Myocardial infarction

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Myocardial infarction

  1. 1. ACUTE CORONARY SYNDROME (A CASE DISCUSSION) BY Dr Ijaz Hussain MBBS , MCPS, MRCGP, Dip Avn Med Prince Sultan Military Medical City Riyadh
  2. 2. Case Presentation• Patient’s Name: Mohammad Al Shahrani• Age: 63 Yrs• Sex: ♂• Nationality: Saudi• Resident of al Oainah
  3. 3. Chief Complaints• Mohammad al Shahrani was brought in the AnE with Brief History of : – Chest Pain – Diaphoresis – Collapse• History of Present Illness: – Patient had an out door BBQ party – While coming back he exerted to pack-up and kept lifting heavy luggage etc. – Since last abt 15 minutes he had been c/o chest “discomfort”. Family rushed to the hospital as he collapsed.• Past History: Known Case if IHD: had undergone cardiac cath one year and a half.
  4. 4. Initial Work-up• Although the patient was in distress but his vital parameters were stable and as following: – B.P: 153/ 86 mm Hg – Pulse: 66 per min – Temp 36.2 ̊C – SPO2 99 % – Reflo: 7.6 mmol/dl• ECG: – St Elevation in II, III, aVf – Reciprocal Changes in aVL, V1 and V2
  5. 5. ECG TRACING
  6. 6. Initial Work-up in PSMMC• Cardiac Enzymes Enzyme 18.11.2012 19.11.2012 Ref Range – Ck 144 651 {50-190 u/L} – Ck MB - 93 {0- 24 u/L } – AST 32 82 {2.0- 37 u/L} – LDH 530 495 {135-255 u/L}• Troponine T Level – 18.11.2012 0.007 1.1 {0.1 ng/ml } – 19.11.2012 1.540• FBC NAD• Renal Functions NAD• CxR NAD
  7. 7. DISCHARGE SUMMARY• Final Diagnosis: – Diabetes ; Hypertension ; IHD e Hx of PCI in Asir 4 Yrs ago• History: – Pt is 63 yrs old saudi male with Dx as above. Presented in A’nE with C/O acute onset chest pain of few hrs duration with no SOB, Orthopnoea, Paraxysmol Nocturnal dyspnoea or Palpitaion.• Physical Examination: – Chest clear, CVA Ex S1+S2+0 ; Abdomen soft lax ; CNS intact ; B.P was normal• Investigation Results : – Showed ST elevation in Inf leads with still having pain
  8. 8. DISCHARGE SUMMARY• Hosp Course & Mngmnt: Pt was taken directly from A’nE to cath Lab. Shown tight mid RCA lesion ,with aspiration of thrombosis. Echo was done which shown slight irregularity. Pt was kept under observation for 24 hrs. Was discharged in a good condition, with no complaints and was doing fine.• Drugs on Discharge: – Aspirin 81 mg 1xTab PO OD – Plavix 75 mg 1xTab PO OD – Prindopril 2.5 mg 1xTab PO OD – Isordil 20 mg 1xTab PO OD – Lipitor 40 mg 1xTab PO OD – Lasix20 mg 1xTab PO OD – Pantoperazole 40 mg 1xTab PO OD• Future Plan : Pt was given an appt 24/52 to be seen in OPD
  9. 9. Case Discussion
  10. 10. • Heart is capable of pumping blood to every cell in the body in under one minute• During the course of the day, your heart will beat approx 100,000 times driving 2,000 gallons of oxygen-rich blood through 60,000 miles of blood vessels.
  11. 11. DEFINITIONMyocardial infarction, commonly known as aheart attack, is the irreversible necrosis ofheart muscle secondary to prolongedischemia. This usually results from animbalance in oxygen supply and demand,which is most often caused by plaquerupture with thrombus formation in acoronary vessel, resulting in an acutereduction of blood supply to a portion of themyocardium.
