Atherosclerosis Mi 2010


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Atherosclerosis Mi 2010

  1. 1. Coronary Artery Disease and Myocardial Infarction
  2. 2. Coronary Artery Disease <ul><li>Cardiovascular diseases are the major cause of death in NZ (40% of all deaths) </li></ul><ul><li>Heart attacks are still the leading cause of all cardiovascular deaths and deaths in general </li></ul><ul><li>Maori are disproportionately at risk </li></ul><ul><li>Male deaths twice that of females </li></ul>
  3. 3. Atherosclerosis <ul><li>Major cause of CAD </li></ul><ul><li>Begins as soft deposits of fat that harden with age </li></ul><ul><li>Referred to as the “hardening of the arteries” </li></ul><ul><li>Abnormal accumulation of lipid, or fatty, substances and fibrous tissue in the vessel wall </li></ul><ul><li>Can occur in any artery of the body </li></ul><ul><li>Atheromas (fatty deposits) have a preference for the coronary arteries </li></ul><ul><li>Substances create blockages or narrow the vessel in a way that reduces blood flow </li></ul>
  4. 4. 3 Types of Lesions Associated with Atherosclerosis <ul><li>Fatty streaks </li></ul><ul><li>Fibrous atheromatous plaque – basic lesion </li></ul><ul><li>Characterised by accumulation of lipids, proliferation of smooth muscle cells & formation of scar tissue </li></ul><ul><li>3. Complicated lesion – characterised by haemorrhage, ulceration & scar tissue formation </li></ul>
  5. 5. Pathophysiology <ul><li>Endothelial lining altered as a result of injuries – hyperlipidaemia & hypertension </li></ul><ul><li>Platelets are activated </li></ul><ul><li>Smooth muscle cell proliferation entraps lipids, which are calcified over time & form an irritant to the endothelium on which platelets adhere & aggregate </li></ul><ul><li>Fibrin formation & thrombi occur </li></ul>
  6. 7. Atherosclerosis
  7. 8. Atherosclerosis
  8. 9. Collateral Circulation <ul><li>Normally some arterial branching, termed collateral circulation exists within the coronary circulation </li></ul><ul><li>Growth of collateral circulation is attributed to 2 factors </li></ul><ul><li>- The inherited predisposition to develop new vessels </li></ul><ul><li>-The presence of chronic ischaemia </li></ul>
  9. 10. Collateral Circulation <ul><li>When atherosclerotic plaque occludes the normal flow of blood through a coronary artery & ischaemia is chronic, increased collateral circulation develops </li></ul>
  10. 12. Coronary Artery Disease (CAD) <ul><li>Other causes of heart disease include: </li></ul><ul><li>Vasospasm (sudden constriction or narrowing) of coronary artery </li></ul><ul><li>Myocardial trauma </li></ul><ul><li>Structural disease </li></ul><ul><li>Congenital abnormalities </li></ul><ul><li>Decreased oxygen supply (acute blood loss) </li></ul><ul><li>Increased demand for oxygen (e.g.. rapid heart rate) </li></ul>
  11. 13. Non-modifiable Risk Factors <ul><ul><li>Increasing age </li></ul></ul><ul><ul><li>Gender (more common in men than premenopausal women) </li></ul></ul><ul><ul><li>Genetic predisposition & family history of heart didease </li></ul></ul><ul><ul><li>Ethnicity (Maori) </li></ul></ul>
  12. 14. Modifiable Risk Factors <ul><li>Major </li></ul><ul><ul><li>Elevated serum lipid levels (serum cholesterol of more than 5.2mmol/L) </li></ul></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Cigarette smoking </li></ul></ul><ul><ul><li>Physical activity </li></ul></ul><ul><ul><li>Obesity </li></ul></ul><ul><ul><li>Contributing </li></ul></ul><ul><ul><li>Diabetes mellitus </li></ul></ul><ul><ul><li>Stressful lifestyle </li></ul></ul><ul><ul><li>Lack of oestrogen in women </li></ul></ul>
  13. 15. NHF – Risk Tables <ul><li> </li></ul>
  14. 16. Clinical Manifestations of CAD <ul><li>Angina pectoris </li></ul><ul><li>Acute coronary syndrome </li></ul><ul><li>Sudden cardiac death </li></ul><ul><li>They all result from ischaemia (lack of oxygen supply to the heart) </li></ul>
  15. 18. Angina Pectoris <ul><li>Episodes or paroxysms of pain or pressure in anterior chest </li></ul><ul><li>Caused by insufficient coronary blood flow </li></ul><ul><li>Insufficient flow results in decreased oxygen supply to meet an increased myocardial demand for oxygen in response to physical exertion or emotional stress </li></ul><ul><li>Usually associated with significant obstruction of a major coronary artery </li></ul>
