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Chapter 9 CARDIOVASCULAR DISORDERS BY Dr. Uche Amaefuna- Obasi •THERE ARE MORE TO LECTURES THAN JUST SLIDES…. An Epidemiological Overview • Cardiovascular disease (CVD) is the leading cause of death in the U.S. • In 2005 CVD accounted for approximately 38 percent of all deaths • CVD has been the number one killer in the U.S. since 1900 except for 1918 (influenza) • More that 2,500 Americans die from CVD each day • Among women, 1 in 2.6 deaths from CVD Death Rates for Cardiovascular Disease, Including CHD and Stroke for Selected Countries Understanding The Cardiovascular System • Cardiovascular system includes: the heart, arteries, arterioles, capillaries, venules, and veins • The heart – – – – – Muscular, four chambered pump Contracts 100,000 times per day Two upper chambers: atria Two lower chambers: ventricles Tricuspid, pulmonary, mitral, and aortic valves Heart Function • Deoxygenated blood enters the right atrium • From the right atrium blood moves to the right ventricle, pumped through the pulmonary artery to the lungs • Oxygen blood enters the left atrium • Blood from the left atrium is forced into the left ventricle • The left ventricle pumps blood through the aorta to various parts of the body Overview • Diagnostic Tests for Cardiovascular Function • General Treatment Measures for Cardiac Disorders • Coronary Artery Disease (CAD) – Arteriosclerosis – Atherosclerosis – Myocardial Infarction (MI) • Cardiac Arrhythmias – Sinus node abnormalities – Atrial conduction abnormalities – Cardiac arrest • Congestive Heart Failure (CHF) • Arterial Diseases – Hypertension • Shock Diagnostic Tests for Cardiovascular Function • ECG – Monitors arrhythmias, MI, infection, pericarditis – Studies conduction activation and systemic abnormalities • Auscultation – Studies heart sounds using stethoscope • Exercise stress test – Assess general cardiovascular function – Checks for exercise-induced problems • Chest X-ray Film – Shows shape, size of heart – Evidence of pulmonary congestion associated with heart failure – Nuclear imaging Diagnostic Tests • Cardiac Catheterization – Visualize inside of heart, measure pressure, assess valve and heart function – Determine blood flow to and from heart Diagnostic Tests • Angiography – Visualization of blood flow in coronary artery – Obstruction assessed and treated • Basic catheterization • Balloon angioplasty Diagnostic Tests • Doppler Studies – Assessment of blood flow in peripheral vessels – Microphone records sounds of blood flow • Can detect obstruction • Blood tests – Assess triglyceride and cholesterol levels – Electrolytes – Hb, hematocrit, cbcs • Arterial Blood Gas Determination – Essential for pts with shock, MI – Check current oxygen levels, acid-base balance General Treatment Measures for Cardiac Disorders • • • • Dietary modification Regular exercise program Quit smoking Drug therapy Drug Therapy • Vasodilators (Nitroglycerin) – Provide better balance of oxygen supply and demand in heart muscle – May cause low bp • Beta-blockers (Metoprolol or Atenolol) – Treats angina, hypertension, arrhythmias – Blocks beta1-adrenergic receptors in heart • Prevent epine from increasing heart activity Drug Therapy • Calcium ion channel blockers – Block movement of calcium – Decrease heart contraction • Antiarrhytmatic for excessive atrial activity • Antihypertension and vasodilator • Digoxin – Treats heart failure – Increases efficiency of heart • Decreases conduction of impulses and HR • Increases contraction of heart – Pts must be checked for toxicity • Antihypertensive drugs – Decrease bp to normal levels – Include: • Adrenergic blocking agents • Calcium ion blockers • Diuretics • Angiotensin-converting enzyme (ACE) inhibitors – Used to treat hypertension, CHF, after MI Drug Therapy • Adrenergic Blocking drugs – Act on SNS (sympathetic nervous system), block arteriole alpha adrenergic receptors, or act directly as vasodilator • ACE Inhibitors – Treat hypertension, CHF (congestive heart failure) • Diuretics – Remove excess water, sodium ions – Block resorption in kidneys – Treat high bp, CHF Drug Therapy • Anticoagulant – Decrease risk of blood clot formation – ASA (acetylsalicylic acid) decreases platelet adhesion – Block coagulation process • Cholesterol or lipid reducing drugs – When diet and exercise fail – Decrease LDL and cholesterol Anatomy of the Heart Types Of Cardiovascular Disease • • • • • • • Atherosclerosis Coronary heart disease (CHD) Chest pain (angina pectoris) Irregular heartbeat (arrhythmia) Congestive heart failure (CHF) Congenital and