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

0
Q

diastole. where is pressure greatest during this time?

A

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

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1
Q

Pacemaker cells

A

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)

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2
Q

systole. where is pressure greatest during this time?

A

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

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3
Q

How is rapid impulse conduction/depolarization achieved across myocardium?

A

Direct ELECTRICAL COUPLING between cells via intercalated disks with gap junctions

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4
Q

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

A

much broader (almost 300x longer)

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5
Q

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

A

they spontaneously depolarize and produce their own APs

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6
Q

sarcolemma =

A

myocardial cell membrane

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7
Q

2 most important physiological characteristics of the myocardial cell membrane

A

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

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8
Q

Resting membrane potential of cardiac myocytes is fx of:

A

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

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9
Q

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

A

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

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10
Q

Nernst Equation

A

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

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11
Q

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

A

little effect

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12
Q

increased extracellular K+ —> myocardial cells

A

depolarize the RMP of cardiac muscle fibers

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13
Q

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

A

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

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14
Q

2 types of action potentials in myocardial cells

A

fast type and slow type

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15
Q

Why is AP of myocardial cells longer than normal cells?

A

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

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16
Q

Most common type of AP in myocardial cells

A

fast response AP

17
Q

Where do fast response APs occur?

A

atrial and ventricular myocytes + Purkinje fibers

18
Q

Where do slow response AP occur?

A

pacemaker cells of SA and AV nodes

20
Q

What do myocardial cells have a high concentration of?

21
Q

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

A

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
Q

Where are “backup” pacemakers located?

23
Q

4 phases of typical fast response cardiac AP

A

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
Q

decrease in extracellular K+ –> myocardial cells

A

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