Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular & Respiratory Medicine > Cardiovascular Mechanics > Flashcards

Cardiovascular Mechanics Flashcards

1
Q

What is the length and width of ventricular cells?

A

100um long

15 um wide

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

What are T-tubules?

A
  • transverse tubules
  • finger-like invaginations from the cell surface
  • 200nm diameter
  • carry surface depolarisation deep into the cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How are T-tubules spaced?

A

-spaced (approx 2um apart) so that a T-tubule lies alongside each Z-line of every myofibril

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

What are the main component of heart cells?

A
  • myofibrils (46%)
  • mitochondria (36%)
  • sarcoplasmic reticulum (4%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the process of excitation-contraction coupling in the heart (calcium induced calcium release) ?

A
  • L-type Ca channels open in response to AP and Ca moves into the cell down its concentration gradient
  • some of the Ca goes to activate myofilaments
  • most of the Ca binds to SR Ca release channel, undergoes conformational change which opens the channel
  • Ca goes from stores in SR into cytosol to bind to myofilaments for contraction

Relaxation:
-Ca pumped into SR via Ca ATPase- restored to be released at next excitation

Na/Ca exchange system:

  • the same amount of Ca that enters the cell to trigger SR release is removed via Na/Ca exchanger
  • no ATP, uses downhill gradient of Na to remove Ca
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where are the L-type Ca channels found?

A

-in the T-tubules

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

What is the SR Ca release channel also known as?

A

-ryanodine receptor

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

What is the relationship between cytoplasm Ca concentration and force (% max) ?

A
  • sigmoidal relationship

- force increases as more myofilaments are activated

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

What is the length-tension relation in cardiac muscle?-

A
  • as the length of the cardiac muscle increases, there is more passive and active force produced
  • like elastic band, it stretches
  • isometric contraction

-only ascending limb of the relation between length and force is important is important for cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Is cardiac or skeletal muscle more resistant to stretch, and why?

A

-cardiac muscle is more resistant to stretch
-due to properties of the extracellular matrix and cytoskeleton
-

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

Is cardiac or skeletal muscle more complaint, and why?

A
  • skeletal muscle is more complaint

- due to properties of the extracellular matrix and cytoskeleton

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

What is isometric contraction?

A

-muscle fibres do not change length but pressures increase in both ventricles

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

What is isotonic contraction?

A

-shortening of fibres and blood is ejected from ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why can’t you overstretch cardiac tissue?

A

-because the heart is contained in the pericardium sac (membrane), prevents overstretching

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

What is the preload?

A

-weight that stretches muscle before it is stimulated to contract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is afterload?

A

-weight not apparent to muscle in resting state; only encountered when muscle has started to contract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens to the amount of shortening as the after load is increased (in isotonic contraction)?

A

-shortening decreases

18
Q

What effect do longer muscle lengths have on the the amount of stretch?

A

-at longer muscle lengths, there is more stretch and shortening for the same amount of load

19
Q

What are the in vivo correlated of preload?

A
  • as blood fills during diastole, it stretched the resting ventricular walls
  • this stretch (filling) determines the preload on the ventricles before ejection
  • measures of preload include end-diastolic volume, end-diastolic pressure and right atrial pressure

-important as then heart pumps exactly how much blood is coming back

20
Q

What is preload in the heart dependent on?

A

-venous return

21
Q

How can preload in the heart be measured?

A
  • end-diastloic volume
  • end-diastolic pressure
  • right atrial pressure
22
Q

What are the in vivo correlates of afterload?

A
  • afterload is the load against which the left ventricle ejects blood after opening of the aortic valve
  • any increase in afterload decreases the amount of isotonic shortening that occurs and decreases the velocity of shortening
23
Q

How can afterload in the heart be measured?

A

-diastolic blood pressure

24
Q

What affects isometric contraction of the heart?

A

-ventricular filling

25
Q

What affects isotonic contraction of the heart?

