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Acute coronary syndrome

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Acute coronary syndrome

  1. 1. EPIDEMIOLGY • Main cause of death • The highest rate is in south India. • It has been estimated that India had the highest number of deaths in the world due to CAD in 2002, nearly 1.5 million and which is expected to double by 2015. • Atherosclerosis remains the major cause of death and premature disability
  2. 2. MEANING • Atherosclerosis : athere=fatty mush, skleros = hard. • Atherosclerosis = “hardening of the arteries”
  3. 3. MEANING ACS no ST elevation Unstable angina NSTEMI ST elevation MI
  4. 4. Coronary circulation
  5. 5. Coronary circulation
  6. 6. Risk factors
  7. 7. Non modifiable Risk Factors • Heredity • Age • Personality factors • Gender
  8. 8. Modifiable Risk Factors • Smoking • Hypertension • Elevated serum cholesterol level • Diabetes • Obesity • Physical Inactivity
  9. 9. Contributing Risk Factors • Response to stress • Homocysteine Level • Inflammatory Level • Menopause • Type A Behavioural Patterns, TABP • Hemostatic factors
  10. 10. Novel risk factors • Homocysteine • CRP • Plasma fibrinogen • Fibrin D dimer • Lipoprotein
  11. 11. CAUSES OF ACS • Decrease in the oxygen available to the myocardium – Nonobstructive clot on an atherosclerotic plaque. – Coronary vasospasm. – Atherosclerotic obstruction without clot or vasospasm. – Inflammation or infection. – Unstable angina due to a non cardiac cause. – Thrombus formation with subsequent coronary artery occlusion
  12. 12. CAUSES OF ACS • Increase in the oxygen demand
  13. 13. PATHOPHYSIOLOGY • Initiation of Atherosclerosis • Leukocyte Recruitment • Foam-Cell Formation • Atheroma Evolution and Complications • Microvessels • Calcification • Plaque Evolution
  14. 14. Deterioration of a stable atherosclerotic plaque Exposing the intima to blood Stimulating platelet aggregation Local vasoconstriction Thrombus formation Partially occluded by the thrombus (manifesting UA/NSTEMI) or totally occluded by a thrombus (STEMI) A C S A C S
  15. 15. Criteria for diagnosis of ACS Major criteria Minor criteria A diagnosis of ACS can be made if one or more of the following major criteria are present:  ST elevation or LBBB in the setting of recent (<24hrs) or ongoing angina  New or presumably new, ST segment depression (≥0.05mV) or T wave inversion (≥ 0.2mV) with rest symptoms  Elevated serum markers of myocardial damage (ie, Troponin I, T and CK-MB) In the absence of a major criterion, a diagnosis of ACS requires the presence of at least one item from both column 1 and 2 1 2  Prolonged (ie, >20mts) chest, arm/shoulder, neck or epigastric discomfort  New onset chest, arm/ shoulder, neck, or epigastric discomfort at rest , minimal exertion or ordinary activity  Previously documented chest, arm/ shoulder, neck, or epigastric discomfort which has become distinctly more frequent or longer in duration  Typical/ atypical angina  Male> 40yrs or female>60yrs  Known CAD  HF, hypotension or transient mitral valve regurgitation by examination  DM  Extracardiac disease  Pathologic Q wave on ECG  Abnormal ST segment or T wave abnormalities not known to be new
  16. 16. NSTE ACS
  17. 17. Definition Stable angina pectoris is characterized by chest or arm discomfort that may not be described as pain but is reproducibly associated with physical exertion or stress and is relieved within 5–10 minutes by rest and/or sublingual nitroglycerin.
  18. 18. Unstable Angina is defined as angina pectoris or equivalent ischemic discomfort with at least one of three features: (1) it occurs at rest (or with minimal exertion), usually lasting >10 minutes; (2) it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or (3) it occurs with a crescendo pattern
  19. 19. The diagnosis of NSTEMI is established if a patient with the clinical features of UA develops evidence of myocardial necrosis, as reflected in elevated cardiac biomarkers.
