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Cardiovascular System > Regulation of Stroke Volume > Flashcards

Regulation of Stroke Volume Flashcards

1
Q

What is the function of pacemaker cells?

A

Responsible for the autorhythmicity of the heart

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2
Q

How does the sympathetic systemic increase heart rate?

A

Release of noradrenaline and adrenaline (form adrenal medulla) which act on B1 receptors win the SA node

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3
Q

What is the effect of activated B1 receptors in the SA node?

A

Increases ion flow through If (Na+ channel) and Ca channels which increases depolarisation so cells reach threshold faster -> increases slope of pacemaker potential which increases HR = tachycardia

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4
Q

Which nerve supplies the heart with parasympathetic supply?

A

Vagus nerve

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5
Q

What neurotransmitter does the vagus nerve release and what receptors does it act on?

A

Releases acetylcholine which acts on muscarinic receptors on SA node

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6
Q

What is the effect of activated muscarinic receptors on the SA node?

A

Increase K+ permeability, hyper polarising cell, and Ca2+ permeability decrease, which slows down the rate of depolarisation of pacemaker potential. Takes longer to reach threshold, decreasing slope and HR

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7
Q

What is stroke volume?

A

The volume of blood pumped per ventricle per contraction and is related to the force of contraction

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8
Q

What is the force of contraction dependent one?

A

Length of muscle fibres at the beginning of contraction

The contractility of the heart

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9
Q

Define Starling’s Law

A

The energy of contraction is proportional to the initial length of the cardiac muscle fibre

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10
Q

What is the relationship between the tension and the length of the sarcomere?

A

Tension increases steadily with increase of length, and then the increase slows until the peak tension is reached
After this the tension decreases

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11
Q

Why does increased preload increase force of contraction?

A

Stretch of ventricular wall increases with increased EDV which causes the contraction to be more forceful in order to eject more blood

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12
Q

What is preload?

A

The stretch prior to contraction and represents the land placed on the cardiac muscle before they contract

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13
Q

In vivo, what affects preload?

A

End diastolic volume (EDV)

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14
Q

How does increased venous return affect stroke volume?

A

Increases in EDV which causes an increased preload and so an increased SV

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15
Q

How does decreased venous return affect stroke volume?

A

Decreased the EDV, which decreases the preload, and thus SV

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16
Q

What does preload allow, in terms of cardiac output from left and right sides of the heart?

A

It ensures self-regulation - the resting EDV is not at the maximum for the max stroke volume, nor is at its minimum. This means stroke volume can vary to match the SV on the other side of the heart

17
Q

What is afterload?

A

The load against which the muscle tries to contract

18
Q

What determines the after load in vivo?

A

The arterial pressure against which the blood is expelled (this in dependent on TPR)

19
Q

What are two factor which affect the aortic pressure?

A

How much blood is being pushed into aorta

How easy it is for the blood to get out of the aorta (the total peripheral resistance)

20
Q

How does an increase in TPR affect SV?

A

Increase TPR, increase aortic pressure and so the ventricles have to work harder and use energy to build up sufficient pressure to open the aortic valve
This leaves it will less energy to contract to eject the blood, and therefore decreases SV

21
Q

What pathological conditions increase afterload?

A

High BP in arteries

Loss of compliance in aorta

22
Q

What occurs in after load becomes chronic?

A

Hypertrophy of myocardium

23
Q

What are 4 factors with regulate SV?

A

Preload
Afterload
Neural
Pathological

24
Q

What is an inotropic agent?

A

Any chemical that effects contractility (the inotropic effect)

25
Q

Describe the inotropic effect of the sympathetic nervous system?

A

Positive - Noradrenaline and adrenaline act on B1 receptors on myocytes and increase contractility - stronger but shorter contraction

26
Q

What are two general factors that will increase contractility?

A

Amount of Ca2+ available increases

Increase in preload which makes myocardium more sensitive to Ca2+

27
Q

Why does activation on B1 receptors increase contractility?

A

Phosphorylates voltage-gated Ca2+ channel, which increases how long they’re open for so more Ca can diffuse in

28
Q

What are 3 pathological conditions which can regulate SV and their affects on the curve?

A

Hypercalcemia - up and left
Hypocalcemia - down and right
Ischaemia - down and right
Babituates (anaesthetic) - down and right

29
Q

What are 4 factors that affect venous return?

A

Contraction or compression of veins
Pressure changes in the abdomen and thorax during breathing (respiratory pump)
Skeletal muscle pump
Sympathetic innervation of veins

30
Q

What is the skeletal muscle pump?

A

Contraction of skeletal muscle compresses veins and pushes blood back to the heart - increased VR

31
Q

What is the respiratory pump?

A

As the thorax expands during inspiration, it develops a sub-atmospheric pressure
This decreases pressure in the IVC, drawing blood into the IVC from abdominal veins
The descend of the diaphragm also compresses abdominal veins to push blood back to heart

32
Q

How does sympathetic innervation increase venous return?

A

Venoconstriction by sympathetic activity causes volume of veins to decrease, squeezing more blood from them and into the heart

33
Q

How does Starlings Law let the heart compensation for a reduced pumping ability?

A

The heart compensates by producing a larger EDV, resulting in a lower ejection fraction and reduced exercise capacity

34
Q

Why can an increase in HR decrease SV?

A

Shortened cardia interval between contraction cuts into rapid filling phase -> reduced EDV
Reduced EDV -> decrease preload -> reduced SV

Cardiovascular System (37 decks)

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