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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
Effect of sympathetic stimulation on SA node
Increases the rate of depolarisation to threshold; increases the heart rate
25
Effect of parasympathetic stimulation on AV node
Decreases excitability; increases the AV nodal delay
26
Effect of sympathetic stimulation on AV node
Increases excitability; decreases the AV nodal delay
27
Effect of parasympathetic stimulation on ventricular conduction pathway
No effect
28
Effect of sympathetic stimulation on ventricular conduction pathway
Increases excitability; decreases the AV nodal delay
29
Effect of parasympathetic stimulation on atrial muscle
Decreases contractility; weakens contraction
30
Effect of sympathetic stimulation on atrial muscle
Increases contractility; strengthens contraction
31
Effect of parasympathetic stimulation on ventricular muscle
No effect
32
Effect of sympathetic stimulation on ventricular muscle
Increases contractility strengthens contraction
33
Effect of parasympathetic stimulation on adrenal medulla
No effect
34
Effect of sympathetic stimulation on adrenal medulla
Promotes secretion of epinephrine
35
Effect of parasympathetic stimulation on veins
No effects
36
Effect of sympathetic stimulation on veins
Increases venous return, which increases the strength of cardiac contraction via intrinsic control
37
At rest SV
approx 70ml
38
Major factors that influence SV x 3
- Preload (intrinsic mechanism) - Contractility (extrinsic and intrinsic influences) - Afterload (extrinsic mechanism)
39
Describe preload (intrinsic mechanism)
Increased filling pressure/volume → ↑EDV → cardiac stretch and increased contractility
40
Describe contractility (as an influence on SV)
Inotropic factors including sympathetic stimulation → ↑[Ca2+] i and contractility
41
Describe afterload as an influence on SV
Pressure against which the left ventricle works | Primarily aortic pressure: resistance to outflow
42
Frank-Starling Law
Relationship between EDV, Contraction Strength, and SV
43
Frank-Starling Mechanism
‒ Length Tension Relationship | ‒ Varying Degree of Stretching of Myocardium by EDV
44
As EDV increases... (Frank Starling)
‒ Myocardium increasingly stretched and contracts more forcefully ‒ Therefore increased preload (EDV), increases contractility, increases SV
45
Length tension curve
46
Frank-Starling relationship diagram
47
Preload: Frank Starling law of the heart
48
Ventricular contractility
The force of contraction achieved from a given initial fibre length
49
Describe sympathetic nervous input to ventricular muscle (acts via,
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
Sympatetic stimulation - increased contractiity Frank Sterling curves x 2
51
knk
hng
52
Normal stroke volume diagram
53
Stoke volume during sympathetic stimulation
54
Stroke volume with combination of sympathetic stimulation and increased end-diastolic volume
55
Factors influencing cardiac output positive effects
56
Factors influencing cardiac output negative effects
57
What is heart failure
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
Normal, heart failure with & without diagram
59
What occurs in the early stages of systolic HF ?
Sympathetic stimulation helps to compensate (augmented by expanded blood volume, controlled by kidneys)
60
SV in systolic heart failure
A smaller than normal SV is ejected (the heart’s contractility is weakened)

Physiology Hilary (12 decks)

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