3 Mechanical Properties of the Heart I Flashcards

1
Q

Q: What are single ventricular cells? Shape? Can be stimulated to? Process? (3)

A

A: can dissociate myocytes into single ventricular cells

rod shaped

stimulated to contract (process)

  • Electrical event
  • Calcium Transient (the amount of calcium in the sarcoplasm has increased for a short period of time)
  • Contractile event
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2
Q

Q: How long and wide is a typical ventricular cell? What’s on surface? Role?

A

A: -Length: 100 micrometres
-Width: 15 micrometres

T-tubules= finger like invaginations from the cell surface

carry surface depolarisation: allow excitation from surface to be conducted down into middle of cell

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3
Q

Q: What does the heart not contract without? skeletal muscle?

A

A: won’t beat without external calcium

skeletal muscle can contract without external calcium

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4
Q

Q: What size are T tubule openings? How far are they spread? reason?

A

A: their openings can be up to 200 nanometres in diameter

about 2 micrometres apart so that a T-tubule lies alongside each Z-line of every myofibril

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5
Q

Q: What is the structure of a ventricular cell? (4)

A

A: -sarcoplasmic reticulum: doesn’t take up large proportion of cell

  • mitochondria: very energy demanding cell + takes up around 30% of cell space
  • myofibrils: take up 50% of cell
  • low calcium levels are maintained in normal conditions
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6
Q

Q: How does the sarcoplasmic reticulum relate to myofilaments?

A

A: terminal part of SR wraps around myofilaments

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7
Q

Q: Describe the process of Excitation-Contraction Coupling in the Heart. (9)

A

A: 1. cardiac AP-> depolarisation (membrane potential)

  1. sensed by the L-type calcium channel (LTCC)
  2. calcium from outside enters the cell
  3. Some of this calcium can directly cause contraction
  4. rest of calcium binds to Ryanodine Receptors (also called Sarcoplasmic Reticulum Calcium Release Channel)
  5. causes release of calcium from the sarcoplasmic reticulum
  6. more contraction
  7. after it has had its effect, some of the calcium is taken back up into the SR by Ca ATPase channels (also called SERCA - SARCO/ENDOPLASMIC RETICULUM CALCIUM ATPase) =uses ATP
  8. same amount of calcium that came into the cell is effluxed by a Sodium-Calcium Exchanger
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8
Q

Q: How much energy does the efflux of calcium out of the cell (after Excitation-Contraction Coupling) require? Calcium taken back up by SR?

A

A: does NOT need energy - it uses energy from the concentration gradient of sodium (high to low) to expel calcium form the cell

needs ATP as uses ATPase channels (also called SERCA - SARCO/ENDOPLASMIC RETICULUM CALCIUM ATPase)

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9
Q

Q: What is an important ion channel in a cardiomyocyte?

A

A: L-type calcium channel

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10
Q

Q: What is the relationship between force production and intracellular calcium concentration? Draw a cytoplasmic calcium concentration (x)- force (y) graph.

A

A: force-calcium relationship is SIGMOIDAL

Around a 10 micromolar intracellular concentration of calcium is sufficient to produce maximum force

force= y= %
conc= x= micromolar (μM)= logorhythmic
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11
Q

Q: What is the Length-Tension Relation in Cardiac Muscle? (3)

A

A: This is ISOMETRIC CONTRACTION = muscle doesn’t shorten - just pulling on the force transducer (in experiment set up)

An increase in muscle length causes an increase in force

As you keep stretching the muscle, you get to a point where further stretching DOES NOT generate more force - this is because there is not enough overlap between the filaments to produce force

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12
Q

Q: How do you produce a graph to represent the Length-Tension Relation in Cardiac Muscle? Draw the resulting graph (muscle length X by force Y). Additional plotted line?

A

A: cardiac muscle cell/tissue is attached to force tranducer (measures) and some stimulating electrodes -> when stimulated produces a rise and fall in force

  1. non stretched
  2. stretched preparation = longer but everything else is the same (=produces a slightly larger force)
  3. stretch a little more (=produces even larger fore)
    - > this relationship= active force production= due to the formation of cross bridges= steeper than x=y then peaks and dips

=plotted baseline= passive force line= stretch in preparation caused by elasticity= less that x=y and remains straight

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13
Q

Q: What is the length-tension relation in cardiac and skeletal muscle? (show on graph)

A

A: REFER. similar curve but cardiac has steeper passive line which makes total force higher

Skeletal muscle has much less passive force produced but there is still a bell-shaped curve

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14
Q

Q: How does cardiac and skeletal muscle differ? (2) Why?

