* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Cardiovascular System & Disease
Saturated fat and cardiovascular disease wikipedia , lookup
Lutembacher's syndrome wikipedia , lookup
Management of acute coronary syndrome wikipedia , lookup
Cardiac surgery wikipedia , lookup
Quantium Medical Cardiac Output wikipedia , lookup
Jatene procedure wikipedia , lookup
Cardiovascular disease wikipedia , lookup
Antihypertensive drug wikipedia , lookup
Coronary artery disease wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
Course Contents Section 1 Exercise and the cardiovascular system 1.1 Structure and function of the cardiovascular system 1.2 Pathology of cardiovascular diseases (CVD) 1.3 Role of exercise in prevention and treatment of CVD Section 2 Exercise and Metabolism 2.1 Energy 2.2 Body composition & Weight Control 2.3 Diabetes Mellitus 2.4 Osteoporosis BHF Survey, 2007 Scottish Stats Deaths from CHD The CVS is subject to disease processes e.g. Atherosclerosis & hypertension are disease processes that lead to the development of : Structure/ Function of CVS 2 parts: Pump Vessels Heart Heart external view Double pump Right side – pumps to lungs (pulmonary circulation) BICUSPID Left side – pumps to body (systemic (mitral) circulation VALVE Left side > right side TRICUSPID VALVE Heart Valves prevent backflow of blood Coronary arteries supply heart muscle with blood (food & oxygen) SEMILUNAR VALVE Heart & Blood Supply Pulmonary artery – deoxygenated blood Pulmonary N.B. Hepatic Portal vein Vein – oxygenated Coronary arteries – heart. supply heart does not return blood to Coronary veins – drain into the right atrium Supplies liver with products of digestion. Aorta - blood body (from L. ventricle) Important in firstto pass metabolism Vena cava (sup./toxins inf.)to -bedrain (into – allowing broken body down before systemic circulation R atrium) Heart Beat Heart beat is endogenous (continues to beat if removed from body) Rhythmical contraction of muscles Under nervous/ hormonal control Influence strength & frequency of contraction Heart beat originates in SinoAtrial node Max. rate limited (refractory period) AV node collects signal and initiates ventricular contraction via Bindle of His after a short delay. In disease, arrythmia can develop in damaged tissue Extra heart beat can occur initiated by damaged tissue Heart beat signal propagated through heart by bundle of His (atria – ventricles), & Purkinje fibres (nerves through muscle tissue) Heart Sounds Stethoscope Listen to heart sounds Lub dub (closing of valves) Lub – closure of AV valves Dub – closure of semilunar valves Diagnostic of valvular disease Leaky – indistinct lub/ dub Heart & ECG ECG is a record of the electrical signals producing the heart beat ECG= ElectroCardioGram Used diagnostically to show heart problems Cardiac Cycle DIASTOLE (relaxed phase) Venous filling of atria Atria distend Some passive flow into ventricles SYSTOLE (contractile phase) SA initiates atrial contraction Blood expelled from atria into ventricles Bundle of His conducts excitation to ventricles/ propagated rapidly by Purkinje fibres Ventricle contracts expels blood into arteries Contraction ends, relaxes (refractory period) Blood Vessels Arteries Must withstand high pressure Thick walled Mainly elastic fibres near heart Arteries more distant from heart less elastic fibres/ more muscle (under nervous control) Stretch to absorb pressure of blood expelled by heart At diastole stretched arteries relax so maintain blood flow (120/80 mmHg) Muscles regulate blood flow into capillary beds Arteries lead to arterioles Can have pre-capillary sphincters to completely close blood flow e.g to skin in cold Blood Vessels Capillaries Wall single cell thick Allows exchange of soluble substances No cell more than few cell widths from a capillary Diffusion rapid over these short distances Blood vessels Veins Less muscle/ elastic fibre than arteries Floppy Low pressure in vein – requires valves to stop backflow Muscle pumping in calves helps venous return (Economy Class Syndrome) Blood Pressure High arterial blood pressure (80-120 mmHg (systolic/ diastolic) Rapid fall in BP in arterioles/ capillaries Very low BP in veins Blood Pressure BP quoted as Systolic / diastolic Measure with a sphygmomanometer Block all blood flow Slowly release pressure Systoliic BP = pressure when sound of artery closing (snap) is heard Diastolic BP = pressure when all noises stop Summary of Structure Cardiovascular Disease Coronary Heart disease Angina pectoris Myocardial infarction CVD s Cerebrovascular disease Stroke (cerebrovascular accident (CVA)) Cardiovascular disease pathology Two major pathological processes lead to CVD Atherosclerosis Narrowing & hardening of arteries (claudication/ angina) Damage to endothelium – promotes blood clot formation blocking arteries – thrombosis/ embolism Hypertension Prolonged, elevated blood pressure – Primary – no known cause – Secondary – caused by pathology Kidney disease Phaeochromacytoma (excess epinephrine produced) Atherosclerosis Typically starts in childhood, progresses in adulthood. Damage to the arterial wall caused by e.g. elevated levels of cholesterol and triglyceride in the blood high blood pressure. tobacco smoke diabetes Atherosclerosis Fat accumulates under inner lining of arteries As disease progresses, fibrous material / calcium/ lipids (inc. cholesterol) accumulates (atheroma) Bulges into lumen of vessel Starts to reduce diameter of artery Restricts blood flow Reduces elasticity of arterial wall Can lead to high blood pressure Atherosclerosis Progression accelerated by: High blood cholesterol (especially LDL or "bad" cholesterol over 100 mg/dL) Cigarette smoking and exposure to tobacco smoke High blood pressure Diabetes mellitus Obesity Physical inactivity Cholesterol & CVD Cholesterol – steroid – Cell membranes, hormones, bile salts Most cholesterol in blood is synthesised by liver Dietary cholesterol acts to suppress liver biosynthesis Dietary cholesterol NOT important risk factor for CVD (overall cholesterol should be less than 200mg/dl) Saturated fats (animal) are used by liver to produce cholesterol High dietary saturated fat INCREASES blood cholesterol levels!! Cholesterol & CVD Cholesterol – insoluble in blood Transported attached to a protein LIPOPROTEIN Two types of LIPOPROTEIN HDL – High density lipoprotein LDL – Low density lipoprotein HDL – transports cholesterol to liver for destruction LDL – transports cholesterol to body cells for deposition GOOD BAD In abnormal circumstances LDL will deposit cholesterol in arteries Cholesterol & CVD LDL (bad) – 60-70% blood cholesterol As LDL increases risk of atherosclerosis increases HDL (good) – 20-30% blood cholesterol AS HDL increases risk of atherosclerosis decreases Risk of CHD is predicted from HDL:LDL ratio High HDL (40mg/dl or more):LDL is GOOD Exercise, low fat diet, not smoking improve HDL:LDL ratio Atherosclerosis – Heart - AP Narrowing of coronary arteries leads to ischaemia (inadequate blood flow) Pain - angina pectoris (AP) due to ischaemia in heart muscle AP only during exertion of heart (when O2 needs are high) Glycerol trinitrite tablets release Nitric oxide (dilates blood vessels) Angioplasty/ Stents Bypass surgery Atherosclerosis – Embolism Clots thrombus-attached embolus-travelling Embolus/ thrombus can cause blood supply to a region of the heart muscle (myocardium) to become blocked, causing myocardial infarction Thrombosis/ embolus may occur in cerebral artery – stroke (cerebrovascular accident-CVA) or lungs pulmonary embolus Myocardial Infarction Myocardial infarction – MI (death of heart tissue) Caused by a sudden blockage to a coronary artery. Due thrombosis/ embolis Atherosclerosis (may cause angina symptoms) leads to increased likelihood that thombosis will occur. Causes pain (15 min) in arm, neck, jaw; nausea. If large artery blocked – collapse, sudden death Tissue dies forming a scar, can cause: Heart failure (weak pumping action) Arrythmia, irregular contraction Cardiac arrest – ventricular fibrillation Hypertension Persistently high resting blood pressure e.g. diastolic >90mmHg (normal 120/80; high 140/90) Often caused by atherosclerosis leading to narrowing of arteries or loss of elasticity Risk factor for majority of CVDs (incl. CHD) Hypertension – risk factors Diet (high salt (Na+), high fat) Nicotine (vasoconstrictor) Smoking Obesity Genetic predisposition Stress Risk Factors for CVD- SQA Modifiable Diet, Smoking, Activity, Obesity Non modifiable Age, Gender, Race, Heredity Risk factors Summary What other factors contribute to heart disease risk? •Diabetes•The mellitus —heart disease in people who drink risk of •Obesity andseriously overweight — of alcohol •Diabetes increases your risk developing moderate amounts (anofaverage of one drink cardiovascular disease. for who women or excess two drinks forfat men per day) isiflower than •People have body — especially a lot of it is at •risks in arenondrinkers. even greater if blood sugar is notas well controlled. One drink is defined 1-1/2 fluid the waist — are more likely to develop heart disease and stroke Physical inactivity •Aboutounces three-quarters of people spirits with diabetes of some form of (fl oz) ofother 80-proof (such asdie bourbon, even if they have no risk factors. Regular, moderate-to-vigorous physical activity helps prevent heart heart or blood vessel gin, disease. Scotch, vodka, etc.), 1 fl oz of 100-proof spirits, 4 fl High blood pressure High cholesterol and blood blood vessel disease. •Excess weight increases the heart's work. Itworkload, also raises blood oz of wine or 12 fl oz of beer. It's not recommended High blood pressure increases the heart's causing As blood cholesterol rises, so does risk of coronary heart The more vigorous the activity, thetriglyceride greater your benefits. pressure and blood cholesterol and