The Heart as a Pump And Control of Cardiac Output

Question 1

What do capacitance vessels do?

Answer 1

Enable the system to vary the amount of blood pumped through the body.

Question 2

What do resistance vessels do?

Answer 2

Restrict blood flow to drive supply to hard to perfuse areas of the body.

Question 3

What are auricles?

Answer 3

Appendages of the atria.

Question 4

Define systole.

Answer 4

Contraction and ejection of blood from ventricles.

Question 5

Define diastole.

Answer 5

Relaxation and filling of ventricles.

Question 6

What are the typical values for stroke volume, heart rate and cardiac output at rest?

Answer 6

70/80L X 70bpm = 5L

Question 7

Describe some features of heart muscle and its action potential.

Answer 7

Discrete cells interconnected electrically (functional syncytium via gap junctions), striated, cells contract in response to an action potential in membranes causing a rise in intracellular calcium concentration - cardiac action potential is long - lasts duration of single contraction (280ms) - triggered by spread of excitation from cell to cell.

Question 8

Name the 4 valves of the heart and state how many cusps they each have.

Answer 8

Tricuspid valve, pulmonary valve and aortic valve - 3 cusps. Mitral valve - 2 cusps, unless congenital abnormality.

Question 9

What determines whether a valve is open or closed?

Answer 9

The differential blood pressure on either side of it.

Question 10

What are the cusps of the mitral and tricuspid valves attached to and why?

Answer 10

Chordae tendineae connected to papillary muscles to prevent inversion of valves at systole.

Question 11

Describe the path of the cardiac action potential.

Answer 11

Pacemaker cells in the SAN generate the AP, then activity spreads over the atria for atrial systole and is delayed at the AVN for 120ms, then excitation spreads down the septum then through ventricular myocardium from inner/endocardium to out/epicardial surface.
Ventricles contract from apex up.

Question 12

How does the heart respond to an increased heart rate in terms of systole and diastole?

Answer 12

Time taken for systole remains constant, but diastole is quicker.

Question 13

Name the 7 phases of the cardiac cycle.

Answer 13

1. Atrial contraction
2. Isovolumetric contraction
3. Rapid ejection
4. Reduced ejection
5. Isovolumetric relaxation
6. Rapid filling
7. Reduced filling

Question 14

What makes phases 2 and 5 of the cardiac cycle ‘isovolumetric’?

Answer 14

The volume in the ventricles does not change, because both the aortic and mitral valves are closed, so there’s nowhere for blood to get in or out.

Question 15

What is the ‘a wave’ and what is its counterpart shown in an ECG?

Answer 15

When atrial systole raises the pressure in the atrium and a ‘p wave’ is shown in an ECG to signify atrial depolarisation.

Question 16

What does QRS complex on an ECG show and when?

Answer 16

It shows ventricular depolarisation during isovolumetric contraction.

Question 17

What does isovolumetric contraction do to the pressure inside the ventricle and how is this expressed graphically?

Answer 17

Increases it, as shown by the ‘C wave’ on a graph.

Question 18

What is the ‘X descent’ of atrial pressure?

Answer 18

When atrial pressure decreases during rapid ejection, because the ventricles contract and decrease in volume and pull down on the base of the atria. Blood is still flowing in.

Question 19

Why does the rate of ejection fall?

Answer 19

Depolarisation of the ventricles reduces tension. A ‘T wave’ is shown on an ECG.

Question 20

During reduced ejection, a ‘V wave’ is shown in relation to pressure, why?

Answer 20

Continual venous return raises atrial pressure.

Question 21

What causes the dicrotic notch?

Answer 21

Intraventricular pressure

Question 22

When is end systolic volume reached?

Answer 22

At the end of isovolumetric relaxation when both valves are shut, enclosing the ventricle - the only blood left is what it did not eject during systole.

Question 23

When and why might you hear S3?

Answer 23

Rapid filling when ventricular pressure

Question 24

What is diastasis?

Answer 24

During reduced filling when the rate slows as the ventricles have reached their inherent relaxed volume. Further filling driven by venous pressure will bring the ventricles up to ~90% full.

Question 25

What heart pathology results in a crescendo-decrescendo murmur and what may cause it?

Answer 25

Aortic valve stenosis may be caused by degeneration (senile calcification/fibrosis), congenital configuration of 2 not 3 cusps, fusing of cusps caused by inflammation from chronic rheumatic fever.

Question 26

What can be the result of an aortic stenosis?

Answer 26

Sheer stress may cause microangiopathic haemolytic anaemia and increased left ventricle pressure may lead to hypertrophy, left-sided heart failure -syncope or angina.

Question 27

What heart pathology can produce an early decrescendo diastolic murmur and what can cause this?

Answer 27

Aortic valve regurgitation (insufficiency/incompetency) may be caused by aortic root dilation (leaflets pulled apart) or valvular damage, which may be caused by endocarditis from rheumatic fever.

Question 28

What are the consequences of aortic valve regurgitation?

Answer 28

Blood flows back into the left ventricle during diastole, increasing the stroke volume and systolic pressure, decreasing diastolic pressure, resulting in left ventricle hypertrophy and a bounding pulse - perhaps head bobbing and Quinke’s sign.