  16. 19. Types of Angina <ul><li>Stable Angina Pectoris </li></ul><ul><li>Pain usually lasts 3-5 minutes </li></ul><ul><li>Subsides when precipitating factor is relieved </li></ul><ul><li>Pain at rest unusual </li></ul><ul><li>2. Unstable Angina Pectoris </li></ul><ul><li>Occurs at rest </li></ul><ul><li>Has a worsening pattern </li></ul><ul><li>Unpredictable </li></ul><ul><li>Considered to be an acute coronary syndrome </li></ul>
  17. 20. Anginal Pain <ul><li>Chest pain or discomfort </li></ul><ul><li>Sometimes referred to as a vague sensation, strange feeling, pressure or ache in chest </li></ul><ul><li>Unpleasant feeling – constrictive, squeezing, heavy, choking, or suffocating sensation </li></ul><ul><li>Usually not sharp or stabbing </li></ul><ul><li>Does not change with position or breathing </li></ul><ul><li>Pain usually located substernally but may occur in neck or radiate to jaw, shoulders & down arms </li></ul>
  18. 21. Factors associated with Anginal Pain <ul><li>Physical exertion (  myocardial oxygen demand) </li></ul><ul><li>Exposure to cold (vasoconstriction &  BP, with  oxygen demand) </li></ul><ul><li>Eating a heavy meal (  blood flow for digestion, therefore reducing blood supply to heart muscle) </li></ul><ul><li>Stress or any emotion-provoking situation (causes release of adrenaline &  BP, increases heart rate & myocardial workload) </li></ul>
  19. 23. Clinical Manifestations of Angina <ul><li>Feeling of anxiety or impending doom </li></ul><ul><li>Shortness of breath </li></ul><ul><li>Cold sweat </li></ul><ul><li>Weakness </li></ul><ul><li>Paraesthesia of one or both arms </li></ul><ul><li>Usually relieved by rest </li></ul><ul><li>Doesn’t usually wake pt from rest </li></ul>
  20. 24. Myocardial Infarction (MI) <ul><li>Death of heart tissue caused by lack of oxygenated blood flow </li></ul><ul><li>Reduced blood flow in coronary artery usually due to atherosclerosis & occlusion of an artery by an embolus or thrombus </li></ul><ul><li>Area of infarction takes time to develop </li></ul><ul><li>As cells are deprived of oxygen, ischaemia develops, cellular injury occurs, then lack of oxygen results in death of tissue </li></ul><ul><li>Most infarcts involve left ventricle </li></ul><ul><li>Location & area of infarct correlate with part of coronary circulation involved </li></ul>
  21. 26. Myocardial Infarction <ul><li>Contractile function of the heart stops in the area of myocardial necrosis </li></ul><ul><li>Transmural MI </li></ul><ul><li>Involves the entire thickness of the myocardium </li></ul><ul><li>Subendocardial MI </li></ul><ul><li>The damage has not penetrated through the entire thickness </li></ul>
  22. 27. Healing Process <ul><li>Body’s response to cell death is inflammation. Within 24 hrs, leucocytes infiltrate the area </li></ul><ul><li>Enzymes are released from dead cardiac cells (important indicators of MI) </li></ul><ul><li>Proteolytic enzymes of neutrophils & macrophages remove all necrotic tissue by 2 nd or 3 rd day </li></ul><ul><li>Development of collateral circulation improves area of poor perfusion </li></ul><ul><li>By 6 weeks after MI, scar tissue has replaced necrotic tissue & area is healed </li></ul>
  23. 28. Clinical Manifestations of MI <ul><li>Sudden chest pain, unrelieved by rest & medication </li></ul><ul><li>May have no previous symptoms (sudden death) </li></ul><ul><li>Increased or decreased BP </li></ul><ul><li>ECG may show tachycardia, bradycardia & dysrhythmias </li></ul><ul><li>Dyspnoea, tachypnoea </li></ul><ul><li>Nausea & vomiting </li></ul><ul><li>Cool clammy skin </li></ul><ul><li>Anxiety, restlessness, feeling of impending doom </li></ul>
  24. 29. Pain of MI <ul><li>Severe & immobilizing </li></ul><ul><li>Described as a heaviness, pressure, tightness, burning, constriction or crushing </li></ul><ul><li>Common locations are substernal, retrosternal or epigastric </li></ul><ul><li>May radiate to neck, jaw, arms or back </li></ul><ul><li>Occurs while active or at rest, or asleep or awake </li></ul><ul><li>Commonly occurs in early morning hrs </li></ul><ul><li>Lasts for 20 mins or more & more severe than anginal pain </li></ul><ul><li>Some may not experience pain but may have ‘discomfort’, weakness or shortness of breath </li></ul>
  25. 30. Complications of MI <ul><li>Arrhythmias </li></ul><ul><li>- present in 80% of MI pts </li></ul><ul><li>- common cause of death in pre-hospital period </li></ul><ul><li>Congestive Heart Failure </li></ul><ul><li>- pumping power of heart has diminished </li></ul><ul><li>Cardiogenic Shock </li></ul>