Cardiac Muscle Flashcards

0
Q

What are some properties unique to cardiac mm?

A

Cells are short, branch and interdigitate

Presence of intercalated disks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What are some properties that are common for cardiac and skeletal mm?

A
Striated
Sarcomeres (thick, thin filaments)
Same sliding filament mechanism
Crossbridge cycling is similar
T-tubules and SR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cardiac muscle cells are similar to _________skeletal muscle fibers

A

Type I (slow oxidative)
because -depend on oxidative phosphorylation
- numerous mitochondria
- highly resistant to fatigue
- BUT highly dependent on continuous supply of O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 3 types of connections b/n cardiac myocytes?

A

Zonula Adherens
Macula Adherens (Desmosomes)
Gap Junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the two connections that make up intercalated discs?

A
Macula Adherens (Desmosomes)
Gap Junction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define physical and functional coupling?

A

Physical coupling: points where cells mechanically pull on each other-Zonula adherens, Macula adherens (Desmosomes)
Functional coupling: allow electrical signals to pass between cells-Gap junctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define sliding filament mechanism of muscle contraction.

A

Thin filaments sliding over thick filaments causing muscle contraction.
NOTE: during muscle contraction the H and I-bands shorten. While the A-band doesn’t change.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the different states of crossbridge cycling?

A

Attached state-Released state (ATP attaches to myosin)-Cocked state (ATP is hydrolyzed, myosin at resting conformation)-Crossbridge state (myosin head binds to a new position on actin)-Power-stroke state (P is released, shortening and force development)-Attached state (ADP is released)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are two molecules essential for crossbridge cycling?

A

Ca

ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the difference b/n cardiac and skeletal muscle at the membrane system for E-C (excitation-contraction) coupling?

A

Cardiac mm:

  • more sparse SR,
  • dyad-SR, TT (triad-1T-tubule b/n 2SR’s in SK mm),
  • d/f T-tubule position cardiac mm @ z-line (SK mm A-I band junction), -bigger T-tubule (200 nm vs. 30 nm in SK mm)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How are cardiac mm d/f from skeletal mm in handling Ca during E-C coupling?

A

Skeletal mm: AP gets to the T-tubule–DHPR (on T-tubule) senses Vm–change in conformation of DHPR results in change in conformation of RyR of the SR–Voltage (depolarization)-dependent Ca release from SR to the cytosol–CONTRACTION
Cardiac mm: AP gets to the T-tubule–DHPR acts as Ca channel–[Ca] in the cytosol increases–Ca-Induced Ca Release from the SR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

T/F Cardiac mm can NOT contract in the absence of extracellular Ca.

A

T. Unlike SK mm., Cardiac mm need CICR to generate contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is another name for DHPR in cardiac mm?

A

L-type Ca channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 3 ways that DHPR regulates cardiac function?

A

DHPR (L-type Ca channel) regulates cardiac function:

  • physiologically (ex. sympathetic stimulation)
  • pharmacologically (ex. calcium channel blockers)
  • pathologically (ex. ischemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T/F Ca influx during AP must not be balanced by a Ca efflux b/n APs.

A

F. It must be balanced. There are different channels responsible for the entry and exit of Ca.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the key players in Ca balance (entry and exit)?

A

Entry: DHPR, RyR
Exit: SR ATPase, Surface ATPase, Surface Na-Ca Exchanger (3Na in for 1Ca out), Mitochondrial uniporter
NOTE: refer to pp. 11

16
Q

What 3 factors affect the [Ca] in the cytoplasm?

A

1) Amount of Ca stored in SR
2) Amount of Ca entering the cell from the extracellular space
3) Heart rate

17
Q

Compare and contrast the gradation of contractile force b/n SK mm and Cardiac mm?

A

SK mm:
recruitment,
summation and tetanus,
length-tension relationship (bell curve)
Cardiac mm:
-all or none (all the muscles work as a unit),
-no summation and tetanus b/c the duration of the AP is comparable to the duration of mm contraction,
-length-tension relationship (resting cardiac mm length is less than optimal length, cardiac muscle does not normally operate within the descending limb safety factor i.e., much stiffer)

18
Q

Define Frank-Starling’s Law.