Question 29

What heart pathology results in a holosystolic murmur and what may cause this?

Answer 29

Mitral valve regurgitation. Usually the chordae tendineae supported by the papillary muscles prevent prolapse in systole, but Myxomatus degeneration weakens CT, or there may be damage to the papillary muscles after an MI. Left-sided heart failure which leads to ventricle dilation may stretch the valve or rheumatic fever may lead to leaflet fibrosis and disrupt the seal formation.

Question 30

What are the consequences of mitral valve regurgitation?

Answer 30

Blood leaking back into the atria will increase the preload, so more blood enters the left ventricle, perhaps causing hypertrophy.

Question 31

What heart pathology may produce a snapping sound as the valve shuts and then a diastolic rumble and what may cause this?

Answer 31

Mitral valve stenosis is mainly caused by RHEUMATIC FEVER - commissural fusion of valve leaflets.

Question 32

What are the consequences of mitral valve stenosis?

Answer 32

Because it’s harder for blood to flow from the left atria to ventricle, the atrial pressure increases. This may result in atrial fibrillation and perhaps thrombus formation. Also possible in oesophagus compression leading to dysphagia. Pulmonary oedema may result, with dyspnea, pulmonary hypertension and right ventricle hypertrophy.

Question 33

What’s the difference between afterload and preload?

Answer 33

Afterload is the load the heart must eject blood against (roughly aortic pressure), whereas preload is the amount the ventricle is stretched/filled in diastole - related to EDV or central venous pressure.

Question 34

Define total peripheral resistance and state the main contributor.

Answer 34

Total peripheral resistance (systemic vascular resistance) is the resistance to blood flow offered by all systemic vasculature. The pressure that blood exerts drops as it flows through ‘resistance’ -arterioles are the main supplier, causing arterial pressure to rise but that in capillaries and veins to fall.

Question 35

What is the consequence when TPR rises but CO (cardiac output) is unchanged?

Answer 35

Venous pressure drops and arterial pressure rises. The opposite is true if TPR were to fall.

Question 36

What would happen in CO increased but TPR was unchanged?

Answer 36

Arterial pressure would increase, but venous pressure would fall. Opposite is true if CO were to decrease.

Question 37

How the the CVS respond when tissues need more blood?

Answer 37

Arterioles and precapillary sphincters dilate, so TPR falls, which means the heart must pump more to maintain arterial pressure and to stop venous pressure from rising. The heart notices changes in arterial BP and CVP and responds to changes via intrinsic and extrinsic mechanisms.

Question 38

What is a typical stroke volume and how can it be increased?

Answer 38

A typical SV is 70ml(67% EDV) and it may be increased by raising EDV or decreasing ESV, as it is EDV-ESV.

Question 39

Why does the ventricular compliance curve show?

Answer 39

In diastole, ventricles are isolated from arteries and will fill/stretch until IV pressure = CVP, so with a higher venous pressure, the heart will fill more. The graph shows this relationship and perhaps how compliance is increased/decreased in disease states.

Question 40

What does the Frank-Starling Law of the Heart tell us?

Answer 40

If you stretch fibres more before contracting, the heart will contract harder, so up to a limit, the more the heart fills, the harder it contracts and the bigger SV obtained.
Increased venous pressure fills the heart more (depending on compliance).

Question 41

What does the Starling curve show?

Answer 41

LVEDP (left ventricle end diastolic pressure) 8mmHg and SV at 70ml. Length tension curve for cardiac muscle shows that if sarcomere length is too short, filament overlap interferes with contraction and stretching of fibres here brings an increase sensitivity to calcium.

Question 42

What is the intrinsic mechanism of the heart and what is the purpose?

Answer 42

Increased SV with increased filling ensures both sides of the heart maintain the same output.

Question 43

What is contractility?

Answer 43

The force of contraction for a given fibre length. A change in contractility shows a change in the slope of the Starling Curve. Increasing contractility increases the force of contraction for a given EDP.

Question 44

How do extrinsic factors affect contractility?

Answer 44

Sympathetic stimulation and circulating adrenaline increase contractility, so reducing sympathetic stimulation will reduce contractility.

Question 45

What is the effect of aortic impedance (which represents afterload) on cardiac output?

Answer 45

May bring an inappropriate increase in arterial pressure causing hypertension and reducing cardiac output.

Question 46

What affects cardiac output?

Answer 46

Heart rate and stroke volume(so ESV and EDV).

Question 47

What controls SV?

Answer 47

ESV - contractility and EDV, how difficult it is to eject blood (aortic impedance ~ arterial pressure).

Question 48

What determines heart rate?

Answer 48

Controlled by ANS (as in contractility) - extrinsic mechanism.

Question 49

What might cause postural hypotension?

Answer 49

Standing up causes a ‘pooling’ of blood in legs because of gravity, venous and arterial pressures both decrease. If extrinsic mechanism of baroreceptors & ANS increasing HR and TPR fail, postural hypotension results. Often happens with the elderly.