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KNES 433 (2)
Ebba Kurt (1)
Midterm

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Department
Kinesiology
Course
KNES 433
Professor
Ebba Kurt
Semester
Fall

Description
433 Midterm #2 Review: Worth 30 % Lindsey Wlasuk LECTURE #10 HYPERTENSION: Risk taker: Not exercising or eating healthy we are taking our own life into our hands (high risk lifestyle) 1) Hypertension: Increases the work of the heart, damages the arterial wall and increases the possibility that a small blood vessel in the brain will rupture causing a stroke. Decreases exercise = increases risk of a stroke * Also known as high blood pressure! 2) According to the Heart and Stroke Foundation of Canada, elevated blood pressure is the #1 correctable risk factor for stroke and a major risk factor for heart disease. Hypertension is on the rise in Canadians 18-35 years of age due to rising rates of obesity in children and teens. * This is why we should understand our values, will be different for everyone! Recent Recommendations: -Most people should be 140/90 or lower -Home values 135/85 or lower (More relaxed in home environment) -People with diabetes or kidney disease should be 130/80 or lower  Normal 120/80 mmhg  Pre hypertension 120-139/80-89 mmhg  High/hypertension 140/90 mmhg Canadian Hypertension Society Lowering blood pressure can reduce: - Heart attacks by 25% - Stroke by 40% - Heart Failure by 50% 3) Measurement Error Blood Pressure: -Patient position -Stimulating environment (people or noise) -Unexposed arms or arm not being supported 4) Blood Pressure checked once a year! -Because it can vary minute-to-minute, day-to-day, hydrated vs. non-hydrated - Get it done by a physician. - One reading not enough to determine your true blood pressure 5) White coat syndrome: Latrophobia (fear of going to the doctor’s office, which actually causes people to get elevated blood pressure) 6) Acute and Chronic Effects of Exercise: - Single sessions (aerobic exercise) = Lowering of bp -Lower bp for 22 hours in elderly hypertensive patients - Increase in bp temporarily with resistance training - Systolic (End of ventricular ejection) increases during exercise, diastolic (Prior to ventricular ejection, filling) stays the same during exercise. 7) Mechanism for Lowering BP: - Reduced sympathetic nervous system activity with training and possible normalization of arteriole morphology which decreases peripheral resistance to blood flow and lowers BP. (Decrease peripheral resistance via sympathetic nerve activity) -Endothelial cells exert their effects by secreting various agents that diffuse to the adjacent vascular smooth muscle and induce their vasodilation or vasoconstriction. -Nitric oxide (vasodilator) is released continuously in the basal state, but its secretion can be rapidly increased in response to chemical stimulants such as those releases during exercise. - Increase in cross sectional area= less resistance to blood flow -Baroreceptors, which are sensitive to pressure changes in the vessels, are reset to lower levels through exercise (more blood flow needed hence less resistance) * Endothelial dysfunction (inability to facilitate vasodilation and therefore increase blood flow) is thought to occur in the early stages of atherosclerosis and is a trigger of myocardia ischemia (heart attack) 8) Effect of cumulative exercise: - Mild Hypertension; Exercise sufficient to lower bp below hypertensive cutoffs, but may not be able to get it to normal/optimal levels. - Exercise prescription 3-5 days a week at 40-60% VO2 max. 9) Should BP remain low throughout our lifetime? - Ex. Kung Bushman of the Kalahari Desert where thei mode of life has prevailed over 95% of human history -Diet low in salt, sat fats and carbs -Diet high in polyunsaturated oils, roughage, vitamins and minerals -Physically active and have a tension free lifestyle -15-20 hours a week hunting/ gathering rest of time for relaxing and visiting. -Systolic and Diastolic both remain low throughout their lifetime in both M & F - Developed countries we see a rise in both BP’s Hypertension and physical Activity: -Harvard Alumni Study - Looked at people who played on varsity sports teams vs those who didn’t -Followed up to 40 +45 years -Elite Sports developed more heart attacks - Elite more likely to stop after playing rather than have a lifetime of physical activity. Aerobics Center Longitudinal Study:  Increase in PA = decrease or less chance of hypertension  Meta analysis:  Reduction systolic 3.4mmHg  Reduction of diastolic 7.58 mmHg  Meta analysis means statistical results of a bunch of studies to get a summary of the results. 