Cardiovascular L4: Regulation of Heart Rate and Cardiac Output Flashcards

1
Q

What is cardiac output?

A

volume of blood pumped by each ventricle per minute

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2
Q

What 2 things determine cardiac output?

A

Heart rate (HR) Stroke volume (SV)

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3
Q

What stimulation increases heart rate and what stimulation decreases heart rate?

A

Heart rate is decreased by parasympathetic stimulation and increased by sympathetic stimulation

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4
Q

What are 2 things that determines stroke volume?

A

Stroke volume is determined by:

  1. sympathetic activity
  2. venous return (how much blood coming back to heart from veins)
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5
Q

What is the equation for cardiac output (CO)?

A

Heart rate (bpm) x stroke volume (ml) = Cardiac output (CO)

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6
Q

On average at rest, what is the CO (cardiac output) for each ventricle?

A

72 bpm x 70 ml = 5040 ml/min 5.04 L

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7
Q

Overview of the autonomic nervous system. What does the sympathetic and parasympathetic nervous system do?

A

To all organs, glands,blood vessels and tissues (other than skeletal muscle)

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8
Q

What are 3 key facts about the autonomic nervous system?

A
  1. Most organs dually innervated
  2. Mostly opposite effects
  3. Balance shifts to meet demands
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9
Q

What is the sympathetic nervous system? Specify length of pre and post fibres.

A
  • ganglia are close to spinal column
  • short pre and long post
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10
Q

What is the parasympathetic nervous system? Specify length of pre and post fibres.

A
  • ganglia are close to effector organ
  • long pre and short post
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11
Q

Diagram of Autonomic nervous system

A
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12
Q

What does the sympathetic nervous system innervate?

A

Innervates SA and AV nodes, myocardium &conduction system

MORE TO ADD

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13
Q

What does the parasympathetic nervous system innervate?

A

Innervates SA and AV nodes &atrial muscle

MORE TO ADD

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14
Q

How is cardiac output affected by autonomic control (heart rate and stroke volume)?

A

Cardiac output = Heart rate x Stroke volume Heart rate: influenced by both parasympathetic and sympathetic nervous systems Stroke volume: influenced by sympathetic nervous system only (but in two ways…)

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15
Q

How is heart rate controlled by the nervous system?

A

Parasympathetic & Sympathetic innervation: both have chronotropic effects (changing heart rate) and ionotropic effects (activating or deactivating voltage-gated ion channels)

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16
Q

Heart rate is a balance between parasympathetic (______) and sympathetic (______) control

A

inhibitory; excitatory

  • Sympathetic- keeps it going If left to own devices, heart rate would speed up
  • Thus, is constantly slowed down by the parasympathetic system
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17
Q

What is ‘vagal tone’?

A

The heart has an intrinsic rate of 100-110 bpm, but at rest, HR is 60-80 bpm, suggesting that it is under constant inhibitory control

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18
Q

An increase in HR would ______ (increase/decrease) parasympathetic activity and ______ (increase/decrease) sympathetic

A

decrease; increase

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19
Q

What happens to HR if the vagus nerve is cut?

A

Lose vagal tone –> accelerate HR

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20
Q

What is produced by the parasympathetic nervous system to control heart rate (change the pacemaker)? What does that cause?

A

Acetylcholine decreases slow inward Na+ and Ca2+ (slower depolarisation); increases K+ out in AP (more hyperpolarisation) = longer time to reach threshold Take longer to reach threshold –> decrease/slower HR

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21
Q

What happens to AP in normal self induced contraction?

A
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22
Q

What is produced by the sympathetic nervous system to control heart rate (change the pacemaker)? What affect does it have on HR?

A

Noradrenaline

increases slow inward Na+ and Ca2+ (faster depolarisation); decreases K+ out in AP (less hyperpolarisation) = shorter time to reach threshold

Takes faster to reach threshold –> increased/faster HR

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23
Q

What are the 2 ways that the sympathetic stimulation has of influencing stroke volume?

