4 Cardiac Output Flashcards

1
Q

In what 3 ways can cardiac output be modulated?

A

HR
EDV
ESV

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2
Q

What is stroke volume equal to?

A

SV = EDV - ESV

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3
Q

What is the ESV usually?

Why?

A

50ml

this is maintained by Starling’s Law

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4
Q

How can contraction force be increased on a cellular level?

A

increasing the Ca2+ sensitivity of the contractile apparatus

increasing Ca2+ concentration in the cell

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5
Q

What is the principle behind Starling’s Law of the Heart?

A

‘Force of ventricular contraction is dependent on the length of ventricular muscle fibres in diastole’

so, when the ventricle fills with more blood in diastole, its’ contraction force in systole will be greater, forcing more blood out, maintaining that ESV of 50ml

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6
Q

How can we measure sarcomere length?

A

we can’t, so we just use EDV as a proxy measurement instead

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7
Q

How does stroke volume change with EDV (ie stretching) ?

A

proportionally(ish)

an increase in EDV of 30ml will increase stroke volume by 30ml

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8
Q

Can the sarcomere keep stretching?

A

no, and at this theoretical point, stroke volume will not be increased by EDV

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9
Q

What does Starling’s Law of the heart ensure?

A

R SV = L SV

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10
Q

How can right side venous return affect left side SV?

A

as right venous return increases, right ventricular EDV increases, increasing R SV

after a couple of pumps, this will have gone through pulmonary circulation, and there will hence be more blood and a higher pressure on the Left side of the heart

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11
Q

Why is it important that R SV = L SV?

A

prevent blood pooling in either the systemic or pulmonary circulations

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12
Q

Name 5 main factors affecting venous return to the right ventricle

A
Blood Volume
skeletal muscle pump
respiratory pump
venous tone
gravity
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13
Q

how does blood volume affect venous return to the right ventricle?

A

increased BV leads to increased VR (renal failure)

decreased BV leads to decreased VR (haemorrhage / dehydration)

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14
Q

How does a skeletal muscle pump increase venous return to the right ventricle?

A

the presence of semilunar valves means that skeletal muscle contraction forces blood proximally, not distally,

this only requires a small bit of skeletal muscle

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15
Q

How does the respiratory pump affect venous return to the right ventricle?

A

inspiration increases abdominal pressure and decreases thoracic pressure (diaphragm moves down)

this pushes blood from the abdominal vena cava to the thoracic vena cava

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16
Q

How does venous tone affect venous return to the right ventricle?

A

mediated by sympathetic activity, veins can mobilise some blood stored in venous circulation by contracting to move it along (semilunar valves important here)

17
Q

How does gravity affect venous return to the heart?

A

when you stand up, blood accumulates in the lower body as less is being returned to the heart, this causes thoracic venous volume to decrease, decreasing central venous pressure

18
Q

Name 2 minor factors contributing to Pre-Load

A

Atrial contraction

HR (>180bpm)

19
Q

How does atrial contraction increase venous return to the venricle

A

innervated sympathetically, increasing total atrial force, and increasing EDV

20
Q

Why is atrial contraction important?

A

important for maintaining EDV at high heart rates when the passive filling phase of diastole is shortened

21
Q

What happens when HR >180

A

passive filling and atrial contraction are no longer enough to maintain EDV, and stroke volume won’t be able to be maintained

22
Q

How can ESV be regulated?

A

increased contractility / inotropy

After-load

23
Q

How does increased inotropy work?

A

sympathetic nerve / ciruclating NAd stimulated beta-1 receptors, increases Ca influx —stronger contraction, ESV decreases, stroke volume increases

24
Q

How does after-load affect ESV?

A

peripheral resistance will increase aortic pressure, increasing ESV as the ventricle has to work harder to pump a given amount of blood into the aorta

25
Q

Why do patients with hypertension get left ventricular hypertrophy?

A

the left ventricle has to overcome a greater aortic pressure created by increased peripheral pressure