A

A: -cardiac muscle is less compliant than skeletal muscle
-cardiac muscle is much more resistant to stretch= CM exerts more passive force

=> due to properties of the extracellular matrix and cytoskeleton

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15
Q

Q: What happens if you overstretch muscle? skeletal muscle? Cardiac muscle? in relation to graph?

A

A: get a decrease in force - this is what happens in skeletal muscle when you pull a muscle

can’t overstretch cardiac tissue because it’s contained within the pericardium -> only ascending limb of the relation is important for cardiac muscle as all cardiac function takes place on that part of the force-length curve

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16
Q

Q: What is passive forced based on?

A

A: resistance to stretch of the muscle

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17
Q

Q: Why does the descending limb of the length-tension graph not occur in physiological conditions?

A

A: pericardium restricts the stretching

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18
Q

Q: What are the 2 forms of contraction that the heart uses?

A

A: ISOMETRIC contraction resists the high pressure - there is NO CHANGE IN LENGTH but there is a change in tone

ISOTONIC contraction is the shortening of fibres (no change in tension) when blood is ejected from the ventricles

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19
Q

Q: How can you change muscle load before contraction? 2 ways.

A

A: using a [little weight] to stretch the preparation as awell as attaching it to a [larger weight] that sits on the table and what the muscle doesn’t see

[1] PRELOAD - the weight that stretched the muscle BEFORE it is stimulated to contract (i.e. the filling of the ventricles with blood makes it stretch before it is stimulated to contract)

[2] AFTERLOAD - weight that is NOT APPARENT to the muscle in the resting state - only encountered ONCE MUSCLE HAS STARTED TO CONTRACT

20
Q

Q: What is preload? What does a force-preload graph look like? Increased preload?

A

A: Preload causes stretching and so the Force-Preload graph is the SAME as the Force-Length graph

The more preload you have, the more you stretch the muscle so the MORE FORCE is produced

MORE PRELOAD = MORE FORCE (up to a certain point)

21
Q

Q: What is afterload? Increasing afterload?

A

A: Afterload is the back pressure on the aortic valves (when considering the left ventricle)

The more afterload you have, the less shortening you get

MORE AFTERLOAD = LESS SHORTENING

22
Q

Q: What happens if you have the same afterload with a larger preload?

A

A: you can shorten the muscle more

=similar

23
Q

Q: What’s the relationship of after load with velocity of shortening?

A

A: ->MORE AFTERLOAD = LOWER VELOCITY OF SHORTENING

24
Q

Q: What does preload govern?

A

A: the amount of force the muscle is capable of producing

25
Q

Q: For the same afterload, if you stretch the muscle prior to excitation, what will happen?

A

A: it will generate more force

26
Q

Q: What are the in vivo correlates of preload? What determines preload? Dependence?

A

A: As blood fills the ventricles during diastole - it stretched the resting ventricular walls

This stretching/filling determines the PRELOAD on the ventricles before ejection (if more blood fills=more stretch=more preload=more powerful contraction)

So preload is dependent upon venous return to the heart (filling of ventricles)

27
Q

Q: What are the 3 measures of preload?

A

A: End-diastolic volume (EDV)

End-diastolic pressure (EDP)

Right atrial pressure

28
Q

Q: What are the in vivo correlates of afterload? Hypertensive? Increasing afterload results? (2)

A

A: afterload is basically blood pressure - the pressure that the heart must overcome to eject blood

So if you are hypertensive, the heart has to work harder to eject the blood and pump it around the body

INCREASE AFTERLOAD = DECREASE SHORTENING + DECREASE VELOCITY OF SHORTENING

29
Q

Q: What is a simple measure of afterload?

A

A: DIASTOLIC ARTERIAL BLOOD PRESSURE

30
Q

Q: Draw an afterload-shortening graph with large preload and small.

