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CRAAB 1 > Nordgren: Cardiac muscle > Flashcards

Nordgren: Cardiac muscle Flashcards

1
Q

What triggers a contraction in striated muscle cells?

A

Rapid voltage change that leads to an AP

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2
Q

What are the three ways cardiac muscle APs differ from skeletal?

A
  1. self generating
  2. conducted directly from cell to cell
  3. long duration
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3
Q

What is a membrane potential?

A

electrical potential created by separation of electrical charges across a membrane

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4
Q

What is the only way for a membrane potential to change?

A

When a current flows through the cell membrane.

The rate of change is directly proportional to net current across the membrane.

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5
Q

What is the transmembrane voltage stable?

A

Only when there is no net current.

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6
Q

What is current?

A

Movement of ions through the cell membrane

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7
Q

What are the three most important ions? Which are interstitial and which are intracellular?

A

Interstitial: Na and Ca
Intracellular: K

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8
Q

How do these ions pass through the lipid bilayer membrane?

A

Via transmembrane proteins like ion channels

ions are very insoluble in lipids

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9
Q

How does membrane permeability relate to ion channels?

A

Permeability is the “net status” of the ion channels

i.e. “high permeability to Na”–> many of the Na channels open

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10
Q

Which two ions play a major role in determining membrane potential?

A

Na and K…the membrane potential will lie between their two equilibrium potentials

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11
Q

Why do Na and K play a minor role in determining membrane potential?

A

Low/unchanging permeability

Low concentration

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12
Q

What ion participates in cardiac muscle AP?

A

Ca

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13
Q

What is the equilibrium potential for Ca?

A

100 mV

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14
Q

The resting membrane potential is typically close to what ion’s equilibrium potential?

A

K (-90 mV)

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15
Q

What are the two types of cardiac muscle cells?

A

Myocardial CONTRACTILE cells

Myocardial AUTORHYTHMIC/PACEMAKER cells

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16
Q

What is the main difference in AP between myocardial contractile cells and cells of neurons/skeletal muscle?

A

They are similar, but myocardial cells have longer AP due to Ca entry.

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17
Q

Describe the AP of Pacemaker cells. Do these cells ever reach a “resting” state? What are the three areas with pacemaker cells?

A

Generate APs spontaneously due to unstable membrane potential (pacemaker potential.

NO

SA node, AV node, Bundle of His

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18
Q

How do the APs of pacemaker cells and contractile cells differ?

A

Pacemaker- slow response

Conractile cells- fast response

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19
Q

What accounts for the difference in AP between contractile and pacemaker cells?

A

Differences in how ion permeability changes during excitation

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20
Q

Describe the AP of a myocardial contractile cell.

A

4 phases (4, 0, 1, 2, 3, 4)

  1. Resting mp at -90 mV, Na channels open, K channels close
  2. Depolarization (influx Na), Na
    PEAK- Na channels close, Fast K channels open (K outward)
  3. Initial repolarization (K channels close, Ca channels open (slow inward).
  4. Plateau: Slow K channels open, Ca channels close.
  5. Rapid repolarization
  6. K channels close, K channels open (inward rectifier)
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21
Q

Describe the AP of a myocardial pacemaker cell.

A

3 phases (4, 0, 3, 4)

  1. Funny current is open allowing for large influx of Na and efflux of K. MP rises.
  2. As it reaches threshold the transient Ca channel opens leading to rapid depolarization and you get activation of long lasting Ca channel.
  3. Once you reach the peak, you get opening of K channels and net efflux that causes repolarization down to -60 mV.
  4. Funny channels open again and gradually depolarize.
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22
Q

What are the main differences in AP between the contractile and the pacemaker cells?

A

0- Mediated by Na in contractile cells, Ca in pacemaker cells
1/2- ABSENT in pacemaker cells
3- SAME
4- Resting vs pacemaker potential

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23
Q

What is unique about the refractory state in APs of cardiac cells and what does this mean for the cell?

A

They are in the refractory state during MOST of the AP.

They cannot be stimulated for another firing.
Precludes summated or tetanic contractions.

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24
Q

What is a refractory period?

A

Time after an AP when a normal stimulus can’t trigger a second AP

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25
Q

What is summation?

A

The tension of the muscle fiber INCREaSES w/ repeated AP

26
Q

What is tetanus?

A

A state of MAXIMAL conraction

27
Q

When does tetanus occur?

A

When AP continue to stimulate a muscle fiber repeatedly at short intervals (hi f) so that the relaxation period between contractions diminishes until nearly (unfused tetanus) or completely (fused tetanus) absent.

28
Q

How does skeletal muscle AP compare to the length of contraction?

A

SHORT AP compared to the length of contraction (Refractory also short) –> Allows for tetanus/sustained muscle contraction to occur

29
Q

What is unique about AP compared to the length of contraction in a cardiac cell? What causes this? Why is this important?

A

AP is almost as long as the actual muscle contraction.

