SM 115a - Cardiac Output and Venous Return Flashcards

1
Q

What is “stressed volume,” as it refers to the circulatory system?

Can it change based on physiological signals?

A

The volume in the blood vessels beyond the unstressed volume

If vasoconstriction occurs, the unstressed volume will decrease, and the stressed volume will increase. The total volume will remain constant.

(The opposite occurs with vasodilation)

Note: Unstressed volume is the volume of fluid it takes to fill the vascular bed to the point where its presence exerts force on the vessel walls, while stressed volume is anything past that (thank you Nathan Shlobin!)

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2
Q

What may have caused the shift in the venous return curve (purple -> yellow)?

A

Transfusion of blood into the person (increased plasma volume) or increased venous tone

This increases the stressed volume of the circulation.

Note: increased venous tone (just the veins constricting) is not the same as increased vascular resistance (arteriole constriction to decrease blood flow to certain areas, increase afterload)

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3
Q

In this image, what is the significance of points A and B?

A

The points A and B represent equilibirium points between cardiac output and venous return.

Point A is the control; cardiac output and venous return match at baseline levels

Point B is the shift in equillibrium due to the shift in cardiac output. Increased contractility (the green line) must be matched by an increase in venous return (from point A to point B along the purple line) in order for the system to remain at equilibrium

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4
Q

What are the 4 major changes to the cardiac and vascular function curves with heart failure?

A
  1. Increased plasma volume
  2. Venoconstriction
  3. Increased systemic vascular resistance
  4. Decreased contractility
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5
Q

What may have caused the shift in the cardiac output curve (red -> green)?

A

Increased contractility

Increasing contractility increases cardiac output for every RAP; even if filling remains the same, more blood will be pumped out of the heart (Think higher ejection fraction)

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6
Q

When increased TPR shifts the curve down (solid to dashed lines), why don’t the x intercepts of the cardiac function and venous return curves change as well?

A

The x intercept of the venous return (red) curve does not change, becuase the unstressed volume in the veins does not change appreciably

The x intercept of the cardiac function (purple) curve also remains fixed, because the cardiac output cannot decrease below zero

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7
Q

What may have caused the shift from the black lines to the red lines?

A

Acute exercise

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8
Q

What may have caused the shift from the black lines to red?

A

Chronic heart failure

  1. Increased plasma volume -> shift vasc. function right and up
  2. Venoconstriction -> shift vasc. function right and up
  3. Increased systemic vascular resistance -> saves perfusion for vital organs. This theoreticaly shifts both curves down, but there are other factors contributing to an upward and right shift in the vascular function curve
  4. Decreased contractility -> Shift cardiac performance down
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9
Q

How does exercise affect the cardiac function and venous return curves?

A
  • Increased CO for every RAP
    • Shift the cardiac performance curve up
  • Venoconstriction to force blood into the arteries and therefore, into the exercising muscles
    • This increases the stressed volume of the circulation
    • Shifts the vascular function curve right and up
  • Decreased peripheral vascular resistance due to vasodilation in the arteries to get blood to exercising muscle
    • Steeper negative slope of the vascular function curve
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10
Q

What may have caused the shift in this graph (solid -> dashed lines)

A

Increased vascular resistance (increased total peripheral resistance).

This increases afterload, resulting in decreased CO. Decreased CO results in decreased venous return.

Note: The x intercept of the venous return (red) curve does not change, becuase the unstressed volume in the veins does not change

The x intercept of the cardiac function (purple) curve also remains fixed, because the cardiac output cannot decrease below zero

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11
Q

What is mean systemic filling pressure (MSFP)?

A

MSFP = the mean pressure in the circulatory system when there is no blood in motion

It is usually ~7 mmHg in the normal circulation, becuase the total circulating volume is more than enough to just barely fill up the blood vessels

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12
Q

What is “unstressed volume,” as it refers to the circulatory system?

Does it change based on physiological signals?

A

The volume that is just barely enough to fill up the floppy blood vessels (but not to distend them)

The unstressed volume can decrease if vascular tone increases; vasoconstriction decreases the volume needed to just barely fill up the blood vessels

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13
Q

What is the physiologic significance of the x-axis of this graph?

A

When venous return is 0, the right atrial pressure is equal to the mean systemic filling pressure (MSFP)

MSFP = the mean pressure in the circulatory system when there is no blood in motion

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14
Q

How does increasing plasma volume affect…

  1. The stressed volume of the circulation
  2. The mean systemic filling pressure
  3. Cardiac output
A

Increasing plasma volume ->

  1. The stressed volume of the circulation increases
  2. The mean systemic filling pressure increases
  3. Cardiac output increases
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15
Q

What is the physiologic significance of the flattening of the curve near the Y-intercept?

A

First look in the middle of the curve: as the right atrial pressure (RAP) decreases, venous return increases. This makes sense, because as pressure in the RA drops, more blood will flow in

However, when the RAP drops below zero, the superior and inferior vena cava collapse, so there is no additional increase invenous return even as the RAP drops.

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16
Q

What is the difference between venoconstriction and vasoconstriction?

How are their effects on cardiac output and venous return different?

A

Venoconstriction = decreased compliance of venous capacitance beds

  • Increased stressed volume of the circulation
  • Blood is dumped into the arterial side
    • Increased venous return -> increased preload
      • Increased CO
    • Decreased total peripheral resistance (in arterioles) -> Decreased afterload
      • Increased CO

Vasoconstriction = increased total peripheral resistance (in aterioles)

  • Increased afterload
    • Decreased cardiac output
    • Decreased venous function (rotate counterclockwise)