Control of Cardiac Output 2.2 Flashcards Preview

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Flashcards in Control of Cardiac Output 2.2 Deck (17):

What is afterload?

The load the heart must eject blood against (roughly equivalent to aortic pressure(impedance))


What is preload?

Amount the ventricles are stretched in diastole (related to the end diastolic volume or central venous pressure)


What is total peripheral resistance?

Also known as systemic vascular resistance
Resistance to blood flow offered by all the systemic vasculature


Which blood vessel offers the greatest resistance to blood flow?



What effect will constricting arterioles have on resistance?

Increased pressure in arterioles, decreased in capillaries and venules


What effect does changing cardiac output or total peripheral resistance have, whilst not changing the other? E.g., increase CO but TPR remains the same

Both of these circumstances follow the same rules:
CO/TPR changes directly correlate to arterial pressure changes
Arterial pressure changes inversely correlate to venous pressure changes
E.g. increased CO means that arterial pressure increases, so the venous pressure falls


What is the Ventricular Compliance Curve?

Relationship between LV pressure and volume, related to compliance (how easily the chamber expands)
The higher the venous pressure, the more the heart fills
As heart fills, LV pressure increases
In diseased states compliance can change, eg. decreased compliance means EDV is the same but EDP will increase and curve will shift to left and up


What is the Frank - Starling Law of the heart?

The more the heart fills, the more the fibres stretch before contracting, so the harder it contracts, so the bigger the SV (up to a limit) (intrinsic control mechanism)
An increase in venous pressure will fill the heart more, and the amount it fills depends on the compliance


What is the 'normal' operating point at rest of LVEDP and SV?

8 mm Hg


What is the Starling Curve?

LVEDP (filling pressure) against SV
Direct correlation at first (straight line), then curves down to a flat line
Increasing venous return leads to increased preload and increased LVEDP, causing an increase in SV so extra blood is pumped out of ventricle


How does the length of sarcomeres affect contractile force?

Shorter sarcomeres decrease contractile force, as filament overlap interferes with contraction
As cardiac muscles are stretched, calcium sensitivity increases


What is contractility?

Force of contraction for a given fibre length
Can be increased by extrinsic factors such as circulating adrenaline and sympathetic stimulation
Change in contractility is seen as a change in the slope of the Starling curve


How does the heart 'see' changes in eg. demand for blood in the tissues?

Through arterial blood pressure (aBP) and central venous pressure (CVP)
Responds to changes via extrinsic and intrinsic mechanisms


What factors determine the Cardiac Output?

Heart rate, stroke volume (EDV, contractility, aortic impedance (after load))


How are the contractility and heart rate controlled?

A decrease in arterial BP will reduce parasympathetic NS activity and stimulate sympathetic NS, to increase heart rate and contractility


What happens to the CVS when metabolism of the body increases?

TPR falls as more blood needs to be supplied
Therefore, the arterial pressure falls and venous pressure increases, and the heart responds by pumping more


How is postural hypotension caused, in terms of blood pressure?

Standing up cause 'pooling' of blood in legs due to gravity
The venous pressure falls, as does CO and arterial pressure
The heart cannot use intrinsic mechanisms to try to fix it, so the baroreceptor reflex and the ANS try to by increasing HR and TPR
If it doesn't work, it results in postural hypotension