rheumatic heart disease Stroke CAD—Arteriosclerosis: Pathophysiology • General term for all types of arterial changes • Best for degeneration in small arteries and arterioles • Loss of elasticity, walls thick and hard, lumen narrows CAD—Atherosclerosis: Pathophysiology • Presence of atheromas – Plaques • Consist of lipids, cells, fibrin, cell debris – Lipids usually transported with lipoproteins Artherosclerosis • Characterized by deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin in the inner lining of the artery • Hyperlipidemia – abnormally high blood lipid level • Plaque – the buildup of deposits in the arteries Coronary atherosclerosis Coronary atherosclerosis Atherosclerosis--Pathophysiology • Analysis of serum lipids: – Total cholesterol, triglycerides, LDL, HDL • LDL – High cholesterol content – Transports cholesterol liver cells – Dangerous component • HDL – “good” – Low cholesterol content – Transports cholesterol cells liver Consequences of Atherosclerosis Atherosclerosis—Etiology • • • • • • • • • Age Gender Genetic factors Obesity, diet high in cholesterol, animal fats Cigarette smoking Sedentary life style Diabetes mellitus Poorly controlled hypertension Combo of BC pills and smoking Atherosclerosis—Diagnostic Tests • Serum lipid levels • Exercise stress test • Radioisotope Atherosclerosis—Treatment • • • • • • Decrease cholesterol and LDL Decrease sodium ion intake Control primary disorders Quit smoking Oral anticoagulant Surgical intervention – Percutaneous transluminal coronary angioplasty (PTCA) – Cardiac catheterization – Laser beam technology – Coronary artery bypass grafting CABG Coronary Heart Disease • Myocardial infarction (MI) or heart attack – blood supplying the heart is disrupted • Coronary thrombosis – blood clot in the artery • Embolus – when the blood clot is dislodged and moves through the circulatory system • Collateral circulation - if blockage to the heart is minor, an alternative blood flow is selected Angina Pectoris • Ischemia – reduction of the heart’s blood and oxygen supply • The more serious the oxygen deprivation the more severe the pain • Nitroglycerin – drug used to relax (dilate) the veins • Beta blockers control potential over activity of the heart muscle Angina Pectoris • This is a symptom complex. Symptoms caused by transient myocardial ischaemia that falls short of inducing the cellular necrosis that defines myocardial infarction. • Three variants:– Stable angina – Prinzmental angina – Unstable angina Angina Pectoris • Stable Angina – Most common form. Chronic stenosing coronary atherosclerosis, reaching a critical level, leaving the heart vulnerable to increased demand. • Typically relieved by rest or a vasodilator Prinzmental Angina • • • • Uncommon pattern Occurs at rest Documented to be due to arterial spasm Unrelated to physical activity, heart rate or blood pressure. • Generally responds to vasodilators. Unstable Angina • Pattern here is the pain, occurs with progressively increasing frequency and tends to be more prolonged • Associated with disruption of the atherosclerotic plaque, with superimposed thrombosis, embolisation or spasm. • Predictor of Myocardial Infarction Effects of ischaemia on myocytes • Onset of ATP Depletion • Loss of contractility • ATP reduced – to 50% of normal – To 10% of normal • Irreversible injury • Microvascular injury • Seconds • < 2 minutes • • • • 10 minutes 40 minutes 20-40 minutes > 1 hour Arrythmias • An irregularity in heart rhythm • Tachycardia – racing heart in the absence of exercise or anxiety • Bradycardia – abnormally slow heartbeat • Fibrillation – heart beat is sporadic, quivering pattern Cardiac Arrhythmias • Alteration in HR or rhythm • ECG monitors – Holter monitors • decreases efficiency of heart’s pumping cycle – Slight increase in HR increases CO – Very rapid HR prevents adequate filling in diastole – Very slow HR reduces output to tissues • Irregular contraction inefficient – Interferes with normal filling/emptying cycle CA: Sinus Node Abnormalities • Brachycardia – Regular but slow HR • Less than 60 beats/min – Results from vagus nerve stimulation or PNS stimulation • Tachycardia – Regular rapid HR • 100-160 beats/min – SNS stimulation, exercise, fever, compensation for low blood volume CA: Atrial Conduction Abnormalities • Premature Atrial Contractions (PAC) – Extra contraction or ectopic beats of atria – Irritable atrial muscle cells outside conduction pathway • Interfere with timing of next beat • Atrial flutter – HR 160-350 beats/min – AV node delays conduction • Slower ventricular rate Treatment of CA • • • • Cause should