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ALL the time nervous control is more rapid than hormonal control

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when you talk about adaptative mechanism of heart failure

COP = HR x SV

1. nervous ( sympathetic )
aim : to increase HR ( heart rate ) --- increase COP ( cardiac output )

2. : hormonal secretion
ranging from RAS ( renin angiotensin aldosterone system ) to Vasopressin , endothelin , hANP ( human atrial natriuretic factor ) , hBNP ( human brain natriuretic factor )

aim : to increase SV ( stroke volume ) ---- increase ciculating volume

so the main compensatory mechanism is neurohormonal activation : sympathetic then hormonal

Now ventricular remodling ( hypertrophy ) this will result from angiotensin

but there is a draw back here :
that increased cardiac muscle will increase contractility yes , but the blood supply wont be increased to the same degree so this will lead to ischemia

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Okay the first point

if SV ( stroke volume-volume ejected by each ventricle per beat ) = EDV ( Venous return VR -preload ) - ESV ( Arterial blood pressure ABP - afterload )

SV = EDV-ESV

then force of contraction is proportional with intial lenght of cardiac muscle ( EDV ) within limits

increase in Force of contraction -- increase SV --- increase COP

so we can say : force of contraction is proportional with venous return ( EDV )

I mean : the more increase in VR --- increase RAP ( right atrial pressure ) --- increase stretch of atrial wall --- increase force of contraction ---increase SV---increase COP

WINTHIN LIMITS
IN OTHER WORDS : starling law

NOW

From the ventricular function curve

( not vascular fxn curve )

see the relation between preload=EDV=VR=RAP and COP or SV

normal curve : increase preload=VR=EDV --- increase SV --- increase COP

at the hypoeffective curve ( heart failure ): now at any EDV=preload=VR=RAP the COP will be less than normal

and this is the problem , COP is too low , i mean ejection fraction is less than 55 %

thats why i have sympathetic stimulation and hormonal secretion

this is both ventricular and vascular fxn curve and from it u can conclude that VR normally = COP = 5 L / min

this balance is altered in Heart failure

There are some mechanisms which couse increase HR (which is an Adaptive mechanism in heart failure )
What are these mechanisms?