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Cardiovascular system > Cardiac Output - L5 > Flashcards

Cardiac Output - L5 Flashcards

1
Q

What is cardiac output?

A

The volume of blood ejected by each ventricle each minute

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2
Q

Do pulmonary and systemic circuits receive similar volumes?

A

Yes, the right and left output may vary from beat to beat, but over short period periods “ventricular balance” is maintained

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3
Q

What is venous return?

A

The volume of blood returning to atrium each minute
It must be equivalent to cardiac output

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4
Q

What are the key factors that affect cardiac ouput?

A

Metabolism, age, body size

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5
Q

How does metabolism affect Cardiac output (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)
No sex difference at rest

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6
Q

How does age influence CO?

A

Metabolic activity declines with increasing age and metabolism influences CO

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7
Q

What is body size referring to?

A

Body surface area - BSA

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8
Q

How does BSA affect CO?

A

CO increases approximately in proportion to BSA and this gives rise to the cardiac index
The larger the individual the greater the CO will be
CO must increase/decrease according to size of the body

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9
Q

What is the Cardiac Index?

A

Cardiac output per square metre of BSA

=> CO/BSA

BSA (m^2) = 0.007184 <-> Height (cm)^0.725 <-> Weight (kg)^0.425

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10
Q

What is CO controlled by?

A

Heart rate and stroke volume

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11
Q

What is HR?

A

The number of times the heart beats per minute
How many cardiac cycles that happen per minute

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12
Q

What is SV?

A

The volume of blood ejected by each ventricle per heart beat
SV = EDV-ESV
With each cardiac cycle what is the volume of blood that leaves these ventricles - SV

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13
Q

CO = HR <-> SV, what is this?

A

70 beats/min <-> 70 ml/beat
= 4900 ml/min U 5 litres/min

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14
Q

What is the autonomic nervous system?

A

It is an involuntary branch of PNS with sympathetic and parasympathetic branches (often opposing effects)

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15
Q

Effect of SA node on ANS- parasympathetic and sympathetic systems on heart activity?

A

Parasympathetic stimulation: the SA node decreases the rate of depolarisation to threshold and thus decreases the heart rate

Sympathetic stimulation: the SA node increases the rate of depolarisation to threshold which increases the heart rate

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16
Q

Effect of AV node on ANS- parasympathetic and sympathetic systems on heart activity?

A

Parasympathetic: the AV node decreases excitability, and increases the AV nodal delay

Sympathetic: the AV node increases excitability and decreases the AV nodal delay

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17
Q

Effect of Ventricular conduction pathway on ANS- parasympathetic and sympathetic systems on heart activity?

A

Parasympathetic: no effect

Sympathetic: increases excitability, hastens conduction through the bundle of His and Purkinje cells

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18
Q

Effect of atrial muscle on ANS- parasympathetic and sympathetic systems on heart activity?

A

Parasympathetic: Decreases contractility, thus weakening contraction

Sympathetic: Increases contractility, thus strengthening contraction

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19
Q

Effect of ventricular muscle on ANS- parasympathetic and sympathetic systems on heart activity?

A

Parasympathetic: No effect

Sympathetic: Increases contractility and strengthens contraction

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20
Q

Effect of adrenal medulla (endocrine gland) on ANS - parasympathetic and sympathetic systems on heart activity?

A

Parasympathetic: no effect

Sympathetic: Promotes secretion of adrenaline, a hormone that increases sympathetic nervous system action

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21
Q

Effect of veins on ANS- parasympathetic and sympathetic systems on heart activity?

A

Parasympathetic: no effect

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

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22
Q

Frank starling law of the heart?

A

The Frank-Starling Law states that the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction. This assumes that other factors remain constant.

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23
Q

Key determinants of CO?

A

Heart rate and stroke volume

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24
Q

End diastolic volume?

A

Amount of blood within ventrciels after atria filling after atria have passed contents in through AV valves

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25
Q

End systolic volume?

A

Amount of blood that remains within the ventricles after contraction
ventricle normally ejects 1/2 the volume of the heart

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26
Q

Does the vagus nerve of the parasympathetic system innervate the ventricles?

A

The vagus nerve does not innervate the ventricles

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27
Q

What is ventricular innervation done by? What else does this nerve discharge into?