  12. 12. DEFINITION Myocardial infarction is considered part of aspectrum referred to as acute coronary syndrome (ACS). The ACS continuum representing ongoingmyocardial ischemia or injury consists ofunstable angina, non–ST-segment elevationmyocardial infarction (NSTEMI), and ST-segmentelevation myocardial infarction (STEMI). Patientswith ischemic discomfort may or may not have ST-segment or T-wave changes denoted on theelectrocardiogram (ECG). ST elevations seen on theECG reflect active and ongoing transmuralmyocardial injury
  13. 13. Types• STEMI : OR New Onset LBBB ACUTE MI• NSTEMI : ECG MAY SHOW ST- DEPRESSION,T-WAVE INVERSION, NON- SPECIFIC CHANGES OR NORMAL (NON-Q WAVE MI OR SUBENDOCARDIAL MI)• UA : ANGINA OF INCREASING FREQUENCY OR SEVERITY, OCCURS ON MIN; EXERTION OR AT REST. ASSOCIATED WITH INCREASED RISK OF MI
  14. 14. Clinical Spectrum of Acute Coronary Syndromes Stable angina Unstable Non-STE MI STE MI angina None Positive PositiveEvidence of necrosis ST-segment ST-segment ST-segmentECG early depression depression elevation and/or and/or T-wave inversion T-wave inversionECG late No Q No Q Q develops
  15. 15. UnstableAngina N-STEMI STEMINon Occludingocclusive thrombus Complete thrombus sufficient to cause occlusionthrombus tissue damage & mild ST elevations onNon myocardial necrosis ECG or new LBBBspecificECG ST depression +/- Elevated cardiac T wave inversion on enzymes ECGNormal More severecardiac Elevated cardiac symptomsenzymes enzymes
  16. 16. EPIDEMIOLOGY OF ACS
  17. 17.  Single largest cause of death  515,204 US deaths in 2000  1 in every 5 US deaths Incidence  1,100,000 Americans will have a new or recurrent coronary attack each year and about 45% will die*  550,000 new cases of angina per year Prevalence  12,900,000 with a history of MI, angina, or both INCIDENCE IN UK=5/1000/ANNUM FOR STEMI
  18. 18. PATHOPHYSIOLOGY
  19. 19. Understanding Myocardial Ischemia Imbalance
  20. 20. Understanding Myocardial IschemiaDec O2 supply Inc. Demand INCREASED CARDIAC OUTPUT….. (THYROTOXICOSIS) MYOCARDIAL HYPERTROPHY (AS,HTN)
  21. 21. PATHOPHYSIOLOGY• RUPTURE OR EROSION OF THE FIBROUS CAP OF A CORONARY ARTERY PLAQUE.• PLATELETS AGGREGATION AND ADHESION.• LOCALIZED THROMBOSIS.VASOCONSTRICTION.• DISTAL THROMBUS EMBOLIZATION.• THROMBUS FORMATION AND VASOCONSTRICTION PRODUCED BY PLT RELEASE OF SEROTONIN & THROMBOXANE A2, RESULT IN MYOCARDIAL ISCHEMIA DUE TO REDUCTION OF CORONARY BLOOD FLOW.
  22. 22. Plaque Rupture, Thrombosis, and Microembolization Quiescent plaque Process Marker Lipid core Plaque formation Cholesterol LDL Vulnerable plaque C-Reactive Protein Inflammation Adhesion Molecules TF → Clotting Multiple factors Interleukin 6, TNFα, Inflammation Cascade ? Infection sCD-40 ligand Collagen → platelet Plaque Rupture MDA Modified LDL activation Foam Cells ? Macrophages Macrophages Metalloproteinases Metalloproteinases Platelet-thrombin micro-emboli Plaque rupture Thrombosis D-dimer, Platelet Activation Complement, Thrombin Fibrinogen, Troponin, CRP, CD40L
  23. 23. Pathogenesis of Acute Coronary Syndromes: The integral role ofPlaque plateletsFissureor PlateletRupture Adhesion Platelet Activation Platelet Aggregation Thrombotic Occlusion
  24. 24. Thrombus Formation and ACS Plaque Disruption/Fissure/Erosion Thrombus FormationOldTerminology: UA NQMI STE-MINew Non-ST-Segment Elevation Acute ST-SegmentTerminology: Coronary Syndrome (ACS) Elevation Acute Coronary Syndrome (ACS)
  25. 25. RISK FACTORS MODIFIABLE NON-MODIFIABLE
  26. 26. RISK FACTORS• AGE. • INCIDENCE INCREASES WITH AGE. • RARE IN CHILDHOOD EXCEPT IN FAMILIAL HYPERLIPIDEMIA.• MALE GENDER. • MEN > PREMENUPAUSAL WOMEN. • AFTER MENUPAUSE INCIDENCE IS ALMOST SAME. • REASON ??? LOSS OF PROTECTIVE EFFECT OF OESTROGEN~~~~• FAMILY Hx OF IHD.
