ACUTE CORONARY SYNDROME (A CASE DISCUSSION)
BY
Dr Ijaz Hussain MBBS , MCPS, MRCGP, Dip Avn Med
Prince Sultan Military Medical CityRiyadh
Case Presentation
• Patient’s Name: Mohammad Al Shahrani• Age: 63 Yrs• Sex: ♂• Nationality: Saudi• Resident of al Oainah
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.
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
ECG TRACING
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
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
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
Case Discussion
•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.
DEFINITION
Myocardial infarction, commonly known as a heart attack, is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.
DEFINITION
Myocardial infarction is considered part of a spectrum referred to as acute coronary syndrome (ACS). The ACS continuum representing ongoing myocardial ischemia or injury consists of unstable angina, non–ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Patients with ischemic discomfort may or may not have ST-segment or T-wave changes denoted on the electrocardiogram (ECG). ST elevations seen on the ECG reflect active and ongoing transmural myocardial injury
Types
•STEMI : OR New Onset LBBB
•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
ACUTE MI
Clinical Spectrum of Acute Coronary Syndromes
Evidence of necrosis None Positive Positive
ECG earlyST-segment depression
and/orT-wave inversion
ST-segment elevation
ECG late No Q No Q Q develops
Stable anginaStable angina UnstableUnstableanginaangina
Non-STE MINon-STE MI STE MISTE MI
ST-segment depression
and/or T-wave inversion
Unstable Angina STEMI N-STEMIN-STEMI
Non occlusive thrombus
Non specific ECG
Normal cardiac enzymes
Occluding thrombus sufficient to cause tissue damage & mild myocardial necrosis
ST depression +/- T wave inversion on ECG
Elevated cardiac enzymes
Complete thrombus occlusion
ST elevations on ECG or new LBBB
Elevated cardiac enzymes
More severe symptoms
EPIDEMIOLOGY OF ACS
Single largest cause of deathSingle largest cause of death 515,204 US deaths in 2000515,204 US deaths in 2000 1 in every 5 US deaths1 in every 5 US deaths
IncidenceIncidence 1,100,000 Americans will have a new or recurrent 1,100,000 Americans will have a new or recurrent
coronary attack each year and about 45% will die*coronary attack each year and about 45% will die* 550,000 new cases of angina per year550,000 new cases of angina per year
PrevalencePrevalence 12,900,000 with a history of MI, angina, or both12,900,000 with a history of MI, angina, or both
INCIDENCE IN UK=5/1000/ANNUM FOR STEMIINCIDENCE IN UK=5/1000/ANNUM FOR STEMI
PATHOPHYSIOLOGY
Understanding Myocardial Ischemia
Imbalance
Understanding Myocardial Ischemia
Dec O2 supply Inc. Demand
INCREASED CARDIAC OUTPUT….. (THYROTOXICOSIS)
MYOCARDIAL HYPERTROPHY (AS,HTN)
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.
Plaque Rupture, Thrombosis, and MicroembolizationPlaque Rupture, Thrombosis, and Microembolization
Quiescent plaqueQuiescent plaque
Platelet-thrombin micro-emboliPlatelet-thrombin micro-emboliPlaquePlaque rupturerupture
ProcessPlaque formation
InflammationMultiple factors? Infection
Plaque Rupture? MacrophagesMetalloproteinases
ThrombosisPlatelet ActivationThrombin
ProcessPlaque formation
InflammationMultiple factors? Infection
Plaque Rupture? MacrophagesMetalloproteinases
ThrombosisPlatelet ActivationThrombin
MarkerCholesterolLDL
C-Reactive ProteinAdhesion MoleculesInterleukin 6, TNFsCD-40 ligand
MDA Modified LDL
D-dimer, Complement,Fibrinogen, Troponin, CRP, CD40L
MarkerCholesterolLDL
C-Reactive ProteinAdhesion MoleculesInterleukin 6, TNFsCD-40 ligand
MDA Modified LDL
D-dimer, Complement,Fibrinogen, Troponin, CRP, CD40L
Vulnerable plaqueVulnerable plaque
MacrophagesFoam Cells
Collagen platelet activation
TF TF ClottingClotting CascadeCascade
Lipid coreLipid core
Metalloproteinases
InflammationInflammation
Pathogenesis of Acute Coronary
Syndromes:The integral role of
plateletsPlaqueFissure or Rupture
PlateletAggregation
PlateletActivation
PlateletAdhesion
ThromboticOcclusion
Thrombus Formation and ACS
UA NQMI STE-MI
Plaque Disruption/Fissure/Erosion
Thrombus Formation
Non-ST-Segment Elevation Acute Coronary Syndrome (ACS)
ST-Segment Elevation Acute Coronary Syndrome (ACS)
Old Terminology:
NewTerminology:
RISK FACTORS
MODIFIABLE
NON-MODIFIABLE
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.
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
DIAGNOSIS OF ACS
TYPICAL HISTORY ECG CHANGES INC CARDIAC ENZYMES
Focused History• Aid in diagnosis and
rule out other causes
– Palliative/Provocative factors
– Quality of discomfort– Radiation– Symptoms associated
with discomfort– Cardiac risk factors– Past medical history -
especially cardiac
• Reperfusion questions
– Timing of presentation
– ECG c/w STEMI – Contraindication to
fibrinolysis– Degree of STEMI
risk
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
SIGNS• DISTRESS.• ANXIETY.• PALLOR.• SWEATINESS.• TACHYCARDIA/BRADICARDIA• HYPO/HYPERTENSION• S4• SIGNS OF HEART FAILURE• PANSYSTOLIC MURMUR• LOW GRADE PYREXIA• PERICARDIAL FRICTION RUB• EDEMA
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,
Targeted Physical Examination
– Vitals– Cardiovascula
r system– Respiratory
system– Abdomen– Neurological
status
Recognize factors that increase risk
•Hypotension•Tachycardia•Pulmonary rhales,
JVD, pulmonary edema
•New murmurs/heart sounds
•Diminished peripheral pulses
•Signs of stroke
DIFFERENTIAL DIAGNOSIS
ANGINAPERICARDITISMYOCARDITISAORTIC DISSECTIONPULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM
Differential Diagnosis
• CHEST PAIN HEAVY,GRIPPING,TIGHTNESS
• CENTRAL • RETROSTENAL• MAY RADIATE TO JAW/ARM• MAY PROVOKE SWEATING AND
FEAR• ASSOCIATED SOB• PROVOKED BY PHYSICAL
EXERTION,AFTER MEALS, IN COLD AND WINDY WEATHER
• AGGRAVATED BY ANGER AND EXCITEMENT
• FADES QUICKLY WITH REST OR NITROGLYCERINE.
ANGINAPERICARDITISMYOCARDITISAORTIC DISSECTIONPULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM
Differential Diagnosis
• SHARP CENTRAL CHEST PAIN• EXACERBATED BY
MOVEMENT,RESPIRATION,AND LYING DOWN.
• RELIEVED BY SITTING FORWARD• MAY BE REFERRED TO NECK OR
SHOULDER• PERICARDIAL FRICTION RUB IN
THREE PHASES OF CARDIAC CYCLE– Atrial systole– Ventricular systole– Ventricular diastole
• BIPHASIC ‘TO AND FRO’ RUB• FEVER• LEUCOCYTOSIS• LYMPHOCYTOSIS• FEATURES OF PERICARDIAL
EFFUSION
ANGINA
PERICARDITISMYOCARDITISAORTIC DISSECTIONPULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM
Differential Diagnosis
• ASYMPTOMATIC • FATIGUE• PALPITATIONS• CHEST PAIN• DYSPNOEA• CCF• SOFT HEART SOUNDS• S3• TACHYCARDIA• PERICARDIAL FRICTION
RUB
ANGINAPERICARDITIS
MYOCARDITISAORTIC DISSECTIONPULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM
Differential Diagnosis
• SEVERE CENTRAL CHEST PAIN.
• RADIATES TO BACK.• SIGNS OF SHOCK• NEUROLOGICAL
SYMPTOMS• RENAL FAILURE• LOWER LIMB ISCHEMIA• VISCERAL ISCHEMIA
ANGINAPERICARDITISMYOCARDITIS
AORTIC DISSECTIONPULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM
Differential Diagnosis
PULMONARY EMBOLISM
SYMPTOMS •COUGH•UNEXPLAINED DYSPNOEA•PLEURITIC CHEST PAIN•HAEMOPTYSIS•DVT ~~~~~******•FEVER
SIGN •TACHYPNEA•TACHYCARDIA•SHOCKED•PALE•SWEATY•LOCALISED PLEURAL RUB•CREPTS•FEBRILE•HYPOTENSION•PERIPHERAL SHUTDOWN•RAISED JVP•RV HEAVE•GALLOP RHYTHM•WIDELY SPLIT S2
INVESTIGATIONS CXR------NORMAL,,,LINEAR ATELECTASIS,,BLUNTING OF CP ANGLE,,RAISED HEMIDIAPHRAGM,,,WEDGE-SHAPED PULM INFARCT,,
ECG-------NORMAL,,SINUS TACHY,,AF,,,,RV STRAIN,,,CBC-------PMN LEUCOCYTOSISESR-----RAISEDLDH-----RAISEDPL D-DIMERSV/Q SCANUS SCANECHOCARDIOGRAPHYSPIRAL CT SCANMRI
ANGINAPERICARDITISMYOCARDITISAORTIC DISSECTION
PULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM
ANGINAPERICARDITISMYOCARDITISAORTIC DISSECTIONPULMONARY EMBOLISM
ESOPHAGEAL REFLUX/ SPASM
