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Personalised Medicine - Cardiovascular > L3 - Physiology of the Heart II > Flashcards

L3 - Physiology of the Heart II Flashcards

1
Q

When the atria contract how much of its blood volume does it eject?

A

60%
- Continuous supply of blood from circulation
If the heart doesn’t eject correctly it doesn’t have time to catch up

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2
Q

What is the equation for cardiac output?

A

Cardiac Output = Heart Rate x Stroke Volume
4.9 litres/min = 70 beats/min x 70mls
Blood volume = 5 litres – entire blood volume pumped every minute

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3
Q

What is the cardiac output during exercise?

A

35 litres /min

7 fold increase in blood circulation compared to rest

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4
Q

What is the ejection fraction?

A

Refers to the percentage volume of blood ejected with each cardiac contraction
Normally 55-60% at rest

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5
Q

What % is the ejection fraction?

A

60%

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6
Q

What bpm is the heart rate?

A

70bpm

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7
Q

What l/min is cardiac output?

A

5 l/min

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8
Q

What ml is stroke volume?

A

70ml

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9
Q

What 4 factors affect heart rate?

A

Sympathetic nervous system
Parasympathetic nervous system –> through vagus nerve
Circulating catecholamines
Drugs

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10
Q

How do circulating catecholamines affect the heart rate?

A

Extension of the sympathetic nervous system Circulate in bloodstream so slower to act
Come from the adrenaline gland
- Sympathetic nervous system through noradrenaline acts instantaneously

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11
Q

What 4 factors affect stroke volume?

A 
Intrinsic contractility 
Extrinsic factors 
- preload 
- afterload 
- sympathetic activity
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12
Q

How does intrinsic contractility affect stroke volume?

A

The heart tissue needs to be in good condition with the correct conditions

  • Intracellular calcium
  • Oxygen, free fatty acids, ATP
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13
Q

How does preload affect stroke volume?

A

Filling pressure

Venous return - how much blood volume is coming back to the heart immediately before it contracts

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14
Q

How does after load affect stroke volume?

A

Resistance to ejection

Blood vessels can restrict and contract

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15
Q

What are the two supplies of Ca for muscle contraction?

A

One from inside SR
One from outside SR
One Ca pathway at cell membrane, one at SR membrane

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16
Q

What are the two Ca channel receptors involved in muscle contraction?

A

L-type

Ryanodine

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17
Q

What are L-type calcium channels?

A

Small amount of Ca enters the cell - not enough to trigger contraction itself

18
Q

What are Ryanodine receptors?

A

Activated by small amount of Ca entering through L-type calcium channels
Triggers an all or nothing response - large Ca influx

19
Q

How does Ca affect actin and myosin?

A
  1. Actin is a filamentous molecule wrapped in troponin and tropomyosin
  2. Tropomyosin and troponin cover myosin binding sites on actin
  3. Ca bind to troponin
  4. Conformational change
  5. Binding sites are now free so myosin binds
  6. Physical movement of the two molecules - requires ATP
20
Q

What is the structure of cardiac muscle?

A

Cross linking

21
Q

What is the importance of cross linking in cardiac muscle?

A

Help to transmit depolarisation across the heart quickly

When the heart contracts it help it contract as one functional unit

22
Q

What is the Frank-Starling mechanism?

A

Heart muscle cells – how much they contract depends on their basal state
before the stimulus
The more you stretch the ventricles the more they contract
The more it fills the more it pumps - depends on pre-load
- Intrinsic property of the heart

23
Q

Where do healthy people lie on the Frank Starling curve?

A

Steep part of the curve

Small increases in filling pressure dramatically increase cardiac output

24
Q

How do increases in filling pressure affect stroke volume and cardiac output?

A

Increases in volume of blood returning to the heart during diastole - preload
Increases LV end-diastolic pressure –> myocardial fibre stretching
Increases force of contraction –> increased stroke volume and cardiac output

25
Q

Frank-Starling - changes in preload (venous return)

A

If venous return increases –> end diastolic pressure increases –> stroke
volume increases –> will eventually equilibrate

26
Q

Frank-Starling - changes in afterload and contractility

A

If contractility decreases / afterload increases –> heart starts failing –> curve flattens –> decrease in cardiac output –> large preload needed to get same cardiac output
Healthier to be on steep curve at top left

27
Q

Frank-Starling - effect of sympathetic stimulation

A

Small stimulation
Small increase in Ca
Small contraction

28
Q

Frank-Starling - effect of sympathetic stimulation - Isoprenaline

A

Sympathetic catecholamine
Give isoprenaline and small stimulation
- Stimulus gives greater Ca influx
- Enhanced contraction

29
Q

Frank-Starling - effect of sympathetic stimulation - noradrenaline

A

Infuse fluid –> for a smaller change in pressure –> greater change in stroke volume

30
Q

In a heart failure patient what leads to them operating on high pressure hearts?

A

Can increase filling pressure but cannot change cardiac output
Cannot survive on normally filling pressures

31
Q

What can a high end diastolic pressure in a heart failure patient lead to?

A

High end diastolic pressure –> high pulmonary venous pressure –> breathless
If pressure increases further –> fluid leaks into lung tissue –> pulmonary oedema

32
Q

How does a diuretic change preload?

A

Lowers preload –> filling pressure decreases In heart failure patient –> filling pressure decreases without little impact on cardiac output

33
Q

What happens if cardiac output drops too much?

A

Start to feel unwell

Don’t want to be in bottom left of curve

34
Q

What happens if ventricular pressure increases too much?

A

Breathlessness, pulmonary tension

Don’t want to be too far to the right on the curve

35
Q

In a heart failure patient how do you change their high filling pressure?

A

Diuretics

Can do it without dropping cardiac output too much

36
Q

In a heart failure patient how do you change their high after load?

A

ACE inhibitor

37
Q

What is an example of a cardiac glycoside?

A

Digoxin

38
Q

How does digoxin impact the heart?

A

Causes increase in heart contractility
Greater Ca influx –> greater contraction (compared to control)
Increases ionotropic effects of the muscle
Moves curve
- May be enough to get you out of low cardiac state
- Puts you on a curve where you can now use diuretics to avoid high pulmonary venous congestion

39
Q

When the heart starts to fail why does it dilate?

A

Because pressure increases –> volume increases –> stroke volume increases –> heart equilibrates
Tends to be
- Large volumes
- Increased pressures

40
Q

Overall, what do heart failure drugs tend to do?

A

Decrease after load
Decrease preload –> diuretics
Decrease sympathetic drive on the heart
These are only used for chronic heart failure not acute

41
Q

Why is thrashing the heart not a good idea?

A

Oxygen demand of the heart increases more than its output does

Personalised Medicine - Cardiovascular (11 decks)

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