CVS session 6: control of cardiac output and response of the whole system

Question 1

Effect of TPR on arterial and venous pressures

Answer 1

Rise in TPR increases arterial pressure and decreases venous pressure
Fall in TPR decreases arterial pressure and increases venous pressure

Question 2

Effect of cardiac output on arterial and venous pressures, when TPR is constant

Answer 2

CO rises: arterial pressure will rise and venous pressure will fall, because a larger pressure is needed to move more blood and less is being stored in veins

CO falls: arterial pressure will fall and venous pressure rise, as a smaller volume of blood is being moved but more is stored in veins

Question 3

Demand

Answer 3

TPR proportional to 1/demand
If body needs more blood the heart needs to pump more to meet demand, AP and VP brought back to normal once demand is met

Question 4

Calculation of cardiac output

Answer 4

CO= stroke volume x heart rate

Arterial and venous pressures affect both SV and HR

Question 5

What is stroke volume and how does venous and arterial pressure affect it?

Answer 5

The amount of blood remaining after contraction, therefore the difference between end diastolic volume and end systolic volume:
SV=EDV - ESV

VP increase causes increased SV and heart rate
AP fall causes increased SV (less resistance) and heart rate

Question 6

Ventricular filling

Answer 6

In diastole the ventricle is isolated from arteries and connected to veins. The ventricles will therefore fill until their walls stretch enough to produce an intraventricular pressure which is equal to venous pressure

Higher venous pressure=more heart fills in diastole

• more blood enters atria increasing atrial pressure
• therefore more ventricle will fill
• relationship between venous pressure and ventricular volume shown on VENTRICULAR COMPLIANCE CURVE (draw)

Question 7

Describe Starling’s law in relation to contractility

Answer 7

If muscle is stretched before contracting, it contracts harder due to increased binding of actin and myosin as the sarcomere stretches. Therefore, the more the heart fills, the harder it contracts (up to a point: fibrous pericardium). The harder it contracts, the bigger the stroke volume. So rises in venous pressure lead to rises in stroke volume. This is an intrinsic cardiac property

Increase in EDV (=venous pressure) causes SV to increase, because preload is increased

On graph shows LVEDP (left ventricular end diastolic pressure) against stroke volume: as LVEDP=filling pressure

Question 8

Frank-Starling mechanism

Answer 8

The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.
Increased venous return increases the ventricular filling (end-diastolic volume) and therefore preload, which is the initial stretching of the cardiac myocytes prior to contraction. Myocyte stretching increases the sarcomere length, which causes an increase in force generation and enables the heart to eject the additional venous return, thereby increasing stroke volume.

Question 9

What is ESV and what does it depend on?

Answer 9

End systolic volume: how much the ventricle empties. Depends on:
1. Force of contraction: determined by EDV (Starling’s law) and contractility (increased by sympathetic activity). Can be affected by neurotransmitters, hormones or drugs

2. Difficulty of ejecting blood: “aortic impedance”. Depends mainly on TPR. Harder to eject=increased arterial pressure; if AP falls from lower TPR then ESV will fall and SV will increase

Question 10

What is preload?

Answer 10

The initial stretching of cardiac myocytes prior to contraction. Related to sarcomere length but this can’t be determined in situ, so measure by ventricular EDV or EDP. Can be applied to atria or ventricles
When venous return increased, EDV and ventricular volume increased, so sarcomere stretched, so preload increased
Increased preload increases stroke volume; decreased preload decreases it by decreasing force of contraction

Question 11

What increases ventricular preload?

Answer 11

Increased central venous pressure due to decreased compliance or hypervolaemia
Increased atrial force of contraction from sympathetic stimulation or increased filling
Bradycardia (more filling time)
Increased aortic pressure: first increases afterload then reduces SV so increases preload secondarily
Heart failure e.g. aortic stenosis

Question 12

What decreases ventricular preload?

Answer 12

Haemorrhage: decreased CVP
Atrial arrhythmias e.g. AF
Atrial tachycardia: increases ventricle filling time
Decreased ventricular afterload as enhances ejection so reduces ESV and EDV
Mitral and tricuspid valve stenosis

Question 13

What is afterload?

Answer 13

The resistance the left ventricle must overcome in order to circulate blood. Higher afterload = higher cardiac workload. Closely related to aortic pressure

Question 14

How is afterload increased?

Answer 14

When aortic pressure and systemic vascular resistance is increased, causing increased ESV and decreased SV:

• hypertension
• vasoconstriction
• aortic valve stenosis

Question 15

Affect of increased afterload on Starling curve?

Answer 15

Shifts it down and to the right: decreased SV, increased LVEDP

Question 16

Describe the autonomic control of heart rate

Answer 16

Decreased arterial pressure:

1. Arterial pressure sensed by BARORECEPTORS in the CAROTID SINUS and AORTIC ARCH
2. Sends signals to MEDULLA OBLONGATA
3. Increases heart rate by reducing parasympathetic and increasing sympathetic activity (so increases contractility) [vv. for decreasing HR]

Rises in venous pressure:

• sensed in RIGHT ATRIUM
• lead to decreased parasympathetic activity so increases HR
• Bainbridge reflex: not very important, little clinical relevance

Question 17

What determines stroke volume?

Answer 17

• venous return: CVP-RAP drives ventricular filling
• aortic pressure: drives baroreceptor sensor output
• ANS and hormones
• cardiac fitness: ventricular distensibility/contractility

Question 18

Where are baroreceptors found and what do they do?

