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Anatomy and Physiology for the Heart!
Cardiac Anatomy and Physiology Geraldine Innes Development Co-ordinator for Phase III in the Community Have a Heart Paisley Please Note: The information contained in this presentation is accurate as of production in May 2006. Subsequent changes to clinical or other guidelines since this date should be incorporated into any adaptation of this material. Topics • Cardio-Respiratory Fitness • Disease Process • Cardiac Physiology • Pharmalogical Therapy Cardiorespiratory Fitness • VO2 Max (Maximum amount of oxygen used, litres consumed per minute) = Heart Rate x Stroke Volume x a-Vo2 diff • Oxygen Uptake: Normal Resting 3.5ml 02/kg/min = 1 Met • Healthy Un-conditioned maximum = 10 METS (Metabolic Equivalents) • WHAT IS THIS INFLEUNCED BY? – Age, Gender, Exercise Training, De-training, Medication, Illness, Different Environments • Effects of Training – Can increase 10-30% with the greatest improvements occurring in the most de-conditioned. CARDIAC PERFORMANCE Maximum Oxygen Consumption With Coronary Heart Disease • People with CHD have below average age and gender predicted Cardiorespiratory fitness levels • In Coronary Heart Disease peak VO2 is reduced due to reduced cardiac output • Benefits of exercise training? – Improved stamina – An ability of tolerate routine - Active Daily Living – Less fatigue – Decrease in angina symptoms Myocardial Blood Flow and Metabolism • Normal contraction requires adequate supply of Adenosine Tri Phosphate(ATP) in aerobic oxidation • Myocardium extracts nearly all available oxygen from the capillary blood flow (unlike skeletal muscle) • Blood flow is determined by Blood Pressure and Vascular Resistance • A significant decrease in flow can be caused by Arteriosclerosis Disease Process • Arteriosclerosis • Endothelial injury and Dysfunction • Artery Occlusion – Plaques • Progression of Plaques Arteriosclerosis Disease Progression Injury to the Artery • Tobacco smoke and other chemical irritants from tobacco • Low Density Lipoprotein (LDL) • Hypertension • Glycated substances resulting from hyperglycaemia and Diabetes Mellitus • Infectious agents (Herpes, Chlamydia) Ischaemia • What is it? – When myocardial blood flow is inadequate to provide the required amount of oxygen for ATP regeneration • Ischaemic Cascade – Diastolic Dysfunction – Systolic Dysfunction – Electrocardiogram (ECG) Abnormalities – Symptoms of Angina Cardiac Physiology – Heart Rate – Stroke Volume – Cardiac output – Rate Pressure Product – Blood pressure = Cardiac Output (CO) x Total Peripheral Resistance (TPR) – Arteriovenous Oxygen (a-v02) Difference Heart Rate • Normal acute heart rate response to exercise • Abnormal Response • Chronotropic Incompetence – Failure of the heart rate to achieve predicted maximum in absence of a beta blocker • Chronic Exercise heart rate response – Heart Rate at rest and at any given submax workload is less. Stroke Volume • Stroke Volume is a function of: – Preload, Afterload and Myocardial Contractility • Normal resting 60-100ml/beat, Maximum 100-200ml/ beat • Ejection Fraction is 57-73% • Acute Response to Exercise – Increases curvilinear up to 50% of maximum aerobic capacity • Chronic Response to Exercise – Increased Force of Contraction (FOC) and increased Ejection Fraction (EF) – Increased Central blood volume which increases End Diastolic Volume (EDV)and Stroke Volume (SV) Cardiac Output (CO) • = Heart Rate x Stroke Volume • Normal 5 litres per minute • Acute Exercise – approx max 20 litres . Linear increase from both HR and SV up to 50% of oxygen capacity • In untrained individual heart rate plays a bigger role than stroke volume • Chronic Exercise: CO remains unchanged • In CHD clients CO may be reduced due to chronotropic incompetence or Left Ventricular Dysfunction. Rate Pressure Product • RPP= Systolic Blood Pressure x Heart Rate • Normal Resting 5400-14000 • Normal Exercise Response >25000 • Chronic Exercise adaptations – Reduced myocardial workload due to decrease in Heart Rate and Blood Pressure and any given submax workload Blood Pressure • BP= CO x TPR – Normal >140/90. Max <220/115 • Acute Exercise – Systolic Linear increase with Cardiac Output. Diastolic remains the same – 10mm Hg / MET • Abnormal Response – A drop in systolic BP or failure to increase with increasing workloads – Client with significant CHD may exhibit exercise hypotension • Chronic Training response – Reduction of BP at rest and during exercise AVo2 Difference • Greater exchange of gases • Increased mitochondria • More ATP • Improved blood flow Pharmacological Therapy – Beta Blockers – Nitrates • Used for angina, hypertension • Vasodilate the Coronary and arrhythmia Arteries which increases flow to heart muscle • Blocks the action of norepinephrine • Reduces preload and afterload • Reduces Heart Rate and Blood • Possibility of Postural pressure Hypotension • Slows metabolism • Increase in exercise tolerance by preventing angina and • Risk of Postural Hypotension increasing the ischaemic threshold DRUGS – Ace Inhibitors – Statins – Used for hypertension, heart – Inhibits an enzyme that failure and post Myocardial catalyses a step in the Infarction (MI) synthesis of cholesterol in – Stops angiotension I converting the liver to angiotension II which lowers – Reduces LDL, Triglycerides blood pressure and reduces fluid and increases High Density retention Lipoprotein (HDL) – Reduces afterload enabling the – No effect on exercise but Left Ventricular to pump more side effect is muscle pains easily – Possible increase in exercise capacity for Heart Failure patients Drugs • Anti-Platelet • Anti-Arrhythmic • Aspirin/Clopidogrel • Digoxin and Amiodarone – Works by decreasing – Controls heart rate and enhances contractility platelet aggregation – Lengthens the refractory period, – Used for Secondary prolonging the period of re-excitation Prevention of and therefore suppressing arrhythmia’s Cardiovascular and – Possible slower heart-rate response to Cerebrovascular thrombosis exercise – Possible risk of bleeding, – Reduced exercise capacity due to safe advise when using depressant effect on the myocardium Gym Equipment Selected References • Clinical Exercise Physiology: Ehrman et al (2003) • Exercise Physiology: McArdle, Katch and Katch (1996) Fourth Edition • American College of Sports Medicine (ACSM) Guidelines for Exercise Testing and prescription. Seventh Edition 2006
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