levels, and that nondrinkers start using alcohol or that drinkers the heart to thicken and become stiffer. disease. Physical activity can help control blood cholesterol, diabetes and lowers HDL ("good") cholesterol levels. increase the amount they drink. Tobacco It also smoke increases your risk of stroke, heart attack, kidney failure When other highpressure blood pressure and tobacco obesity, as risk wellfactors as help(such loweras blood in some people. and • congestive Smokers' heart risk failure. ofrisk developing coronary disease is obese 2–4 times that •It can also make diabetes more likelymore. toheart develop. Many smoke) are present, this increases even of nonsmokers. highcholesterol blood pressure exists with obesity, smoking, highby and overweight people may have difficulty losing weight. AWhen person's level is also affected by age, sex, But blood • cholesterol riskdiet. factor forfew sudden oras diabetes, thedeath: risk about heart twice attack the orheart risk stroke of losing evenlevels as 10cardiac pounds, youof can lower your heredity and increases nonsmokers. several times. disease risk. • Exposure to other people's smoke increases the risk of heart disease even for nonsmokers. Exercise & CVS Cardiovascular system (CVS) delivers oxygen & nutrients to body tissues, removes wastes During exercises more O2 & nutrients required by exercising tissues (muscles), wastes removed Exercise effects Cardiovascular system function Cardiac output increased Circulation redistributed to important tissues Cardiac Output Cardiac output (C.O.) = volume of blood pumped per min. by the heart Regulated by: – Heart rate (H.R.) – Stroke volume (S.V.) C.O. = H.R. x S.V. Exercise effects on Heart Exercise causes HR & SV to increase i.e. CO Meets needs of muscles Athlete’s Heart Regular exercises strengthens heart muscle Ventricular mass (echocardiography) increases (210-300g) Force of contraction , more blood expelled per beat (SV ) Ventricular volume also increases (100-180ml) (SV ) Consequently HR at rest of a trained athlete (Bjorn Borg – 32bpm, Miguel Induraine, 29bpm) CO of trained heart increased so more O2 and food delivered at max. HR Therefore max. level of activity greater Redistribution of Blood flow During exercise blood flow directed away from non-essential needs (gut, kidney) Redirected to heart, muscles, skin (cooling) Vasodilation/ vasoconstriction of supplies to these tissues. Exercise & Blood Pressure Cardiac Output increased (HR/ SV) Tends to increase BP Vasodilation of blood supply to muscles Increases volume of vascular system Peripheral vascular resistance reduced Tends to reduce BP Overall slight increase in BP Systolic increase > diastolic Exercise & Hypertension Regular exercise, produces long term, moderate fall in BP Offsets age related hardening of arteries Acutely, a fall in BP is also found following exercise. Role of exercise - in preventing CVD Decreases a number of risk factors: HDL , LDL Resting HR Arterial blood pressure Body fat (i.e. obesity ) Reduces development of atheroma Reduces stress Moderate exercise 3-5 times per week lasting more than 20mins Exercise testing - Introduction Monitor recovery from MI Monitor improvement in athletic training programme Measure aerobic capacity Assess performance of respiratory and cardiovascular systems in delivering oxygen Exercise testing - Principles Oxygen required by body to work Maximum work rate – determined by body’s ability to deliver oxygen to body VO2max – maximal oxygen uptake Higher the VO2max, the greater the aerobic fitness Measure by exercising to exhaustion and directly measure O2 uptake and CO2 ouput Exercise testing – Direct Method Treadmill/ bicycle ergometer Using online gas analysis Progressively increase workload until no further increase in O2 consumption i.e. exercise to exhaustion Oxygen consumption at that point = VO2max Suitable for fit people Exercise testing – Indirect Method Shuttle test Run between two cones (20m apart) Rate determined by a tape (beep) Subject continues until they can’t maintain pace Number of completed shuttles can be used to predict VO2max Exercise Testing – Sub maximal If exercise to exhaustion clinically contraindicated Submaximal testing used Patient O2 consumption measured at various levels of work intensity (submaximal) Graph of O2 consumption vs. HR plotted Theoretical max. HR calculated (220-age) Graph extrapolated to estimate theoretical max. O2 consumption Exercise Testing – Sub maximal Assumptions: Direct relation between HR and O2 consumption and intensity of exercise Sources of error: HR affected by other factors: – Emotion – Temperature – Anxiety Predicted HR may be inaccurate for a given individual Exercise Stress Testing Used to diagnose heart abnormality only present under stressed conditions Bruce Protocol Treadmill speed/gradient increased incrementally Exercise to exhaustion ECG can be monitored to evaluate effect of exercise on heart