A

Ventricular innervation is done by sympathetic nerve, but also this sympathetic nerve discharge is going into the atria

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28
Q
A

1% of cardiomyocytes are those autorhythmic cells

29
Q

Does the SA node have intrinsic firing rate?

A

Yes the SA node has an intrinsic firing rate, i.e. without neuro-humoral input and this is about 100 impulses/min

30
Q

How come our heart rate is not as high as this 100 impulses per min?

A

At rest the increased vagal activity inhibits this SA node and thus slows amount of action potentials and this is what brings our resting heart rate from about 70 beats per minute

31
Q

How is this 70bpm brought about?

A

Achieved via parasympathetic (vagus) cholinergic input increased potassium ion permeability
Hyperpolarisation and slowed drift to threshold
constant cycle of drift threshold and fire and comes back to this hyperpolarised state

1st part of slow depolarisation to allow sodium influx and decrease potassium

2nd stage open up calcium trasneint fast acting cahnnels and close funnu channels

parasymapthetic when it is increased to slow this down, we do the reverse of this: close the unique funny channels and reduce how many are open and and open more postassium channels and this will bring about the natural slowing to get to this threshold slower

32
Q

what happens when we open potassium channels? and what does this mean?

A

when we open potassium channels it hyperpolarises it even further, meaning threshold takes even longer to get to for cardiac cycle

33
Q

When we need heart rate to increase initially example durong exercise of 100-110bpm at the warm up what causes this?

A

Purely by vagal withdrawal
Allows SA node to bounce back to its inherent action of action potentials at 100/110 impulses per minute
SA to AV
Initial increase in heart rate occurs

34
Q

What happens when exercise increases even more so heart rate is more then 110bpm?

A

Achieved via sympathetic stimulation:
Stimulates SA node more rapidly
Need to accelerate this
so more sodium funny channels open
close these potassium channels
SA node: ↓K+ permeability: depolarising effect & faster drift to threshold
More rapid action potential translating to an increased heart rate

AV node: more systolic instead of diastolic
AV node: reduced AV node delay via ↑Ca2+ flux
Conduction pathways (Bundle of His, Purkinje cells) Relying on long lasting calcium channels being opened
This is neuronal component^
We also have humoural component:
Chronotropic- increase heart rate
The effect of catecholamines
Adrenaline etc to help increase heart rate

35
Q

What is age predicted max HR?
What is HR reserve?

A

220 - age
Max HR - Resting HR

36
Q

EXAM Q
Talk about key determinants of cardiac output in relation to genration action potentials this is what you need ^^^

A
37
Q

Major factors that influence Stroke Volume?

A

Preload - intrinsic mechanism
Contractility

38
Q

Determines cardiac ouput?

A

Amount of venous return - the amount of blood available for ejection

39
Q

How is venous return meditaed?

A
  1. Skeletal muscle pump: veins embedded in muscles, when muscles contract for any movement, they physically squeeze vein and helps to propel blood back to heart
  2. Sympathetic stimulation of veins which enhances constriction so gets pressure to bring blood back to the heart
40
Q

Stroke volume is another key determinant of cardiac output - stroke volume is typically what value?
How is this calculated?

A

70mL
EDV - ESV: 140 - 70

41
Q

3rd factor that influences SV?

A

Afterload

42
Q

Preload? balloon idea

A

Pressure that the blood exerts on the ventricular myocytes: Intrinsic mechanism that increases filling, and increases EDV which causes more cardiac stretch and increased contractility

-> The amount of blood that is within the ventricle is what puts pressure on ventricle itself

43
Q

What is stretch governed by?

A

Frank Starling mechanism

44
Q

What are the extrinsic and intrinsic influences that influence SV?

A

Contractility
Inotropic factors including sympathetic stimulation: adrenaline which increases calcium ion influx and increased contractility

45
Q

What impact do inotropic factors have?

A

They increase or decrease contractility

46
Q

What do chronotropic factors do?

A

They increase or decrease heart rate

47
Q

Afterload - extrinsic mechanism that influences SV, how?

A

Pressure exert after contraction
Pressure against which the left ventricle works
Primarily aortic pressure which is restitance to outflow

48
Q

Frank starling law - what does it represent?

A

Represents the relationship between EDV, contraction strength and stroke volume

49
Q

Mechanism?

