Which compensatory mechanism is involved in both chronic heart failure and decompensated heart failure, leading to fluid retention and edema?

A. Ischemia and neuronal death – Cerebral perfusion pressure (CPP) is the pressure needed to ensure adequate blood flow to the brain. If CPP drops too low, the brain doesn't receive enough oxygen and glucose, leading to ischemia and eventually neuronal death.
B. Improved cognitive function – Low CPP results in decreased oxygen and nutrient delivery, which impairs cognitive and neurological function.
C. Increased blood flow to the brain – Low CPP means reduced blood flow, not increased.
D. Undetectable intracranial glucose levels – While glucose delivery may decrease, levels are not necessarily undetectable and this is not the primary concern with low CPP.

A. Increased systemic blood pressure – While systemic vasoconstriction may occur to maintain perfusion, it is a result of compensatory mechanisms like RAAS, not a primary mechanism leading to fluid retention and edema.

B. Renin-angiotensin-aldosterone activation – RAAS leads to:

Sodium and water retention via aldosterone

Vasoconstriction via angiotensin II

These changes increase intravascular volume, contributing to fluid overload and edema.

C. Ventricular hypertrophy – This is a structural adaptation to increased workload (pressure overload), not directly responsible for fluid retention.

D. Ventricular dilation – Dilation occurs as a result of chronic volume overload, not as a compensatory mechanism causing fluid retention.