NSTEMI DrHafiz

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NSTEMI DrHafiz

  1. 1. NON-ST ELEVATION MI BBH, Bangalore Ahmad Hafiz Nov 2011
  2. 2. ACUTE CORONARY SYNDROME SPECTRUM ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  3. 3. WHAT IS NSTEMI? <ul><li>Unstable angina = angina pectoris with at least one of three features : </li></ul><ul><li>it occurs at rest (or with minimal exertion) usually lasting more than 20 minutes (if not interrupted by nitroglycerin) </li></ul><ul><li>it is severe and described as frank pain and of new onset (i.e., within 1 month); and </li></ul><ul><li>it occurs with a crescendo pattern (i.e., more severe, prolonged, or frequent than previously). With or without ischemic ECG changes </li></ul><ul><li>NSTEMI = UA with evidence of myocardial necrosis on the basis of the release of cardiac markers </li></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  4. 4. Davidson pg. 589
  5. 5. PATHOPHYSIOLOGY <ul><li>UA/NSTEMI is caused by reduction in oxygen supply and/or increased myocardial oxygen demand superimposed on an atherosclerotic coronary plaque with varying degrees of obstruction </li></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  6. 6. <ul><li>Plaque rupture or erosion with superimposed non-occlusive thrombus </li></ul><ul><li>Dynamic obstruction </li></ul><ul><li>Progressive mechanical obstruction </li></ul><ul><li>Secondary unstable angina related to increased myocardial oxygen demand and/or decreased supply </li></ul>
  7. 10. CLINICAL PRESENTATION <ul><li>SYMPTOMS: </li></ul><ul><ul><li>chest discomfort </li></ul></ul><ul><ul><li>epigastric discomfort </li></ul></ul><ul><ul><li>shortness of breath </li></ul></ul><ul><ul><li>nausea and vomiting </li></ul></ul><ul><ul><li>excessive sweating </li></ul></ul><ul><ul><li>palpitation, anxiety, sense of impending doom, and feeling of being acutely ill </li></ul></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  8. 11. PHYSICAL EXAMINATION <ul><li>Resembling that of stable angina </li></ul><ul><li>Large NSTEMI may resemble that of large STEMI e.g. diaphoresis, pale cool skin, sinus tachycardia, S3 or S4, basilar rales and sometimes hypotension </li></ul><ul><li>Signs of co-morbidities e.g. peripheral or cerebrovascular diseases </li></ul><ul><li>Autonomic disturbances e.g. pallor, sweating </li></ul><ul><li>Complications e.g. arrhythmia or heart failure </li></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  9. 12. ECG CHANGES <ul><li>ST depression (70-80%) </li></ul><ul><li>T wave inversion (10-20%) </li></ul><ul><li>Both ST depression and T wave inversion </li></ul><ul><li>Post MI NSTEMI  - ECG changes variable (Ironically, even a residual  ST elevation may be present) </li></ul><ul><li>Normal ECG </li></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  10. 15. CARDIAC MARKERS ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  11. 16. TROPONIN-T <ul><li>Peak – 12 hours </li></ul><ul><li>Troponin is released during MI from the cytosolic pool of the myocytes </li></ul><ul><li>Its subsequent release is prolonged with degradation of actin and myosin filaments </li></ul><ul><li>Differential diagnosis of troponin elevation includes acute infarction, severe pulmonary embolism causing acute right heart overload, heart failure, myocarditis </li></ul><ul><li>Troponins can also calculate infarct size but the peak must be measured in the 3rd day. released in 2–4 hours and persists for up to 7 days. </li></ul>
  12. 17. BNP <ul><li>B-type   natriuretic peptide is a cardiac neurohormone released upon   ventricular myocyte stretch as proBNP, which is enzymatically   cleaved to the N-terminal proBNP (NT-proBNP) and, subsequently,   to BNP. The usefulness of assessing this neurohormone was first   shown for the diagnosis and evaluation of HF. </li></ul>
  13. 18. GLYCOGEN PHOSPHORYLASE ISOENZYME BB <ul><li>Peak – 7 hours </li></ul><ul><li>Glycogen phosphorylase isoenzyme BB (abbreviation: GPBB) is an isoenzyme of glycogen phosphorylase </li></ul><ul><li>Glycogen phosphorylase exists in 3 isoforms. One of these Isoforms is GP-BB. This isoform exists in heart and brain tissue </li></ul><ul><li>Because of the blood-brain barrier GP-BB can be seen as heart muscle specific. During the process of ischemia, GP-BB is converted into a soluble form and is released into the blood. This isoform of the enzyme exists in cardiac (heart) and brain tissue. GP-BB is one of the &quot;new cardiac markers&quot; which are discussed to improve early diagnosis in acute coronary syndrome. A rapid rise in blood levels can be seen in myocardial infarction and unstable angina. GP-BB elevated 1–3 hours after process of ischemia. </li></ul>