  27. 27. MODIFIABLE RISK FACTORS•SMOKING•HYPERLIPIDEMIA•HTN•DM•LACK OF EXERCISE•BLOOD COAGULATION FACTORS•CRP•HOMOCYSTEINAEMIA•PERSONALITY•OBESITY•GOUT•SOFT WATER•DRUGS……OCP,COX-2 INHIBITORS•HEAVY ALCOHOL CONSUMPTION
  28. 28. DIAGNOSIS OF ACS INC CARDIACTYPICAL HISTORY ECG CHANGES ENZYMES
  29. 29. Focused History• Aid in diagnosis and • Reperfusion rule out other causes questions – Palliative/Provocative – Timing of factors presentation – Quality of discomfort – ECG c/w STEMI – Radiation – Contraindication to – Symptoms associated fibrinolysis with discomfort – Degree of STEMI – Cardiac risk factors risk – Past medical history -especially cardiac
  30. 30. SYMPTOMS• ACUTE CENTRAL CHEST PAIN.• NAUSEA.• SWEATING.• DYSPNOEA.• PALPITATION.• SYNCOPE.• PULM;EDEMA.• EPIGASTRIC PAIN.• VOMITING.• POST-OP HYPOTENSION.• OLIGURIA.• ACUTE CONFUSIONAL STATE.• STROKE.• DIABETIC HYPERGLYCEMIC STATES. BE-AWARE OF SILENT
  31. 31. SIGNS• DISTRESS.• ANXIETY.• PALLOR.• SWEATINESS.• TACHYCARDIA/BRADICARDIA• HYPO/HYPERTENSION• S4• SIGNS OF HEART FAILURE• PANSYSTOLIC MURMUR• LOW GRADE PYREXIA• PERICARDIAL FRICTION RUB• EDEMA
  32. 32. Clinical Presentation Substernal chest pain or pressure (>20-30 min)• Localization or radiation to arms, back, throat, jaw• Accompanying features – Dyspnea – Nausea/vomiting – Diaphoresis – Weakness• Atypical: syncope ,
  33. 33. Targeted Physical Examination Recognize factors that– Vitals increase risk– Cardiovascul • Hypotension ar system • Tachycardia– Respiratory • Pulmonary rhales, system JVD, pulmonary– Abdomen edema • New murmurs/heart– Neurological sounds status • Diminished peripheral pulses • Signs of stroke
  34. 34. DIFFERENTIALDIAGNOSISANGINAPERICARDITISMYOCARDITISAORTIC DISSECTIONPULMONARYEMBOLISMESOPHAGEALREFLUX/SPASM
  35. 35. Differential Diagnosis • CHEST PAIN HEAVY,GRIPPING,TIGHTNESS • CENTRAL • RETROSTENALANGINA • MAY RADIATE TO JAW/ARM • MAY PROVOKE SWEATING ANDPERICARDITIS FEARMYOCARDITIS • ASSOCIATED SOBAORTIC DISSECTION • PROVOKED BY PHYSICALPULMONARY EMBOLISM EXERTION,AFTER MEALS, INESOPHAGEAL COLD AND WINDY WEATHERREFLUX/SPASM • AGGRAVATED BY ANGER AND EXCITEMENT • FADES QUICKLY WITH REST OR NITROGLYCERINE.
  36. 36. DifferentialDiagnosis • SHARP CENTRAL CHEST PAIN • EXACERBATED BY MOVEMENT,RESPIRATION,AND LYING DOWN.ANGINA • RELIEVED BY SITTING FORWARDPERICARDITIS • MAY BE REFERRED TO NECK OR SHOULDERMYOCARDITIS • PERICARDIAL FRICTION RUB INAORTIC DISSECTION THREE PHASES OF CARDIACPULMONARY EMBOLISM CYCLEESOPHAGEAL – Atrial systoleREFLUX/SPASM – Ventricular systole – Ventricular diastole • BIPHASIC ‘TO AND FRO’ RUB • FEVER • LEUCOCYTOSIS • LYMPHOCYTOSIS • FEATURES OF PERICARDIAL EFFUSION
  37. 37. DifferentialDiagnosis • ASYMPTOMATIC • FATIGUEANGINA • PALPITATIONSPERICARDITIS • CHEST PAINMYOCARDITIS • DYSPNOEAAORTIC DISSECTION • CCFPULMONARY EMBOLISM • SOFT HEART SOUNDSESOPHAGEALREFLUX/SPASM • S3 • TACHYCARDIA • PERICARDIAL FRICTION RUB
  38. 38. DifferentialDiagnosis • SEVERE CENTRAL CHEST PAIN. ANGINA • RADIATES TO BACK. PERICARDITIS MYOCARDITIS • SIGNS OF SHOCK AORTIC • NEUROLOGICAL DISSECTION SYMPTOMS PULMONARY EMBOLISM • RENAL FAILURE ESOPHAGEAL • LOWER LIMB ISCHEMIA REFLUX/SPASM • VISCERAL ISCHEMIA
