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Changes in CO can be....

Physiological (exercise/posture) or pathophysiological (HF, haemorrhage)


Why to we not just try increase the preload if someone has heart failure

Because although they need to raise their CO, they have ALREADY got volume overload.


SO what do we focus on in HF patients

-Cardiac function
-Vascular function
-Blood volume (kidneys


What are the differing factors that impact CO?

Cardiac Factors : HR and Myocardial contractility

Coupling Factors: preload and afterload (dependent of vascular function)


CO =

CO = SV x HR
CO = change P x TPR

Although HR and SV do impact CO, we need to remember SV is dependent on venous return! Look at the bigger picture.


CO is more becuase of the tissue needs, instead of the

heart pumping


CO must match (within a beat or two) ...

Venous return


Draw and explain CO curve



Three main determinants of Venous Return

1) Right atrial pressure (back pressure)
2) Degree of filling (blood volume and venous capacitance) ~ mean systemic filling pressure
3) Systemic vascular resistance

ie: the pressure gradient (Ps - Pv) and vascular resistance > "vascular function"

VR= Pa-Pv/ R


Draw Venous function curve (venous return)

-as we change venous return the right atrial pressure (preload) is affected.

As Right atrial pressure increases, venous return decreases, due to pressure gradient driving flow (Pa-Pv)

-So as MRAP falls, flow increases but the curve level off due to the large veins collapsing (inc R), so no further increase in VR


usually Pressure gradient =

PG = 102 (aortic) - 2 (venous)
= 100mmHg
this is required to ensure venous return is maintained!


What happens when CO= 0L/min (when right atrial P = 7mmHg)

Arterial Pressure drops
Venous Pressure rises due to large diference in compliance (19mmHg drop in arterial P = 1mmHg rise in venous P)

This is because veins are very compliant and already have lots of blood in them, can handle volume change BUT arteries are not and so small volume change > big pressure change.

Meet at 7mmHg "mean systemic filling pressure"


Main determinant of mean systemic filling pressure (Psf)

Blood volume (inc)
venous compliance (dec)

as MSFP increases, venous return increases at any given R atrial pressure


What would an increase in vascular/resistance do to venous return

Drops venous return curve as its harder to get blood back to the heart.

Still plateau at 0/-2 right atrial pressure.


An increase in blood volume leads to...

> increase in mean systemic filling pressure = increase in venous return > increased CO at a high right atrial pressure

eg) transfusions


What happens in heart failure?

Heart is unable to effective pump. This decrease in peripheral perfusion > synmpathetic activation and increase in fluid retention > increased MSFP. CO remains normal

So the patient will have a higher Right atrial pressure just to compensate /maintain CO


is the increase ing R atrial pressure/ MSFP a good thing

No as you have a higher workload on the heart!! Bad long term


Because of increasing MSFP in heart failure, whats a good treatments

-reduce venous pressure
-reduce oedema

ACE inhibitors
-reduces remodelling
-reduces bloodvolume

-Reduce energy demand