Lecture 02: Basic Structural and Electrical Chars. of Myocardial Cells (Hayward) Flashcards Preview

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Flashcards in Lecture 02: Basic Structural and Electrical Chars. of Myocardial Cells (Hayward) Deck (40):
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Pacemaker cells

specialized myocardial cells in SA node that undergo spontaneous depolarization (produces SELF-GENERATED action potentials) to instigate sequential depolarization of heart muscle, followed by synchronized rhythmic contractions of the heart chambers (systole)

1

diastole. where is pressure greatest during this time?

period of ventricle relaxation as blood from atria fill ventricles. Pressure outside ventricle is greater than inside ventricle

2

systole. where is pressure greatest during this time?

period of ventricular contraction as ventricle pump blood out to pulmonary and systemic circulation. Pressure is greater inside ventricle than outside

3

How is rapid impulse conduction/depolarization achieved across myocardium?

Direct ELECTRICAL COUPLING between cells via intercalated disks with gap junctions

4

How do action potentials of myocardial cells compare to those generated by skeletal muscle cells?

much broader (almost 300x longer)

5

Why do pacemaker cells not have input from external control system?

they spontaneously depolarize and produce their own APs

6

sarcolemma =

myocardial cell membrane

7

2 most important physiological characteristics of the myocardial cell membrane

1) ability to maintain appropriate ion concentration gradients b/w intracellular and extracellular environments
2) ability to respond to electrical depolarization

8

Resting membrane potential of cardiac myocytes is fx of:

1) high permeability of membrane to K+
2) low permeability of membrane to other ions (i.e. Na, Ca)
3) high concentration of K+ in myocardial cells at rest

9

Why is K+ concentration in myocardial cells higher than extracellular environment at rest? (3 main reasons)

1) Myocardial cells have high permeability to K+
2) negatively charged proteins in cells draw K+ in
3) Na+/K+ contributes to negative balance inside cell, which also draws more K+ in

10

Nernst Equation

used to determine the equilibrium potential for different ions across a semi-permeable membrane at rest

11

Changes in extracellular concentrations of Na+ and Ca++ --> myocardial RMP

little effect

12

increased extracellular K+ ---> myocardial cells

depolarize the RMP of cardiac muscle fibers

13

What does Na/K pump pump in/out of cell?

3 Na+ out, 2 K+ in. Driven by ATP

14

2 types of action potentials in myocardial cells

fast type and slow type

15

Why is AP of myocardial cells longer than normal cells?

due to large influx of Ca++ during depolarization IN ADDITION to normal Na+ influx

16

Most common type of AP in myocardial cells

fast response AP

17

Where do fast response APs occur?

atrial and ventricular myocytes + Purkinje fibers

18

Where do slow response AP occur?

pacemaker cells of SA and AV nodes

20

What do myocardial cells have a high concentration of?

glycogen

21

Phase 0: Rapid Depolarization (precursor + 2 main events)

Before Phase 0, pacemaker cells fire in wave of membrane depolarization. Causes:
1) opening of abundant fast-type voltage sensitive Na+ channels of myocardial cells
2) rapid influx of Na+ down Na+ concentration and charge gradient

*RAPID Na+ INFLUX*

22

Where are "backup" pacemakers located?

AV node

23

4 phases of typical fast response cardiac AP

0) Rapid depolarization
1) Initial repolarization
2) Plateau phase
3) Rapid repolarization
4) Resting membrane potential

RAPID Na+ INFLUX --> Ca++ INFLUX --> K+ EFFLUX --> return to RMP

24

decrease in extracellular K+ --> myocardial cells

hyperpolarizes

25

Phase 1: Initial repolarization (2 main events)

1) Na+ channels rapidly close
2) Transient K+ outward current activated by the depolarization

26

Phase 2: Plateau phase (3 main events)

1) Ca++ channels SLOWLY open
2) Ca++ influx according to its conc. gradient
3) Decreased K+ efflux

27

Phase 3: Rapid Repolarization (3 main events)

1) Ca++ channels slowly close/Ca++ conductance decreases
2)K+ efflux increases via delayed rectifier channel that was activated in plateau phase
3) Cell is repolarized/hyperpolarized as membrane potential returns to original resting negative potential

28

Why is plateau phase a plateau?

Low conductance of K+ during this time.

Also, slow Ca++ channel opening and closing(<--main regulator)

29

Why is slow nature of Ca++ channel opening/closing important?

Allows for prolonged AP in cardiac cells. Length of AP is directly related to the rate of intracellular sequestering of Ca++

30

When do delayed rectifier channels become activated?

During plateau phase

31

Phase 4: Resting membrane potential (3 main events)

1) High K+ conductance, low Na+ and Ca++ conductance
2) Na+/K+ pumps correct Na+/K+ concentrations from preceding AP
3) Na/Ca++ channels and sarcolemma restore internal Ca++ concentration

32

Long AP is associated with long:

refractory period

33

refractory period fx

allows for sufficient time between heart beats for adequate cardiac filling time and Ca++ reuptake into intracellular stores

34

When does absolute/effective refractory period occur?

Phase 1-3

35

When does relative refractory period occur?

phase 3

36

When is cell completely unexcitable to new input?

During phase 1-2 in absolute/effective refractory period

37

Stimulation of myocardial cell in beginning of phase 3 will result in:

local AP only with no propagation

38

Stimulation of myocardial cell during middle/end of phase 3 during relative refractory period will result in:

AP conducted, but with slower velocity. AP may not depolarize the rest of the heart and generate a heart beat.

39

What is amplitude of AP directly relate to?

Driving force to open Na+ channels

40

Normal RMP of myocardial cell

-90mV

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