  39. 39. PULMONARY EMBOLISMDifferentialDiagnosis SYMPTOMS •COUGH •UNEXPLAINED DYSPNOEA •PLEURITIC CHEST PAIN •HAEMOPTYSIS •DVT ~~~~~****** •FEVER SIGN •TACHYPNEA •TACHYCARDIA ANGINA •SHOCKED •PALE PERICARDITIS •SWEATY •LOCALISED PLEURAL RUB MYOCARDITIS •CREPTS •FEBRILE AORTIC DISSECTION •HYPOTENSION •PERIPHERAL SHUTDOWN •RAISED JVP PULMONARY •RV HEAVE •GALLOP RHYTHM •WIDELY SPLIT S2 EMBOLISM INVESTIGATIONS CXR------NORMAL,,,LINEAR ATELECTASIS,,BLUNTING ESOPHAGEAL OF CP ANGLE,,RAISED HEMIDIAPHRAGM,,,WEDGE- SHAPED PULM INFARCT,, REFLUX/SPASM ECG-------NORMAL,,SINUS TACHY,,AF,,,,RV STRAIN,,, CBC-------PMN LEUCOCYTOSIS ESR-----RAISED LDH-----RAISED PL D-DIMERS V/Q SCAN US SCAN ECHOCARDIOGRAPHY SPIRAL CT SCAN MRI
  40. 40. DifferentialDiagnosis ANGINA PERICARDITIS MYOCARDITIS AORTIC DISSECTION PULMONARY EMBOLISM ESOPHAGEAL REFLUX/ SPASM 20% OF THE PTS; ADMITTED INTO CCU HAVE GORD
  41. 41. ECG CHANGES
  42. 42. 12-Lead ECG Variations in AMI and Angina Baseline Ischemia—tall or inverted T wave (infarct), ST segment may be depressed (angina) Injury—elevated ST segment, T wave may invert Infarction (Acute)—abnormal Q wave, ST segment may be elevated and T wave may be inverted Infarction (Age Unknown)—abnormal Q wave, ST segment and T wave returned to normal
  43. 43. ECG FINDINGS IN ACS• NORMAL • REPEAT ECG WHEN PATIENT IS IN PAIN• ST-DEPRESSION • CONTINUOUS ST –• T-WAVE SEGMENT INVERSION MONITORING• PERSISTANT ST- ELEVATION OR• LBBB PATTERN
  44. 44. ECG AssessmentST Elevation or new LBBB STEMI ST Depression or dynamic T wave inversions NSTEMI Non-specific ECG Unstable Angina
  45. 45. TYPICAL ECGCHANGES IN STEMI
  46. 46. Normal or non-diagnostic EKG
  47. 47. ST-Segment Elevation MI
  48. 48. New LBBB Prominent R wave V1-V3QRS > 0.12 sec Prominent S wave 1, aVL, V5-V6L Axis deviation with t-wave inversion
  49. 49. Case 13. A 53 year old man with 3 hours of "crushing" chest pain. InterpretationAcute inferior myocardial infarctionST elevation in the inferior leads II, III and aVFreciprocal ST depression in the anterior leads
  50. 50. Case 16. 51 yr old male with no prior cardiac history presents with mid-sternal chest discomfortQuestions1. Is there ECG evidence of injury or ischemia?2. Is this patient having an MI? If so, in what anatomic distribution? Interpretation 1. YES 2. YES, ANTEROSEPTAL
  51. 51. post thrombolysis ECG
  52. 52. BIOCHEMICAL MARKERS
  53. 53. BIOCHEMICAL MARKERS • TROP. I CARDIAC TROPONONS I T C • TROP T • CK-MB • MYOBLOBIN • FBC OTHER • S ELECTROLYTES BLOOD • BGLINVESTIG ATIONS • LIPID PROFILE • TRANSTHORACIC ECHO CARDIOGRAPHY (TTE)
  54. 54. Cardiac Markers• Troponin ( T, I) • CK-MB isoenzyme – Very specific and – Rises 4-6 hours after more sensitive than injury and peaks at 24 CK hours – Rises 4-8 hours after – Remains elevated 36-48 injury hours – May remain elevated – Positive if CK/MB > 5% for up to two weeks of total CK and 2 times – Can provide normal prognostic – Elevation can be information predictive of mortality – Troponin T may be – False positives with elevated with renal exercise, trauma, dz, muscle dz, poly/dermatomyositis MYOGLOBIN RAPID DIAGNOSIS BUT POOR SPECIFICITY
  55. 55. Troponins for Evaluation and Management of ACS Advantages Disadvantages• Risk Stratificaton • Low sens. early (< 6h)• Sens/Spec > CKMB • Repeat at 8-12 h if neg.• Detect Recent MI • Limited ability to detect late minor reinfarction• Selection of Rx• Detect Reperfusion Recommendation• Useful as single test to efficiently Dx NSTEMI• Clinicians should familiarize themselves with Dx “cutoffs” in local lab
  56. 56. Cardiac Markers Initial Peak NormalMyoglobin 1-4hr 6-7hr 24hr NonspecificCK-MB 3-12hr 24hr 48-72hr Also elevated with Sk muscleTroponinI 3-12hr 24hr 5-10d Highly sensitive/ specific
  57. 57. MANAGEMENT