A

-pressure in the aorta

26
Q

What is Frank-Starling relationship?

A
  • as filling of the heart increases, the force of contraction also increases
  • increased diastolic fibre length increases ventricular contraction

Consequence: ventricles pump greater stroke volume so that (at equilibrium), cardiac output exactly balances the augmented venous return

27
Q

What are the two factors causing the Franklin-Starling relationship?

A
  1. Changes in the number of myofilament cross bridges that interact
    - at shorter lengths than optimal the actin filaments overlap on themselves so reducing the number the number of myosin cross bridges that can be made
  2. Changes in the Ca sensitivity of the myofilaments
    -hypothesis 1:
    At longer sarcomere lengths, the affinity of TnC for Ca is increased due to conformational change in protein (since less Ca required for same amount of force)

-hypothesis 2:
With decreasing myofilament lattice spacing, the probability of forming strong binding cross-bridges increases (produced more force of the same amount of activating Ca)

28
Q

What is troponin C (TnC) ?

A
  • thin filament protein that binds Ca

- regulates formation of cross-bridges between acting and myosin

29
Q

What is lattice spacing?

A
  • the spacing between myosin and actin filaments

- decreases with stretch

30
Q

What is stroke work?

A

-work done by the heart to eject blood under pressure into aorta and pulmonary artery

stroke work = volume of blood ejected during each stroke (SV) x the pressure at which the blood is ejected (P)

SW = SV x P

31
Q

What greatly influences stroke volume?

A
  1. preload:
    - more stretch in ventricles produces larger SV
  2. after load:
    - if after load is larger, the SV is smaller as it is having to push blood out against a higher pressure
32
Q

What greatly affects the pressure at which the blood is ejected (P) ?

A

-cardiac structure

33
Q

What is the stroke volume?

A

-the volume of blood ejected during each stroke

34
Q

What is Law of LaPlace?

A

-when the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius

35
Q

What is the wall tension?

A

wall tension = pressure in vessel x radius of vessel

T = P x R

incorporating wall thickness (h):

T= (PxR)/h

36
Q

Link the Law of LaPlace with the heart.

A

-the radius of curvature of walls of LV less than that of RV allowing LV to generate higher pressure with similar wall stresses.

37
Q

What happens as muscle length increases to passive force?

A

-passive forces increases continuously (unlike active force)

38
Q

What often happens to failing hearts?

A

-failing hearts often become dilated, increasing the radius and os the tension (wall stress) increases

39
Q

Does increased adrenaline secretion during fight or flight response affect the preload, and why?

A

-expect more blood to be coming back to the heart, increased venous return

40
Q

Arrange the following events into the correct order.

A. Ca enters cell
B. Ca binds to TnC
C. AP travels down T-tubules
D. Muscle fibres shorten 
E. Ca enters cytoplasm from sarcoplasmic reticulum
F. The sinoatrial node depolarises 
G. Myosin heads bind to actin 
H. Ca binds to ryanodine  receptor
A 
F
C
A
H
E
B
G
D
41
Q

lecture slides

A

https://d3c33hcgiwev3.cloudfront.net/vWzHzxW1SkCsx88VtapAfg_a1a5d45165ce4b50b567f74c2c248805_Final_SV_CVR_LE02Cardiovascular_mechanics.pdf?Expires=1582070400&Signature=cGop8-DVZ7rRZ9xp-y0~NDbtsqmU~wmLWcWpxeZrG1-E49mw-13gGsxnXojNeEC2YZ1ev~Jl7mwnSep54xDXMIhuz3OD-9WreSFDB63ioVlsnA9i9nUCj~GU6CE3Bb~8ZtnQxtA4PTIGlZ0A~JA-hH-93Yq3hev1o2dA6Wt~RiE&Key-Pair-Id=APKAJLTNE6QMUY6HBC5A

Cardiovascular & Respiratory Medicine (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions