myocardial infarction

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my case discussion in CPD


  • 1.ACUTE CORONARY SYNDROME(A CASE DISCUSSION)BY Dr Ijaz Hussain MBBS , MCPS, MRCGP, Dip Avn Med Prince Sultan Military Medical City Riyadh

2. Case Presentation Patients Name: Mohammad Al Shahrani Age: 63 Yrs Sex: Nationality: Saudi Resident of al Oainah 3. Chief Complaints Mohammad al Shahrani was brought in the AnE withBrief 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 undergonecardiac cath one year and a half. 4. Initial Work-up Although the patient was in distress but hisvital 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. ECG TRACING 6. Initial Work-up in PSMMC Cardiac EnzymesEnzyme 18.11.2012 19.11.2012 Ref Range Ck 144651{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 18.11.20120.007 1.1 {0.1 ng/ml } 19.11.20121.540 FBC NAD Renal Functions NAD CxR NAD 7. DISCHARGE SUMMARY Final Diagnosis: Diabetes ; Hypertension ; IHD e Hx of PCI in Asir 4 Yrsago History: Pt is 63 yrs old saudi male with Dx as above.Presented in AnE with C/O acute onset chest pain offew 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. DISCHARGE SUMMARY Hosp Course & Mngmnt: Pt was taken directly fromAnE to cath Lab. Shown tight mid RCA lesion ,with aspirationof thrombosis. Echo was done which shown slight irregularity.Pt was kept under observation for 24 hrs. Was discharged in agood condition, with no complaints and was doing fine. Drugs on Discharge: Aspirin 81 mg1xTab POOD Plavix 75 mg 1xTab POOD Prindopril 2.5 mg1xTab POOD Isordil 20 mg 1xTab PO OD Lipitor 40 mg 1xTab PO OD Lasix20 mg1xTab PO OD Pantoperazole 40 mg 1xTab PO OD Future Plan : Pt was given an appt 24/52 to be seen in OPD 9. Case Discussion 10. Heart is capable of pumping bloodto every cell in the body in underone minute During the course of the day, yourheart will beat approx 100,000times driving 2,000 gallons ofoxygen-rich blood through 60,000miles of blood vessels. 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. 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,nonST-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. Types STEMI : OR New Onset LBBBACUTE 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. Clinical Spectrum of Acute Coronary SyndromesStable anginaUnstable Non-STE MI STE MIanginaNonePositive PositiveEvidence of necrosisST-segment ST-segment ST-segmentECG earlydepression depressionelevation and/or and/orT-wave inversion T-wave inversionECG lateNo QNo QQ develops 15. UnstableAnginaN-STEMISTEMINon Occludingocclusive thrombusComplete thrombussufficient to cause occlusionthrombustissue damage &mildST elevations onNon myocardial necrosis ECG or new LBBBspecificECG ST depression +/- Elevated cardiacT wave inversion on enzymesECGNormalMore severecardiac Elevated cardiacsymptomsenzymes enzymes 16. EPIDEMIOLOGY OFACS 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 recurrentcoronary 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. PATHOPHYSIOLOGY 19. Understanding Myocardial Ischemia Imbalance 20. Understanding Myocardial IschemiaDec O2 supply Inc. DemandINCREASEDCARDIACOUTPUT..(THYROTOXICOSIS)MYOCARDIALHYPERTROPHY(AS,HTN) 21. PATHOPHYSIOLOGY RUPTURE OR EROSION OF THE FIBROUS CAPOF A CORONARY ARTERY PLAQUE. PLATELETS AGGREGATION AND ADHESION. LOCALIZEDTHROMBOSIS.VASOCONSTRICTION. DISTAL THROMBUS EMBOLIZATION. THROMBUS FORMATION ANDVASOCONSTRICTION PRODUCED BY PLTRELEASE OF SEROTONIN & THROMBOXANEA2, RESULT IN MYOCARDIAL ISCHEMIA DUE TOREDUCTION OF CORONARY BLOOD FLOW. 22. Plaque Rupture, Thrombosis, and MicroembolizationQuiescent plaque ProcessMarker Lipid corePlaque formation CholesterolLDL Vulnerable plaqueC-Reactive Protein Inflammation Adhesion Molecules TF Clotting Multiple factors Interleukin 6, TNF,Inflammation Cascade ? InfectionsCD-40 ligand Collagen plateletPlaque Rupture MDA Modified LDL activation Foam Cells? MacrophagesMacrophagesMetalloproteinases