Control of Cardiac Output Flashcards
What type of system is the cardiovascular system + what is the sig of this?
- closed
- amount of blood leaving the heart (CO) must = amount entering it (venous return) so blood isn’t building up in parts of body
What situations does CO =/= VR?
- transient events
- e.g. when you stand up CO > VR as ~ 500ml of blood pools in the extremities - quickly reg by body to balance once again
What type of circ are systemic + pul circ?
series
What must the outputs of LV + RV be?
- equal
- both sides need to pump same amount
What mech exist to ensure LV CO = RV CO?
Starling mech
Which heart is adjusted to cope with inc/dec VR?
R
Which 4 things directly influence CO?
- Preload
- Afterload
- HR
- Contractility
What is preload?
- degree of stretch of heart immediately before it contracts (at end of diastole just before systole)
- P filling R vent
- blood flowing back to heart
What is afterload?
- P against heart must pump to eject blood into aorta (due to aortic P)
- R to outflow from LV due to aortic/arterial P
Which factors inc CO?
- inc contractility
- inc HR
- inc preload
Which factor dec CO?
afterload
What is contractility + HR controlled by?
ANS
What is contractility?
heart beat more/less strongly
Why is CVP = R vent EDP?
no valves sep venous circ from R vent as R vent filling
Which factors that influence CO are intrinsic mech?
- preload
- afterload
What causes the degree of stretch in preload?
blood coming in from the veins
How is preload related to EDV?
- as P inc due to more blood filling vent
- EDV inc due to higher P - stretches heart + cardiac cells
What is EDV related to?
filling P aka R atrial P of heart
What is preload closely affected by?
- CVP
- EDP of R atrium
What is afterload mainly due to + why?
- aortic P bc as it inc e.g. hypertension - more diff for heart to pump blood into aorta - has to work harder which inc afterload
What is afterload influenced by + why?
- TPR: inc peripheral R where small arteries + arterioles constricted - inc aortic P
- aortic stiffness: as get older, aorta gets more fibrous - less blood expelled into heart as its less expandable - inc work to get blood into aorta so inc afterload
Describe the Starling curve
- as inc P going into vent, tension dev during systole inc
- inc P inc P the vent could gen + amount of blood it could have pumped
What relationship does the Starling curve have + why?
- sigmoidal
- ability of vent to pump (gen P) v. sensitive to filling P
- degree of stretch had big effect on vent work
- but reaches sat point where inc filling P no longer has effect on vent P
What is the sig of phys range of F-S relationship of vent function curve?
- Physiologically, we operate in range where inc in vent stretch would not get sat which is at low levels so small in vent stretch have large effect on SV and CO
What does the F-S relationship/cardic/vent function curve show?
- cardiac myocytes gen more force (SV/vent work) when stretched (vent stretch/EDV)
Why is EDP plotted instead of EDV on the vent function curve?
easier to measure
Are EDP + EDV linearly related?
- normally are but not in certain cases
- e.g. in case of stiffness of vent in heart failure
- harder to expand heart as in P doesn’t cause in in vol - curve shifts slightly
