Control Of Cardiac Output Flashcards

1
Q

What is the definition of cardiac output (CO)? What is its normal value in a 70kg male?

A

The volume of blood pumped by each ventricle per minute (L/min)

OR

CO = SV x HR

SO SV (70ml) x HR (72bpm) = 5L/min typically

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2
Q

Define the ejection fraction (EF).

A

SV / EDV x 100

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3
Q

How much circulating blood is there in total and how much is in the heart and lungs?

A

Total: 5L

Heart & lungs: 1.5L

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4
Q

How much blood is in the heart when it is filled and empty?

A

Filled (EDV) = 140ml

Empty (ESV) = 50ml

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5
Q

Define stroke volume (SV). What is a typical value for a 70kg male?

A

The volume of blood ejected from each ventricle during each ventricular contraction

OR

SV = EDV - ESV

SO

EDV ~ 140ml - ESV ~ 50ml = SV = 90ml typically

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6
Q

What is End Systolic Volume (ESV)?

A

Filled volume of L ventricle prior to contraction + pushing of blood into the aorta

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7
Q

What is End Diastolic Volume (EDV)?

A

Residual volume of blood remaining in L ventricle after contraction + pushing of blood into aorta just before the L atrium empties into it

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8
Q

What is diastasis?

A

When volume of blood in the L ventricle is basically static just after the AV valves open

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9
Q

Define cardiac preload.

A

Initial stretching of cardiac myocytes prior to contraction i.e. volume load on L ventricle before contraction (directly measured via sarcomere length)

SO Higher EDV = higher preload

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10
Q

Define cardiac afterload.

A

Arterial pressure represents a ‘load’ OR resistance on the L ventricle

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11
Q

What factors influence stroke volume?

A

Preload 1: systemic venous return
Preload 2: R heart function
Preload 3: pulmonary vascular resistance
Preload 4: inlet i.e. mitral valve

Afterload 1: outlet i.e. aortic valve diameter
Afterload 2: arterial BP
Afterload 3: arteriolar tone

Contractility

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12
Q

What factors affect heart rate?

A

Venous return -> atrial reflex -> ANS innervation (e.g. SNS)

Venous return

Hormones

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13
Q

What factors affect preload and afterload?

A

Preload: venous return + filling time

Afterload: vasodilation or vasoconstriction

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14
Q

What factors affect contractility?

A

Hormones

ANS

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15
Q

What factors affect End Diastolic Volume (EDV) and End Systolic Volume (ESV)?

A

Contractility + afterload -> ESV

Preload -> EDV (+ ESV as it increases contractility)

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16
Q

When is filling time more rapid? Why?

A

First 1/2 of ventricular filling time as ventricle is more compliant

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17
Q

What effect does an increased heart rate (HR) have on cardiac output (CO)?

A

Reduced filling time impinges on early diastole so ventricular filling is reduced + CO is reduced (made worst by mitral stenosis obstruction/AF where atrial contraction removed)

18
Q

What is the autonomic nervous system (ANS) impact on heart rate (HR)? Why?

A

PNS: vagus nerve decreases HR via hyperpolarization causing slower depolarization i.e. harder to reach AP threshold

SNS: sympathetic cardiac nerves increase HR + force of contraction via reduced repolarization causing faster depolarization i.e. easier to reach AP threshold

19
Q

Where are the arterial baroreceptors in the body?

A

Aortic arch (afferent fibres of vagus nerve)

Carotid sinus R + L (afferent of glossopharyngeal nerve)

20
Q

How does the baroreceptor reflex work?

A
  1. Increased BP stimulates baroreceptors increasing firing of glossopharyngeal + vagal afferent nerves
  2. Nerves go to cardiac + vasomotor centres in medulla of brain to SA node
  3. Increased efferent vagal nerve firing
  4. Decreased sympathetic nerve firing to veins, arteries + AV node
  5. Adrenal medulla releases NA + RAAS system
  6. BP decreased
21
Q

How does the atrial receptor (Bainbridge) reflex work?

A
  1. Increased atrial pressure detected by atrial stretch receptors
  2. Increased vagal afferent nerve firing to cardiac + vasomotor centres in medulla of brain
  3. Decreased PS efferent firing to SA node
  4. Increased S efferent firing to SA node
  5. HR increased to deal with higher blood volume
22
Q

How does the chemoreceptor reflex work?

A
  1. Increased pCO2 or decreased O2 stimulate chemoreceptors increasing firing of glossopharyngeal + vagal afferent nerves
  2. Nerves go to cardiac + vasomotor centres in medulla of brain
  3. Decreased efferent vagal nerve firing to SA node
  4. Increased sympathetic nerve firing to veins, arteries + AV node
  5. BP increased
23
Q

Where are the chemoreceptors of the body?

A

Aortic arch (afferent fibres of vagus nerve)

Carotid sinus R + L (afferent of glossopharyngeal nerve)

Medulla of brain

24
Q

Why is cardiac preload the major way in which stroke volume is increased?

A

Starling’s law: the more a muscle is stretched the more powerfully it will contract i.e. w/o other control mechanisms, heart’s intrinsic property results in what comes in will be pumped out response

25
Q

What factors increase pre-load i.e. ventricular filling?

A

Increased aortic pressure which decreases HR

Increased atrial contractility

Increased ventricular compliance

Increased CVP

26
Q

What factors increase CVP?

A

Decreased venous compliance

Increased thoracic venous BV: TBV, venous return (respiration, muscle contraction + gravity)

27
Q

What is used as a surrogate for preload?

A

End-Diastolic Volume (EDV)

28
Q

What happens to the stroke volume (SV) as End-Diastolic Volume (EDV) increases?

A

Increases + then drops

29
Q

What will happen to the heart’s stroke volume (SV) in short-term and long-term increased pre-load?

A

Short-term: Increases SNS, contractility + HR

Long-term: contraction of heart muscle reduced due to myocardial injury or overload (increased pre-load or afterload) due to long-term adverse remodelling

30
Q

What are the 2 reasons why preload may be increased in disease?

A
  1. Regional e.g. heart attack

2. Global e.g. dilated cardiomyopathy

31
Q

What will to stroke volume (SV) if afterload is increased? Give an example of when this can occur.

A

The greater the load/resistance, the less muscle fibres can contract

E.G. hypertension

32
Q

What can be used as a surrogate for afterload?

A

End Systolic Volume (ESV)

33
Q

Define contractility.

A

Force of contraction of myocardium

34
Q

What agents affect contractility?

A

Positive inotropic agents increase it

Negative inotropic agents decrease it

35
Q

What factors affect total peripheral resistance?

A

Capacitance: vena cava, vein + venule
Exchange: capillaries
Resistance: small arteriole + small artery
Distribution: large artery + aorta

36
Q

What is the main determinant of cardiac output (CO)?

A

Total venous return

37
Q

What are indirect local control mechanisms of total venous return?

A

Local control in each organ system

38
Q

Why is cardiac output controlled by indirect local control mechanisms?

A

As different organs need different amounts of blood when the body is doing different things e.g. rest + exercise

39
Q

Where is most of the bodies blood being pumped to at rest?

A

Liver, kidneys + brain

40
Q

Where is most of the bodies blood being pumped to during exercise?

A

Muscle