  20. 20. Canadian Cardiovascular Society - Classification of Angina CLASS ACTIVITY EVOKING ANGINA LIMITS TO ACTIVITY I II III IV Prolonged exertion Walking>2 blocks Walking<2 blocks Minimal or rest None Slight Marked Severe
  21. 21. Pathophysiology A reduction in oxygen supply and/or by an increase in myocardial oxygen demand superimposed on a lesion that causes coronary arterial obstruction, usually an atherothrombotic coronary plaque
  22. 22. (1) plaque rupture or erosion with a superimposed nonocclusive thrombus  NSTEMI may occur with downstream embolization of platelet aggregates and/or atherosclerotic debris; (2) dynamic obstruction [e.g., coronary spasm, as in Prinzmetal's variant angina (PVA) (3) progressive mechanical obstruction [e.g., rapidly advancing coronary atherosclerosis or restenosis following percutaneous coronary intervention (PCI)] (4) UA secondary to increased myocardial oxygen demand and/or decreased supply (e.g., tachycardia, anemia).
  23. 23. Clinical Presentation • Typical chest and associated symptoms (not related to trauma):
  24. 24. Atypical symptoms • Neck, throat, jaw or tooth discomfort • Shoulder or arm pain • Numbness or tingling in the chest or related area • Fullness or burning in the chest • Epigastric discomfort which is described as indigestion • Discomfort between scapula or in the midback region • Dizziness/ light headedness with or without syncope • Fatigue or weakness not related to neurologic problems • Palpitation of new onset with no history of dysrhythmia • Mid back pain (not related to degenerative joint diseases)
  25. 25. Diagnostic Pathways • Clinical history • ECG • Cardiac markers • Stress testing (coronary imaging is an emerging option).
  26. 26. Clinical history
  27. 27. Electrocardiogram
  28. 28. Electrocardiogram
  29. 29. Biochemical cardiac markers • Creatine kinase (CK-MB) • Troponin I and T and/ or • Myoglobulin
  30. 30. Medical Treatment • Bed rest • Continuous ECG monitoring for ST- segment deviation and cardiac arrhythmias. • Ambulation is permitted if the patient shows no recurrence of ischemia and does not develop a biomarker of necrosis for 12–24 h.
  31. 31. TREATMENT Medical therapy Anti-ischemic treatment Antithrombotic treatment.
  32. 32. Anti-ischemic treatment • To provide relief and prevention of recurrence of chest pain • Initial treatment should include – bed rest – nitrates, and – beta blockers
  33. 33. Antithrombotic Therapy: • Other main component of treatment for UA/NSTEMI • Initial treatment should begin with the platelet cyclooxygenase inhibitor aspirin. • The typical initial dose is 325 mg/d, with lower doses (75–162 mg/d) recommended for long-term therapy.