  58. 58. Cardiac Care Goals• Decrease amount of myocardial necrosis• Preserve LV function• Prevent major adverse cardiac events• Treat life threatening complications
  59. 59. MANAGEMENT OF ACS1 2 KEY QUESTIONS 2IS THERE IS THERE AST- RISE INSEGMENT TROPONINS?ELEVATION? RIGHT ANSWER LEADS TO SUCCESSFUL MANAGEMENT
  60. 60. Acute Management • Initial evaluation & stabilization • Efficient risk stratification • Focused cardiac care
  61. 61. ACS RISK CRITERIA Low Risk ACSNo intermediate or highrisk factors<10 minutes rest pain • ASA • CLOPIDOGRAL • BETA-BLOCKERNon-diagnostic ECG • NITRATESNon-elevated cardiac markersAge < 70 years
  62. 62. ACS RISK CRITERIA • LOW RISK ACS• ELEVATED TROPS.• DYNAMIC ST OR T WAVE CHANGES.• DM EARLY <72 HOURS> CORONARY• RENAL DYSFUNCTION ANGIOGRAPHY.• REDUCED LVF + INTERVENTION• EARLY POST- INFARCTION ANGINA.• PCI WITHIN 6 M• PREVIOUS CABG
  63. 63. ACS RISK CRITERIA HIGH RISK ACS• PTS WITH PERSISTENT OR RECURRENT ANGINA.• ST CHANGES > 2MM• OR DEEP NEGATIVE T URGENT CORONARY WAVE CHANGES. ANGIOGRAPHY• CLINICAL SIGNS OF HEAR FAILURE.• HAEMODYNAMIC INSTABILITY.• LIFE THREATENING ARRHYTHMIAS (VT,VF)
  64. 64. Chest pain suggestive of ischemia Immediate assessment within 10 Minutes Initial labs Emergent History & and tests care Physical– 12 lead ECG  IV access  Establish– Obtain initial  Cardiac diagnosis cardiac monitoring  Read ECG enzymes  Oxygen  Identify– electrolytes,  Aspirin complication cbc lipids, s  Nitrates bun/cr, glucose,  Assess for coags reperfusion– CXR
  65. 65. REPERFUSION GOALS EMS-TO- <30 MIN DRUGS EMS-TO- BALLOON <90 MINSYMPTOM ONSET –TO- <120 REPERFUSION MIN REPERFUSION HOSP EMS ARRIVAL PRE-HOSP ONSET OF ARRIVAL ECGSYMPYOMS INCREASING LOSS OF MYOCYTES
  66. 66. STEMIEARLY MEDICAL MANAGEMENT• ARRANGE EMERGENCY AMBULANCE• ASPIRIN 300MG.• GTN S/L. 0.3-1 MG.----REPEAT• OXYGEN 2-4 L/M• ANALGESIA IV DIAMORPHINE 2.5-5MG+ METOCLOPRAMIDE 10 MG.(NOT IM ~~~RISK OF BLEEDING WITH THROMBOLYSIS.• BETA-BLOCKER (IF NO C/I ) FOR ONGOING CHEST PAIN,HTN,TACHYCARDIA• IF PRIMARY PCI AVAILABLE GIVE GP11b/111a INHIBITOR.• ALTERNATIVELY GIVE THROMBOLYSIS. PRE-HOSPITAL TREATMENT INCLUDING THROMBOLYSIS CAN BE GIVEN BY TRAINED HEALTHCARE PROFESSIONAL UNDER GUIDELINES
  67. 67. IN-HOSPITAL MANAGEMENT OF ACS IN STEMI• THROMBOLYSIS OR PRIMARY ANGIOPLASTY.• BETA-BLOCKER (ATENOLOL 5MG IV). – CONTRAINDICATION IN ASTHMATICS• ACE-INHIBITORS. – CONSIDER (LISINOPRIL 2.5 MG) IN ALL NORMOTENSIVE PATIENTS WITHIN 24 HRS OF ACUTE MI ESPECIALLY IF THERE IS EVIDENCE OF HEART FAILURE OR ECHO EVIDENCE OF LV DYSFUNCTION.
  68. 68. MANAGEMENT OF AMI THRMBOLYSIS INDICATIONS(PRESENTATION WITHIN 12 H) • ST Elevation>2mm IN 2 OR MORE CHEST LEADS. OR • ST elevation>1mm IN 2 OR MORE LIMB LEADS. OR• EFFECTIVE IN REDUCING • POSTERIOR MORTALITY. INFARCTION (DOMINANT R• GREATEST BENEFIT IF WAVES & ST DEPRESSION IN V1- GIVEN <12 H OF ONSET OF V3) PAIN. • NEW ONSET OF LBBB• BEST TIME <60MIN (BHF)
  69. 69. THRMBOLYSIS CONTRAINDICATIONS• HAEMORRHAGIC STROKE OR STROKE OF UNKNOWN ORIGIN AT ANY TIME• ISCHEMIC STROKE IN PRECEDING 6 MONTHS• CNS DAMAGE OR NEOPLASM• RECENT MAJOR TRAUMA/SURGERY/HEAD INJURY/ WITHIN PRECEDING 3 WEEKS• GI BLEEDING WITHIN LAST MONTH• KNOWN BLEEDING DISORDER• AORTIC DISSECTION
  70. 70. THRMBOLYSIS RELATIVE CONTRAINDICATIONS• H/O SEVERE HTN (SBP >180 mmHg.)• PREGNANCY OR <1 WEEK POSTPARTUM• ORAL ANTICOAGULANT THERAPY.• NON-COMPRESSIBLE PUNCTURES.• TRAUMATIC RESUSSITATION• ADVANCED LIVER DISEASE• TRANSIENT ISCHEMIC ATTACK IN PRECEDING 6 MONTHS.