A
  1. Directly by excitatory innervation of the myocardium (atria & ventricles), increases strength of contraction, results in larger stroke volume = ‘extrinsic control
  2. Indirectly by stimulating the Adrenal Medulla to produce Adrenaline, acts on veins to cause venoconstriction
    • increases venous return (more blood returned to heart)
    • increases ventricular filling and leads to increased EDV
    • results in a larger stroke volume, through length–tension relationship called the ‘Frank–Starling law’ = ‘intrinsic control’
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24
Q

When controlling stroke volume, the sympathetic control as extrinsic and intrinsic effects to increase SV. Explain this.

A
  1. Extrinsic: direct increase in muscle contractility = increase SV
  2. Intrinsic: indirectly causes increase in venous return, increased EDV = increase SV
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25
Q

What is the Frank Starling Law?

A

The heart has the capacity to automatically adjust its output (Stroke Volume) to match its input (End Diastolic Volume)

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26
Q

Cardiac muscle fibre length depends on the extent of _______. Normally, fibre length is _____ (more/less) than optimal length for developing max tension. What happens to SV when there is an increase in venous return?

A

venous filling; less

Increased venous return → increased EDV → stretches fibres closer to optimal length → increased tension → stronger contraction → increased SV.

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27
Q

What is different when it comes to stretch cardiac and skeletal muscles.

A

Cardiac- the more the heart fills (stretch), the more it will contract (linear) Skeletal- there is an optimal length (inverted parabola)

28
Q

How is EDV increased in the Frank-Starling Law?

A

This would be the effect if only EDV increases, but we also get effects of extrinsic control

29
Q

How to increase contractility (extrinsic control) in the Frank-Starling Law?

A

Extrinsic control shifts the curve to the left: same EDV, more SV (to meet the demands of the body)

30
Q

How does intrinsic and extrinsic effects affect the Frank-Starling Law to increase SV?

A
  • Intrinsic effect shifts up curve through increased EDV Extrinsic effect shifts curve to the left through increased contractility Combined together to give a larger response
31
Q

How is the Frank-Starling Law important in heart failure? What happens to the curve?

A

Frank–Starling curve shifts downward and to the right - SV decreases at normal EDV Damage = decrease contraction = decrease SV = weaker

32
Q

How does the Frank-Starling Law compensate in heart failure?

A

Sympathetic stimulation increases contractility, shifting curve to the left Increase in blood volume increases EDV, increases muscle fibre length = able to get normal SV

33
Q

Summary of Frank-Starling Law. What happens to the curve normally?

A

Shift to left

34
Q

Summary of Frank-Starling Law. What happens to the curve in heart failure?

A

Shift to right

35
Q

Summary of Frank-Starling Law. What happens to the curve when compensating for heart failure?

A

Shift back to left

36
Q

Summary: What are 2 things that the parasympathetic innervation does?

A
  1. inhibits SA and AV nodes, decreasing heart rate and increasing AV node delay
  2. inhibits atrial muscle, weakening atrial contraction
37
Q

Summary: What are 4 things that the sympathetic innervation does?

A
  1. stimulates SA and AV nodes, increasing heart rate and decreasing AV node delay
  2. excites conduction pathways, increasing conduction
  3. stimulates myocardium increasing atrial &ventricular contractility and stroke volume
  4. causes venoconstriction increasing venous return & EDV = increased SV
38
Q

What is the effect of parasympathetic stimulation on SA node?

A

Decrease the rate of depolarisation to threshold Decrease the heart rate

39
Q

What is the effect of parasympathetic stimulation on AV node?

A

Decreased excitability Increases the AV nodal delay

40
Q

What is the effect of parasympathetic stimulation on ventricular conduction pathway?

A

No effect

41
Q

What is the effect of parasympathetic stimulation on atrial muscle?

A

Decreases contractility Weakens contraction

42
Q

What is the effect of parasympathetic stimulation on ventricular muscle?

A

No effect

43
Q

What is the effect of parasympathetic stimulation on adrenal medullar (an endocrine gland)?

A

No effect

44
Q

What is the effect of parasympathetic stimulation on veins?

A

No effect

45
Q

What is the effect of sympathetic stimulation on SA node?

