BIOM 3090 Study Guide - Final Guide: Sodium Nitroprusside, Vascular Resistance, Beta Blocker

• School: University of Guelph
• Department: Biomedical Sciences
• Course: BIOM 3090
• Professor: Bettina Kalisch

Document Summary

Most common cardiovascular disease (23% canadian adults) Leads to damaged blood vessels, coronary disease, renal failure, stroke. Treatment slows vessel damage and decreases morbidity and mortality. Blood pressure = cardiac output x peripheral vascular resistance. Venules: capacitance (can hold extra volume is necessary) Stretch/pressure baroreceptor stimulation vasomotor center sns activity to decrease bp. Long term regulation by controlling blood volume (slower to respond) Main player is angiotensin 2 (potent vasoconstrictor) Ace cleaves angiotensin 1 to angiotensin 2. Angiotensin triggers: vasoconstriction ( bp, release of aldosterone ( sodium retention water retention bp) Goal of treatment: bp to prevent further organ damage. Interfere with regulation mechanisms: balance between toxicity and risk of not treating, combined therapy more common than monotherapy. Ne in cns sns and pns activity. Co and pvr ( heart rate, force of contraction, bp) Propranolol (non-selective, blocks 1 and 2: toxi(cid:272)ities asso(cid:272)iated (cid:449)ith 2 blocking (asthma) Blo(cid:272)k 1 in jga of kidney will renin pvr.