A

Increased stretching of the myocardial filaments results in a stronger contraction-Fundamental property of cardiac mm.
Ex: Increased venous return->increased stroke volume (SV)

19
Q

______gives the precise arrangement of thick and thin filaments, and gives rise to passive mm stiffness

A

Titin

20
Q

What are the factors that alter the length of ventricular cardiac mm fibers?

A

Increase the length: stronger atrial contraction, increased (total blood volume,venous tone, pumping action of SK mm, negative intrathoracic pressure)

Decrease the length: standing, increased intraventricular pressure, ventricular compliance

21
Q

Define preload and afterload.

A

Preload: the amount of blood (chamber volume) before contraction (extent to which the mm is stretched).

Afterload: the tension against which the ventricle must contract (the load lifted by the mm in isotonic contraction)

REVIEW:CO=HR(SV). SV depends on: preload, afterload and inotropic state. Inotropic state depends on: # functional myocytes, the cytosolic [Ca] and coronary O2 supply.

22
Q

Describe what each of the ff. situations signify:

1) No PL, AL acting on the mm
2) PL added on the mm
3) PL, AL added without additional stretch
4) AL lifted

A

1) Relaxed state after ventricular contraction
2) End of filling of the ventricle
3) Ventricle contraction has started, both valves are closed
4) Left Ventricular ejection into aorta
NOTE: refer to pp. 18

23
Q

What factors can affect preload and afterload?

A
  • Cardiac factors (HR, or SV)

- Vascular factors (vascular tone and peripheral resistance)

24
Q

What is contractility?

A

a measure of the force generated (strength of contraction) of the mm fibers at a given INITIAL FIBER LENGTH (inotropic state)

25
Q

What inputs can alter contractility?

A

nervous inputs (ex: sympathetic increases contraction while parasympathetic decreases contraction)
hormonal inputs,
drugs

26
Q

Mention 3 factors that will change the rate of cycling of crossbridges.

A

1) The amount of Ca release into the cytosol
2) The affinity of the myofilament to Ca
3) # functional myocytes

27
Q

Give examples of positive and negative inotropic agents.

A

Positive Inotropic Agents (increase strength of contraction)

  • Catecholamines (Epinephrine or Norepinephrine which increase Ca influx)
  • Cardiac glycosides (Digitalis-inhibit Na/K ATPase; digioxin)
  • Xanthines (Caffeine and theophylline-inhibit breakdown of cAMP)

Negative Inotropic Agents (weaken force of contraction)

  • Beta blockers (block B-Adrenergic receptors)
  • Dilatiazem, Verapamil (block DHPR Ca channels)
28
Q

Explain the cellular results of B-Adrenergic stimulation by Isoproterenol.

A

Increase in Ca in SR->Increase Ca release from SR->Increased contraction
B1-receptor also decrease the sensitivity of the contractile machinery to Ca->shorten duration of contraction (tachycardia)
Thus, increased speed of contraction and relaxation= SHORTER BUT STRONGER CONTRACTIONS

29
Q

How does cardiac glycoside work?

A

Cardiac glycoside (ex: digoxin) inhibit Na/K ATPase->increased cytosolic Na->Increase Na/Ca exchanger (this time 3Na out and 1Ca into the cell)->Increase Ca inside SR->Increase Ca release from SR->Increase contraction

30
Q

Compare and contrast increased and decreased contractility.

A

Increased: Decreased:
-higher myocardial fiber -lower shortening velocity
shortening velocity
-highly developed tension peak - lower tension peak
-steeper pressure rise - blunted pressure rise

31
Q

What is a widely used clinical tool measured by ECG, MRI, CT, nuclear medicine scan, measuring pressure/volume loops)?

A

Ejection fraction

32
Q

What are the 2 physiological means of controlling the inotropic state of the heart?

A
  • Sympathetic Nervous System (Positive Inotropic Effect)

- Parasympathetic Nervous System (Negative Inotropic Effect)

33
Q

Define ejection fraction.

A

Ejection fraction is a measurement of the percentage of blood leaving your heart each time it contracts.

The left ventricle is the heart’s main pumping chamber, so ejection fraction is usually measured only in the left ventricle (LV).
An LV ejection fraction of >55 percent=normal.
An LV ejection fraction of <50 percent=reduced.