Advanced Medical Life Support Practice Exam 2025 – Complete Study Guide

The renin-angiotensin-aldosterone system (RAAS) plays a critical role during compensatory shock by activating mechanisms that help maintain blood pressure and fluid balance. When the body senses a decrease in blood flow or blood pressure, the kidneys release renin, which triggers a cascade leading to the production of angiotensin II. This peptide has several important effects.

Firstly, angiotensin II acts as a potent vasoconstrictor, which increases systemic vascular resistance. This contributes to an increase in afterload, as the heart has to work harder against the elevated pressure in the arteries to pump blood.

Secondly, angiotensin II stimulates the adrenal cortex to release aldosterone, which promotes sodium reabsorption in the kidneys. This effect leads to an increase in blood volume as water follows sodium, effectively raising the preload. An increase in preload enhances cardiac output, helping to stabilize blood pressure during shock.

Overall, the combined effects of RAAS during compensatory shock enhance fluid retention and vascular resistance, crucially supporting the cardiovascular system’s response to decreased perfusion.