The influx of Ca during Phase 2 lengthens total duration of AP to 200ms

30
Q

What prevents cardiac muscle from tetnus?

A

Long refractory periods

31
Q

What is an intercalated disk?

A

structure that connects ends of two adjacent cells

32
Q

What do disks contain?

A
  1. firm mechanical attachments (desmosomes made out proteins called adherens)
  2. Low-resistance electrical connections (channels formed of proteins called connexins in structures called gap junctions)
33
Q

What causes local current to flow between the depolarized membrane of cell A and the polarized membrane of cell B?

A

Electrostatic attraction!

POSITIVE Ion movement in cell A depolarizes cell B triggering an AP. Cell B evokes an AP in BOTH C and D. (how depolarization rapidly spreads between tissue and amplifies)

34
Q

What is an electrocardiogram?

A

Record of how the voltage between two points on the body surface changes with time as a result of the electrical events of the cardiac cycle.

35
Q

In an electrocardiogram what does the_____ stand for?

P wave

A

P wave- Atrial depolarization

36
Q

In an electrocardiogram what does the_____ stand for

PR interval

A

PR interval- Conduction time through atria and AV node

37
Q

In an electrocardiogram what does the_____ stand for?

QRS

A

QRS- Ventricular depolarization (LARGE peak)

38
Q

In an electrocardiogram what does the_____ stand for?

QT

A

QT- total duration of ventricular systole

39
Q

In an electrocardiogram what does the_____ stand for?

ST

A

ST- Plateau phase of ventricular AP

40
Q

In an electrocardiogram what does the_____ stand for?

T

A

T- Ventricular repolarization

41
Q

How does parasympathetic activity affect heart beat rate?

A

Parasympathetic activity leads to a release of ACh resulting in an initial hyperpolarization. This means the heart rate SLOWS because you are prolonging the time to depolarization.

42
Q

What does sympathetic activity do to the heart beat rate?

A

It INCREASES the rate of depolarization leading to a net effect of speeding up the heart rate.

43
Q

What do cardiac parasympathetic fibers do? Nerve? Release? End result?

A

Via vagus nerve
Release Ach
Increases permeability of resting membrane to K
Decreases diastolic funny current through HCN channels

44
Q

What do cardiac sympathetic fibers do?

A

Release NE and increase diastolic inward currents through HCN channels.

45
Q

Describe Excitation Contraction Coupling….Yea it’s a long process, but you can do it!

A
  1. AP enters from adjacent cell
  2. VG Ca channels open. Ca enters cell.
  3. Ca induces Ca release through RyR channels.
  4. Local release causes Ca spark.
  5. Summed Ca sparks create a Ca signal.
  6. Ca ions bind to troponin to initiate contraction.
  7. Relaxation occurs when Ca unbinds from troponin.
  8. Ca is pumped back into the SR for storage
  9. Ca is exchanged with Na by the NCX antiporter.
  10. Na gradient is maintained by the Na K ATPase.
46
Q

What are isometric contractions?

A

fixed LENGTH

Activation of muscle whose ends are held rigidly means it can develop tension, but can’t shorten.

47
Q

What is isotonic contraction?

A

fixed TENSION

Activation of unrestrained muscle causes it to shorten without force development because it has nothing to develop force against.

48
Q

What is required to strech a resting muscle to different lengths?

A

Force!

49
Q

What is active tension?

A

It develops when a muscle is stimulated to contract while at a fixed length

50
Q

What is total tension?

A

The sum of active and resting tensions

51
Q

What does active tension developed during isometric contraction depend on?

A

The muscle length at which contraction occurs

52
Q

How does weight affect a resting muscle?

A

It shortens the length

53
Q

What happens to contractile potential as a muscle shortens?

A

It decreases

54
Q

What is Inotrope?

A

Influences the amount of tension the muscle can develop and the amout of shortening the muscle can achieve

55
Q

What is NE?

A

Positive inotrope
Increases isometric tension
Increases afterload shortening

( you get more shortening of the muscle fiber and a stronger force of contraction)

56
Q

What determines the volume and pressure tensions in the heart champer?

A

Length-tension relationships of cardiac muscle fibers in the ventricular wall

57
Q

What does an increase in ventricular volume lead to?

A

An increase in ventricular circumference and an increase in the length of cardiac muscle cells. An increase in tension of individuals cells in the wall causes an incarease in intraventricular pressure.

58
Q

What happens as ventricular volume decreases?

A

Lesser total force is required by the muscle cells in the ventricular walls to produce any given intraventricular pressure.

59
Q

What is the law of laplace?

A

The total ventricular wall tension T depends on both intraventricular pressure P and the internal ventricular radius (r). T= PxR

60
Q

What is the implication of the law of laplace?

A

It is easier for muscle cells to produce adequate internal pressure at the end of ejection (small radius) than beginning of ejection (large radius).

CRAAB 1 (11 decks)

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