Control of cardiac output

Question 1

What is the Fick Principal

Answer 1

The amount of oxygen in the pulmonary vein is derived from the amount of oxygen in the pulmonary artery and the amount of oxygen uptake across the lungs

Question 2

What is Q1

Answer 2

Volume of blood to the lungs x the volume of oxygen in the pulmonary artery

Question 3

What is Q2

Answer 3

Oxygen uptake per unit time

Question 4

What is Q3

Answer 4

Volume of blood in the pulmonary vein x conc of oxygen in the pulmonary vein

Question 5

What is the relationship between Q1,2 and 3

Answer 5

Q1 + Q2 = Q3

Question 6

How is cardiac output measured using the Fick principal

Answer 6

CO (flow) = Q2 (O2 uptake) / ([O2]pv - [O2]pa)

Question 7

How is O2 uptake measured in an individual

Answer 7

Measure the conc of oxygen in their expired air

Question 8

How is O2 conc measured in pulmonary artery

Answer 8

Directly measured using a catheter placed in the right atria or ventricle or the pulmonary artery itself

Question 9

How is O2 conc measured in the pulmonary vein

Answer 9

Can be estimated using peripheral arterial blood

Question 10

How is cardiac output measured using dilution methods?

Answer 10

A fluorescent tracer is inserted at point A - injected into vein or right ventricle - Blood is sampled at point B (arterial blood) Use equation - CO = amount of indicator/(average concentration x time interval) Do the example

Question 11

What is a heterometric control of cardiac output

Answer 11

End diastolic volume is regulated by venous return

Question 12

Give 4 ways in which venous return is effected

Answer 12

1. If blood volume rises then so does venous return and CO
2. If vascular storage decreases VR increases as does CO
3. In haemorrhages - blood loss causes reduced CO - followed by a reduction in vascular storage….
4. Vascular resistance goes up - VR goes down

Question 13

What is atrial “sucking”

Answer 13

Pressure in atria when emptied is less than that of the atmosphere so sucks blood from the vena cava

Question 14

What is a homeometric control of CO

Answer 14

A positive inotropic effect not related to the nervous or endocrine system e.g. TREPPE - strength of contraction increases when the rate of contraction increases

Question 15

What is the extrinsic control of CO from the parasympathetic NS

Answer 15

Negative chronotropic effects (bradycardia) - Ach muscarinic receptors - vagal input slows node firing rates - right vagal nerve - SAN left vagal node - AVN - Also slows conduction through the AVN

Question 16

How is parasympathetic control of CO blocked

Answer 16

Using muscarinic receptor antagonists such as atropine

Question 17

What is the extrinsic control of the sympathetic nervous system on CO

Answer 17

Both inotropic and chronotropic effects (tachycardia)
Noradrenaline acts on B1 receptors which are present on both the nodes and myocardium
Nodes - Increased SAN firing rate and increased speed of conduction - increased heart rate
Myocardium - Increased contractility - More calcium - more stimulation of cAMP/PKA due to the action of adenylate cyclase
PKA phosphorylates calcium channels so they become more open

Question 18

How is sympathetic control of CO blocked

Answer 18

Using beta blockers - propranolol/atenolol

Question 19

Which extrinsic system is more dominant at rest?

Answer 19

Parasympathetic

Question 20

What are the humoral factors that affect CO

Answer 20

Adrenaline release increases rate and force of contraction

Question 21

What affect do thyroid hormones have on CO

Answer 21

Increased rate and force

Question 22

What are the genomic actions of hyperthyroidism

Answer 22

Promotes cardiac gene expression of e.g. myosin and ATPases - non genomic action on transport proteins e.g. increase calcium channel activity