Control of cardiac output Flashcards

1
Q

what is the definition of cardiac output?

A

→amount of blood ejected from the heart per minute

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2
Q

what is the equation for cardiac output?

A

→CO = HR x SV

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3
Q

what is the equation for blood pressure?

A

→BP = CO x TPR (total peripheral resistance)

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4
Q

what does cardiac output determine?

A

→blood pressure

→blood flow

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5
Q

what is cardiac output proportional to?

A

→ how often the heart beats PM

→ how much blood is ejected per beat

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6
Q

what controls stroke volume? (list)

A

→ preload
→ heart rate
→ contractility
→ afterload

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7
Q

what is the equation for blood flow (CO)?

A

CO = BP/TPR

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8
Q

what is preload?

A

→ The stretching of the heart at rest

→ Increases stroke volume due to Starling’s Law

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9
Q

what is afterload?

A

→ Opposes ejection

→Reduces stroke volume due to Laplace’s law

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10
Q

what controls heart rate?

A

→ sympathetic and parasympathetic nerves control heart rate

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11
Q

What is energy of contraction and what does it depend on?

A

→ amount of work done required to generate stroke volume

→ depends on Starling’s Law and contractility

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12
Q

What two functions does stroke work carry out?

A

→ Increases chamber pressure to make it greater than aortic pressure (isovolumetric contraction)
→ Ejection from the ventricle

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13
Q

what do afterload and preload do to the stroke volume?

A

→ Preload increases the stroke volume and afterload opposes the stroke volume

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14
Q

State Starling’s law

A

→ Energy of contraction in cardiac muscle is relative to the muscle fibre length at rest

→the greater the stretch of the ventricle in diastole (blood entering)
→the greater the energy of contraction
→ a greater stroke volume is achieved in systole

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15
Q

what is the equation for stroke volume?

A

→ SV = end diastolic volume - end systolic volume

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16
Q

Describe an unstretched fibre

A

→ overlapping actin/myosin
→ mechanical interference
→ Less cross-bridge formation available for contraction

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17
Q

Describe a stretched fibre

A

→ Less overlapping actin/myosin
→ Less mechanical interference
→ potential for more cross-bridge formation
→ Increases sensitivity to Ca2+ ions

18
Q

What are the roles of Starling’s law during preload?

A

→ Balances the output of the right and left ventricle which is very important

→ responsible for the fall in cardiac output during a drop in blood volume

→ Restores cardiac output in response to IV fluid transfusions

→ Responsible for fall in cardiac output during orthostasis leading to postural hypotension + dizziness

→ contributes to increased stroke volume and cardiac output during upright exercise

19
Q

What is afterload determined by?

A

→ it is determined by wall stress directed through the heart wall

→stress through the wall of the heart prevents muscle contraction

20
Q

What is the equation for Laplace’s law?

A

→ P = 2t/r
T = wall tension
P = pressure
R = radius

21
Q

what is the equation for wall tension?

A

→ T = S (wall stress) x ( wall thickness) W

22
Q

How is afterload increased and how it it reduced ?

A

→ by increasing pressure + radius and reduced by increasing wall thickness

23
Q

what happens if there is a small radius (in terms of afterload)?

A

→ greater wall curvature
→ more wall stress directed towards the center of the chamber
→ less afterload
→ better ejection

24
Q

what happens if there is a big radius (in terms of afterload)?

A

→ less wall curvature
→ more wall stress directed through heart wall
→more afterload
→ less ejection

25
Q

How does Laplace’s law oppose Starling’s law at rest?

A

→ Increased preload gives increased stretch of chamber
→increases chamber radius and decreases curvature
→ increases afterload
→ opposes ejection of blood from a full chamber

26
Q

What law takes precedence in a healthy heart?

A

→Starling’s law overcomes Laplace’s

27
Q

How does Laplace’s law facilitate ejection during contraction?

A

→ Ventricular contraction reduces the chamber radius and increases curvature

→Laplace’s law states there will be less afterload in the emptying chamber

→ This aids expulsion and increases stroke volume

28
Q

what do the chambers look like in a failing heart?

A

→ In a failing heart the chambers are often dilates - increased radius

29
Q

How does Laplace’s law contribute to a failing heart at rest and during contraction?

A

→ In a failing heart the chambers are often dilated

→increased afterload opposing ejection

30
Q

What does Laplace’s law state about blood pressure and wall stress?

A

→ Increased blood pressure will increase wall stress

31
Q

What is an acute rise in blood pressure offset by?

A

→ Starling’s law
→ Local positive inotropes
→ Baroreflex

32
Q

What is the baroreflex?

A

→ decreased sympathetic tone

→ decreasing blood pressure

33
Q

What is chronic increase in arterial blood pressure caused by?

A

→ increased energy expenditure to maintain stroke volume

→ ultimately decrease in stroke volume

34
Q

what does decreasing blood pressure do to the heart?

A

→ increases the efficiency of the heart

35
Q

What happens if there is an increased radius in the heart?

A

→Heart failure where the heart does not contract properly (MI, cardiomyopathies, mitral valve re-gurgitation)
→ blood is left in the ventricle leading to eventual volume overload

36
Q

What happens if there is increased pressure in the heart?

A

→ pressure overload heart failure due to increased pressure

37
Q

What happens with increase in radius and pressure?

A

→ wall stress increases which opposes ejection

38
Q

how does the heart compensate for an increase in radius + pressure?

A

→ the heart compensates with ventricular hypertrophy (greater myocyte size and more sarcomeres)
→ Increasing wall thickness
→ decreases wall stress per sarcomere and therefore afterload so maintains SV and CO

39
Q

why does ventricular hypertrophy eventually cause heart failure?

A

→ the more sarcomeres used the more O2 is used
→ amount of energy required continues to increase
→ contractility decreases and produces more heart failure

40
Q

describe Laplace’s law and the ventricular pressure-volume loop with high blood pressure

A

→ increased afterload
→ a longer time is spent in isovolumetric contraction to increase pressure in the chamber to be > aorta to open the valve
→ this uses more energy and lowers the force of contraction and SV
→end systolic volume increases

41
Q

describe Starling’s law and the ventricular pressure-volume loop during exercise

A
→ increased venous return leads to an increase in EDV 
→increased preload 
→more stretch 
→shorter isovolumetric contraction phase
→ increase in SV due to Starlings law.  
→More blood back to the heart
→ more blood ejected from the heart