Control of Cardiac Output Flashcards

1
Q

What is cardiac output ? Give a formula for it.

A

“effective volume of blood expelled by either ventricle of the heart per unit of time”

Cardiac Output = Stroke volume x heart rate

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2
Q

What is the average stroke volume ? average heart rate ? Deduce the average cardiac output from this information.

A

70 mL
70 bpm
5 L/min

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3
Q

If the demands of tissues increase, what is the maximum stroke volume the heart can produce ? maximum heart rate ? maximum cardiac output ?

A

140 mL
200 bpm
30 L/min

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4
Q

Describe the main ways in which stroke volume can be controlled.

A

INTRINSIC (Self-Regulating)
1) FRANK STARLING MECHANISM (change in pre-load)
↑EDV and ↑force of contraction (Increased pre-load results in an increased EDV due to increased amount of blood flowing to ventricles. Increased EDV results in a direct increase in force of contraction (because different EDVs, walls achieve different levels of stretch) which increases stroke volume through increase in ejection fraction (an increase in force of contraction results in an increase in ejection fraction even if EDV does not increase)
2) CHANGES IN AFTERLOAD
“If afterload is increased (e.g., increasing aortic pressure by increasing systemic vascular resistance; red loop in figure), the stroke volume is reduced and the end-systolic volume increased. The increased end-systolic volume, however, leads to a secondary increase in end-diastolic volume because more blood is left inside the ventricle following ejection and this extra blood is added to the venous return, thereby increasing ventricular filling. This secondary increase in preload enables the ventricle to contract with greater force (Frank-Starling mechanism), which partially offsets the reduction in stroke volume caused by the initial increase in afterload (Consequently, in a normal heart, changes in aortic pressure have relatively little affect on stroke volume.)”

EXTRINSIC
Sympathetic nerves (increase force of contraction and thus stroke volume/ejection fraction)
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5
Q

Define pre-load and afterload.

A

PRELOAD = Venous pressure or venous return to heart (If increase EDP, increase amount of blood flowing to ventricles)

AFTERLOAD = Aortic/pulmonary artery pressure (Force heart is exerting against when it contracts, main components being vascular resistance and ventricular wall tension)

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6
Q

Show, in graphical form, EDV, ESV and stroke volume in normal conditions, with intrinsic control, and with extrinsic control.

A

Refer to slide 4 in lecture on “Control of Cardiac Output”

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7
Q

State Frank Sterling’s Law of the Heart. Explain its role in balancing between L and R sides of the heart.

A

” strength of the heart’s systolic contraction (i.e. stroke volume) is directly proportional to its diastolic expansion” (hence, by increasing pre-load increase force of contraction and vice versa when decreasing pre-load)

“Hence, this allows for automatic balancing between CO from left-side of heart to volume returning to right-side because:
-increase in stroke volume leads to an increase in cardiac output and arterial pressure; therefore, the afterload on the ventricle increases. This partially offsets the increased stroke volume by increasing the end-systolic volume. The reason for this is that the increased afterload reduces the velocity of fiber shortening and therefore the ejection velocity. “
VICE VERSA “a decrease in preload reduces stroke volume, but this reduction is partially offset by the decreased afterload (reduced aortic pressure) so that the end-systolic volume decreases slightly”

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8
Q

Show Frank Sterling’s Law of the Heart in graphical form (as muscle force as a function of muscle length), including lines denoting total force, active force and resting force, explaining what each of these stands for.

A
Refer to slide 5 in lecture on "Control of Cardiac Output"
Total force = Resting force + Active force
Resting force (diastolic) = Recoil resulting from natural elasticity of heart
Active force (systolic) = Force generated by muscle contracting itself
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9
Q

Can extrinsic and intrinsic controls of cardiac output work together ?

A

Yes they can (both can contribute at the same time to increased force of contraction), but it’s mainly just the SNS and intrinsic control (not the PSNS)

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10
Q

Graph the effect of SNS control on force of contraction, comparing it to “normal” force of contraction and a theoretical negative inotropic control of force of contraction.

A

Refer to slide 6, lecture on “Control of Cardiac Output”

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11
Q

Summarise the main ways in which cardiac output may be altered.

A

Three main things:

  1. Increase EDV (intrinsic control, through preload) results in increased force of contraction, and hence stroke volume
  2. Increase Sympathetic activity (as well as increase in adrenaline) increase force of contraction and hence stroke volume + increase heart rate
  3. Decrease parasympathetic activity increases HR (chronotropic effect)

Anything that changes either stroke V or heart rate will change cardiac output since
CO = HR x SV

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12
Q

Draw an illustrating showing the oscillation in pressure in the different vessels and heart chambers. Explain the shape of the graph.