Answer 18

Sense arterial blood pressure by responding to change in stretch of the arterial wall:

• in aortic arch (innervated by aortic nerve, combines with vagus nerve) increase firing of AP when pressure >100 mmHg
• in carotid sinus (innervated by sinus nerve of Hering; branch of glossopharyngeal nerve) increase firing when pressure >50 mmHg most important as threshold close to normal level so keeps at set point
• set point can change with exercise, hypertension, heart failure: explains how arterial pressure remains elevated during chronic hypertension

and decreased stretch decreases AP firing (most importantly during loss of blood or when stand up)

Modulates activity of S and P neurones in medulla, either increasing or decreasing activity to affect heart rate and force of contraction: this alters cardiac output. Also affects TPR. So after blood loss, baroreceptors cause increase in cardiac output and TPR to try to restore arterial blood pressure

Question 19

Role of arterioles

Answer 19

Control TPR
Vascular smooth muscle cells in tunica media/pre-capillary sphincters precisely regulate flow under SNS or metabolite autacoid control
Interaction causes vasodilatation

Question 20

Role of veins and great veins

Answer 20

Control stroke volume
Act as a reservoir for blood
Large volume, low pressure: CVP usually between 2 and 10 mmHg

Question 21

Mean arterial blood pressure

Answer 21

At rest is ~ 95 mmHg: this provides adequate pressure to perfuse and drive blood through whole vasculature, ensuring a positive CVP
Significant functional reserve available: many capillary beds are not perfused
If hypotensive, MABP is

Question 22

Describe the effects of rapid orthostasis

Answer 22

Gravity redistributes blood: mainly moves from intrathoracic vessels into the legs (legs take up an extra 500ml i.e. 10%)
CVP falls directly, so RA filling drops, so SV decreases by 10-25% and MABP falls by 20-25 mmHg. Arterial and venous pressures fall acutely

Question 23

Describe the baroreceptor response to rapid orthostasis

Answer 23

• Drop in MABP increases heart rate by 10-25 bpm
• TPR briefly drops, then increases to offset MABP drop, but then decreases venous return so affects stroke volume. The increased TPR increases vasoconstriction and venoconstriction
• Veins limit gravitational pooling (leg vein distensibility lower than great veins), so muscular contraction when standing up forces venous blood upwards to increase CVP

A complex response involving at least 15 factors; usually stabilises after about 30 seconds

Question 24

Syncope?

Answer 24

Conflict between differing flow demands (e.g. temperature/food) and delay in response time can cause dizziness and syncope:

• acute decrease in cerebral flow leads to loss of conscioussness
• need to maintain CVP by balancing response

Question 25

Describe the responses involved in supplying the GI tract to digest a large meal

Answer 25

Flow to abdomen increases at the sight of food, as GI demand after a large meal becomes 25-30% of cardiac output. There is a phased response along the duodenum/jejunum as digestion takes place

Effect on CVS:

• ANS increases parasympathetic activity
• local autacoids and vasodilators
• local GI vasodilatation decreases TPR

Effect on venous supply:

• TPR decreases so arterial pressure initially decreases arterial pressure
• flow out via liver increases so CVP increases
• CVP and RA filling increase, so CO increases

Response of CVS:

• baroreceptors detect fall in MABP, modest increase in CO via HR and SV
• increased CVP then decreases by extra pumping of the heart
• arterial pressure returned to normal
• GI demand met: CVS goes back to normal MABP operating range by adjusting CO
• perfusion pressure maintained for other tissues

Question 26

Why should strenuous exercise not take place immediately after eating?

Answer 26

After eating there is a high GI demand however is used for exercise instead, so high SNS activity on the GI renders digestion unpleasant: can cause vomiting

Question 27

Effects of exercise on the heart (in terms of HR etc)

Answer 27

At rest: total muscle demand is ~ 15-20% of cardiac output (so 0.75-1 litre per minute)
During exercise demand is ~70% of CO (12-17.5 L per min)
-HR increases to >180 bpm
-SV increases to 150-200 ml [max SV higher when fitter]

Question 28

Acute effects of exercise on the CVS

Answer 28

Increased peak flow demand so:

• increase substrate demand: need higher CO
• decrease in TPR: vasodilators in metabolising tissue (K+, H+, adenosine, lactate), plus endothelial autacoids which reduce the local SNS effect
• exercise-induced hyperaemia
• decreased TPR will initially increase CVP (so increase SV) and initially decrease MABP

Question 29

Response of the CVS to exercise

Answer 29

Central voluntary control: brain increases HR with expectation of exercise, avoids CVP overfilling

Baroreceptors: signal acute exercise-induced increase in BP so increase HR and SV

Skeletal muscle: contractile activity actively aids the whole circulation. Not as pulsatile as in the heart

Other effects:

• increased SNS to gut
• initially skin decreases supply then increases for heat loss
• brain and heart spared
• kidney perfusion drops by nearly 1/2

Question 30

What happens if residual blood volume drops below 3.5-4L?

Answer 30

Hypovolaemic shock

• cannot perfuse tissues
• MABP

Question 31

Effect of hypovolaemic shock on the CVS

Answer 31

• rapid drop in CVP
• SV, CO and MABP all decrease
• tissues react badly: build up of metabolites so would decrease TPR
• conflict as need to preserve systemic systemic MABP

Question 32

Response of the CVS to hypovolaemic

Answer 32

• baroreceptors signal drop in blood pressure, so very large SNS output to increase HR and SV, and increase in TPR of arterioles to keep MABP up and to veins to keep CVP and SV up
• tachycardia
• all systems decrease supply except to the heart and brain, can cause kidney failure
• conserving heart and blood perfusion: need adequate CVP and MABP. If can;t maintain=organ failure and death