  34. 34. Anticoagulant therapy • Unfractionated heparin (UFH • The low-molecular-weight heparin (LMWH), enoxaparin • The indirect Factor Xa inhibitor, fondaparinux • Bivalirudin
  35. 35. Unstable Angina Risk Stratification o Low risk – New-onset exertional angina – Minor chest pain during exercise – Pain relieved promptly by nitroglycerine o Management – Can be managed safety as an outpatient (assuming close follow-up and rapid investigation)
  36. 36. Unstable Angina Risk Stratification o Intermediate risk – Prolonged chest pain – Diagnosis of rule-out MI o Management – Observe in the ER or Chest Pain Unit – Monitor clinical status and ECG – Obtain cardiac enzyme (troponin T or I) every 8 to 12 hours
  37. 37. Unstable Angina Risk Stratification o High risk – Recurrent chest pain – ST-segment change – Hemodynamic compromise – Elevation in cardiac enzyme o Management – Monitor in the coronary Care Unit
  38. 38. Risk Stratification by ECG The risk of death or MI at 30 days is stongly related to the ECG at the time of chest pain • ST depression 10 % • T-wave inversion 5 % • No ECG changes 1~2 %
  39. 39. PRINZMETAL'S VARIANT ANGINA (PVA) • A syndrome of severe ischemic pain that occurs at rest but not usually with exertion and is associated with transient ST- segment elevation. • This syndrome is due to focal spasm of an epicardial coronary artery, leading to severe myocardial ischemia
  40. 40. Clinical and Angiographic Manifestations
  41. 41. Treatment of PVA • Nitrates and calcium channel blockers • Aspirin may actually increase the severity of ischemic episodes, possibly as a result of the exquisite sensitivity of coronary tone to modest changes in the synthesis of prostacyclin. • The response to beta blockers is variable. • Coronary revascularization
  43. 43. DEFINITION • A dynamic process by which one or more regions of the heart experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood flow; subsequently, necrosis or death•to the myocardial tissue occurs.
  44. 44. Pathophysiology slowly developing high grade stenosis of epicardial coronary arteries complete occlusion , but do not precipitate MI Development of collateral circulation atherosclerotic plaque rupture exposure of substances that promote platelet activation and aggregation thrombin generation thrombus formation interrupt blood supply and leads imbalance between O2 demand and supply myocardial necrosis contractile function of the heart stops at necrotic area
  45. 45. • The coronary plaques prone to disruption are those with a rich lipid core and a thin fibrous cap. disrupted plaque Formation of an initial platelet monolayer activation of various agonists promote platelet activation release of thromboxane A2 further platelet activation potential resistance to fibrinolysis develops.
  46. 46. Platelet activation change in the glycoprotein IIb/IIIa receptor develops a high affinity for soluble adhesive proteins (i.e., integrins) such as fibrinogen platelet cross-linking and aggregation
  47. 47. Disrupted plaque exposure of tissue factor in damaged endothelial cells at the site coagulation cascade is activated Factors VII and X are activated the conversion of prothrombin to thrombin converts fibrinogen to fibrin autoamplification reaction further activation of the coagulation cascade Artery is occluded by a thrombus containing platelet aggregates and fibrin strands.
  48. 48. The amount of myocardial damage caused by coronary occlusion depends on (1) the territory supplied by the affected vessel (2) whether or not the vessel becomes totally occluded (3) the duration of coronary occlusion (4) the quantity of blood supplied by collateral vessels to the affected tissue (5) the demand for oxygen of the myocardium whose blood supply has been suddenly limited (6) endogenous factors that can produce early spontaneous lysis of the occlusive thrombus, and (7) the adequacy of myocardial perfusion in the infarct zone when flow is restored in the occluded epicardial coronary artery.
  49. 49. Location of Infarction Location of MI Primary siteof occlusion Inferior MI RCA (80-90%), LCX (10- 20%) Inferolateral MI LCX Posterior MI RCA/ LCX Anterior MI LAD Anterior septal MI LAD Lateral MI LAD/LCX Right ventricular RCA
  50. 50. KILLIPS CLASSIFICATION Killip class I Individuals with no clinical signs of heart failure Killip class II Individuals withrales or crackles in the lungs , an S3, and elevated JVP Killip class III Individuals with frank acute pulmonary edema Killip class IV Individuals with cardiogenic shock/ hypotension and evidence of peripheral vasoconstriction (oliguria, cyanosis or sweating)
  52. 52. Involved layers of heart muscle – Transmural (Q wave) infarction - area of necrosis occurs throughout the entire thickness of the heart muscle. – Subendocardial (nontransmural/non Q-wave) infarction area of necrosis is confined to the innermost layer of the heart lining the chambers.
