lOMoARcPSD|15362186 Cardiovascular Disease Notes Integrated Pathophysiology and Pharmacology (California State University Fullerton) StuDocu is not sponsored or endorsed by any college or university Downloaded by Carolina Landa Perez (landaperezc@gmail.com) lOMoARcPSD|15362186 Concept Details Right Heart Failure (Patho) ● ● ● RV impaired resulting in systemic venous overload Usually caused by left-sided failure Symptoms ○ fatigue/weakness ○ Bilateral leg swelling ○ Abdominal bloating/pain (right) ○ Weight gain ○ Loss of appetite Left Heart Failure (Patho) ● LV is weakened or over loaded resulting in pulmonary congestion Symptoms ○ fatigue/weakness ○ Dyspnea ○ Orthopnea ○ PND ○ Sudden orthopnea that awakens from sleep ● Nitrates ● Used to treat (stable) angina ADH and BP Regulation ● The release of ADH regulates hypotension by causing reabsorption of water by kidney With reabsorption, blood plasmas volume inc (raising BP) ● Preload ● ● ● ● ● Afterload ● ● ● ● Hypertension ● Pressure generated in LV at end of diastole (LVEDP) Reflects the amount of stretch of the muscle fibers Greater stretch means greater CO (Starling’s law) Factors that inc ○ Hypervolemia Factors that dec ○ Hypovolemia, inc intrathoracic pressure, vasodilation due to inc temp/sepsis/meds, atrial fibrillation, cardiac tamponade Resistance to ejection of blood from LV Pressure the ventricle must overcome in order to eject its contents SVR is a reflection of LV afterload Normal: 800-1200 dynes sec cm-5 BP >140/>90 (intermittent or sustained elevation) ○ Normal- <120/<80 ○ Prehypertension- 120-139/80-89 Downloaded by Carolina Landa Perez (landaperezc@gmail.com) lOMoARcPSD|15362186 ● ● ● Myocardial Ischemia (MI) -lack of O2 ● ● ● ● ● ● Angina -chest pain ● ● ○ Hypertension 1- 140-159/90-99 ○ Hypertension 2- >160/>100 Associated Factors ○ Insulin (sensitivity) ○ RAAS activity ○ Cell membrane sodium/calcium transport ○ Sympathetic response to neurogenic hormones ○ Family hx ○ Age ○ Gender ○ Race ○ DM ○ Diet/ETOH/Tobacco Primary ○ Most common ○ Begins insidiously, asymptomatic Secondary ○ Related to systemic disease that raises peripheral vascular resistance (PVR) or SV Develops if the supply of coronary blood cannot meet the demand of myocardium for oxygen and nutrients Myocardial cells become ischemic within 10 seconds of coronary occlusion Causes conduction abnormalities Anaerobic process take over and lactic acid accumulates If fow not restored, infarction occurs Silent ischemia ○ Occur with presence of abnormal global or regional symptomatic afferent innervation of LV Stable angina ○ recurrent/predictable ○ Transient (3-5 mis approx) Unstable angina ○ Form of ACS that results in reversible myocardial ischemia ○ Signal that atherosclerosis plaque has become complicated ○ Small fissuring or superficial erosion of plaque leads to vessel occlusion/vasoconstriction at site of plaque damage Downloaded by Carolina Landa Perez (landaperezc@gmail.com) lOMoARcPSD|15362186 ■ ● ● ● ● Ejection Fraction (EF) ● ● ● ● Arteriosclerosis ● ● ● ● ● Atherosclerosis ● ● Unstable plaques have ore with oxidized LDL and thin fibrous cap Prinzmetal angina ○ CP attributable to transient ischemia of myocardium that occurs unpredictably and almost exclusively at rest (common during REM sleep) ○ Pain secondary to vasospasm of 1+ major coronary arteries with or without associated atherosclerosis Experienced as substernal chest pain Pain most likely from lactic acid build-up or abnormal myocardial fibers stretching causing myocardial nerve fibers to be irritated Caused by gradual narrowing and hardening of arterial walls (arteriosclerosis) preventing vasodilation when more blood flow is needed Estimate of the amount of blood pumped from LV to the rest of the body with each heartbeat Used as determinant of LV function Reflects systolic function of heart Normal: 50-75% Abnormal thickening and hardening of vessel walls Tunica intima undergoes changes that decrease the artery’s ability to change lumen size Smooth muscle cells and collagen fibers migrate into intima, causing it to stiffen/thicken Worsened by ○ HTN ○ Ischemia ○ Weakening and outpouching of arterial walls ○ Changes in lipid/cholesterol/phospholipid metabolism within intima Chronic Clogging of arteries with plaque and lipids Pathophys ○ Injury to endothelial cell leads to inflammatory rxn ○ Inflamed endothelial cells express adhesion molecules ○ Neutrophils/lymphocytes attach to them ○ Oxidized LDL is engulfed by macrophages, which penetrate into intima of vessel Downloaded by Carolina Landa Perez (landaperezc@gmail.com) lOMoARcPSD|15362186 ○ ○ ○ ○ “Good” cholesterol vs “Bad” cholesterol ● ● RAAS ● ● ● ● ● ● ● RAAS and hypertension ● ● Foam cells: lipid-laden macrophages When foam cells accumulate, they form a lesion called a fatty streak (which prod more toxic O2 radicals and cause further inflammatory changes which progressively damage vessel wall Macrophages release growth factors which stimulate smooth muscle cell proliferation Smooth muscle cells produce collagen and migrate over the fatty streak forming a fibrous plaque LDL is “bad” cholesterol ○ Greatest contributor to CHD HDL is “good” cholesterol ○ Cardioprotective Sodium depletion, reduced BP, and dehydration stimulate renin release Renin reacts with angiotensin (liver enzyme) and converts it to angiotensin I (inc preload/afterload) Angiotensin I converts to angiotensin II in lungs (potent vasoconstrictor targeting arterioles) Angiotensin II causes structural changes in BV (inc PVR and makes vessels at risk for endothelial dysfunction and platelet aggregation) Circulating angiotensin II also works to inc preload/afterload by stimulating adrenal cortex to secrete aldosterone (inc BV by conserving sodium/water) Aldosterone causes sodium retention Inc BV causes inc BP Patients with hypertension already have high BP RAAS highers BV → highers BP (which we do not want to further heighten in pts with HTN) Downloaded by Carolina Landa Perez (landaperezc@gmail.com)