  14. 19. MYOGLOBIN (MB) <ul><li>Myoglobin is used less than the other markers </li></ul><ul><li>Myoglobin is the primary oxygen-carrying pigment of muscle tissue </li></ul><ul><li>It is high when muscle tissue is damaged but it lacks specificity. It has the advantage of responding very rapidly, rising and falling earlier than CK-MB or troponin. It also has been used in assessing reperfusion after thrombolysis </li></ul>
  15. 20. CK-MB <ul><li>Peak – 10-24 hours </li></ul><ul><li>CK-MB resides in the cytosol and facilitates high energy phosphates into and out of mitochondria </li></ul><ul><li>It is distributed in a large number of tissues even in the skeletal muscle </li></ul><ul><li>Since it has a short duration, it cannot be used for late diagnosis of acute MI but can be used to suggest infarct extension if levels rise again </li></ul><ul><li>This is usually back to normal within 2–3 days. </li></ul>
  16. 21. MANAGEMENT GUIDELINE <ul><li>Suspicion </li></ul><ul><li>Early management </li></ul><ul><li>-Emergency management </li></ul><ul><li>-Hospital phase management </li></ul><ul><li>-Pharmacotherapy </li></ul><ul><li>Late Management </li></ul><ul><li>-Risk stratification </li></ul><ul><li>-Life style modification </li></ul><ul><li>-Secondary prevention drug therapy </li></ul>
  17. 22. ALGORITHM FOR EVALUATION AND MANAGEMENT OF PATIENTS SUSPECTED OF HAVING ACS
  18. 23. EMERGENCY MANAGEMENT <ul><li>ABC, Pulse Oximeter, Attach ECG monitor and record 12-lead ECG, </li></ul><ul><li>High flow O2 by face mask </li></ul><ul><li>IV access [bloods for CBC, U&E, glucose, lipids, cardiac enzymes] </li></ul><ul><li>Brief assessment </li></ul><ul><li>History of CVS disease, risk factors for IHD </li></ul><ul><li>Examination: pulse, BP, JVP, cardiac murmurs, scar from previous cardiac surgery </li></ul><ul><li>Aspirin 300 mg or Clopidogrel 75mg </li></ul><ul><li>Morphine 5-10 mg IV + metoclopramide 1 mg IV </li></ul><ul><li>GTN sublingually </li></ul><ul><li>Thrombolysis management </li></ul><ul><li>Beta blockers + ACEI </li></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  19. 24. ACUTE REPERFUSION THERAPY <ul><li>Thrombolysis </li></ul><ul><li>PCI </li></ul><ul><li>CABG </li></ul><ul><li>Aim : </li></ul><ul><li>Restore coronary patency </li></ul><ul><li>Preserves left ventricular function </li></ul><ul><li>Improves survival rate and reduced mortality rate. </li></ul>
  20. 25. THROMBOLYSIS <ul><li>Indication: </li></ul><ul><ul><li>Ischaemic chest pain > 30 minutes duration </li></ul></ul><ul><ul><li>Less than 12 hours from the onset of pain </li></ul></ul><ul><ul><li>ECG changes: </li></ul></ul><ul><ul><ul><li>new ST elevation of at least 2 mm in two consecutive chest leads; </li></ul></ul></ul><ul><ul><ul><li>or ST elevation of at least 1 mm in two consecutive limb leads; </li></ul></ul></ul><ul><ul><ul><li>or a new left bundle branch block. </li></ul></ul></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  21. 27. <ul><li>Fibrinolysis </li></ul><ul><li>Streptokinase </li></ul><ul><li>Dosage : 1.5 million units in 100 ml saline </li></ul><ul><li>Route of administration : IV infusion over 1 hour </li></ul><ul><li>Mode of action : Catalyze the conversion of plasminogen to active plasmin which further lyse the clots. </li></ul><ul><li>Side effects : </li></ul><ul><ul><li>-Allergic manifestations </li></ul></ul><ul><ul><li>-Hypotension </li></ul></ul><ul><ul><li>-Systemic bleeding </li></ul></ul><ul><li>Note: production of circulating neutralizing antibodies following therapy may cause subsequent infusion with streptokinase ineffective </li></ul>
  22. 28. <ul><li>Alteplase </li></ul><ul><li>Tissue plasminogen activators </li></ul><ul><li>MOA : specifically bound to fibrin-bound plasminogen </li></ul><ul><li>Route of administration: </li></ul><ul><li>IV infusion over 90 minutes duration </li></ul><ul><li>Side effects : </li></ul><ul><li>less compared to streptokinase </li></ul><ul><li>risk of intracranial bleeding </li></ul><ul><li>Other drugs: </li></ul><ul><li>Tenecteplase –longer plasma half life </li></ul><ul><li>Reteplase - given as double bolus instead of infusion </li></ul>First 30 mins Bolus dose 15mg Followed by 0.75mg/kg Next 60 mins 0.5mg/kg (not > 35mg)
  23. 29. FULL THERAPEUTIC ANTICOAGULATION <ul><li>Use either an infusion of  unfractionated heparin  or  low molecular weight heparin (e.g., enoxaparin sodium). </li></ul><ul><li>In the context where pathology is not readily available, low molecular weight heparin is often easier to use </li></ul>
  24. 30. ADJUNCTIVE THERAPY <ul><li>Consider intravenous beta-blocker (metoprolol 5 mg IV slow bolus at 0 min, 5 min and 10 min to give a total dose of 15 mg) then oral therapy (2). </li></ul><ul><ul><li>IV beta-blockers decreases mortality when given early in acute myocardial infarction though the evidence is less clear in the reperfusion therapy setting; </li></ul></ul><ul><ul><li>it is more commonly used in the United States and parts of Europe and is routine therapy in Scandinavia. </li></ul></ul><ul><li>ACE-inhibitors: when started within 24 hours reduce morbidity and mortality. </li></ul>
