Cardiac output regulation Flashcards
Define cardiac output
the total flow of blood out of the LV
* small portion flows to the heart itself via coronary circulation
CO is thus the total available flow to perfuse all the tissues in the body
Why does CO need to increase during exercise?
to meet the metabolic demands of the body, and maintain arterial pressure
How much can CO increase?
4-5 fold
How much can HR and SV increase?
HR - up to 3 fold
SV - up to 1.5 fold
*HR more important
What does the increase in HR and SV enable?
an increse in overall O2 consumption up to 12 times
Why is and increase in CO essesntial to maintain MAP during exercise?
TPR will decrease to as little as 1/3 resting value
What changes are required to produce an increase in CO?
in both heart and systemic vasculature
What are the cardiac factors of CO?
characteristics of heart tissue
- HR
- myocardial contractility
What are the coupling factors of CO?
constitute a functional coupliung between the heart and blood vessels
- preload
- afterload
What are cardiac function curves?
expression of the frank starling relationship and reflects the dependece of CO on preload (central venous or RA pressure)
What does the vascular function curve define?
the dependence of central venous pressure on CO
- depends on peripheral resistance, arterial and venous compliance, and blood volume
- independent of characteristics of the heart
What is the relationship between preload and CO?
greater preload = greater CO
What will determine preload in intact circulation?
pressure in the great veins
In the whole heart what will determine the strength of subsequent contraction?
the stretch of the ventricles prior to systole
How does preload in RV determine CO?
filling pressure on right side of the heart will determine the output of the left side
What is the filling pressure on the right side of the heart functionally equal to?
central venous pressure
What is the relationship between preload and SV?
decreased preload = decreased SV through decreasing EDV
increased preload = increased SV through increasing EDV
What is the primary way CO is increased physiologically?
through increased cardiac contractility produced by norepinephrine and epinephrine
How do norepinephrine and epinephrine acto to increase contractility?
by the cellular mechanisms and having the effect of rasing peak pressure that can be developed at a given LV volume
How is increased contractility relfected in ESPVR?
shifted upward and to the right (increase slope)
*opposite for decreased contractiltiy
What is the relationship between contractility and SV?
increased contractility = increased SV by decreasing ESV
* at each preload SV will increase with increased contractility = cardaic function curve increase upwardly
What is afterload related to?
the arterial BP and hemodynapic properties of arterial system
How does afterload affect pressure?
increased afterload = increased pressure throughout ejection phase
* when diastolic arterial BP is elevated, isovolumic contraction must develop a higher pressure in LV before aortic valve will force open
What occurs to SV is contractility and ESPVR are not altered?
SV will decreased because the heart is not able to achieve a lower ESV
What does a decrease in afterload cause in SV if contractility and ESPVR are not altered?
increased SV because the heart is able to sqeeze down more, achieveing a lower ESV
What are characteristics of HFrEF?
generally secondary MI
right shift PV relationship
*eventially SV will narrow
increased EVD to offset decreased SV
How does exercise training effect HFrEF?
increased heart function and AVO2 diff
may cause anti remodeling
How does a HFrEF heart remodel?
eccentric
becomes larger
ballooned and dialated
increases wall stress (volume loading driven - kidneys hold fluid)
What are characteristics of HFpEF?
ESVPR generally normal
EDP always elevated
increased pressure at any given volume
SV often decreased
slow/stiff to relax
highly associated with hypertension
How does exercise training effect HFpEF?
only peripheral adaptation
AVO2 diff
How does a HFpEF heart remodel?
concentric
hypertrophied and small chambered heart (decreased volume)
hypertension major remodeling stimulus
What is aortic stenosis?
aortic valvue not opening well = decrease in flow and increase in systolic pressure
What are contributors to HFrEF?
MI *
smoking *
male *
hyperlipidemia
diabetes
What are contributors to HFpEF?
diabetes
hyperlipidemia
female
obesity
hypertension
What are therapies for HFrEF?
ivabradine
ACEi/ARB
beta blocker
MRA
ARNI
What are therapies for HFpEF?
currently non available