  71. 71. SIDE-EFFECTS OF THROMBOLYTICS• NAUSEA• VOMITING• BLEEDING• REPERFUSION ARRHYTHMIA• RECURRENT ISCHEMIA• ANGINA• CEREBRAL EDEMA• PULM EDEMA• HYPOTENSION• FEVER• CONVULSIONS• ALLERGIC REACTIONS----RASH, FLUSHING,UVEITIS• ANAPHYLAXIS• GB SYNDROME
  72. 72. ACUTE MANAGENT OF N- STEMI )• ADMIT TO CCU• MONITOR CLOSELY• O2:• ANALGESIA: MORPHINE 2.5-5mg +METOCLOPRAMIDE 10 mg. IV• NITRATES:GTN SPRAY OR S/L TABS• ASPIRIN: 300mgPO• BETA-BLOCKER: METOPROLOL 50-100mg/8H OR ATENOLOL 50-100mg/24H• IF B-BLOCKER IS CI THEN GIVE RATE LIMITING Ca; Channel ANTAGONIST. • VERAPAMIL 80-120 mg/8H PO DON’T USE VERAPAMIL » OR AND • DILTIAZEM 60-120 mg/8H PO B-BLOCKER TOGATHER CAN CAUSE ASYSTOLE
  73. 73. ACUTE MANAGENT OF N- STEMI ) Cont…..• LMW HEPARIN • ENOXAPARIN 1mg/kg SC/12h• Or • Dalteparin 120u/kg/12h sc• Alternatively :unfractionated heparin 5000u iv bolus then IVI infusion @0.25 UNITS/KG/H. • Check APTT 6-hourly. • Alter IVI rate to maintain APTT @ 1.5-2.5 times control.• Nitrates IV if pain continues • GTN 50mg in 50 ml 0.9%saline @2-10ml/h titrate to pain and maintain SBP >100mmHg.• Record ECG while in pain.
  74. 74. ACUTE MANAGENT OF ACS WITHOUT ST-SEGMENT ELEVATION (NSTEMI) CONTD: •No further pain •Flat or inverted T- waves or normal ECGLOW Risk Pts. •Negative Troponins• May be discharged if a repeat troponin (>12h) is negative.• Treat medically.• Arrange further investigations: • Stress test • angiography
  75. 75. POST-MI DRUG THERAPY• ASA 75-100MG./D• A BETA-BLOCKER TO MAINTAIN HR <60/MIN. (METOPROLOL 50MG BID)• ACE-INHIBITORS (RAMIPRIL 2.5MG BID TITRATED TO MAX TOLERATED OR TARGET DOSE)• IF INTOLERANT OF ACE-INH USE ARB (VALSARTAN 20MG BID)• STATINS(SIMVASTATIN 20-80MG/D)• CLOPIDOGREL 75MG/D FOR 9-12 MONTHS.(FOR MODERATE – HIGH RISK Pts. WITH NST- ACS• GTN SPRAY FOR SYMPTOMATIC RELIEF OF ANGINA• ALDOSTERONE ANTAGONIST(EPLERENONE 25MG/D FOR REDUCED EF AND HF PTS
  76. 76. SUBSEQUENT MANAGEMENT IN ACS CONTD;• ADDRESS MODIFIABLE RISK FACTORS. – DISCOURAGE SMOKING – ENCOURAGE EXERCISE 20-30MIN/DAY – DIAGNOSE AND TREAT DM,HTN & HYPERLIPIDEMIA – ENCOURAGE TO CONSUME >7 GRAMS OF OMEGA 3 FATTY ACIDS/WEEK FROM OILY FISH OR >1 GRAM/D OF OMEGA -3-ACID ETHYL ESTERS. – WEIGHT REDUCTION
  77. 77. SUBSEQUENT MANAGEMENT IN ACS CONTD; GENERAL ADVICE• DISCHARGE FROM HOSPITAL AFTER 5-7 DAYS IF UNCOMPLICATED.• MAY RETURN TO WORK AFTER 2 MONTHS.• FOLLOWING OCCUPATIONS SHOULD NOT BE RESTARTED POST-MI. – AIRLINE PILOTS – AIR-TRAFFIC CONTROLLERS – DIVERS