  25. 31. CONTRAINDICATIONS TO THROMBOLYTIC THERAPY <ul><li>Active internal bleeding </li></ul><ul><li>Previous history of subarachnoid or intracerebral bleeding </li></ul><ul><li>Uncontrolled hypertension </li></ul><ul><li>Recent surgery (less than 1 month) </li></ul><ul><li>Recent trauma </li></ul><ul><li>High probability of active peptic ulcer </li></ul><ul><li>Pregnancy </li></ul>
  26. 32. PRIMARY PERCUTANEOUS CORONARY INTERVENTION <ul><li>Primary percutaneous intervention is more effective than thrombolysis for treatment of AMI. </li></ul><ul><li>Death, non fatal reinfarction and stroke reduced from 14% with thrombolytic therapy to 8% with primary PCI </li></ul><ul><li>Keeley EC, et al. Lancet 2003;361:13-20 </li></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  27. 34. <ul><li>Treatment of choice to prevent reinfarction </li></ul><ul><li>Avoid hemostatic problems encounter with thrombolytic therapy </li></ul><ul><li>Preferred in case of presence of cardiogenic shock, bleeding risk, symptoms of more than 2-3h </li></ul><ul><li>Disadvantage </li></ul><ul><li>Expensive in terms of facilities and personnel, limited availability. </li></ul>
  28. 35. CORONARY ARTERY BYPASS GRAFTING (CABG) <ul><li>surgical procedure performed to relieve angina and reduce the risk of death from coronary artery disease. </li></ul><ul><li>  Arteries or veins from elsewhere in the patient's body are grafted to the coronary arteries to bypass atherosclerotic  </li></ul><ul><li>narrowing and improve the blood supply to the coronary circulation supplying the myocardium. </li></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  29. 36. HOSPITAL PHASE MANAGEMENT <ul><li>Coronary care units- provide intensive care. Duration of stay depends on the condition of patient. </li></ul><ul><li>Activity – advise bed rest for first 12 hours, as increase workload to the heart may cause increase size of the infarct. </li></ul><ul><li>Diet – clear liquids for first 4-12 hours due to risk of emesis and aspiration. Diet should contain 50% complex carbohydrate and low fat contents. </li></ul><ul><li>Bowels – prevention of constipation by giving high fiber diet, laxative can be prescribed. </li></ul><ul><li>Sedation – Diazepam, oxazepam or lorazepam is given for sedation to enforced inactivity with tranquility. </li></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  30. 37. LATE MANAGEMENT <ul><li>Risk stratification and investigation </li></ul><ul><li>Left ventricular functions </li></ul><ul><ul><li>Assess by physical findings i.e tachycardia,3 rd heart sounds, crackles at lung bases </li></ul></ul><ul><ul><li>Echocardiography and radionuclide imaging to assess LV ejection fraction. </li></ul></ul><ul><li>Arrhythmias </li></ul><ul><ul><li>Presence of ventricular arrhythmias during convalescence phase may benefit from specific anti arrhythmic therapy such as implantable cardiac defibrillator. </li></ul></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  31. 38. <ul><li>3. Early post MI ischemia is managed like unstable angina </li></ul><ul><li>If no spontaneous ischemia, assess by exercise testing to look for residual ischemia </li></ul><ul><li>-Good exercise tolerance – 1-4% chance of adverse event in 12 months </li></ul><ul><li>-Low exercise tolerance – consider revascularization by CABG </li></ul><ul><li>4. Other risk factors include age >75,diabetic patient, prolonged sinus tachycardia, hypotension and silent ischemia </li></ul>
  32. 39. SECONDARY PREVENTION <ul><li>Long term drug therapy with low dose aspirin, clopidogrel, beta blockers and ACEI </li></ul><ul><li>Cessation of smoking </li></ul><ul><li>Control of hypertension and hyperlipidemia </li></ul><ul><li>Regular exercise </li></ul><ul><li>Diet – diet high in fibers, fruit, oily fish, low in saturated fat, weight control </li></ul><ul><li>Returning to work after 4-6 weeks </li></ul>ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
  33. 40. REFERENCE <ul><li>2011 ACC/AHA Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction </li></ul><ul><li>http://content.onlinejacc.org/cgi/content/short/57/19/e215 </li></ul><ul><li>Harrison's Principles of Internal Medicine, 17e   </li></ul><ul><li>Davidson’s Principles & Practice of Medicine, 20e </li></ul><ul><li>wikipedia </li></ul><ul><li>Medscape http://emedicine.medscape.com/article/811905-overview#aw2aab6b3 </li></ul>
  34. 41. <ul><li>The End </li></ul>

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