NURS 3102 Study Guide - Midterm Guide: Ventricular Remodeling, Angiotensin-Converting Enzyme, Angiotensin

• School: Mount Royal University
• Department: Nursing
• Course: NURS 3102
• Professor: Helena Myllykoski

Document Summary

Des(cid:272)ri(cid:271)e the state(cid:373)e(cid:374)t fro(cid:373) (cid:1006)(cid:1005)(cid:1005)(cid:1007) (cid:862)heart failure (cid:271)egets heart failure(cid:863). The inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients. **heart failure begets heart failure-compensatory mechanisms perpetuate heart failure. Cns a(cid:272)ti(cid:448)it(cid:455) i(cid:374) sympathetic nerves to heart (sns stimulated to release epinephrine and norepinephrine hr and contractility. Causes vasoconstriction of the skin, gi and kidneys. (cid:272)ardia(cid:272) preload (arterioles also constrict to maintain bp kidney receives sns stimulation (cid:449)he(cid:374) co . Release of renin by the kidney (renin promotes the formation on angiotensin i) **all the compensatory mechanisms lead to decreased cardiac output and play a significant role in the development and subsequent progression of chronic heart failure. N a(cid:272)ti(cid:448)atio(cid:374) (cid:448)ia & pressure of baroreceptors (in aorta and carotid arteries), as an early compensatory mechanism to maintain co. Chronic sympathetic activation, however, has deleterious effects, causing a further deterioration in cardiac function.