Physiology: Cardiac Muscle/Function Flashcards

1
Q

How does the shortening of muscle occur?

A

By the sliding filament mechanism :

Actin filaments slide along adjacent myosin filaments by cycling of cross-bridges with myosin

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2
Q

What happens when cardiac muscle shortens?

A

Z lines come closer together and muscle cell shortens

Cardiac muscle produces force/tension

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3
Q

What is the trigger for cardiac muscle contraction?

A

Calcium

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4
Q

What undergoes a conformational change for cardiac muscle contraction?

A

Tropomyosin

This allows actin and myosin to interact

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5
Q

When does the excitation-contraction coupling occur?

A

Occurs in systole

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6
Q

What process occurs in diastole?

A

Relaxation-restitution

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7
Q

Describe what happens as the cell is depolarized.

A

Cells depolarized
Membrane potential rises
Threshold L-type calcium channels open
Ca ions enter the cell

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8
Q

Are the Ca ions released from the L type channels enough?

A

NO

Causes calcium to be released from the SR

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9
Q

What do we call the process whereby calcium released from the L-type channels stimulates calcium release from the SR?

A

Calcium Induced Calcium Release (CICR)

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10
Q

What receptors does the junctional SR have?

A

Ryanodine receptors (RYR)

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11
Q

Name the organization of the RYR that ensures maximal release of Calcium.

A

Density of RYR is maximal near the L-type Ca receptors
Distance between the RYR and L-type channels is short
This facilitates CICR

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12
Q

Describe what happens to tropomyosin when Ca ions bind.

A

Ca ions bind to troponin C in troponin complex
Tropomyosin moves
Actin-myosin interaction occurs
Muscle contraction occurs

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13
Q

What happens at the end of contraction to allow cardiac muscle relaxation?

A

Ca2+ influx ceases and SR is no longer stimulated to release Ca
Intracellular concentration of Ca is reduced:
1 - SERCA
2 - Sodium-calcium exchange pump
3 - Cell membrane ATP dependent Ca pumo

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14
Q

Describe the SERA mechanism.

A

ATP dependent Ca pump

Pumps calcium from the cytoplasm into the SR

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15
Q

What regulates SERCA pump?

A

Regulatory protein - Phospholamban (PLN) = inhibits calcium uptake into the SR (while in its dephosphorylated state)

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16
Q

What powers the sodium calcium exchange pump?

A

Sodium gradient

17
Q

Where does the majority of Ca from the cytoplasm go?

A

Goes back into the SR by SERCA pump
Remainder goes via sodium calcium pump
Very small amount of calcium goes via Ca-ATPase pump

18
Q

Why does cardiac contraction need to be adaptable?

A

1 - make the heart a better pump i.e. improving pumping action
2 - improve operating conditions to give it more to work with

19
Q

What does sympathetic stimulation of cardiac muscle produce?

A

Increase in active tension
Increase in rate of tension development
Increase in rate of relaxation - shorter contraction

20
Q

Describe how sympathetic stimulation has a positive inotropic effect on the heart.

A

Binding of noradrenaline to B1-adrenoreceptors on cardiac muscle cell

  • increased concentration of cAMP
  • activation of protein kinase A (PKA)
  • PKA phosphorylates L-type Ca channel and RYR channel
  • more Ca ions enter cell
  • increases force of contraction
21
Q

Describe how the sympathetic stimulation has a lusitropic effect on the heart.

A

Binding of noradrenaline to B1 adrenoreceptors of the heart

  • increase in cAMP
  • increase in PKA
  • phosphorylation of phospholamban (PLN) = inhibition of SERCA
  • increased uptake of Ca into SR
  • promotes rate of relaxation (lusitropic effect)
  • phosphorylation of troponin-I limits interaction between troponin C and Ca = relaxation
22
Q

What underlies cardiac muscle’s ability to control stroke volume?

A

Increase its contractile force with a slight increase in its length

23
Q

What happens if the heart muscle is overstretched?

A

Its ability to produce active tension is reduced

An overly dilated heart is not a good pump

24
Q

Starlings Law

A

Describes responses to changes in LVEDV

Increase LVEDV = increased SV

25
Q

What does contractility describe?

A

Cardiac performance at a given preload and aferload

SV for a given EDV

26
Q

What happens to sympathetic activity and the Starling Curve?

A

Increased contractility: higher SV for same EDV
Starling’s Law: higher SV when increase EDV
Shift to a higher Starling Curve

27
Q

What happens with decreased contractility?

A

Shift to a lower Starling Curve

28
Q

What causes a positive inotropic effect?

A

Agents that cause in increase in contractility = inotropic agents

29
Q

Name examples of positive inotropic agents.

A

Noradrenaline, adrenaline - increased Ca influx + uptake by SR
Increased intracellular Ca
Digoxin

30
Q

What are negative inotropic agents?

A

Agents that cause a decrease in contractility have a negative inotropic effect.

31
Q

List examples of negative inotropic agents.

A

Hypoxia

Drugs: CCBs, beta adrenergic blockers

32
Q

What is an example of acute cardiac failure?

A

Reduced myocardial mass following an MI

33
Q

What happens to the Starling Curve in acute heart failure?

A

Decrease in contractility

Lower SV for same EDV

34
Q

What happens in a moderate MI?

A

CO goes down
EDV increases to compensate
CO partly maintained
Sympathetic stimulation occurs leading to increased contractility
Go to higher starling curve
MAP will be maintained in the short term.

35
Q

What happens to the curve when SNS cannot maintain contractility?

A
RAA system causes retention of Na and water by kidneys 
Increases plasma volume 
Increases EDV 
CO back to normal 
Sympathetic stimulation stops
Renal output returns to normal
36
Q

What problems still persist even though the patient who had a moderate MI is now stable?

A

Right atrial pressure is high (increased EDV)
EDV is high
Heart is dilated = contraction problems especially during exercise

37
Q

What is a major myocardial infarction?

A

40% of more of left ventricular mass

38
Q

What does myocardial ischaemia and decreased coronary perfusion cause?

A
  • decreased contractile mass
  • decreased LV function
  • decreased MABP
  • decreased contractile mass
  • decreased LV function
  • Decreased MABP

Viscous cycle leading to death