2) Control of Cardiac Output Flashcards

1
Q

What is cardiac output?

A
  • The amount of blood ejected from the heart per minute
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2
Q

What is heart rate?

A
  • How often the heart beats per minute
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3
Q

What is stroke volume?

A
  • How much millilitres of blood is ejected per beat
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4
Q

What factors does cardiac output affect?

A
  • Blood pressure

- Blood flow

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5
Q

What is the equation for blood pressure?

A

Blood pressure = Blood flow (Cardiac output) x Total peripheral resistance (TPR)

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6
Q

What controls heart rate?

A
  • Sympathetic innervation and parasympathetic innervation to the Sino atrial node (SAN) pacemaker
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7
Q

What causes/affects the strength of contraction in the heart?

A
  • Sympathetic innervation and circulating adrenaline causes a rise in intracellular calcium levels
  • Increased calcium leads to increased contraction
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8
Q

What is Preload?

A
  • Stretching of the heart at rest which increases stroke volume
  • Due to Starling’s law
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9
Q

What is Starling’s law of the heart?

A
  • ‘Energy of contraction of cardiac muscle is relative to the muscle fibre length at rest’
  • A greater stretch of the ventricle during diastole (blood entering) causes a greater energy of contraction and so a greater volume in systole (blood leaving)
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10
Q

Explain the effect of an increase in Central venous pressure (CVP) on Stroke volume (SV)?

A
  • Initially as CVP increases there is an increase in SV
  • This is because an increase in CVP means an increase in stretching of the cardiac muscles.
  • This increased stretching causes an increased force of contraction resulting in more volume being pumped out (i.e. a higher stroke volume)
  • However this curve begins to level out
  • Eventually there comes a point where an increase in CVP causes a decrease in SV.
  • This is because when CVP reaches these levels there is an excess filling leading to overstretched cardiac muscles
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11
Q

What is actin linked to in cardiac muscles?

A
  • Z-band
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12
Q

Describe the structure of an un-stretched cardiac muscle fibre?

A
  • Overlapping actin/myosin

- Mechanical interference so less cross-bridge formation available for contraction

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13
Q

Describe the structure of a stretched cardiac muscle fibre?

A
  • Less overlapping of actin/myosin
  • Less mechanical interference so more cross-bridge formation can occur
  • Increased sensitivity to Ca2+ ions
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14
Q

What is the role of Starling’s Law?

A
  • Balances the outputs of the left and right ventricles
  • Responsible for fall in cardiac output during drop in blood volume or vasodilation (for eg: haemorrhage)
  • Restores cardiac output in response to fluid transfusions
  • Responsible for fall in cardiac output after standing for a long time leading to postural hypotension and dizziness as blood pools in legs
  • Contributes to increased stroke volume and cardiac output during exercise
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15
Q

Where does the preload enter the heart and where does it come from?

A
  • Vena cavae (Preload from body)

- Pulmonary vein (Preload from lungs)

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16
Q

Where does the output leave the heart from and where does it go?

A
  • Aorta (Output to body)

- Pulmonary artery (Output to lungs)

17
Q

What is afterload?

A
  • Opposes contraction which ejects blood from the heart.

- It is determined by wall stress directed through the heart wall

18
Q

What prevents cardiac muscle contraction?

A
  • Stress through the wall of the heart (Afterload)
19
Q

How is ejection produced?

A
  • More energy of contraction is put in to overcome wall stress (afterload)
  • This produces cell shortening and ejection
20
Q

What is the relationship between wall tension (T), pressure (P) and radius of ventricle (r)?

A
  • T α Pr

- Tension is increased by increasing Pressure or increasing radius

21
Q

What is the equation for wall stress?

A
  • wall stress (S)= tension(T)/ wall thickness (w)
  • since t=Pr we can also say that S= (Pr)/2w
  • (It is divided by 2w as there are two directions of curvature)
  • Afterload/ stress is increased by increasing pressure, increasing radius of ventricle and decreasing wall thickness
22
Q

Why does radius affect wall stress/ ejection?

A
  • Small radius: Greater wall curvature so more wall stress directed towards centre of chamber. There is less afterload and better ejection
  • Large radius: Less wall curvature so more wall stress directed through heart wall. There is more afterload and less ejection
  • Huge theoretical radius: Negligible wall curvature so all stress is directed through wall.
23
Q

What is the importance of Laplace’s law?

A
  • Opposes Starling’s law at rest. An increase in preload causes the chambers to stretch more. This increases the radius and decreases curvature which increases afterload. (In a healthy heart Starling’s law always overcomes Laplace’s law)
  • Facilitates ejection during contraction: Contraction reduces chamber radius so less afterload when the chamber empties. This increases stroke volume and ensures all blood is expelled
  • Contributes to a failing heart at rest and during contraction: In a failing heart the chambers are often dilated and the radius is large. This increases afterload and opposes ejection
24
Q

What does an acute rise in blood pressure cause?

A
  • It affects Starling’s law as it increases stretch of the cardiac walls giving increased contraction and increased stroke volume
  • This also happens with certain hormones such as noradrenaline
  • Baroreflexes decreases sympathetic tone which decreases blood pressure
25
Q

What does a chronic increase in blood pressure cause?

A
  • When undergoing exercise the body attempts to maintain stroke volume however eventually it will decrease
  • Decrease in blood pressure would increase efficiency of the heart
  • An increase in blood pressure will reduce cardiac output
  • Therefore blood pressure needs to be kept constant during exercise
26
Q

How does heart failure cause increased wall stress?

A
  • In some heart failures the heart does not contract properly and can lead to some blood being left in the ventricle
  • This eventually leads to volume overload causing the increased radius
  • In some heart failures there is an increase in the pressure/afterload in the chamber causing pressure overload.
  • This leads to increased pressure
  • An increase in radius or pressure increases wall stress and opposes ejection
27
Q

How does the heart deal with increased wall stress?

A
  • The heart uses ventricular hypertrophy (increased muscular size) to cope with increased wall stress.
  • It uses greater myocyte size and more sarcomeres to increase wall thickness
  • This decreases wall stress per sarcomere and hence afterload.
  • This maintains SV and CO
28
Q

What is a disadvantage of ventricular hypertrophy?

A
  • It requires more energy as more sarcomeres are used.
  • As the amount of energy required increases the contractility will decrease as the heart will struggle to supply adequate oxygen for respiration.
  • Hence producing more heart failures
29
Q

What is the energy of contraction?

A
  • The amount of work required to generate stroke volume

- It depends on Starling’s law and contractility

30
Q

What is the function of stroke work (the work performed by the left ventricle to eject a volume of blood)?

A
  • Contract until chamber pressure is greater than aortic pressure
  • This causes ejection from ventricle
31
Q

How does an increased preload affect the ventricular pressure-volume loop.

A
  • Increased exercise leads to increased preload and increased EDV.
  • This is because increased exercise leads to an increased venous return. This fills the ventricle more and so we end diastole with a higher volume in the ventricle.
  • This higher volume stretches the walls more leading to a higher force of contraction.
  • After contraction the ventricle will eject the volume of blood to the same end systolic volume (ESV) we started with.
  • Hence there is more blood pumped out leading to a higher SV
32
Q

How does an increased afterload affect the pressure volume loop

A
  • Hypertension leads to increased afterload.
  • There is a longer time spent in the (isovolumetric) contraction phase to increase pressure in the chamber located above the aorta
  • This opens the aortic valve
  • This uses more energy and lowers the force of contraction reducing stroke volume and increases the end-systolic volume (ESV).