L3 - Physiology of the Heart II

Question 1

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

Answer 1

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

Question 2

What is the equation for cardiac output?

Answer 2

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

Question 3

What is the cardiac output during exercise?

Answer 3

35 litres /min

7 fold increase in blood circulation compared to rest

Question 4

What is the ejection fraction?

Answer 4

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

Question 5

What % is the ejection fraction?

Answer 5

60%

Question 6

What bpm is the heart rate?

Answer 6

70bpm

Question 7

What l/min is cardiac output?

Answer 7

5 l/min

Question 8

What ml is stroke volume?

Answer 8

70ml

Question 9

What 4 factors affect heart rate?

Answer 9

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

Question 10

How do circulating catecholamines affect the heart rate?

Answer 10

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

Question 11

What 4 factors affect stroke volume?

Answer 11

Intrinsic contractility 
Extrinsic factors 
- preload 
- afterload 
- sympathetic activity

Question 12

How does intrinsic contractility affect stroke volume?

Answer 12

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

• Intracellular calcium
• Oxygen, free fatty acids, ATP

Question 13

How does preload affect stroke volume?

Answer 13

Filling pressure

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

Question 14

How does after load affect stroke volume?

Answer 14

Resistance to ejection

Blood vessels can restrict and contract

Question 15

What are the two supplies of Ca for muscle contraction?

Answer 15

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

Question 16

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

Answer 16

L-type

Ryanodine

Question 17

What are L-type calcium channels?

Answer 17

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

Question 18

What are Ryanodine receptors?

Answer 18

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

Question 19

How does Ca affect actin and myosin?

Answer 19

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

Question 20

What is the structure of cardiac muscle?

Answer 20

Cross linking

Question 21

What is the importance of cross linking in cardiac muscle?

Answer 21

Help to transmit depolarisation across the heart quickly

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

Question 22

What is the Frank-Starling mechanism?

Answer 22

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

Question 23

Where do healthy people lie on the Frank Starling curve?

Answer 23

Steep part of the curve

Small increases in filling pressure dramatically increase cardiac output

Question 24

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

Answer 24

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

Question 25

Frank-Starling - changes in preload (venous return)

Answer 25

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

Question 26

Frank-Starling - changes in afterload and contractility

Answer 26

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

Question 27

Frank-Starling - effect of sympathetic stimulation

Answer 27

Small stimulation Small increase in Ca Small contraction

Question 28

Frank-Starling - effect of sympathetic stimulation - Isoprenaline

Answer 28

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

Question 29

Frank-Starling - effect of sympathetic stimulation - noradrenaline

Answer 29

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

Question 30

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

Answer 30

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

Question 31

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

Answer 31

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

Question 32

How does a diuretic change preload?

Answer 32

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

Question 33

What happens if cardiac output drops too much?

Answer 33

Start to feel unwell | Don’t want to be in bottom left of curve

Question 34

What happens if ventricular pressure increases too much?

Answer 34

Breathlessness, pulmonary tension | Don’t want to be too far to the right on the curve

Question 35

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

Answer 35

Diuretics | Can do it without dropping cardiac output too much

Question 36

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

Answer 36

ACE inhibitor

Question 37

What is an example of a cardiac glycoside?

Answer 37

Digoxin

Question 38

How does digoxin impact the heart?

Answer 38

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

Question 39

When the heart starts to fail why does it dilate?

Answer 39

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

Question 40

Overall, what do heart failure drugs tend to do?

Answer 40

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

Question 41

Why is thrashing the heart not a good idea?

Answer 41

Oxygen demand of the heart increases more than its output does