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Flashcards in Control of cardiac output Deck (22)
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What is the Fick Principal

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


What is Q1

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


What is Q2

Oxygen uptake per unit time


What is Q3

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


What is the relationship between Q1,2 and 3

Q1 + Q2 = Q3


How is cardiac output measured using the Fick principal

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


How is O2 uptake measured in an individual

Measure the conc of oxygen in their expired air


How is O2 conc measured in pulmonary artery

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


How is O2 conc measured in the pulmonary vein

Can be estimated using peripheral arterial blood


How is cardiac output measured using dilution methods?

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


What is a heterometric control of cardiac output

End diastolic volume is regulated by venous return


Give 4 ways in which venous return is effected

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


What is atrial "sucking"

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


What is a homeometric control of CO

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


What is the extrinsic control of CO from the parasympathetic NS

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


How is parasympathetic control of CO blocked

Using muscarinic receptor antagonists such as atropine


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

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


How is sympathetic control of CO blocked

Using beta blockers - propranolol/atenolol


Which extrinsic system is more dominant at rest?



What are the humoral factors that affect CO

Adrenaline release increases rate and force of contraction


What affect do thyroid hormones have on CO

Increased rate and force


What are the genomic actions of hyperthyroidism

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