MetalloproteinasesPlatelet-thrombin micro-emboli Plaque rupture ThrombosisD-dimer, Platelet Activation Complement, ThrombinFibrinogen, Troponin, CRP, CD40L 23. Pathogenesis of Acute Coronary Syndromes: The integral role ofPlaqueplateletsFissureorPlateletRuptureAdhesion Platelet ActivationPlateletAggregationThromboticOcclusion 24. Thrombus Formation and ACS Plaque Disruption/Fissure/Erosion Thrombus FormationOldTerminology:UA NQMI STE-MINewNon-ST-Segment Elevation AcuteST-SegmentTerminology: Coronary Syndrome (ACS) Elevation Acute Coronary Syndrome (ACS) 25. RISK FACTORS MODIFIABLE NON-MODIFIABLE 26. RISK FACTORS AGE. INCIDENCE INCREASESWITH AGE. RARE IN CHILDHOODEXCEPT IN FAMILIALHYPERLIPIDEMIA. MALE GENDER. MEN > PREMENUPAUSALWOMEN. AFTER MENUPAUSEINCIDENCE IS ALMOSTSAME. REASON ??? LOSS OFPROTECTIVE EFFECT OFOESTROGEN~~~~ FAMILY Hx OF IHD. 27. MODIFIABLE RISK FACTORSSMOKINGHYPERLIPIDEMIAHTNDMLACK OF EXERCISEBLOOD COAGULATION FACTORSCRPHOMOCYSTEINAEMIAPERSONALITYOBESITYGOUTSOFT WATERDRUGSOCP,COX-2 INHIBITORSHEAVY ALCOHOL CONSUMPTION 28. DIAGNOSIS OF ACSINC CARDIACTYPICAL HISTORY ECG CHANGESENZYMES 29. Focused History Aid in diagnosis and Reperfusionrule out other causesquestions Palliative/Provocative Timing offactorspresentation Quality of discomfort ECG c/w STEMI Radiation Contraindication to Symptoms associatedfibrinolysiswith discomfort Degree of STEMI Cardiac risk factors risk Past medical history-especially cardiac 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. SIGNS DISTRESS. ANXIETY. PALLOR. SWEATINESS. TACHYCARDIA/BRADICARDIA HYPO/HYPERTENSION S4 SIGNS OF HEART FAILURE PANSYSTOLIC MURMUR LOW GRADE PYREXIA PERICARDIAL FRICTION RUB EDEMA 32. Clinical PresentationSubsternal 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. Targeted Physical ExaminationRecognize factors that Vitals increase risk Cardiovascul Hypotensionar system Tachycardia Respiratory Pulmonary rhales,systemJVD, pulmonary Abdomen edema New murmurs/heart Neurologicalsoundsstatus Diminishedperipheral pulses Signs of stroke 34. DIFFERENTIALDIAGNOSISANGINAPERICARDITISMYOCARDITISAORTIC DISSECTIONPULMONARYEMBOLISMESOPHAGEALREFLUX/SPASM 35. Differential Diagnosis CHEST PAINHEAVY,GRIPPING,TIGHTNESS CENTRAL RETROSTENALANGINA MAY RADIATE TO JAW/ARM MAY PROVOKE SWEATING ANDPERICARDITIS FEARMYOCARDITIS ASSOCIATED SOBAORTIC DISSECTION PROVOKED BY PHYSICALPULMONARY EMBOLISM EXERTION,AFTER MEALS, INESOPHAGEAL COLD AND WINDY WEATHERREFLUX/SPASM AGGRAVATED BY ANGER ANDEXCITEMENT FADES QUICKLY WITH REST ORNITROGLYCERINE. 36. DifferentialDiagnosis SHARP CENTRAL CHEST PAIN EXACERBATED BYMOVEMENT,RESPIRATION,ANDLYING DOWN.ANGINA RELIEVED BY SITTING FORWARDPERICARDITIS MAY BE REFERRED TO NECK ORSHOULDERMYOCARDITIS PERICARDIAL FRICTION RUB INAORTIC DISSECTIONTHREE PHASES OF CARDIACPULMONARY EMBOLISM CYCLEESOPHAGEAL Atrial systoleREFLUX/SPASM Ventricular systole Ventricular diastole BIPHASIC TO AND FRO RUB FEVER LEUCOCYTOSIS LYMPHOCYTOSIS FEATURES OF PERICARDIALEFFUSION 37. DifferentialDiagnosis ASYMPTOMATIC FATIGUEANGINA PALPITATIONSPERICARDITIS CHEST PAINMYOCARDITIS DYSPNOEAAORTIC DISSECTION CCFPULMONARY EMBOLISM SOFT HEART SOUNDSESOPHAGEALREFLUX/SPASM S3 TACHYCARDIA PERICARDIAL FRICTIONRUB 38. DifferentialDiagnosis SEVERE CENTRAL CHEST PAIN. ANGINA RADIATES TO BACK. PERICARDITIS MYOCARDITIS SIGNS OF SHOCK AORTIC NEUROLOGICAL DISSECTIONSYMPTOMS PULMONARY EMBOLISM RENAL FAILURE ESOPHAGEAL LOWER LIMB ISCHEMIA REFLUX/SPASM VISCERAL ISCHEMIA 39. PULMONARY EMBOLISMDifferentialDiagnosis SYMPTOMS COUGH UNEXPLAINED DYSPNOEA PLEURITIC CHEST PAIN HAEMOPTYSIS DVT ~~~~~****** FEVERSIGN TACHYPNEA TACHYCARDIA ANGINA SHOCKED PALE PERICARDITIS SWEATY LOCALISED PLEURAL RUB MYOCARDITISCREPTS FEBRILE AORTIC DISSECTIONHYPOTENSION PERIPHERAL SHUTDOWN RAISED JVP PULMONARYRV HEAVE GALLOP RHYTHM WIDELY SPLIT S2 EMBOLISM INVESTIGATIONS CXR------NORMAL,,,LINEAR ATELECTASIS,,BLUNTING ESOPHAGEAL OF CP ANGLE,,RAISED HEMIDIAPHRAGM,,,WEDGE- SHAPED PULM INFARCT,, RE