20% OF THE PTS; ADMITTED INTO CCU HAVE GORD
Differential Diagnosis
ECG CHANGES
12-Lead ECG Variations in AMI and Angina
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 wavemay be inverted
Infarction (Age Unknown)—abnormal Q wave,ST segment and T wave returned to normal
ECG FINDINGS IN ACS
• NORMAL• ST-DEPRESSION• T-WAVE INVERSION• PERSISTANT ST-
ELEVATION OR• LBBB PATTERN
• REPEAT ECG WHEN PATIENT IS IN PAIN
• CONTINUOUS ST – SEGMENT MONITORING
ECG Assessment
ST Elevation or new LBBBST Elevation or new LBBBSTEMISTEMI
Non-specific ECGNon-specific ECGUnstable AnginaUnstable Angina
ST Depression or dynamicST Depression or dynamicT wave inversionsT wave inversions
NSTEMINSTEMI
TYPICAL ECG CHANGES IN
STEMI
Normal or non-diagnostic EKG
ST-Segment Elevation MI
New LBBB
QRS > 0.12 secL Axis deviation
Prominent R wave V1-V3Prominent S wave 1, aVL, V5-V6 with t-wave inversion
Case 13. A 53 year old man with 3 hours of "crushing" chest pain.
Interpretation
Acute inferior myocardial infarctionST elevation in the inferior leads II, III and aVF reciprocal ST depression in the anterior leads
Case 16. 51 yr old male with no prior cardiac history presents with mid-sternal chest discomfort
Questions 1. Is there ECG evidence of injury or ischemia? 2. Is this patient having an MI? If so, in what anatomic distribution?
Interpretation 1. YES2. YES, ANTEROSEPTAL
post thrombolysis ECG
post thrombolysis ECG
BIOCHEMICAL MARKERS
• TROP. I• TROP T• CK-MB• MYOBLOBIN
• FBC• S ELECTROLYTES• BGL• LIPID PROFILE• TRANSTHORACIC ECHO CARDIOGRAPHY (TTE)
OTHERBLOOD
INVESTIGATIONS
CARDIAC TROPONONSI T C
BIOCHEMICAL MARKERS
Cardiac Markers
• Troponin ( T, I)
– Very specific and more sensitive than CK
– Rises 4-8 hours after injury
– May remain elevated for up to two weeks
– Can provide prognostic information
– Troponin T may be elevated with renal dz, poly/dermatomyositis
• CK-MB isoenzyme
– Rises 4-6 hours after injury and peaks at 24 hours
– Remains elevated 36-48 hours
– Positive if CK/MB > 5% of total CK and 2 times normal
– Elevation can be predictive of mortality
– False positives with exercise, trauma, muscle dz,
MYOGLOBIN
RAPID DIAGNOSIS BUT
POOR SPECIFICITY
Troponins for Evaluation and Troponins for Evaluation and Management of ACSManagement of ACS
• Risk StratificatonRisk Stratificaton
• Sens/Spec > CKMBSens/Spec > CKMB
• Detect Recent MIDetect Recent MI
• Selection of RxSelection of Rx
• Detect ReperfusionDetect Reperfusion
• Low sens. early (< 6h)Low sens. early (< 6h)
• Repeat at 8-12 h if neg.Repeat at 8-12 h if neg.
• Limited ability to Limited ability to detect late minor reinfarctiondetect late minor reinfarction
AdvantagesAdvantages DisadvantagesDisadvantages
• Useful as single test to efficiently Dx NSTEMIUseful as single test to efficiently Dx NSTEMI
• Clinicians should familiarize themselves with Dx “cutoffs” in local labClinicians should familiarize themselves with Dx “cutoffs” in local lab
RecommendationRecommendation
Cardiac Markers
Initial Peak Normal
Myoglobin 1-4hr 6-7hr 24hr Nonspecific
CK-MB 3-12hr 24hr 48-72hrAlso elevated with Sk muscle
TroponinI 3-12hr 24hr 5-10d Highly sensitive/ specific
MANAGEMENT
Cardiac Care Goals
• Decrease amount of myocardial necrosis
• Preserve LV function
• Prevent major adverse cardiac events
• Treat life threatening complications
MANAGEMENT OF ACS
2 KEY QUESTIONS
IS THERE ST-SEGMENT ELEVATION?
IS THERE A RISE IN TROPONINS?