  78. 78. SUBSEQUENT MANAGEMENT IN ACS GENERAL ADVICE CONTD;• DRIVERS OF HEAVY GOODS VEHICLES AND PUBLIC SERVICE MAY BE PERMITTED TO RETURN TO WORK IF MEET CERTAIN CRITERIA.• LIGHTER JOB PREFERRED AGAINST HEAVY MANUAL LABOUR.• DIET: – HIGH IN OILY FISH LOW IN SATURATED FATS – FRUITS – VEGETABLES – FIBRE• EXERCISE:REGULAR DAILY EXERCISE.• SEX: AVOID INTERCOURSE FOR 1 MONTH.• TRAVEL: AVOID AIR TRAVEL FOR 2 MONTHS.• F/U REVIEW AT 5 WKS POST-MI: IF ANGINA RECURS CONSIDER FOR ANGIOGRAPHY.• REVIEW AT 3 MONTHS : CHECK LIPIDS
  79. 79. MANAGEMENT ECG OF O2 AMI IV ACCESS TAKE LABS BRIEF ASSESSMENT ASPIRIN 300 MG MORPHINE 2.5-5mg IV +METOCLOPRAMIDE 10mG GTN S/L 2 PUFFS OR 1 TAB. THROMBOLYSIS BETA-BLOCKER CXR CONSIDER GLUCOSE,INSULIN,& POTASSIUM INFUSION FOR DM PTs. CONSIDER DVT PROPHYLAXIS CONT;MEDICATION EXCEPT Ca;CHANNEL ANTAGONIST (UNLESS SPECIFIC INDICATIONS)
  80. 80. SUMMARY• ACS includes UA, NSTEMI, and STEMI• Management guideline focus – Immediate assessment/intervention (MONA+BAH) – Risk stratification (UA/NSTEMI vs. STEMI) – RAPID reperfusion for STEMI (PCI vs. Thrombolytics) – Conservative vs Invasive therapy for UA/NSTEMI• Aggressive attention to secondary prevention initiatives for ACS patients • Beta blocker, ASA, ACE-I, Statin
  81. 81. THANK YOU
  82. 82. ACUTE MANAGENT OF ACS WITHOUT ST-SEGMENT ELEVATION (NSTEMI) CONTD: Indications for consideration of invasive intervention:• Poor prognosis, e.g pulmonary edema.• Refractory symptoms.• Positive ETT. At low workload.• Non-Q wave MI.
  83. 83. Timing of Release of Various Biomarkers After Acute Myocardial Infarction Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157Copyright ©2007 American College of Cardiology Foundation. Restrictions may apply.
  84. 84. THRMBOLYTIC AGENTS• STREPTOKINASE – INITIATED WITHIN 12H. – 1.5 MILLION UNITS IN 100 ML N/S IVI OVER 1 HR – S/E: NAUSEA,VOMITING,HAEMORRHAGE,STR OKE, DYSRHYTHMIA,WATCH FOR ALLERGIC REACTIONS, ANAPHYLAXIS – DON’T REPEAT UNLESS IT IS WITHIN 4D OF THE 1st. ADMINISTRATION.
  85. 85. THRMBOLYTIC AGENTS• ALTEPLASE (rt-PA, TISSUE-TYPE PLASMINOGEN ACTIVATOR) – ACCELERATED REGIMEN • INITIATED WITHIN 6 H. OF SYMPTOMS ONSET. • 15 MG IV INJECTION FOLLOWED BY IVI OF 50 MG OVER 30 MIN. THEN 35 MG OVER 60MIN.= TOTAL DOSE= 100MG OVER 90 MIN. • IN PTS <65KG WT==15MG BY IV INJ.FOLLOWED BY IVI OF 0.75MG/KG OVER 30 MIN.==THEN 0.5MG/KG OVER 60 MIN.=MAX TOTAL DOSE 100MG OVER 90 MIN.
  86. 86. THRMBOLYTIC AGENTS• ALTEPLASE – NON-ACCELERATED REGIMEN • INITIATED WITHIN 6-12 H. OF SYMPTOMS ONSET. • 10 MG IV INJECTION FOLLOWED BY IVI OF 50 MG OVER 60 MIN. THEN 4 INFUSIONS EACH OF 10 MG OVER 30MIN.= TOTAL DOSE= 100MG OVER 3 HRS. • IN PTS <65KG WT=MAX TOTAL DOSE 1.5MG/KG.
