Effect does vasodilation have on afterload

Blood pressure is determined by cardiac output and systemic vascular resistance (SVR). Vasodilation decreases SVR, which leads to a decrease in blood pressure. This is because when blood vessels dilate, the total area available for blood flow increases, reducing the pressure exerted on the vessel walls.  

To compensate for the decreased blood pressure caused by vasodilation, the body employs several mechanisms. Tachycardia (increased heart rate) is a common compensatory response. By beating faster, the heart can increase cardiac output and help to maintain blood pressure. Additionally, the body can activate the renin-angiotensin-aldosterone system (RAAS) to increase blood volume and raise blood pressure. Renin, an enzyme released by the kidneys, stimulates the production of angiotensin II, which is a potent vasoconstrictor. Angiotensin II also promotes the release of aldosterone, a hormone that causes the kidneys to retain sodium and water, increasing blood volume.  

In conclusion, vasodilation in sepsis can have significant effects on afterload and blood pressure.

By decreasing afterload and reducing SVR, vasodilation can lead to a decrease in blood pressure. The body compensates for this by increasing heart rate and activating the RAAS to raise blood volume and restore blood pressure to homeostasis.