A

Refer to slide 8, lecture on “Control of Cardiac Output”

Overall pattern: Properties of vascular tree means oscillation gets dampened the further
you go in CVS tree so by time you get to capillaries, near continuous fluid flow going through rather than stop start in ventricles

1) In ventricle, push at high degree of P to get aortic valve to open to get blood into aorta
2) Pressure in aorta (non-compliant vessel) means get peak systolic pressures. However, downstream resistance of CV tree that aorta is trying to get blood into resists that flow (aorta still squeezing to push blood further) hence oscillation where P in diastole settles in region of 80.
3) Large arteries thick and very elastic (hard to stretch) so big peaks of pressure because no compliance
4) As go gown vascular tree (e.g. small arteries, arterioles), start distributing pressure because cross sectional area of vascular tree starts increasing (so pressure starts dropping and pulsatile flow starts to diminish into something that’s fairly low P and continuous)
5) (Then same in pulmonary system but at lower magnitude pressure)

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13
Q

Describe the main features of transmission of Pressure Pulses to the Peripheral Arteries.

A

In systole, arterial system expands to accommodate full ventricular stroke volume. BUT arterial system has limited capacity so SVR limits how fast blood can escape

In diastole, energy stored in arterial walls during systole drives blood forward (without ventricular push)

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14
Q

Describe the main causes of the dampening of pressure pulses in smaller Arteries, arterioles, and capillaries.

A

(1) “resistance to blood movement in the vessels (because a small amount of blood must flow forward at the pulse wave front to distend the next segment of the vessel; the greater the resistance, the more difficult it is for this to occur)”
(2) “compliance of the vessels (the more compliant a vessel, the greater the quantity of blood required at the pulse wave front to cause an increase in pressure)”

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15
Q

Define a compliant vessel, giving examples of compliant vessels.

A

Tube with elastic walls which will stretch easily with increasing volume, with little changes in pressure.

Arteries, veins

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16
Q

Define a non-compliant vessel, giving examples.

A

Tube whose walls do not stretch easily with increasing volume, causing large changes in pressure.

Capillaries, arterioles

17
Q

Describe the relationship between compliance and age.

Which other factor may affect compliance ?

A

Compliance decreases with age and vasoconstriction.

18
Q

What is the clinical effects of the change in compliance with increasing age and vasoconstriction?

A

As you lose compliance in the aorta and vessels, bigger peak pressures because change in volume is generating a higher change in pressure (possible atherosclerosis)

19
Q

Represent the changing compliance with increasing age and vasoconstriction in graphical form.

A

Refer to slide 10 in lecture on “Control of Cardiac Output”

20
Q

What is the formula for Mean Arterial BP ?

A

MAPB = Diastolic pressure + 1/3 pulse pressure

where,
pulse pressure = systolic pressure – diastolic pressure

21
Q

What does the diastolic pressure have more value on the MABP than the systolic pressure ?

A

Because heart spends a little more time in diastole.

22
Q

Represent, in graphical form, Mean Arterial Blood Pressure.

A

Refer to slide 11 in lecture on “Control of Cardiac Output”

23
Q

Identify the main factors determining the magnitude of pulse pressure.

A

1) STROKE VOLUME
- Intrinsic (preload and afterload) and extrinsic (sympathetic innervation) factors

2) SPEED OF EJECTION OF STROKE VOLUME (influenced by sympathetic nerves)
3) ARTERIAL COMPLIANCE (decreases with age)

24
Q

Identify the factors affecting speed of flow of blood.

Which of these are usually constant in the CVS ? Which of these vary ?

A

1) Radius of Vessel (directly proportional)
2) Pressure Gradient Along Vessel (directly proportional)
3) Length of Vessel (inversely proportional)
4) Thickness of Fluid/Viscosity (inversely proportional, influenced by hematrocit)

Length of vessel and thickness of blood do not really vary.
Radius of vessel and pressure gradient along vessel do really vary.

25
Q

Define the Poiseuille equation, showing the workings in order to get it.

A

Flow ∝ (ΔP x (Radius of vessel)⁴) / Length x Viscosity

Length and viscosity are constants so can be reduced to constant K.
Flow = (ΔP x (Radius of vessel)⁴) / K

Radius of the vessel, and the constant K define the resistance to flow by contributing to friction between blood and the walls of the vessels.
Flow = ΔP / Resistance

In other words,
Arterial pressure = cardiac output x total peripheral resistance

26
Q

What is the main determinant of flow within CVS ?

A

Radius of vessels because length and viscosity are constants, and pressure gradient is usually kept within certain working values.

27
Q

Compare the Poiseuille equation with Ohm’s Law.

A

Flow (=current, I) = ΔP (voltage, V) / Resistance (resistance, R)

28
Q

Identify the average pressures for systemic and pulmonary circulations.

A
Systemic = 120/75 
Pulmonary = 26/8
29
Q

How may we calculate the resistance in the pulmonary and systemic circulation ?

A

Based on:
Arterial pressure = cardiac output x total peripheral resistance

We can easily calculate MABP using the average pressures (both systolic and diastolic) for systemic and pulmonary circulations.
Average cardiac output is 5L/min.
We input those values and may then calculate total peripheral resistance.

30
Q

Compare the peripheral resistance in pulmonary and systemic circulations.

A

Resistance much lower in pulmonary circulation.