be determined and treated Easiest to treat are those due to meds SA node problems may require a pacemaker Some may require defibrillators Cardiac Arrest • Cessation of all activity in the heart • No conduction of impulses (flat line) • May occur b/c: – Excessive vagal nerve stimulation (decreases heart) – Drug toxicity – Insufficient oxygen to maintain heart tissue • Blood flow to heart and brain must be maintained to resuscitate Congestive Heart Failure (CHF) • Damaged or overworked heart muscle is unable to keep blood circulating normally • Affects over 5 million Americans • Damage to heart muscle may result from: rheumatic fever, pneumonia, heart attack, or other cardiovascular problem • Lack of proper circulation may allow blood to accumulate in the vessels of the legs, ankles, or lungs • Diuretics relieve fluid accumulation Congenital And Rheumatic Heart Disease • Congenital heart disease affects 1 out of 125 children born • May be due to hereditary factors, maternal diseases, or chemical intake (alcohol) during fetal development • Rheumatic heart disease results from rheumatic fever which affects connective tissue Rheumatic fever • Once the most common cause of valvular heart disease in Hong Kong. • It is an acute immunologically mediated , multi-system inflammatory disease that occurs a few weeks after an episode of Group A (ßhemolytic) streptococcal pharyngitis. Chronic Rheumatic Valvular Heart Disease • Most important consequence of rheumatic fever • Inflammatory deformity of valves – Almost always involve the mitral valve – Involvement of aortic or other valves also common Characteristics of rheumatic valvular disease • Acute phase – Foci of fibrinoid degeneration surrounded by lympocytes – Aschoff bodies – Most distinctive within the heart, but widely disseminated. – Pancarditis • Pericarditis • Myocarditis • Verrucae vegetations (1-2 mm) Characteristics of rheumatic valvular disease • Chronic – Leaflet thickening – Commissure fusion – Shortening, thickening and fusion of chordae tendinae Stroke • Occurs when the blood supply to the brain is interrupted • Thrombus – blood clot • Embolus – free flowing clot • Aneurysm – bulging or burst blood vessel • Transient ischemic attack (TIA) – brief interruptions that cause temporary impairment Common Blood Vessel Disorders CAD: Myocardial Infarction— Pathophysiology • Coronary artery completely obstructed – Prolonged ischemia and cell death of myocardium • Most common cause is atherosclerosis with thrombus • 3 ways it may develop: – Thrombus obstructs artery – Vasospasm due to partial occlusion – Embolus blocks small branch of coronary artery • Majority involve L ventricle – Size and location of infarction determine severity of damage MI—Signs and Symptoms • Pain – Sudden, substernal area – Radiates to L arm and neck – Less severe in females • Pallor, sweating, nausea, dizziness • Anxiety and fear • Hypotension, rapid and weak pulse (low CO) • Low grade fever MI—Treatment • • • • • Rest, oxygen therapy, morphine Anticoagulant Drugs Cardiac rehabilitation Prognosis depends on site/size of infarct, presence of collateral circulation, time elapsed before treatment • Mortality rate in 1st year – 30-40% due to complications, recurrences Myocardial Infarction Transmural Infarction – The ischaemic necrosis involves the full or nearly the full thickness of the ventricular wall in the distribution of a single coronary artery. – Usually associated with chronic coronary atherosclerosis, acute plaque change and superimposed completely obstructive thrombosis. Myocardial Infarction • Subendocardial infarct – Limited to the inner one-third or at most one half of the ventricular wall – May extend laterally beyond the perfusion territory of a single coronary artery – In a majority of cases, there is diffuse stenosing coronary atherosclerosis. Gross changes of myocardial infarction • Gross changes – None to occasional mottling (up to 12 hours) – Dark mottling (12-24 hours) – Central yellow tan with hypereamic border (3-7 days) – Gray white scar (2-8 weeks) Varying gross appearance of myocardial infarction Recent and Old Myocardial Infarcts Microscopic changes of myocardial infarct • Early coagulation necrosis and oedema; haemorrhage (4-12 hours) • Pyknosis of nucleic, hypereosinophilia, early neutrophilic infiltrate (12-24 hours) • Coagulation necrosis, interstitial infiltrate of neutrophils (1-3 days) • Dense collagenous scar (> 2 months) Laboratory detection of myocardial infarction • This is based on the measurement of intracellular macromolecules leaked from the damaged myocytes into the circulation • Creatine kinase – particularly the MB isoenzyme • Lactate dehydrogenase • Troponin – Troponin 1 and Troponin T Other diagnostic tools • • • • Electrocardiogram – Q waves Echocardiogram Radioisotope studies Magnetic Resonance Imaging Electrocardiogram (ECG) changes Acute effects of myocardial infarction • • • • • Contractile dysfunction Arrhythmias Cardiac rupture Pericarditis Sudden death – Invariably this would be due to a lethal arrhythmia (asystole or ventricular fibrillation) Pathological complications of myocardial infarction • • • • Infarct extension Mural thrombus Ventricular aneurysm Myocardial rupture – Ventricular free wall – Septal – Papillary muscle Infarct extension Ruptured Myocardial Infarct Old myocardial infarct showing evidence of thinning of ventricular wall replaced by fibrous scar Fibrous scarring with compensatory hypertrophy of unaffected ventricular wall Ventricular wall aneurysm Anatomy of Heart Valves • Aortic valve – Commonly tricuspid semi lunar valves. Can be congenitally bicuspid. • Mitral valve – Bi-cuspid flaps supported by chordae tendinae attached to papillary muscles • Pulmonary valves – Tricuspid semi lunar valves • Tricuspid valves – Tri-cuspid flaps supported by chordae tendinae. Response to injury • Mechanical injury – superficial fibrous thickening over preserved architecture. • Inflammation – invariably leads to vascularisation of structure, fibrosis leads to decrease in size/surface area. • Degenerative changes – distortion and increase in size due to deposits of material such as calcium salts, cholesterol, etc. Effects of valvular disease • Stenosis – tightening of the valvular opening resulting in decreased flow of blood through the opening. • Incompetence – incomplete closure of the valvular opening, allowing backflow of blood through the valvular opening • Mixed. Infective Endocarditis • Colonisation or invasion of heart valves by microbiologic agent. • Formation of friable vegetations (composed of thrombotic debris and organisms. • Leads to destruction of underlying cardiac tissue. • Source of infective embolisation Infective endocarditis • Most common sites involve the left heart valves • Tricuspid valves typically involved in intravenous drug abusers • Development of infective endocarditis preventable in patients with valvular diseases by provision of antibiotic cover for any surgical or dental procedures. Bacteria Endocarditis Arterial Diseases: Hypertension— Pathophysiology • Increased bp • Insidious onset, mild symptoms and signs • 3 major categories – Essential (primary) – Secondary – Malignant • Can be classified as diastolic or systolic • Develops when bp consistently over 140/90 • Diastolic more important Hypertension—Pathophysiology • Over long time, high bp damages arterial walls – Sclerosis, decreased lumen – Wall may dilate, tear • Aneurysm • Areas most frequently damaged: – Kidneys, brain, retina • End result of poorly controlled hypertension: – – – – Chronic renal failure Stroke Loss of vision CHF Hypertension—Etiology • • • • • • • Increases with age Males more freq and severe Genetic factors High sodium ion intake Excessive alcohol Obesity Prolonged, recurrent stress Hypertension—Signs and Symptoms • Asymptomatic in early stages • Initial signs vague, nonspecific – Fatigue, malaise, morning headache Hypertension—Treatment • Treated in sequence of steps – Life style changes – Mild diuretics, ACE inhibitors – One or more drugs added • Pt compliance is an issue • Prognosis depends on treating underlying problems and maintaining constant control of bp The elements of circulation An effective pump (The heart) An effective return (No peripheral pooling) (Normal blood vessels) A clear channel The elements of circulation Blood Pressure/Heart Rate Effective venous and lymphatic return Intact and unblocked blood vessels The economics of circulation Distribution of blood volume in the circulatory system Heart 7% Arteries 13% Arterioles and capillaries 7% Veins 64% Pulmonary vessels 9% Body Fluid Compartments Plasma 3.0L Interstitial fluid 11.0L Intracellular fluid 28.L Blood volume contains both extracellular fluid (plasma) and intracellular fluid (fluid in RBC). Average blood volume is about 8% of body weight, approximately 5L (60% plasma 40% RBC) What is shock? • A state of generalised hypoperfusion of all cells and tissues due to reduction in blood volume or cardiac output or redistribution of blood resulting in an inadequate effective circulating volume • A systemic (whole body) event resulting from failure of the circulatory system • It is at first reversible, but if protracted