  53. 53. Clinical features • Chest pain
  54. 54. Clinical features • Diaphoresis, cool clammy skin, facial pallor. • Hypertension or hypotension and Bradycardia or tachycardia • Premature ventricular and/or atrial beats • Palpitations, severe anxiety, dyspnea • Disorientation, confusion, restlessness • Fainting, marked weakness • Nausea, vomiting, hiccups
  55. 55. Atypical symptoms • Epigastric or abdominal distress • dull aching or tingling sensations • shortness of breath • extreme fatigue
  56. 56. Physical Signs • Fourth and third heart sounds • Decreased intensity of the first heart sound • Paradoxical splitting of the second heart sound • A pericardial friction rub (transmural STEMI) • Temperature elevations up to 38°C.
  57. 57. Diagnostic Evaluation (1) ECG (2) serum cardiac biomarkers (3) cardiac imaging (4) nonspecific indices of tissue necrosis and inflammation
  58. 58. Physical Examination • muffling of sounds • presence of gallop • arrhythmia, and • accentuation of pulmonary second sound
  59. 59. WHO criteria for diagnosis of MI: It requires atleast two of the following three elements • A history of ischemic type chest discomfort • Evolutionary changes on serially obtained ECG tracing • Typical rise and fall in serum cardiac markers
  60. 60. ECG Changes – ST segment depression and T wave inversion indicate a pattern of ischemia. – ST elevation indicates an injury pattern. – Q waves indicate tissue necrosis and are permanent
  61. 61. Location of MI Primary siteof occlusion Primary ECG changes Complications Inferior MI RCA (80-90%) LCX (10-20%) L II,III, aVF First and second degree AV block, right ventricular infarct Inferolateral MI LCX L II, III, aVF, V5,V6 Third degree heart block, left HF, CMP, left ventricular rupture Posterior MI RCA/ LCX No lead truly looks at posterior surface. Look for reciprocal changes in V1 and V2- tall, broad R waves; ST depression and tall T waves. Posterior leads V7,V8 and V9 may be recorded and evaluated First, second, and third degree heart block, HF, bradydysrhythmias Anterior MI LAD V2- V4 Third degree heart block, HF, bundke branch block Anterior septal MI LAD V1-V3 Second and third degree heart block Lateral MI LAD/LCX V5, V6, I, aVL HF Right ventricular RCA V4R Right precordial leads V1R – V6R may be recorded and evaluated Increased RAP, decreased CO, bradydysthymias, heart blocks, hyptension, cardiogenic shock
  62. 62. ECG leads showing changes Location of infarct V1-V3 Anteroseptal V4- V6, L1 and aVL Anterolateral aVF,L2 and L3, ST depression in V1 and V2 Inferior wall Presence of tall R wave and upright T waves in V1 and V2 True posterior infarct ST elevation in Rt sided chest leads and Q waves (V3R, V4R) Right ventricular infarct
  63. 63. Cardiac Markers • Nonspecific markers – lactate dehydrogenase – aspartate aminotransferase – myoglobin • Specific cardiac markers – Troponin (troponin C, troponin I and troponin T). – Creatine kinase (CK)
  64. 64. Marker Rise in serum level from onset Peak level Time to return to normal Time for blood collection SGOT (5- 40u/l) 8-12 hrs 18-36hrs 3-4 days Once n 12hrs LDH (20- 220IU/L) 10hrs 24-48hrs 10- 14 days 24hrs CK-MB 3-12hrs 24hrs 48-72 hrs Every 12hrs for 3 days C TnT 3-12hrs 12hrs-2 days 5-14 days Once atleast every 12 hrs C TnI 3-12hrs 24hrs 5-10days Once atleast every 12 hrs
  65. 65. • Chest xray: Prominent pulmonary vascular markings on x ray indicate left ventricular failure. Chest film helps to exclude other causes of chest pain such as pneumothorax, pulmonary infarction with effusion, aortic dissection and skeletal fractures. • Echocardiogram: – used to evaluate ventricular function. – used to assist in diagnosing an MI, especially when the ECG is nondiagnostic.
