Final answer:
When heart failure progresses beyond the body's compensatory abilities, it can lead to decreased blood pressure, increased respiratory rate, and decreased kidney function. The body tries to compensate by releasing renin leading to the productions of aldosterone and antidiuretic hormone (ADH), which are meant to help retain sodium and water, thus increasing blood volume and pressure.
Step-by-step explanation:
When the body can no longer compensate for heart failure, several mechanisms fail, leading to a series of symptoms and complications. Firstly, decreased blood pressure can occur as the heart is unable to pump effectively. This reduced blood pressure prompts the liver to release renin, which then converts angiotensinogen into angiotensin I. Angiotensin I is then converted to angiotensin II, which is a potent vasoconstrictor that increases blood pressure and stimulates the release of aldosterone from the adrenal cortex. Aldosterone acts on the kidneys to promote the reabsorption of sodium, which in turn leads to water retention and an increase in blood volume, compensating for the initially decreased blood pressure.
Additionally, angiotensin II stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary gland. ADH works to increase water reabsorption in the collecting ducts of the kidneys, further aiding in the retention of water to increase blood volume. Overall, the release of renin, aldosterone, and ADH are part of a complex regulatory system aimed at maintaining blood pressure and volume. However, if heart failure progresses to a point where these compensatory mechanisms are overwhelmed, it can lead to systemic effects, including increased respiratory rate and decreased kidney function.