Regulation of Cardiac Output Flashcards

1
Q

Input typical values into the following equation:
CO = HR x SR
if SR = EDV-ESV

A

CO = HR x (EDV-ESV)
= 70 x (120-50)
= 70 x70
= 5L/min

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2
Q

How can stroke volume be increased?

A

increase end diastolic volume

decrease end systolic volume

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3
Q

What is meant by excitation-contraction coupling?

In what two ways can the force of contraction be increased?

A
  • Ca2+ regulates the no. of actin-myosin cross-bridges formed and therefore force of contraction
  • Force of contraction (no. of cross bridges) can be increased by:
    1. Increasing the Ca2+ sensitivity of the contractile apparatus (starlings law of the heart - EDV)
    2. increasing the concentration of Ca2+ in the cell (changing contractility/inotropy - ESV)
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4
Q

What is starlings law of the heart?

A
  • intrinsic property of cardiac muscle
  • in isolated muscle cells stretching the sarcomere increases force of contraction
  • length-dependent increases in Ca2+ sensitivity results in greater number of cross-bridges
  • Exact mechanisms unknown
  • “Force of ventricular contraction is dependent on the length of ventricular muscle fibres in diastole”
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5
Q

Explain how an increased EDV leads to increased SV

A

Increased EDV
Heart muscle is more stretched
ventricular muscle fibre length is longer
more sensitive to the same amount of calcium
force of contraction is more forceful
more blood can be ejected per beat

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6
Q

How does Starlings law ensure the relationship between left and right stroke volumes?
What happens when this fails to happen?
List the sequence of events following an increased venous return and central venous pressure/

A

right stroke volume = left stroke volume
RSV>LSV –> congestion of pulmonary circulation
LSV>RSV –> congestion of systemic circulation
1. increased venous return and central venous pressure
2. increased cardiac filling, increased RV EDV
3. increased right stroke volume
4. increased cardiac filing, increased LV EDV
5. increased left stroke volume

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7
Q

What five factors affect venous return to the right ventricle?

A
  1. blood volume
  2. skeletal muscle pump
  3. respiratory pump
  4. venous tone
  5. gravity
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8
Q
  1. Explain how blood volume affects venous return
A
  1. Increased BV (renal failure) leads to increased venous return
  2. Decreased BV (dehydration/haemorrhage) leads to decreased venous return
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9
Q
  1. Explain how skeletal muscle pumps affect venous return
A
  1. skeletal muscle contraction changes pressures between valves in the vein, increasing venous return
    Inactive (decreased skeletal muscle activity) decreased venous return as blood pools in the lower limbs
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10
Q
  1. Explain how the respiratory pump affects venous return
A
  1. Deep breathing helps move blood back towards the heart. inspiration decreases thoracic pressure and increases abdominal pressure. This provides a pressure gradient for blood to flow back to the heart.
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11
Q
  1. Explain how venous tone affects venous return
A
  1. Increases in sympathetic activity will evoke venoconstriction
    This reduces the volume of blood in the veins at a given pressure
    This increases venous return
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12
Q
  1. Explain how gravity affects venous return
A
  1. Supine postion –> uniform distribution of blood across body
    Central venous pressure and venous return maintained

Standing –> redistribution of blood due to gravity, venous pooling in lower extremities, reduction in thoracic blood volume, CVP and VR fall, EDV and SV fall.

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13
Q

What other two factors affect EDV?

A

Atrial contraction
- SNS of atrial muscle increases force of atrial contraction and EDV. Important at high HR’s when the rapid passive filling phase is reduced
Heart rate
- P wave can move a long way to left before ventricular filling is compromised
- >180bpm atrial contraction can no longer compensate

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14
Q

What is preload?

What parameters increase preload?

A

Pre-load = any factor which influences the stretch of the cardiac muscle cells before contraction

  • venous return / central venous pressure
  • atrial contraction
  • heart rate
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15
Q

How is ESV regulated?

A

SEE DIAGRAM IN LECTURE
Increased contractility/inotropy
- increase sympathetic nerve activity and/ or circulating nor/adrenaline stimulates B1 receptors
- increased Ca2+ influx during AP and Ca2+ induced Ca2+ release
- increase cross-bridge formation and binding affinity for TN-C
- increase force of contraction and SV
- decrease ESV

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16
Q

How do beta blockers work?

A

block B1 receptors
decrease contractility
decrease SV

17
Q

The stroke volume is also affected by after-load.

What does this mean?

A

After-load = the load against which the heart must contact to eject the stroke volume
Aortic/pulmonary artery pressure is the most important factor in determining after-load
High pressure makes it more difficult to eject the SV e.g. in hypertension
Increased resistance in peripheral/pulmonary circulation increases pressure upstream and therefore increases after load