  66. 66. • CT Scan: to reveal cavity dimensions, wall thickness, aneurysms and intracardiac thrombi. • Nuclear imaging : to study nature of myocardial lesion, its viability and prognosis • MRI scan: to assess the perfusion of infracted and noninfarcted tissue as well as the state of reperfused myocardium
  67. 67. Other Findings • Elevated CRP and lipoprotein • Abnormal coagulation studies • Elevated white blood cell (WBC) count and sedimentation rate • Radionuclide imaging allows recognition of areas of decreased perfusion. • PET determines the presence of reversible heart muscle injury and irreversible or necrotic tissue; extent to which the injured heart muscle has responded to treatment can also be determined.
  68. 68. Management • Prehospital care: 1) recognition of symptoms by the patient and prompt seeking of medical attention; (2) rapid deployment of an emergency medical team capable of performing resuscitative maneuvers, including defibrillation; (3) expeditious transportation of the patient to a hospital facility that is continuously staffed by physicians and nurses skilled in managing arrhythmias and providing advanced cardiac life support; and (4) expeditious implementation of reperfusion therapy
  69. 69. Emergency department • Goals: – control of cardiac discomfort, – rapid identification of patients who are candidates for urgent reperfusion therapy, – triage of lower-risk patients to the appropriate location in the hospital, and – avoidance of inappropriate discharge of patients with STEMI.
  70. 70. • Aspirin : Rapid inhibition of cyclooxygenase-1 in platelets followed by a reduction of thromboxane A2 • Supplemental O2: when hypoxemia is present, O2 should be administered by nasal prongs or face mask (2–4 L/min) for the first 6–12 h after infarction
  71. 71. Control of Discomfort • Sublingual nitroglycerin • Morphine • Intravenous beta blockers
  72. 72. Management Strategies: Initial 12-lead ECG  ST-segment elevation of at least 2 mm in 2 contiguous precordial leads and 1 mm in 2 adjacent limb leads is present  a patient should be considered a candidate for reperfusion therapy • Gold hour = first 60 mts. Total ischemic time : 120 mts
  73. 73. Primary Percutaneous Coronary Intervention • PCI, usually angioplasty and/or stenting without preceding fibrinolysis, referred to as primary PCI • It is effective in restoring perfusion in STEMI when carried out on an emergency basis in the first few hours of MI.
  74. 74. • Advantage: – patients who have contraindications to fibrinolytic therapy – More effective than fibrinolysis in opening occluded coronary arteries
  75. 75. PCI • Indication: – When the diagnosis is in doubt – Cardiogenic shock is present – Bleeding risk is increased, or – Symptoms have been present for at least 2–3 h when the clot is more mature and less easily lysed by fibrinolytic drugs.
  76. 76. Fibrinolysis • Ideally initiated within 30 min of presentation (door-to-needle time 30 min). • Goal of fibrinolysis is prompt restoration of full coronary arterial patency.
  77. 77. Fibrinolytic agents • Tissue plasminogen activator (tPA), streptokinase, tenecteplase (TNK), and reteplase (rPA) – First generation drugs- streptokinase, urokinase – Second generation- TPA, anioylated plasminogen streptokinase – Third generation- reteplase, TNK • These drugs are promoting the conversion of plasminogen to plasmin, which subsequently lyses fibrinthrombi.
