Control of cardiac output Flashcards
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
- If blood volume rises then so does venous return and CO
- If vascular storage decreases VR increases as does CO
- In haemorrhages - blood loss causes reduced CO - followed by a reduction in vascular storage….
- 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?
Parasympathetic
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
