Control of Cardiac Output Flashcards

1
Q

What is the cardiac output equation

A

Heart Rate x Stroke Volume

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2
Q

What is the cardiac output limited by and why

A

Limited by venous return as the blood is held in a closed system

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3
Q

Name some factors that influence the venous return

A
  • Skeletal Muscle Pump

- Abdomino-Thoracic Pump

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4
Q

What is the skeletal muscle pump

A
  • Veins have one way valves that prevent back flow

- Surrounding muscle activity acts to propel the blood back towards the heart.

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5
Q

What is the abdomen-thoracic pump

A
  • The great veins (vena cavae) and atria are exposed to intrathoracic pressure
  • This pressure is normally negative and becomes more so during inspiration
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6
Q

Why does cardiac output start to decrease if the heart rate does much above 180bpm

A

Not enough time for ventricular refilling and stroke volume is reduced

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7
Q

Up to 180bpm how does an increase in heart rate affect the cardiac output

A

It will increase proportionately

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8
Q

At what exercise intensity does stroke volume usually reach its maximum levels

A

fairly moderate exercise levels

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9
Q

How is the heart rate innervated

A

Dually innervated

Rate of the SAN is modulated by both the sympathetic and parasympathetic nervous systems

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10
Q

The natural intrinsic rate of the SAN is about 110-120bpm so why is the resting rate about 70

A

Parasympathetic inhibition dominates at rest

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11
Q

Small increases in heart rate occur by what nervous system

A

By inhibition of the parasympathetic nervous system.

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12
Q

What neurotransmitters from the SNS act on what receptors on the SAN

A

Noradrenalin released at nerve endings acts on the Beta-receptors in the SAN

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13
Q

How does sympathetic stimulation affect the action potential graph of pacemaker tissues

A

Increases the rate of depolarisation after repolarisation has occurred so the threshold potential is reached quicker and the rate of firing increases

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14
Q

Sympathetic fibres on the Right and Left sides of the body innervate what in the heart

A
RIGHT = SAN, regulates heart rate
LEFT = Innervate the ventricles, regulate cardiac contractility
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15
Q

The left and right branches of what nerve innervate the SAN and AVN

A

Vagus nerve

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16
Q

Where can the parasympathetic ganglia innervating the heart be found

A

On the cardiac surface or in the heart itself

17
Q

The postganglionic fibres release what neurotransmitter and act on what receptors in the SAN

A

Acetylcholine on the muscarinic receptors in the SAN

18
Q

If an individual has a lower resting heart rate how big does their stroke volume tend to be

A

Lower heart rate = bigger stroke volume

19
Q

What is the end-diastolic volume (EDV)

A

This is the filled volume of the ventricle prior to contraction

20
Q

What is the end-systolic volume (ESV)

A

This is the residual volume of blood remaining in the ventricle after ejection

21
Q

What is the definition of ventricular stroke volume

A

The difference between the ventricular end-diastolic volume and end-systolic volume

22
Q

What are the three primary mechanisms that regulate EDV, ESV and therefore SV

A

Preload
Contractility
Afterload

23
Q

What is preload

A

Factors that determine ventricular EDV and end-diastolic fibre length of the ventricular muscle

24
Q

What is Afterload

A

Factors which determine ventricular wall stress (chamber radius, wall thickness and resistance to outflow)

25
Q

What are the 3 things that EDV depend on

A

Filling pressure
Filling time
Ventricular compliance

26
Q

What is filling pressure and how can it affect EDV

A

When venous return increases atrial filling pressure increases and so ventricle filling pressure increases and so EDV rises

27
Q

What is filling time and how can it affect EDV

A

Longer filling time = greater EDV

Heart rate increase = diastole shortens more than systole does so EDV decreases

28
Q

What is ventricular compliance and how can it affect EDV

A

As an ventricular compliance increases, a given filling pressure will produce an increased ventricular volume and result in a greater EDV.

29
Q

What are the 4 things that ESV depend on

A

Preload
Afterload
Heart Rate
Contractility

30
Q

What is pre load and how does it affect stroke volume

A

Starlings law of the heart - increased EDV increases stretch on the cardiac muscle and the force of the contraction and thus the stroke volume

31
Q

What is Starlings law of the heart

A

the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction.

32
Q

What is after-load and how does it affect ESV

A

Afterload of the left ventricle is the mean systemic arterial pressure. increased after-load impedes the hearts ability to empty and so increases the ESV.

33
Q

How does heart rate affect ESV

A

Increased heart rate = greater Ca2+ entry into myocardial cells and increasing contractility and reducing ESV

34
Q

Why is the Frank-Starling mechanism physiological important

A

The heart is able to eject additional blood that was returned to it and keeps the two sides in balance. Otherwise if the RV output exceeds the LV output then blood would be trapped in the lungs, but instead the extra preload in the left means the LV pumps more strongly to keep the sides in balance

35
Q

What is contractility

A

Physiological alterations in contractility are associated with change in intracellular calcium conc in the myocyte.

36
Q

What can increase the force of ventricular contraction without increasing the EDV and stretching the muscle fibres

A

Contractility

37
Q

What is an inotrope

A

a neurotransmitter, hormone or drug that alters the force of contraction of the heart muscle

38
Q

What are positive and negative inotropes

A
Positive = increases contractility
Negative = decreases contractility