Module 9 ML-1 Flashcards
What is cardiac output
the volume of blood coming out of each ventricle per unit time
What is the average CO
5L/min
Cardiac output can be influenced by whay
both divisions of the autonomic nervous system
How does the parasympatheic affect cardiac output?
Ach to muscarinic recpetors within the atria ( SA, AV, and Atrial contractile cells
How does the sumpathetic affect the cardiac output
NE to beta 1 within the whole heart
Epi to beta 1 within the whole heart
In a resting person what is the state of the para and symp
para: on
symp: off
If you increase physical activity what happens
increased symp output
decreased para output
What are the intrinisc rates of the SA node, AV node, his/purkinje
SA: 100
AV: 70
His/purkinje: 30
What are the major affects influencing heart rate
-epi onto beta 1 increased the symp NS which increases HR
-Ach onto alpha 1 will increase the para and decrease heartrate
-ALL EFFECTS EXERTED ONTO THE SA NODE
Pacemaker potential in SA node celss in slowed and quickened by what
slowed: para
quickened: symp
Chronotropic effect
factors that alter the heart rate
How does the symp make depol go faster
-no change in potassium current
-increased funny sodium current
-increased T type calcium current
How does para make depol go slower
-increase of voltage gated potassium current
-decreased funny sodium current
-decreased t type calcium current
True/False: upstroke of AP is also affected by symp and para
true
Dromotropic effects
conduction velocity changes
Symp ion channel change makes upstrok faster
increase in L type calcium current
Para ion channel change makes upstroke slower
decrease of L type calcium current
If you have an increased venous return what occurs
higher ECV and imporved overlap of actin
-heartbeat will be stronger to eject all the blood
What does increased EDV cause
increased length of cells, increased tension and increased SV
EDV
how much we fill
What is an intrinisc mechamisn of regulating SV
if ventricle fills to a large volume than the next beat is stronger to eject the extra blood
What is the frank starling mechanism
contraction force and stroke volume change in response to venous return
Example of frank starling
instead of noraml 135 mL EDV is it 165mL so Sv has to go up 30 to get 65 mL again
Implications of frank starling
-prevents a rise in ESV( prevents clotting)
-matching of LV and RV output; (if venous reutn increased on either side, CO increased)
-prevention of rise in venous pressure
