Control of Cardiac Output Flashcards
What is a normal cardiac output?
What is a a normal return?
(Ignoring transient events)
Both = 5L/min
Volume of blood leaving the heart = volume of blood returning
In a transient event which is bigger and why?
Cardiac output or venous return
Cardiac output, as venous return drops due to around 500ml of blood pooling in the legs due to gravity.
Are the outputs of the systemic and pulmonary systems the same or different?
They are the same as they are in series with one another, therefore ventricular output (70ml) is the same from the left and right.
In summary C.O. Left = C.O. Right = Venous Return
What X4 things control cardiac output?
Preload
Afterload
Inotropy (ANS)
Chronotropy (ANS)
Is the length-tension relationship curve steeper for skeletal or cardiac muscle?
Cardiac, therefore smaller changes in length (due to preload) will result in larger increases in force of contraction (inotropy).
Why do cardiac cells show a steeper curve for their length-tension relationship?
There is a relationship between sarcomere length and calcium sensitivity, probably linked to troponin c (which calcium binds to), although this is not understood fully.
How does starlings law allow the right and left ventricle output to be matched?
If one increases, the other ventricle will fill with more blood (as they are in series) and will therefore contract with more force, allowing its output to now match the first ventricles.
Are the right ventricle and left ventricle starling curves the same? If not how and why?
What does this mean for its length-tension relationship?
The right is more compliant as it is thinner walled and works at a lower pressure.
This means for a given pressure it will increase in length more than the left side would and will therefore contract with more force than the left at a given pressure.
How is cardiac output maintained via the frank-starling mechanism when:
1) afterload increases
2) cardiac contractility decreases
1) As afterload increases, the ejection fraction decreases and the volume of blood left in the ventricle is increased. This means after ventricular filling it will have a larger LVEDV (preload) which will increase its sarcomere length and therefore increase its contractility in the next beat, maintaining cardiac output.
2) the same principle applies with decreased contractility, as LVEDV (preload) will increase due to a lower ejection fraction, meaning stroke volume will increase with the next beat maintaining cardiac output.
Are venous return and CVP the same? If not what are they?
Venous return = volume of blood returning to the heart each minute
CVP = pressure in the vena cavae near the right atrium
Which affects preload and why, CVP or venous return?
CVP, as it is a pressure and venous return is a rate.
What X2 other effects (other than increased cardiac output due to decreased stroke volume compensated for by the starling effect) does an INCREASE in afterload have on the CV system?
Do they inhibit or promote cardiac output?
The ANREP response (promotors cardiac output)
Depression of cardiac output (inhibits) vis the baroreceptor reflex (due to increases in afterload usually being attributed to increases in blood pressure which trigger this response)
What is the ANREP response?
Over a few minutes substances (such as endothelin) are released which increase the calcium concentration within the cardiac myocytes which increases inotropy and therefore cardiac output.
Explain the baroreceptor reflex.
A decrease in blood pressure is sensed by baroreceptors in the aortic arch and the carotid sinus, which stimulates vasoconstriction and increased chronotropy to increase the blood pressure via resistance and cardiac output respectively.
Does afterload (taking into accounts it’s X3 effects on the CV system) have any net effect on cardiac output?
Not in a normal range of blood pressures.