  87. 87. Risk Stratification to Determine the LikelihoodAssessment of Acute Coronary Syndrome Findings Findings indicating Findings indicating indicating INTERMEDIAT LOW likelihood of E likelihood of ACS in ACS in absence of high- HIGH absence of high- or intermediate- likelihood of likelihood findings likelihood findings ACSHistory Chest or left arm pain Chest or left arm pain Probable ischemic or discomfort as chief or discomfort as chief symptoms symptom symptom Recent cocaine use Reproduction of Age > 50 years previous documented angina Known history of coronary artery disease, including myocardial infarctionP New transient mitral Extracardiac vascular Chest discomfort regurgitation, disease reproduced by hypotension, palpation diaphoresis, pulmonary edema or rales
  88. 88. RISK STRATIFICATIONINITIAL RISK LONG-TERM RISK • DEFINED BY CLINICAL RISK • DETERMINED BY FACTORS COMPLICATIONS • AGE • PRIOR MI OF ACUTE • CABG THROMBOSIS. • DM • HF • MAY PRODUCE • CRP RECURRENT MI • FIBRINOGEN • BNP • MARKED ST-DEP • MODIFIED ALBUMIN • S.CREATININE • DYNAMIC ST • LVD CHANGE • LT.MAIN OR 3VD • RAISED TROPS
  89. 89. SCORES USED FOR LONGTERM RISK STRATIFICATION IN ACS GRACETIMI SCORE PREDICTION SCORE • THROMBOLYSIS • GLOBAL IN MYOCARDIAL REGISTRY OF INFARCTION ACUTE CORONARY EVENTS • BASED ON AGE,HR, SBP,S.CREATINI NE,KILLIP
  90. 90. TIMI RISK SCORE IN ACS NSTEMI/UARISK FACTOR SCOREAGE >65 1>3 ARTERY DIS RISK FACTORS 1HTNHLPDFMLY HXDMSMOKINGCORONARY ART STENOSIS >50% 1ASA USE IN LAST 7 DAYS 1SEV ANGINA >2 EPISODES/D @REST 1ST DEVIATION ON ECG(HORIZONTAL 1ST DEPRESSION OR TRANSIENT STELEVATIONELEVATED CARDIAC MARKERS 1CK-MB OR TROPONIN
  91. 91. TIMI RISK SCORE IN ACS NSTEMI/UATOTAL RATE OF RATE OF DEATH / DEATH /MI MI/ URGENTSCORE REVASCULARIZATION IN 14 DAYS % %0-1 3 4.752 3 8.33 5 13.24 7 19.95 12 26.26-7 19 40.9
  92. 92. TIMI RISK SCORE IN ACS STEMIRISK FACTOR SCOREAGE >65 2AGE >75 3HO ANGINA 1HO HTN 1HO DM 1SBP<100 3HR>100 2KILLIP II-IV 2WEIGHT>67KG 1ANT MI OR LBBB 1DELAY TO TREATMENT >4 HRS 1
  93. 93. TOTAL SCORE RISK OF DEATH @30 DAYS %0 0.81 1.62 2.23 4.44 7.35 12.46 16.17 23.48 26.8
  94. 94. LOW INTERMEDIATE HIGH RISK RISK RISK Chest Pain CONSERVATIVE INVASIVE CORONAR Y center THERAPY STENTING THERAPY CABG•ANTIPLATELET •GLYCOPROTEINS IIAGENTS B/IIIA INHIBITORS •MYOCARDIAL ENERGY CONSUMPTION •ASA •ABCIXIMAB •ATENOLOL •CLOPIDOGREL •EPTIFIBATIDE •METOPROLOL •PLAQUE •TICLOPIDINE •TIROFIBAN STIBILIZING/REMO DELLING OF VENT •HMG-CoA•ANTITHROMBINS •CORONARY •ANALGESIA REDUCTASE •HEPARIN VASODILATORS •MORPHINE INHIBITORS •LMWH •GTN •ACE- INHIBITORS
  95. 95. ACUTE MANAGENT OF ACS WITHOUT ST- SEGMENT ELEVATION (NSTEMI) ischemia •Persistent •Recurrent ischemia contd: High Risk Pts. •ST-Depression •DM •Increased Troponins• Infusion of a GP11b/111a antagonist. PREVENT PLT AGGRGN BY – Abciximab (250microgram/kg IV OVER 1 Min. THEN 125 BLOCKING nanogram/kg/min IVI) BINDING OF FIBRINOGEN TO – Aptifibatide RECEPTOR ON PLT. – Tirofiban• Urgent angiography.• Add clopidogrel 300mg po stat •Beta-blocker then 75mg/d •Ca2+; ch antagonist With ASA OPTIMIZE •ACE-I DRUGS •Nitrates •Intensive statin regimens
  96. 96. ACUTE MANAGENT OF ACS WITHOUT ST-SEGMENT ELEVATION CONTD: (NSTEMI) High Risk Pts. IF SYMPTOMS FAIL TO IMPROVE• URGENT ANGIOGRAPHY• URGENT ANGIOPLASTY OR• CABG
  97. 97. ACUTE MANAGENT OF ACS WITHOUT ST-SEGMENT ELEVATION (NSTEMI) CONTD: Further measures:• Wean off GTN infusion when stabilized on oral drugs.• Stop heparin when pain-free for 24h.(give atleast 3-5 days therapy).• Check serial ECGs. For 2-3 days.• Check serial cardiac enzymes for 2-3 days.• Address modifiable risk factors • Smoking • HTN • Hyperlipidemia • DM• Gentle mobilization.
  98. 98. ACUTE MANAGENT OF ACS WITHOUT ST- SEGMENT ELEVATION (NSTEMI) CONTD: Prognosis • Overall risk of death ~1-2% • 15% for refractory angina.Followings are associated with increasedrisk•Haemodynamic instability: • Hypotension, •Pulmonary edema RISK•T-wave inversion or ST segmentdepression on restingECG. STRATIFICATION•Previous MI•Prolonged rest pain.•Older age.•DM

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