leads to irreversible injury and death. Causes of shock • Hypovoleamia • Cardiogenic (pump failure) • Anaphylactic (peripheral pooling) (return failure) • Septic (Septiceamic) – Complex reasons Hypovoleamic shock • Haemorrhage – External (Chop wounds, Gastro-intestinal bleeding, etc) – Internal (Hemoperitoneum due to ruptured aortic aneurysm, ruptured ectopic pregnancy, etc. • Fluid loss – Dehydration (low intake or excessive loss) Shock (Hypotension) • Results from decreased circulating blood vol – General hypoxia – Low CO Classification and Mechanisms of Shock Type Hypovolemic Cardiogenic Mechanism loss of blood or plasma Decreased pumping capability of heart Anaphylactic Systemic vasodilation due to severe allergic reaction Septic Vasodilation due to severe infection Neurogenic Vasodilation due to loss of SNS and vaso-motor tone External loss Internal Bleeding Effect of volume loss on Cardiac Output and Arterial Pressure Stages of hypovoleamic shock • Asymptomatic (< 10%) • Early stage (15-25% loss) – Compensated hypotension • Progressive/Advance Stage – Results when no therapeutic intervention is given for the early stage, compensatory mechanisms become harmful. Autoregulation mechanisms breakdown. • Irreversible shock – Irreversible hypoxic injury to vital organs Compensated hypotension • Hypotension (low volume or low cardiac output) • Sympathetico-adrenal stimulation (fight or fright) • Release of catecholamines – resulting in peripheral vasoconstriction – maintain BP • Activation of renin-angiotensin-aldosterone system and increased anti-diuretic hormone release • Fluid retention by kidneys, further vasoconstriction • Impaired renal perfusion and perfusion to other organs with every effort made to maintain perfusion to brain and heart (autoregulation) Shock—Pathophysiology • Bp decreases when blood vol, heart contraction, or periph resistance fails • Low CO, microcirculation – = decreased oxygen, nutrients for cells • Compensation mechanism – – – – – SNS, adrenal medulla stimulated Renin secreted Increased secretion of ADH Secretion of glucocorticoids Acidosis stimulates respiration Shock—Pathophysiology • Complications of decompensation of shock – – – – – – Acute renal failure Adult respiratory distress syndrome (ARDS) Hepatic failures Hemorrhagic ulcers Infection of septicemia Decreased cardiac function Shock—Etiology • Hypovolemic shock – Loss of blood, plasma • Burn pts, dehydration • Cardiogenic shock – Assoc w/ cardiac impairment • Distributive shock – Blood relocated b/c vasodilation • Anaphylactic shock • Neurogenic shock • Septic shock – Severe infection Shock—Signs and Symptoms • 1st signs – Shock, thirst, agitation, restlessness – Often missed • 2nd signs – Cool, moist, pale skin; tachycardia; oliguria – Compensation – Vasoconstriction • Direct effects – Decrease bp and blood flow – Acidosis • Prolonged – Decreased responsiveness in body – Compensated metabolic acidosis progresses to decompensated – Acute renal failure – Monitoring Shock—Treatment • Primary problem must be treated • Hypovolemic shock – Whole blood, plasma, electrolytes, bicarbonate required • Anaphylactic shock – Antihistamines, corticosteroids • Septic – Antimicrobials, glucocorticoids • • • • • Maximize oxygen supply Epine reinforces heart action and vasoconstriction Dopamine, dubutamine increase heart function Good prognosis in early stages Mortality increases as irreversible shock develops Splenic Infarct Infarct of kidney Replaced by scarred tissue Haemorrhagic infarct of lung Cardiogenic shock • Failure of myocardial pump. – Intrinsic – due to myocardial damage – Extrinsic • Due to external pressure –e.g. cardiac tamponade • Due to obstructed flow – e.g. thrombosis Compensated heart failure • Here the situation is one of a compromised cardiac pump which has been “compensated” by an increase in right atrial pressure ( increased blood volume caused by retention of fluid ). Thus cardiac output is maintained. • It may not be noticed as it would have developed gradually over time. However any strain on the heart, eg sudden increase in exercise would tip the balance and lead to a “decompensated heart failure”. Decompensated heart failure • The pump is so damaged that no amount of fluid retention can maintain the cardiac output. This failure also means that the renal function cannot return to normal, thus fluid continues to be retained and the person gets more and more oedematous with eventual death. In short, failure of the pump to pump enough blood to the kidneys. Anaphylactic shock • Usually due to prior sensitisation • Exposure to specific antigens • Mediated by histamines, complements and prostaglandins • Vasodilatation of micro-circulation associated with pooling and fluid extravasation. Septic shock • Commonly due to gram-negative endotoxin producing bacteria. May also accompany gram+ve bacteria. • Predisposing factors include:– Debilitating diseases – Complications of instrumentation and treatment – Burns Septic shock • Pathogenesis include:– Inflammatory reaction – vasodilatation mediated by histamines and complements – Disseminated intravascular coagulopathy – activation of clotting factors and platelets together with consumption of clotting factors – Endothelial damage – extensive due to endotoxins – Release of interleukin-1 and TNF-alpha (Tumor necrosis factor alpha) from macrophages Possible mechanisms of septic shock Pathological changes • Hypoxic injury to vital organs – infarction • Necrosis of tissues • Lysis of cells • The extent of pathological changes is dependent on the duration of decompensation before death. • In acute deaths, often no significant findings are found. Pathological changes • Brain – Hypoxic and ischaemic damage – Initially found at “boundary” zones – May also be associated with marked cerebral oedema. Pathological changes • Heart – Focal myocardial necrosis – Subendocardial infarction (vulnerable region of blood supply) – If there is pre-existing coronary artery diseases, may also lead to acute transmural myocardial infarction Pathological changes • In cardiogenic shock – Due to previous ischaemic heart diseases – the ventricular chambers may well be dilated and distended. The walls are often thin and may be replaced by non-elastic fibrous scars – In intrinsic myocardial diseases leading to pump failure, the myocardium may be unusually thickened and rigid. Pathological changes • Lungs – Diffuse alveolar damage (adult respiratory distress syndrome) – Damage to Type 1 pneumocytes and to endothelial cells – oedema as well as damage to the hyaline membrane due to decreased surfactant production – Haemorrhages, fibrosis, atelectasis and infection. Pathological changes • Kidneys – Acute tubular necrosis – often associated with remarkably well preserved glomeruli Pathophysiology of Acute Tubular Necrosis Acute Tubular Necrosis, Pathological changes • Gastrointestinal tract – Mucosal ischaemia, haemorrhage, necrosis, gangrene • Liver – Centrilobular necrosis, fatty degeneration • Adrenal glands – Focal necrosis – Diffuse haemorrhagic destruction Pump Failure Cardiogenic Shock Vessel injury Peripheral Pooling Physical injuries such as wounds, ruptures of aneurysms, etc (Hypovoleamic) Hypoalbumineamia, Ascites, Renal failure, Toxins , infection and immunecomplexes (DIC, Anaphylaxis, Septiceamic) Septiceamic, Anaphylaxis (Hypovoleamic) (Capillary pooling) Reducing Your Risk For Cardiovascular Diseases • Risks you can control – Avoid tobacco – Cut back on saturated fat and cholesterol – Maintain a healthy weight – Modify dietary habits – Exercise regularly – Control diabetes – Control blood pressure • Systolic – upper number • Diastolic – lower number – Manage stress Reducing Your Risk For Cardiovascular Diseases • Risks you cannot control – – – – Heredity Age Gender Race New Weapons Against Heart Disease • Techniques for diagnosing heart disease – – – – – – – – Electrocardiogram (ECG) Angiography Positron emission tomography (PET) Single positron emission color tomography (SPECT) Radionuclide imaging Magnetic resonance imaging (MRI) Ultrafast CT Digital cardiac angiography (DSA) Angioplasty Versus Bypass Surgery • Angioplasty – a thin catheter is threaded through the blocked arteries. The catheter has a balloon on the tip which is inflated to flatten the fatty deposits against the wall of the artery • Coronary bypass surgery – a blood vessel is taken from another site and implanted to bypass blocked arteries and transport blood Aspirin For Heart Disease? • Research shows that 81 milligrams of aspirin every other day is beneficial to heart patients due to its blood thinning properties • Some side effects of aspirin: gastrointestinal intolerance and a tendency for difficulty with blood clotting • Should only be taken under the advice of your physician Thrombolysis • If victim reaches an emergency room and is diagnosed quickly, thrombolysis can be performed • Thrombolysis involves injecting an agent such as tissue plasminogen activator (TPA) to dissolve the clot and restore some blood flow Cardiac Rehabilitation • Every year, 1 million people survive heart attacks • Cardiac rehabilitation exercise training increases stamina and strength, and promotes recovery.