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Physiology Hilary > 5. Cardiac Output > Flashcards

5. Cardiac Output Flashcards

1
Q

Cardiac output:

A

Volume of blood ejected by each ventricle each minute

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2
Q

Venous return

A

Volume of blood returning to atrium each minute

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2
Q

Venous return

A

Volume of blood returning to atrium each minute

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3
Q

What must venous return be equivalent to?

A

Cardiac output

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4
Q

List key factors that influence CO

A
  • Metabolism
  • Age
  • Body size
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5
Q

How does metabolism influence CO?

A

CO varies directly with activity level throughout life
Rest: 4.9-5.6 l/min (young, healthy, female-male)
Exercise: 4-5 fold increase (20-25 l/min)

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6
Q

CO

A

Cardiac output

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7
Q

How does age influence CO

A

Metabolic activity declines with increasing age

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8
Q

How does body size influence CO

A

CO increases approximately in proportion to BSA
Gives rise to the Cardiac Index
“cardiac output per square metre of BSA”

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9
Q

Cardiac index diagram

A
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10
Q

What is cardiac output controlled by?

A 
Heart Rate (HR)
Stroke Volume (SV)
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11
Q

What is heart rate?

A

The number of times the heart beats per minute

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12
Q

What is stroke volume?

A

Volume of blood ejected by each ventricle per heart beat

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13
Q

SV

A

Stroke volume ( = EDV - ESV)

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14
Q

What is the intrinsic firing rate of the SA node?

A

100 impulses/min

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15
Q

What happens to SA node at rest?

A

Increase in vagal activity inhibits SA node

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16
Q

Average HR

A

70bpm

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17
Q

How is rest (HR) achieved?

A

Achieved via parasympathetic (vagus) cholinergic input ↑K+ permeability
→ hyperpolarisation and slowed drift to threshold

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18
Q

Exercise HR

A

Initial increases in HR to 100-110 beats/min

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19
Q

How is the initial increase in HR during exercise achieved?

A

Via inhibition of parasympathetic tone (vagal withdrawal)

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20
Q

How is exercise HR > 110bpm achieved?

A

Via sympathetic stimulation of:
SA node: ↓K+ permeability: depolarising effect & faster drift to threshold
AV node: reduced AV node delay via ↑Ca2+ flux
Conduction pathways (Bundle of His, Purkinje cells)
Chronotropic effect of catecholamines

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21
Q

Age predicted max HR =

A

220 – age

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22
Q

HR reserve = eqn

A

Max HR – resting HR

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23
Q

Effect of parasympathetic stimulation of the SA node

A

Decreases the rate of depolarisation to threshold; decreases the heart rate

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24
Q

Effect of sympathetic stimulation on SA node

A

Increases the rate of depolarisation to threshold; increases the heart rate

25
Q

Effect of parasympathetic stimulation on AV node

A

Decreases excitability; increases the AV nodal delay

26
Q

Effect of sympathetic stimulation on AV node

A

Increases excitability; decreases the AV nodal delay

27
Q

Effect of parasympathetic stimulation on ventricular conduction pathway

A

No effect

28
Q

Effect of sympathetic stimulation on ventricular conduction pathway

A

Increases excitability; decreases the AV nodal delay

29
Q

Effect of parasympathetic stimulation on atrial muscle

A

Decreases contractility; weakens contraction

30
Q

Effect of sympathetic stimulation on atrial muscle

A

Increases contractility; strengthens contraction

31
Q

Effect of parasympathetic stimulation on ventricular muscle

A

No effect

32
Q

Effect of sympathetic stimulation on ventricular muscle

A

Increases contractility strengthens contraction

33
Q

Effect of parasympathetic stimulation on adrenal medulla

A

No effect

34
Q

Effect of sympathetic stimulation on adrenal medulla

A

Promotes secretion of epinephrine

35
Q

Effect of parasympathetic stimulation on veins

A

No effects

36
Q

Effect of sympathetic stimulation on veins

A

Increases venous return, which increases the strength of cardiac contraction via intrinsic control

37
Q

At rest SV

A

approx 70ml

38
Q

Major factors that influence SV x 3

A
  • Preload (intrinsic mechanism)
  • Contractility (extrinsic and intrinsic influences)
  • Afterload (extrinsic mechanism)
39
Q

Describe preload (intrinsic mechanism)

A

Increased filling
pressure/volume → ↑EDV
→ cardiac stretch and increased contractility

40
Q

Describe contractility (as an influence on SV)

A

Inotropic factors including
sympathetic stimulation
→ ↑[Ca2+]
i and contractility

41
Q

Describe afterload as an influence on SV

A

Pressure against which the left ventricle works

Primarily aortic pressure: resistance to outflow

42
Q

Frank-Starling Law

A

Relationship between EDV, Contraction Strength, and SV

43
Q

Frank-Starling Mechanism

A

‒ Length Tension Relationship

‒ Varying Degree of Stretching of Myocardium by EDV

44
Q

As EDV increases… (Frank Starling)

A

‒ Myocardium increasingly stretched and contracts more forcefully
‒ Therefore increased preload (EDV), increases contractility, increases SV

45
Q

Length tension curve

A
46
Q

Frank-Starling relationship diagram

A
47
Q

Preload: Frank Starling law of the heart

A
48
Q

Ventricular contractility

A

The force of contraction achieved from a given initial fibre length

49
Q

Describe sympathetic nervous input to ventricular muscle (acts via,

A

Acts via b1 adrenoceptors
→ G-protein coupled increase in cAMP
→ activation of protein kinase A (PKA)
→ activation of surface L-type Ca2+ channels
Increases [Ca2+]i and Enhances CICR
→ greater contractile force of ventricular myocytes
Increased SV

50
Q

Sympatetic stimulation - increased contractiity Frank Sterling curves x 2

A
51
Q

knk

A

hng

52
Q

Normal stroke volume diagram

A
53
Q

Stoke volume during sympathetic stimulation

A
54
Q

Stroke volume with combination of sympathetic stimulation and increased end-diastolic volume

A
55
Q

Factors influencing cardiac output positive effects

A
56
Q

Factors influencing cardiac output negative effects

A
57
Q

What is heart failure

A

A condition where the heart does not pump blood as efficiently around your body as it should - difficulty getting oxygen to body parts that need it.

58
Q

Normal, heart failure with & without diagram

A
59
Q

What occurs in the early stages of systolic HF ?

A

Sympathetic stimulation helps to compensate (augmented by expanded blood volume, controlled by
kidneys)

60
Q

SV in systolic heart failure

A

A smaller than normal SV is ejected (the heart’s contractility is weakened)

Physiology Hilary (12 decks)

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