A

Length tension relationship
-> Muscle fibres have an optimal length to work at: under a stretched environment
Varying degrees of stretch will bring about differences of stroke volume - this variety of stretching of myocardium by EDV

50
Q

As EDV increases, according the Frank Starling law of the heart:

A

Myocardium increasingly stretched and contracts more forcefully
Therefore increased pre load: EDV will increase contractility and SV
The muscle fibre is at optimal length here

51
Q

what is contractility?

A

The force of contraction achieved from a given initial fibre length

52
Q

How is extrinsic control of contractility brought about?

A

Heavily innervated sympathetic nervous input to ventricular muscle: noradrenaline for e.g.
-> Acts by binding to b1 adrenoceptors
→ Then couples to G-protein causes increase in cAMP pathway within cardiomyocyte
-> This cAMP pathway brings about an increased in calcium permeability that increases contractility strength
→ It activates of protein kinase A (PKA): role is to phosphorylate calcium channels
→ activation of surface L-type Ca2+ channels
-> Increases [Ca2+] intracellular
and Enhances CICR: calcium induced calcium release in this sarcoplasmic reticulum
→ Causes a greater contractile force of ventricular myocytes
Ultimately we have an Increased SV

53
Q

EDV: 135ml —SV 70ml–> ESV: 65ml, what is this?

A

Normal stroke volume

54
Q

EDV: 135ml —SV 100ml–> ESV: 35ml, what is this?

A

SV during sympathetic stimulation

55
Q

EDV: 175ml —SV 140ml–> ESV: 35ml, what is this?

A

SV with combination of sympathetic stimulation and increased EDV

56
Q

Ejection fraction?

A

Stroke volume / EDV

57
Q

Healthy heart: ejection fraction?

A

50-75%

58
Q

Failing heart: ejection fraction?

A

Less then or equal to 30%

59
Q

Positive effects influencing cardiac output: 10

A
  1. Increased SV
  2. Increased force of contraction
  3. Increased End diastolic fibre length: Starling law, preload
  4. Increased end diastolic pressure
  5. Increased contractility
  6. Sympathetic stimulation via noradrenaline acting on beta 1 receptors
  7. Circulating adrenaline acting on beta 1 receptors - minor
  8. Intrinsic changes in contractility in response to changes in heart rate and after load
  9. Positive inotropic drugs e.g. digitalis, beta receptor agonists, phosphodiesterase inhibitors
  10. Hypertrophy - of filling is not impaired due to decreased compliance
60
Q
  1. People with Heart failure is Ireland today?
  2. How many are under 65 years of age?
  3. What % of 75-84 year old?
  4. Older than 85 years old?
A
  1. Approx 90,000
  2. Approx 1%
  3. 7%
  4. 15%
61
Q

What is heart failure?

A

It is a condition in which your heart does not pump blood as efficiently around your body as it should, which makes it difficult for your body to get as much oxygen and blood as it needs.

62
Q

In systolic heart failure what happens for any given EDV?

A

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

63
Q

What happens in the early stages of systolic heart failure?

A

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

64
Q

Negative effects that influence cardiac output: 9

A
  1. Decreased ventricular compliance, hypertrophy, cardiac tamponade, scar tissue
  2. Increased after load
  3. Increased ventricular radius
  4. Increased Ventricular systolic pressure
  5. Negative inotropic drugs: Ca^2+ channel blockers, general anaesthetic, beta blockers
  6. Disease: coronary artery disease, myocarditis, cardiomyopathy, etc
  7. Myocardial ischemia
  8. Ventricular and supraventricular tachycardias
  9. Irregular heart beat, atrial fibrillation
65
Q

How many in room get heart failure?

A

1 in 5 in future

66
Q

Types of heart failure?

A

Systolic and diastolic

67
Q

Issue with diastolic heart failure?

A

Issue with refill

68
Q

Heart with exercise - cardiac ouput?

A

Greater increase of SV
Increasing venous return which impacts extrinsic and more important intrinsic controls
increased skeletal pump activity, sympathetic stimulation of vein, increased EDV and heart is beating faster, SA node depolarising faster, increased heart rate, increased stroke volume, increased contractility, increase in cardiac output

Cardiovascular system (13 decks)

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