  78. 78. Thrombolysis in myocardial infarction (TIMI) grading system • Grade 0 - Complete occlusion of the infarct-related artery • Grade 1 - Some penetration of the contrast material beyond the point of obstruction but without perfusion of the distal coronary bed; • Grade 2 - Perfusion of the entire infarct vessel into the distal bed, but with flow that is delayed compared with that of a normal artery • Grade 3 - Full perfusion of the infarct vessel with normal flow
  79. 79. CONTRAINDICATIONS OF FIBRINOLYSIS • History of cerebrovascular hemorrhage, a nonhemorrhagic stroke or other cerebrovascular event within the past year • Suspicion of aortic dissection • Active internal bleeding (excluding menses). • Advanced age associated with an increase in hemorrhagic disorders
  80. 80. Relative contraindications: • Current use of anticoagulants (INR- 2) • A recent (<2 weeks) invasive or surgical procedure or prolonged (>10 min) cardiopulmonary resuscitation • Known bleeding disorders • Pregnancy • A hemorrhagic ophthalmic condition (e.g., hemorrhagic diabetic retinopathy) • Active peptic ulcer disease • A history of severe hypertension that is currently adequately controlled. • Because of the risk of an allergic reaction, patients should not receive streptokinase if that agent had been received within the preceding five days to two years.
  81. 81. Hospital Management • Coronary Care Units • Diet • Bowel Management • Sedation
  82. 82. Interventional Cardiology: • Percutaneous transluminal coronary angioplasty • Intracoronary stent
  83. 83. Surgical Revascularization • Coronary Artery Bypass Graft • Minimal Invasive Coronary Artery Surgery • Transmyocardial revascularization
  84. 84. Cardiac Rehabilitation • Medically supervised program consisting of exercise training, education on heart healthy living, and counseling to reduce stress and help patients return to an active lifestyle and recover more quickly
  85. 85. Components • Physician-prescribed exercise • Cardiac risk factor modification (education, counseling and behavioral intervention) • Psychosocial assessment • Outcomes assessment • Individualized treatment plan
  86. 86. Complications • Ventricular Dysfunction and Congestive Heart Failure STEMI left ventricle begins to dilate results from expansion of the infarct resulting in disproportionate thinning and elongation of the infarct zone lengthening of the noninfarcted segments occurs overall chamber enlargement HEART FAILURE
  87. 87. EARLY COMPLICATIONS • Hypovolemia • Cardiogenic Shock • Right Ventricular Infarction • Arrhythmias • Ventricular Premature Beats • Ventricular Tachycardia and Fibrillation • Sinus Bradycardia
  88. 88. LATE COMPLICATIONS • Left Ventricular Aneurysm • Dressler’s syndrome • Shoulder hand syndrome
  89. 89. Nursing Management of MI
  90. 90. Nursing Assessment • Gather information regarding the patient's chest pain: • Evaluate cognitive, behavioral, and emotional status. • Prior health status with emphasis on current medications, allergies • Analyze information for contraindications for thrombolytic therapy and PCI. • Gather information about presence or absence of cardiac risk factors. • Identify patient's social support system and potential caregivers. • Identify significant other's reaction to the crisis situation.
  91. 91. • Acute pain related to decreased blood supply to the myocardium
  92. 92. • Ineffective tissue perfusion : cardiopulmonary related to reduced coronary blood flow from coronary thrombus and atherosclerotic plaque
  93. 93. • Anxiety related to pain and fear of death
  94. 94. • Risk for decreased cardiac output related to decrease in LV function
  95. 95. • Activity intolerance related to imbalance between oxygen demand and supply
  96. 96. • Ineffective coping related to life threatening diagnosis
  97. 97. • Risk for bleeding
  99. 99. BIBLIOGRAPHY • Braunwald, Fauci,Kasper,Hauser, Longo,Jameson. Harrison’s Principles of Internal Medicine. 15th ed. Vol 1. New York:McGraw-Hill;2001 • K.V Krishnadas. Textbook of Medicine. 5th ed. Delhi: Jaypee brothers;2008 • Bonow. Mann. Zipes, Libby. Braunwald’s Heart disease. 9th ed. India; Elsevier publication; 2011. • Joyce M Black, Jane Hokanson Hawks. Medical Surgical Nursing. 8th ed. Vol-2. India: Saunders Elsevier publishers; 2010