10) Summary CVD and Exercise: - CVD diseases are a major cause of mortality and morbidity in developed countries, and their prevalence is increasing in developing countries -Atherosclerosis is a major cause of CHD. Long clinical history and may well be progressed before symptoms occur. - Inactivity and low fitness are strong risk factors for CHD. Both confer an increase in risk similar to that associated with smoking, hypertension and high blood cholesterol. Being physically active or fit may reduce the risk of having a stroke. - Mechanisms by which PA may modify CVD risk includes effects on lipoprotein metabolism, blood pressure and endothelia function. - Exercise reduces symptoms of claudication and heart failure and may help lower blood pressure in hypertensive individuals. LECTURE #11 CARDIOVASCULAR DISEASE: *Midterm: Damage of endothelial lining, and consequences of a heart attack (atherosclerosis) Heart attack grill: -Promoting obesity, people over 350lbs eat for free…the owner is an enabler! * People who normally wouldn’t consider themselves as risk takers nevertheless take daily risks by smoking, drinking, eating unhealthy and the consequence can be a heart attack. Dyslipidemia: An important risk factor in the context of cardiovascular disease, and appropriate intervention (pharmalogical and non-pharmalogical (ie therapeutic benefits of lifestyle (diet and exercise) can have a significant impact on clinical outcomes. This information will provide a foundation of knowledge on which to base the assessment and treatment of dyslipidemia patients. 1) Cardiovascular disease (CVD): A name given to a group of disorders of the heart and blood vessels (ie diseases) Examples: -Hypertension -High blood pressure -CHD (ischemic heart disease) -Cerebrovascular disease (stroke/brain attack) -Peripheral vascular disease or peripheral artery disease (discoloration, swelling, gangrene) -Heart failure (unable to pump) -Rheumatic heart disease (valves are damaged by rheumatic fever inflammatory disease damages connective tissue, starts like strep throat virus, common age 5-15) -Cardiomyopathies (athletes usually die of hyper-myotrophy increased heart size, highest incidence in US, heart muscle become inflamed, viral infection, hypertension, heart disease) 2) Coronary Artery Disease (CAD synonymous with CHD): Happens when arteries that supply the heart with blood become narrowed and hardened. This is due to the build of cholesterol and other material called plaque, on the inner walls. As the build up grows less blood can flow through the arteries. As a result the heart muscle cant get the blood or oxygen it needs. This can lead to chest pain (angina) or a heart attack. Most heart attacks happen when a clot suddenly cuts off the hearts blood supply, causing permanent heart damage. * decreased BF = decrease o2 to heart. Clots can for from vigorous activity 3) Atherosclerosis: A progressive thickening and hardening of the walls (forms calcium deposits) of medium and large arteries as a result of fat deposits on their inner lining. Atherosclerosis is responsible for much CAD (angina, heart attacks and strokes) * Plaque builds up as we age and our bodies become less efficient with removal * We start life with very little plaque; see a spike when we go through puberty, then a gradual increase over life. Without latent buildup we don’t have as much risk for clot breakoff. (Dr. Merri Knudtson**???) 4) Natural History of Atherosclerosis (diagram) *MIDTERM* 1) between 10-20 we start to see a fatty streak (influence of hormones (puberty) (if we increase the amount of exercise we can decrease the size of the fatty streak) 2) 20-30 we start to see fibrous plaque (infiltration of new muscle cell) 3) 30-40 calcification completed lesion (hemorrhage , ulceration, thrombus) (Platelets in plaque can become a hemorrhage) ---------------------------------Clinical Horizon----------------
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