1 2
RIGHT ANSWER LEADS TO SUCCESSFULMANAGEMENT
Acute Management
• Initial evaluation & stabilization
• Efficient risk stratification
• Focused cardiac care
ACS RISK CRITERIA
Low Risk ACS
No intermediate or high risk factors
<10 minutes rest pain
Non-diagnostic ECG
Non-elevated cardiac markers
Age < 70 years
• ASA• CLOPIDOGRAL• BETA-BLOCKER• NITRATES
•LOW RISK ACS
• ELEVATED TROPS.• DYNAMIC ST OR T WAVE
CHANGES.• DM• RENAL DYSFUNCTION• REDUCED LVF• EARLY POST-INFARCTION
ANGINA.• PCI WITHIN 6 M• PREVIOUS CABG
ACS RISK CRITERIA
EARLY <72 HOURS> CORONARY ANGIOGRAPHY.+ INTERVENTION
HIGH RISK ACS• PTS WITH PERSISTENT
OR RECURRENT ANGINA.
• ST CHANGES > 2MM• OR DEEP NEGATIVE T
WAVE CHANGES.• CLINICAL SIGNS OF
HEAR FAILURE.• HAEMODYNAMIC
INSTABILITY.• LIFE THREATENING
ARRHYTHMIAS (VT,VF)
URGENT CORONARY ANGIOGRAPHY
ACS RISK CRITERIA
Chest pain suggestive of ischemia
– 12 lead ECG
– Obtain initial cardiac enzymes
– electrolytes, cbc lipids, bun/cr, glucose, coags
– CXR
Immediate assessment within 10 Minutes
Establish Establish diagnosisdiagnosis
Read ECGRead ECG Identify Identify
complicationcomplicationss
Assess for Assess for reperfusionreperfusion
Initial labsInitial labsand testsand tests
Emergent Emergent carecare
History & History & PhysicalPhysical
IV accessIV access Cardiac Cardiac
monitoringmonitoring OxygenOxygen AspirinAspirin NitratesNitrates
ONSET OF SYMPYOMS
EMS ARRIVAL PRE-HOSP
ECG
HOSP ARRIVAL
REPERFUSION
REPERFUSION GOALS
EMS-TO-DRUGS
EMS-TO-BALLOON
SYMPTOM ONSET –TO-REPERFUSION
<30 MIN
<90 MIN
<120 MIN
INCREASING LOSS OF MYOCYTES
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
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.
MANAGEMENT OF AMITHRMBOLYSIS
• EFFECTIVE IN REDUCING MORTALITY.
• GREATEST BENEFIT IF GIVEN <12 H OF ONSET OF PAIN.
• BEST TIME <60MIN (BHF)
• ST Elevation>2mm IN 2 OR MORE CHEST LEADS. OR
• ST elevation>1mm IN 2 OR MORE LIMB LEADS. OR
• POSTERIOR INFARCTION (DOMINANT R WAVES & ST DEPRESSION IN V1-V3)
• NEW ONSET OF LBBB
INDICATIONS(PRESENTATION WITHIN 12 H)
• 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
THRMBOLYSIS 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.
THRMBOLYSIS RELATIVE CONTRAINDICATIONS
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
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 » OR
• DILTIAZEM 60-120 mg/8H PO
DON’T USE VERAPAMIL AND
B-BLOCKER TOGATHERCAN CAUSE ASYSTOLE
• 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.
ACUTE MANAGENT OF N-STEMI)Cont…..
ACUTE MANAGENT OF ACS WITHOUT ST-SEGMENT ELEVATION
(NSTEMI) CONTD:
• May be discharged if a repeat troponin (>12h) is negative.
• Treat medically.
• Arrange further investigations:• Stress test• angiography
LOW Risk Pts.
•No further pain•Flat or inverted T-waves or normal ECG•Negative Troponins
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
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
SUBSEQUENT MANAGEMENT IN ACSCONTD;
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
SUBSEQUENT MANAGEMENT IN ACSGENERAL 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
MANAGEMENT OF AMI
ECG
O2 IV ACCESS TAKE LABS
BRIEF ASSESSMENT
ASPIRIN 300 MG
GTN S/L 2 PUFFS OR 1 TAB.
MORPHINE 2.5-5mg IV +METOCLOPRAMIDE
10mG
THROMBOLYSIS
BETA-BLOCKER
CXR
CONSIDER GLUCOSE,INSULIN,& POTASSIUM INFUSION FOR DM PTs.
CONT;MEDICATION EXCEPT Ca;CHANNEL ANTAGONIST (UNLESS SPECIFIC INDICATIONS)
CONSIDER DVT PROPHYLAXIS
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
THANK YOU
Copyright ©2007 American College of Cardiology Foundation. Restrictions may apply.
Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157
Timing of Release of Various Biomarkers After Acute Myocardial Infarction