HELP with pathophysiology of HTN

[Drea1713]

Hey everyone I need help with the patho phys of HTN. Here is what I have so far

Pathophysiology of HTN: Cardiac output is raised with normal total peripheral resistance (TRP) over time the cardiac output drops to normal levels but the TRP levels increase. The kidney plays a role since it excretes sodium and increases fluid reabsorption. This excess fluid causes BP to rise. Decreasing pressure in the renal artery causes the secretion of renin enzyme. Renin in turn causes the formation of Angiotensin I, which causes the kidneys to retain sodium and water. Angiotensin I is converted to Angiotensin II by angiotension converting enzyme found in the lungs. Angiotension II causes vasoconstricts of the arterioles which further increases TRP and elevates the BP further.

My instructor is very hard and i need to know if this will be enough to correctly describe it. Any help or input would be greatly appreciated.

Thanks!

Andrea:nurse:

[Daytonite, BSN, RN]

hypertension is due to

• increased cardiac output
  • any condition that increases heart rate or stroke volume

  [*]increased total peripheral resistance

  • any factor that increases blood viscosity or reduces vessel diameter

  [*]both increased cardiac output and total peripheral resistance

with total peripheral resistance. . .vasoconstriction or high pressures in vessels when prolonged over time will cause vessels to thicken and strengthen in order to tolerate the stress. the smooth muscle of the arteries will hypertrophy and sustain hyperplasia. the tunica intima and tunica media of the arteries will experience fibromuscular thickening that results in permanent narrowing of the vessel's lumen. these changes aggravate an inflammatory response resulting in biochemical mediators entering the areas where these changes are actively occurring (see https://allnurses.com/forums/f50/histamine-effect-244836.html for a description of the pathophysiology of the inflammatory response) which results in the permeability of the vascular endothelium. with this permeability, sodium, calcium, water, plasma proteins and other substances enter the vessel causing further vessel wall thickening and increasing the smooth muscle responsiveness to vasoconstriction.

renin, an enzyme produced and secreted from the kidney becomes angiotensin i which, according to my references does nothing until it is converted to angiotensin ii which stimulates the secretion of aldosterone which, in turn, causes the reabsorption of sodium in the kidneys. this renin-angiotensin system helps to regulate blood pressure. if it goes on the fritz, as it does in renal disease, and the kidneys fail to synthesize renin, the blood pressure becomes elevated.