2 Cardiac Function

Question 1

What is cardiac output?

Answer 1

Cardiac output = stroke volume x Heartbeat

(litres/min) (litres/beat) (beat/min)

Question 2

What is the normal cardiac output at rest?

Answer 2

5 L/min = 70ml/min x 70bpm

Question 3

What is the normal cardiac output during exercise?

Answer 3

22 L/min = 110ml/min x 200bpm

Question 4

What does control of cardiac output depend on?

Answer 4

• Factors affecting heart rate

- Factors affecting stroke volume

Question 5

What keeps the intrinsic rate stable?

Answer 5

Pacemaker - sinoatrial (SA) node - pacemaker cells

Conduction - atrioventricular (AV) node - speed of conduction

Question 6

Describe the factors affecting heart rate

Answer 6

It is influenced by:

Sympathetic nervous system
- activation of B-adrenoceptors causes an increase in heart rate (release of NA)

Parasympathetic nervous system
- activation of muscarinic receptors causes a decrease in heart rate (hyperpolarises cells in SA node - further from threshold potential) - release of ACh

Hormones
- e.g. Adrenaline acting on B-adrenoceptors, causing an increase in heart rate

Extra/intracellular ions
- alteration in membrane potential (e.g. K+)

Question 7

Define stroke volume

Answer 7

Stroke volume is the volume of blood ejected by each Ventricle in a single heartbeat

• Stroke volume represents the difference between the end-diastolic volume (EDV) and end-systolic volume (ESV)

Question 8

Describe what stroke volume is determined by:

Answer 8

• Preload: how much blood is returned to the heart
• Cardiac contractility - force of muscle fibre contraction
• Afterload: how easy it is to push out blood against pressure

Question 9

Define and describe preload,

(what can affect preload)

and how this affects stroke volume

Answer 9

End diastolic volume is dependent upon end-diastolic pressure (PRE-LOAD).

This is influenced primarily by venous return and this depends on several factors:

• Venous tone - contraction to back into the heart
• Blood volume - how much blood there is
• Posture - blood being pushed into the heart (gravity)
• Intrathoracic pressure - increases in exercise (ventilation rate) - squeezes thoracic vein
• Filling time - increased heart rate reduces filling time and hence can limit EDV
• Atrial contractility - as atria contract with more force 0 more blood enters the ventricle

In a normal heart, the more blood that returns to the heart, the more blood is pumped by the heart, based on properties of cardiac muscle fibres -
(length-tension relationship)

SO, INCREASE IN PRELOAD = INCREASE IN SV

Question 10

Explain what a Frank-Starling curve describes

Answer 10

A curve that shows:

• End diastolic volume x stroke volume
• There is a fairly linear relationship
• If there is an increase in EDV, there will be an increase in stroke volume

This is because the force of contraction of the cardiac muscle fibres is proportional to the degree of stretch
- increased stretch (EDV) = increased force of contraction and therefore increased contractility

SO, if more returns, more stretching of ventricles, more contraction

Question 11

Define contractility,

and describe contracility

and describe its effects on stroke volume

Answer 11

The amount of force generated by cardiac muscle fibres can vary independently from the degree of stretch
- i.e. ventricular contractility can vary at any given EDV depending on other influences

e.g. sympathetic nerve activation

Question 12

Define and describe afterload,

and describe its effects on stroke volume

Answer 12

Afterload
- How much force/aortic pressure the heart has to work against - affects SV

• An increase in aortic pressure (caused by increased peripheral resistance, altered aortic stiffness, etc) will increase afterload which will reduce stroke volume at a contact preload

SO
- the velocity of contraction at a fixed length is greatest at low (after) loads and slows as afterload increases

Question 13

Describe the events of a pressure-volume loop, in a normal, healthy individual

Answer 13

1. Onset of ventricular systole
   - EDV (preload) - 140ml,
   - EDP - 0mmHg
   - There is a rise in LVP with no change in volume
2. LVP > aortic pressure
   - causes the aortic valve to open
3. Ejection phase
4. End of systole, the onset of diastole
   - Aortic valve shuts
5. Isovolumetric phase of diastole
   - Fall in LVP with no change in volume
6. AV valve opens
7. Ventricular filling occurs

Question 14

Describe the changes to the pressure-volume loop, when there is an increase in EDV (pre-load)

Answer 14

Increases EDV (pre-load)
- leads to an increase in stroke volume

Question 15

Describe and explain the changes to the pressure-volume loop when there is an increase in aortic pressure

Answer 15

This leads to a decrease in stroke volume

Increase in aortic pressure (after-load):
- Means that the (left) ventricle needs to generate more force and contract more to overcome the aortic pressure

• This increased contraction takes place in a shorter time, meaning there is less time to empty the ventricles (so blood is left behind in L ventricle)
• Extra blood in L ventricle = more stretch in L ventricle = return to normal stroke volume in the next heartbeat
• Eventually, after few heartbeats, the stroke volume returns to normal
  > BUT the heart has to work harder to achieve this

SO, high BP costs more energy to maintain the same stroke volume

AND, there is a decrease in stroke volume

Question 16

Describe and explain the changes to the pressure-volume loop when there is an increase in contracility

Answer 16

Increases in sympathetic NS activity, Ca2+, other drugs
- This makes the heartbeat more efficient - more forceful contraction

• More efficient emptying of the heart

In the next heartbeat - there is less blood left in the ventricle, so less contraction is needed for the next beat

SO, increased contractility = increase in stroke volume