A

Increasess the rate of depolarsiation to threshold Increases the heart rate

46
Q

What is the effect of sympathetic stimulation on AV node?

A

Increases excitability Decreases the AV nodal delay

47
Q

What is the effect of sympathetic stimulation on venticular conduction pathway?

A

Increases excitability Hasten conduction through the bundle of His and Purkinje cells

48
Q

What is the effect of sympathetic stimulation on atrial muscle?

A

Increases excitability Strengthens contraction

49
Q

What is the effect of sympathetic stimulation on ventricular muscle?

A

Increases excitability Strengthens contraction

50
Q

What is the effect of sympathetic stimulation on adrenal medulla (an endocrine gland)?

A

Promotes adrenomedullary secretion of epinephrine, a hormone that augments the sympathetic nervous system’s actions on the heart

51
Q

What is the effect of sympathetic stimulation on veins?

A

Increases venous return, which increases the strength of the cardiac contraction through the Frank-Starling mechanism

52
Q

Although filled with blood, cardiac muscle cannot get oxygen nutrients from the blood within its chambers. Where is it supplied then?

A

This must be supplied by the coronary arteries

53
Q

Heart gets its own blood supply through the ______circulation, but mostly during diastole.

A

coronary

54
Q

Why does the heart get its own blood supply through the coronary arteries? List 3 reasons

A
  1. the coronary arteries branch off the aorta close to aortic valve, but during contraction, the open aortic valve partially blocks their entrances
  2. the contracting myocardium compresses the major branches of the coronary arteries (can get blood when contract)
  3. but, cardiac muscle very good at getting O2 out of blood, and can use multiple sources of energy
55
Q

Coronary blood flow normally _____ to keep pace with cardiac oxygen needs

A

varies

56
Q

Cardiac muscle removes 65% of oxygen from blood even at rest (other tissues remove 25%) and has _____ (large/little) capacity to increase this

A

little

57
Q

During exercise blood flow increases five-fold through vasodilation, due to local increases in ______.

A

adenosine

58
Q

What is coronary artery disease?

A

Coronary artery disease refers to pathological changes within the artery walls that diminish blood flow

59
Q

Coronary artery disease, particularly the development of ______, can occur due to ______, ______ and _______.

A

atherosclerosis (plaque); hypertension; hyperlipidemia; hyperglycaemia

60
Q

Atherosclerotic plaques in coronary arteries can cause partial or full ______, leading to _______, _______ and ______ → _______ of muscle wall

A

obstructions; angina; ischemic heart disease; myocardial infarction (no blood supply which damages tissue); death

61
Q

What is the treatment of coronary artery disease?

A

Heart bypass

62
Q

What are the 4 possible outcomes of acute myocardial infarction (heart attack)?

A

Immediate death Delayed death from complication Full functional recovery Recovery with impaired function

63
Q

What are characteristics of immediate death after acute myocardial infarction (heart attack)?

A

Acute heart failure occurring because the heart is too weakened to pump effectively to support the body tissues Fatal ventricular fibrillation (fist sign of death) brought about by damage to the specialised conducting tissues or induced by O2 deprivation

64
Q

What are characteristics of delayed death from complications after acute myocardial infarction (heart attack)?

A

Fatal rupture of the dead, degenerating area of the heart wall Slowly progressing congestive heart failure (unable to keep going) occurring because the weakened heart is unable to pump out all the blood returned to to

65
Q

What are characteristics of full functional recovery after acute myocardial infarction (heart attack)?

A

Replacement of the damaged area with a strong scar, accompanied by enlargement of the remaining normal contractile tissue to compensate for the lost cardiac musculature

66
Q

What are characteristics of recovery with impaired function after acute myocardial infarction (heart attack)?

A

Persistence of permanent functional defects, such as bradycardia or conduction blocks, caused by destruction of irreplaceable auto-rhythmic or conductive tissue

67
Q

What is produced by the parasympathetic nervous system to control heart rate (change the pacemaker)? What affect does it have on HR?

A

ACh.

Decrease slow influx of Na+ and Ca2+ → Slow depolarisation

Increase K+ efflux → More hyperpolarisation

= Longer time to reach threshold -> Decreased HR