Regulation of Cardiac Output Flashcards

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1
Q

Cardiac Output equation

A

Co = HR x SV

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2
Q

Stroke Volume equation

A

SV = EDV - ESV

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3
Q

What is the heart rate controlled by

A

The number of times the SA node contracts controlled by the autonomic nervous system. A decrease in HR is caused by an increase in parasympathetic nervous system.

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4
Q

How to regulate stroke volume

A
  1. Increase filling to a greater volume = increase SV
  2. Fill to the same volume but eject a greater volume of blood that we fill the heart with = decrease in ESV = increase SV

To increase SV = increase EDV - decrease ESV

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5
Q

How does increasing EDV increase SV

A

By increasing the amount of blood going into the heart by having a physical effect on the ventricle by stretching it as we put more blood into it. By stretching the vertical we increase the force of contraction.

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6
Q

Excitation- contraction coupling explain

A

Ca2+ regulates the number of actin-myosin cross bridges formation and therefore the force of contraction. Number of cross bridges formed can be increased by:

  1. Increasing Ca2+ sensitivity of the contractile apparatus.
  2. Increasing the sensitivity of Ca2+ in the cell.
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7
Q

Starling Law of the Heart

A

“Force of ventricular contraction is dependant on the length of ventricular muscle fibres in diastole.”

In isolated muscle cells stretching the sarcomere increases force of contraction. Length-dependent increase in Ca2+ sensitivity results in a greater number of cross bridges.

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8
Q

What happens if you over stretch the sarcomere?

A

Cause a decrease in contraction force

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9
Q

How does venous return affect SV

A

An increase in venous return (the amount of blood leaving the ventricles and entering the right atrium) determines cardiac filling (CF).
Increase VR = Increase CVP = Increase CF
Increase in heart filling therefore increase EDV will stretch the heart increasing Ca2+ sensitivity will generate cross bridges giving a greater force of contraction = increase in right SV.

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10
Q

What factors affect venous return to the heart?

A
  1. Blood volume
  2. Skeletal muscle pump
  3. Respiratory pump
  4. Venous tone
  5. Gravity
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11
Q

How does blood volume affect VR?

A

Increase in blood volume (renal failure) increases VR

Decrease in blood volume (haemorrhage/dehydration)decreases VR

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12
Q

How does skeletal muscle pump affect VR?

A

Unidirectional valves, when forward propulsion stops, you get a small backflow of blood causing the valves to close. Many blood vessels and veins are between skeletal muscle when they contract it squashes the begins and propels the blood back towards the heart = increase in VR. Very important in exercise or a hot day.

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13
Q

How does the respiratory pump affect VR?

A

Breath in = contracts the diaphragm, therefore pushing down on to blood vessels in the abdomen. Increase in pressure. Pressure gradient is set up (decrease in thoracic pressure and increase in abdominal pressure)moving blood back towards the heart. Reverse during expiration.

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14
Q

How does venous tone affect VR?

A

Increase in sympathetic activity will evoke vasoconstriction as NA is released onto smooth muscle causing the veins to contract reducing the volume of blood in the veins at a given pressure = increasing VR.

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15
Q

How does gravity affect VR?

A

When supine there is uniform distribution of blood across the body. CVP and HR are maintained. When standing up there is redistribution of blood due to gravity, venous pooling in lower extremities, reduction in thoracic blood pressure. CVP and VR falls, EDV and SV falls.

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16
Q

Other factors affecting EDV

A

Atrial Contraction and Heart Rate (>180bpm)

17
Q

Regulation of ESV

A

Increase in contractility/inotropy:
Increase in sympathetic nerve activity and or circulating NAd stimulates B1 receptors (G-coupled receptors) [cAMP} increases which activates protein kinase A which phosphorylates L-type Ca2+ channels to open increasing Ca2+ concentration. Increases cross-bridge formation and binding affinity for TN-C = increase force of contraction and SV = decrease in ESV.

18
Q

Effect of increase change in contractility/inotrophy on the LV P-V loop

A

Increase in SV by decreasing ESV. The loop shifts to the left. Increase in contractility (increase in force of contraction at a given EDV)

19
Q

Effect of increased cardiac filling (EDV) on the LV P-V loop

A

Increase in cardiac filling, increase force of contraction allowing an increase in SV. The loop shifts the right

20
Q

After Load

A

The load against which the heart must contract to eject the SV.

21
Q

How does the after load increase?

A

Increase in arterial blood pressure or increase in resistance in circulation or an increase in stiffness of aorta (in disease). Requires a stronger contraction to eject the same SV.

22
Q

What is the most important factor in determining afterload

A

Aortic/ pulmonary artery pressure is the most important factor in determining afterload.
High aortic/ pulmonary pressure makes it more difficult to eject the SV e.g. in hypertension.
Increase in peripheral/ pulmonary circulation increases pressure upstream and therefore increases after- load.