A

A: straight lines from top left to bottom right

small preload is smaller triangle

31
Q

Q: Draw an afterload-velocity of shortening graph with large preload and small.

A

A: top left to bottom right with a dip

both begin from same point but small decreases faster with earlier dip

32
Q

Q: How does shortening respond to increased aortic pressure?

A

A: INCREASE IN AORTIC PRESSURE (increased AFTERLOAD) = DECREASE IN SHORTENING

33
Q

Q: How does shortening respond to the same aortic pressure with more ventricular filling?

A

A: INCREASE IN SHORTENING

34
Q

Q: What is the sequence of events linking cardiac muscle excitation with contraction and then relaxation?

A

A: 1. AP

  1. T tubules
  2. LTCC activated
  3. Ca influx
  4. RyR activated
  5. SR Ca release
  6. Ca binds to TnC
  7. myofilament activation
  8. SER CA/ Ca exchange
  9. relaxation
35
Q

Q: Define the Frank-Starling relationship. Explain. Consequence?

A

A: Starling’s Law:
-Increased diastolic fibre length increases ventricular contraction

an increase in stretching leads to an increase in shortening and speed of shortening/increase in preload leads to an increase in shortening and speed of shortening

when diastolic fibre length increases, ventricles pump a greater stroke volume so that, at equilibrium, cardiac output exactly balances the augmented venous return

36
Q

Q: What does the amount of blood coming in to the ventricles determine? According to?

A

A: strength of the ventricular contraction and hence determines the amount of blood leaving the ventricles

(frank) Starling Law

37
Q

Q: What are the 2 factors that determine the Frank-Starling relationship?

A

A: Changes in the NUMBER OF MYOFILAMENT CROSS BRIDGES that interact

Changes in the CALCIUM SENSITIVITY OF THE MYOFILAMENTS

38
Q

Q: How does the changes in the number of myofilament cross bridges that interact determine the Frank-Starling relationship? (2) Draw a graph to represent.

A

A: At shorter lengths than optimal, the actin filaments overlap thus reducing the number of myosin cross bridges that can be made

The more you stretch the muscle, the more optimum interdigitation of the actin and myosin filaments you achieve

resting length X by tension Y

middle= max amount of cross bridges that can form = produce max amount of force

39
Q

Q: How does length and myofilament sensitivity to calcium determine the Frank-Starling relationship? (2)

A

A: underlying process is currently unknown

2 possibilities which are not mutually exclusive

  • At longer sarcomere lengths, the AFFINITY OF TROPONIN C (regulates the formation of cross bridges) FOR CALCIUM IS INCREASED due a conformational change in the protein (less calcium is needed for the same amount of force)
  • With decreasing myofilament lattice spacing (space between myosin and actin filaments)- the probability of forming strong binding cross bridges INCREASES (produces more force for the same amount of calcium)
40
Q

Q: What is stroke work?

A

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

(work done by the heart in one contraction)

41
Q

Q: How is stroke work defined mathematically?

A

A: Volume of blood ejected during each stroke (SV) MULTIPLIED BY the pressure at which the blood is ejected (P)

42
Q

Q: What is stroke volume greatly affected by? What is pressure greatly affected by?

A

A: -Preload
-Afterload

heart structure

43
Q

Q: Define the Law of Laplace. Equation. Explain.

A

A: When the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius

T=wall tension
P=internal pressure
R=radius

T=PR in cylindrical vessel

-So when you increase the radius, the force around the sides increases (tension)

44
Q

Q: What is the physiological relevance of the Law of Laplace? Example.

A

A: in order to keep the wall tension the same, if you change radius-> need to find way to change pressure (since it changes with radius)

Radius of curvature of the LV is LESS than the RV

This allows the left ventricle to generate HIGH PRESSURES with similar wall stress (tension)

45
Q

Q: Law of Laplace relevance:

giraffe.
frog.
failing heart.

A

A: Giraffe - wall stress is kept low in giraffe by the long, narrow, thick-walled ventricle - it has a small radius so it can generate high pressure

Frog - pressures are low so the ventricles are almost spherical - large radius so low pressure

Failing Hearts (Dilated Cardiomyopathy) - hearts become dilated which increases wall stress