Brainscape's Knowledge GenomeTM

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


See full index

CVS > 2. Mechanical Properties of the Heart 1 > Flashcards

2. Mechanical Properties of the Heart 1 Flashcards

1
Q

What shape are ventricular cells and what influences their contraction?

A
  • Rod shaped
  • Electrical event
  • Calcium transient - amount of calcium increasing (changing) in the sarcoplasmic reticulum for a short period of time
  • Contractile event - shows sequence of AP => [Ca] => contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the heart muscle differ to the skeletal muscle in terms of the need for external calcium?

A
  • The heart will not beat without external calcium (reliance on calcium channels)
  • The skeletal muscle can contract without external muscle (AP=>DHPR=>internal calcium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Structure of a heart muscle cell

A
  • Length: 100µm
  • Width: 15µm
  • T-tubule diameter - 200nm
  • T-tubule spacing - 2µm apart (lie on each Z-line of every myofibril)
  • Sarcoplasmic reticulum (junctional in T-tubules - terminal part) - stores calcium (very low concentration inside the cell under normal conditions)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What 2 components make up most of the ventricular myocyte?

A
  • Myofibrils (46%)

* Mitochondria (36%) - energy heavy

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

Excitation-Contraction Coupling in the Heart

A
  • Depolarisation sensed by L-type calcium channel
  • Ca2+ from outside enters through LTCC
  • Some of this calcium directly causes contraction
  • The rest binds to RyR - release of more calcium from SR
  • Some calcium taken back up into SR by Ca ATPase channels (SERCA - sarco/endoplasmic reticulum calcium ATPase)
  • Calcium enters = calcium leaves (leaving via sodium-calcium exchanger - not energy needed, concentration gradient from sodium used)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the relationship between intracellular calcium concentration and force production?

A
  • Sigmoidal (force on y axis)
  • Logarithmic [Ca] scale
  • around 10 micromolar [Ca] sufficient to produce maximum force (100%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is active force production?

A
  • Force of (ISOMETRIC) contraction
  • Muscle doesn’t shorten but pulls on the force transducer
  • Get to a point where further stretching => no force (not enough overlap between filaments)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is passive force?

A
  • Due to the elasticity of muscle when stretching - resistance to the stretch
  • Linear relationship - Hooke’s law
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the overall relationship between muscle length and force production?

A
  • As muscle length increases, active and passive force increase (active above passive)
  • At greater lengths, active force starts to decrease but passive force keeps increasing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does the force-muscle length relationship compare in skeletal muscle?

A
  • Overstretch skeletal muscle - decrease in force (pulling a muscle)
  • Skeletal - much less passive force, still bell-shaped active/total curve
  • Cardiac - much more resilient to stretch - much more passive force - less compliant
  • Resilient due to the properties of its extracellular matrix and cytoskeleton
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which limb of the cardiac length tension curve is important and why?

A
  • Ascending limb
  • Descending limb doesn’t happen in physiological conditions
  • Pericardium restricts stretching
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens during the isometric contraction of the heart?

A
  • Muscle fibres don’t change in length
  • Occurs when heart fills up and contracts initially
  • Change in tone but not length as contraction resists the high pressure
  • This increases the blood pressure in the ventricles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens during the isotonic contraction of the heart?

A
  • Shortening of fibres
  • Blood ejected from ventricles
  • Happens once the heart is full - enough pressure to eject blood (ventricular pressure > arterial pressure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is preload and afterload?

A

• Preload - weight that stretched the muscle before it is stimulated to contract i.e. ventricles filling with blood makes it stretch before stimulation
- governs the amount of force the muscle is capable of producing
• Afterload - weight that is not apparent to the muscle in the resting state, only during contraction e.g. back pressure of aortic valves in left ventricle
- the weight that the muscle is trying to overcome

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

What is the relationship between preload and force?

A
  • More preload = more force
  • More stretch
  • Up to a certain point
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the relationship between afterload and force?

A
  • More afterload = less shortening
  • Same afterload - larger preload => more shortening + force
  • More afterload = lower velocity of shortening
17
Q

What happens in the ventricles during preload with reference to pressure/volume?

A

• Blood fills the ventricles during diastole - stretching the resting walls
• Stretching/filling determines preload - dependent upon venous return to the heart
• Measures of preload:
- End-diastolic volume (EDV)
- End-diastolic pressure (EDP)
- Right atrial pressure

18
Q

What happens in the heart during afterload and how is it measured?

A
  • The load against which the left ventricle ejects blood after opening of the aortic valve
  • Hypertension - heart has to work harder against a greater pressure
  • Simple measure - diastolic arterial blood pressure
  • Increase in aortic pressure => increased afterload => less shorterning
  • Same aortic pressure + more ventricular filling => increase in shortening
19
Q

What is the Frank-Starling relationship?

A
  • aka Starling’s Law
  • Increased diastolic fibre length increases ventricular contraction
  • in other words, increase in stretching/preload leads to an increase in shortening and speed of shortening
  • Consequence - ventricles pump a greater stroke volume - cardiac output exactly balances augmented venous return
  • Strength and volume of output determined by blood coming into ventricles
  • Independent of nervous input
20
Q

What are the 2 factors (in myocytes) affecting The Frank-Starling Relationship and explain how?

A

• Changes in the number of myofilament cross bridges that interact
- at shorter lengths than optimal, actin filaments overlap each other - reduced number of myosin cross bridges
- more stretch - more optimum interdigitation of actin and myosin
- overstretch - actin too far from myosin, less cross-bridges
• Changes in the calcium sensitivity of the myofilaments
- calcium sensitivity increases when myofilaments are stretched

21
Q

Why does the calcium sensitivity increase when myofilaments are stretched?

A

• Unknown but 2 possibilities
1) • Troponin C binds to calcium and regulates the formation of cross-bridges between actin and myosin
• At longer sarcomere lengths - affinity of troponin C for calcium increases due to a conformational change
• Less calcium needed for same amount of force at greater lengths
2) • Space between myosin and actin decreases when stretched (lattice spacing)
• Decreasing myofilament lattice spacing => probability of forming strong binding cross bridges increases
• More force for the same amount of calcium (less linked to the sensitivity of calcium)

22
Q

What is stroke work?

A
  • Work done by the heart to eject blood under pressure into the aorta and pulmonary artery (in one contraction)
  • stroke volume x pressure
  • Preload and afterload influence SV
  • Structure influences pressure at which blood is ejected
23
Q

What is The Law of Laplace?

A
  • Constant pressure within cylinder
  • Increase radius = increase tension on walls
  • Tension/force around the side = pressure x radius
24
Q

What is the physiological relevance of The Law of Laplace (comparing different scenarios)?

A
  • Radius of curvature of LV is less than RV (LV is round, RV is like a crescent)
  • LV can generate high pressures but have similar wall stress (tension) to the right ventricle
  • Giraffe - long, narrow, thick-walled ventricle => small radius => high pressure
  • Frog - almost spherical ventricles => large radius => low pressure
  • Failing hearts (dilated myopathy) - dilated heart => increases radius => increases wall stress => heart needs to work harder to maintain same pressure, but CO decrease when unable

CVS (21 decks)

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