases as a result of their opening, resulting in a slow ______ current.

Back 44

inward

Front 45

Entering Ca2+ triggers release of more Ca2+ by _________.

Back 45

sarcoplasmic reticulum

Front 46

Slow channel opening is not affected by less _____ resting potentials as
much as are fast sodium channels.

Back 46

negative

Front 47

Ca2+ influx is increased by ___________.

Back 47

catecholamines

Front 48

Certain ______ block slow Ca2+ channels (e.g., verapamil, nifedipine).

Back 48

drugs

Front 49

In phase 2, ________ is lower than Phase 4, but not zero.

Back 49

K+ conductance (gK)

Front 50

in phase 2, a small_____ K+ current balances the Ca2+ _______ , prolonging the plateau at about 0 mV.

Back 50

outward (efflux)
influx

Front 51

During phase 3, gK increases, allowing _______ to increase (repolarizing effect, IKr).

Back 51

K+ efflux

Front 52

During phase 3, ______ channels close, and gCa decreases; Ca2+ influx is shut off.

Back 52

Slow

Front 53

During phase 3, Recovery of ability of ____ channels to open occurs (see above).

Back 53

fast

Front 54

In cells with slow responses, fast channels are probably always ______ .

Back 54

inactivated

Front 55

Fast responses in fast response cells can be ______ to slow responses by pharmacologically blocking the fast channels (e.g., with tetrodotoxin).

Back 55

converted

Front 56

_____ does not affect the amplitude of a slow response action potential.

Back 56

[Na+]o

Front 57

Depolarization of phase 0 of a slow response is due to influx of ___ ions through slow _____channels

Back 57

Ca2+
Ca2+

Front 58

Depolarization of phase 0 of a slow response cannot be blocked by tetrodotoxin, but can be blocked by ____ channel blockers.

Back 58

Ca2+

Front 59

During depolarization of phase 0 of a slow response, Action potential amplitude is directly dependent upon ____.

Back 59

[Ca2+]o

Front 60

Conduction velocity is directly proportional to __________and __________

Back 60

action potential amplitude
rate of depolarization.

Front 61

Conduction velocity decreases when ________ becomes less negative (via the effects of resting potential on action potential amplitude and rate of depolarization).

Back 61

resting potential

Front 62

Since slow response action potentials are smaller and slower in depolarization rate, they are conducted slower than fast responses. Slow responses are also more easily _______.

Back 62

blocked

Front 63

_______ slow responses/unit time can be conducted compared to fast responses.

Back 63

Fewer

Front 64

Influences which change cardiac conduction velocity are called ________ influences.

Back 64

dromotropic

Front 65

During the __________vno propagated depolarizations are possible

Back 65

effective refractory period (ERP)

Front 66

Effective refractory period (ERP)lasts from _______ to _______

Back 66

From beginning of phase 0 to middle of phase 3 (Vm ~ -50mV).

Front 67

By the end of ERP, some ____ channels can reopen.

Back 67

fast

Front 68

During the _________ strong stimuli can result in propagated action potentials.

Back 68

relative refractory period (RRP)

Front 69

Duringt the relative refractory period (RRP),the number of fast channels able to reopen depends upon ___

Back 69

Vm (voltage membrane)

Front 70

During slow response, ERP may extend beyond phase ___.

Back 70

3

Front 71

During slow response, RRP extends into phase ___

Back 71

4

Front 72

Slow response, significantly prolongs recovery of ______.

Back 72

excitability

Front 73

During slow response, conduction velocity is proportional to level of _________.

Back 73

excitability

Front 74

Refractory period duration (and action potential duration) decrease as heart rate ______ (interval-duration relationship).

Back 74

increases

Front 75

Pacemaker Cells of the SA Node have several characteristics in common with the slow response:
1. Resting potential is less ________ than ventricular cells.
2. Phase 0 is relatively ____ .
3. A distinct ______is not seen.
4. Phase 3 is relatively ___.
5. Depolarization of phase 0 appears to be due to ___ influx

Back 75

negative
slow
plateau
slow
Ca2+

Front 76

Spontaneous phase 4 depolarization is called the ________ .

Back 76

pacemaker potential

Front 77

_____________ results from unstable membrane ionic permeabilities and conductances.

Back 77

Spontaneous phase 4 depolarization

Front 78

a gradual increase in slow ___ influx begins during phase 3.

Back 78

Na+

Front 79

during spontaneous phase 4 depolarization, A slow ____ of Ca2+ begins in phase 4 (T-type channels and possibly a contribution by L-type channels also, ICa).

Back 79

influx

Front 80

during spontaneous phase 4 depolarization, ______ of K+ (IK1) gradually decreases throughout phase 4.

Back 80

efflux

Front 81

When pacemaker potential reaches the threshold voltage, an action potential occurs. Phase 0 results mainly from ____ channels.

Back 81

Ca++

Front 82

Rate of pacemaker potential depolarization and action potential amplitude are decreased by:
a. Decreased external ___ concentration.
b. ____ channel blocking agents.

Back 82

Ca2+
Ca2+

Front 83

Mechanisms which can change heart rate by changing SA node depolarization rate:
1. Change the rate of phase __ depolarization
2. Change the ______ voltage.
3. Change the _______ of membrane potential at the end of phase 3

Back 83

4

threshold

negativity

Front 84

Influences which change heart rate are called ___________ .

Back 84

chronotropic influences

Front 85

Major Types of Ion Channels in Cardiac Cell Membranes:
(give type & role)

Fast Na+ (INa)

Back 85

Voltage-gated

Opening results in Phase 0 of fast response cells.

Front 86

Slow Na+ (If)

Back 86

Voltage-gated &
Ligand-gated

Contribute to Phase 4 of pacemaker cells.

Front 87

L-type Ca++ (ICa)

Back 87

Voltage-gated

Long-lasting, slow inward current during Phase 2 of fast response cells and Phases 4 and 0 of slow response and pacemaker cells.

Front 88

T-type Ca++ (ICa)

Back 88

Voltage-gated

Channel opening is transient. Contribute to Phase 4 of pacemaker cells.

Front 89

Inward rectifier K+ (IK1)

Back 89

Voltage-gated

Open channels are major contributors to Phase 4 potential. Depolarizations close them. Contribute to Phases 2 & 3 of fast response cells. Slow closure contributes to Phase 4 depolarization of pacemaker cells.

Front 90

Transient outward K+ (Ito)

Back 90

Voltage-gated

Contribute to Phase 1, of fast response cells., also Phases 2 & 3 to some extent.

Front 91

Delayed rectifier K+ (IKr)

Back 91

Voltage-gated

Opening results in Phase 3 repolarization. Also contribute to lesser extent to Phases 2 & 4.

Front 92

ATP-sensitive K+ (IK, ATP)

Back 92

Ligand-gated

ATP inhibits opening. Reduced ATP results in greater opening, e.g., during hypoxia.

Front 93

ACh-activated K+ (IK, ACh)

Back 93

Ligand-gated

ACh opens channel via Gi protein. Occurs with increased vagal activation