Seminar iHD
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Transcript of Seminar iHD
8/13/2019 Seminar iHD
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ACUTE CORONARY SYNDROME (ACS)
INTAN NADRAH BINTI IDRIS
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ACUTE CORONARY SYNDROME (ACS)
unstable angina (UA) Myocardial infarction
NSTEMI
STEMI
Share a common underlying pathology – plaquerupture, thrombosis, and inflammation
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RISK FACTORS
NON-MODIFIABLE
Age, male, family history of IHD (MI in 1st degreerelative <55yrs)
MODIFIABLE
Smoking, hypertension, DM, hyperlipidemia,obesity, sedentary lifestyle
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PATHOPHYSIOLOGY
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UNSTABLE ANGINA/NSTEMI -
Clinical Presentation
History:
Angina on minimal exertion/at rest
Crescendo angina
chest pain, located in the substernal region or sometimes at the
epigastrium, that frequently radiates to the neck, left shoulder,and left arm.
Dyspnoea
Physical Examination:
diaphoresis
pale cold skin sinus tachycardia
a third and/or fourth heart sound
basilar rales
hypotension
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UA or NSTEMI:
Unstable Angina NSTEMI Clinical Presentation(at least 1 of these 3features)UA Feature:
1. Discomfort occurs at rest or atminimal exertion,
2. Much severe and of new onset (i.e.within the prior 4-6 weeks)
3. Crescendo pattern (distinctly moresevere, prolonged, or frequent withthe previous)
Develops UA features+
↑ cardiac biomakers
1. ST-segment depression2. Transient ST-segment elevation3. And/or T-wave inversion
Similar finding in ECG
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Risk stratification
RISK STRATIFICATIONHigh Risk Low Risk
Clinical Post- infarct anginaRecurrent pain at restHeart Failure
No history of MIRapid resolution ofsymptoms
ECG ArrhythmiaST depression
Transient ST elevationPersistent deep T-waveinversion
Minor or no ECGchanges
Biochemistry Troponin T > 0.1 µg/l Troponin T < 0.1 µg/l
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MYOCARDIAL INFARCTION
Myocardial necrosis as a result of critical
imbalance between coronary blood supply &
myocardial demand
Acute myocardial infarction refers to two
subtypes of acute coronary syndrome,namely non-ST-elevated myocardial infarction
(NSTEMI) and ST-elevated myocardial
infarction (STEMI)
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Clinical history of ischaemic type chest painlasting for more than 20 minutes
Changes in serial ECG tracings (ST segment , Twave, Q wave)
Rise and fall of serum cardiac biomarkers such
as creatine kinase-MB fraction and troponin (I/T)
MAJOR RISK FACTORS Hyperlipidemia, (inc TG, LDL, dec in HDL)
HT Cigarette smoking
Diabetes mellitus
Family history
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DIAGNOSIS of MI
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CLINICAL PRESENTATIONHistory:
1. Chest Pain Central portion of chest and/or epigastrium >20 minutes Heavy, squeezing, crushing, sometimes stabbing and
burning. Radiates to arms(common), less commonly to abdomen,back, lower jaws and neck
When pain begins after exertion, it doesn’t subside withcessation of activity or also by GTN
2. Breathlessness3. Weakness4. Sweating/ Anxiety5. Collapse/syncope
6. Nausea/ Vomiting 10
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CLINICAL PRESENTATION
Physical Examination:
1. Sympathetic activation: pallor, sweating,
tachycardia2. Vagal activation: sometimes bradycardia3. Impaired myocardial function: inc. JVP, narrowed
pulse pressure, lungs crepitation
4. Tissue damage: fever, pericardial rub
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INVESTIGATION ACS
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ECGST-segment elevation. (STEMI)Normal or show minor ST-T changes or occasionally ST segmentdepression (NSTEMI)
Plasma Biochemical Markers :Raised cardiac enzyme Widely used biochemical marker in detection of MI is creatinekinase (CK). Also present in skeletal muscle.More sensitive and cardiospecific isoform of this enzyme is CK-MB.Cardiospecific protein, troponin T and I.
Imaging techniques such as echocardiography and radionuclidetechniques - identify non-ischaemic conditions ,prognostic information
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CARDIAC BIOMARKERS
Cardiac
Biomarker
Troponin I Detectableafter 3-6H
after AMI
Remainedelevated 14d
CK-MB Rising within
4 H after
injury
Peak 18-24H Subside 2-3d
LDH Rising within
24H after MI
Peak 3-6d Return to
baseline 8-
12d
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Assessment and stabilization of the patients'
haemodynamics.
Bed rest, Continuous ECG monitoring.
Aspirin. A dose of 150-300mg crushed or chewed toachieve rapid action.
Oxygen by nasal prongs / facemask.
Sublingual GTN (unless systolic arterial pressure < 90
mmHg). Venous access established and blood taken for cardiac
markers, full blood count, renal profile, sugar and lipid
profile. Preferably 2 intravenous lines should be set up.
Pain relief - morphine should be administeredintravenously 2-5mg every 5-15 minutes until pain is
relieved or there is evidence of toxicity - hypotension,
respiratory depression or severe vomiting. Anti-emetics
(IV metoclopromide 10mg or promethazine 25mg) may
be given simultaneously.
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ORAL ANTIPLATELET AGENTS-
1. Aspirin(platelet cyclooxygenase inhibitor) – 300mg initial@ 75daily
Block formation of thromboxane A2→prevent platelet
aggregation
its anti-inflammatory properties, which could reduce plaque
rupture and its sequelae2. Clopidogrel (Plavix) - 300mg initial@ 75 daily
Inhibit ADP-dependent activation of the GP II/IIIa complex
→prevent platelet aggregation
ANTICOAGULANTS
1. Unfractionated heparin/ low molecular weight heparin
(enoxaparin)
PLATELET GP IIb/IIIa receptor inhibitor
1. abciximab - for high risk patient
UA/NSTEMI – ANTI THROMBOTIC
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REPERFUSION THERAPY (THROMBOLYTIC OR
PCI) thrombolytic therapy (Streptokinase & Tissue
Plasminogen Activator (tPA))
PCI – Percutaneous Coronary Intervention
Depends on: Time from onset of symptoms
Contraindication to thrombolytic therapy
High risk patients
STEMI
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COMPLICATION OF MI
Arrythmias CHF
Cardiogenic shock when 40+% of LV infarcted
Cardiac rupture- external or interventricular
Ventricular rupture – pericardial h’age and tamponade Rupture of septum – L-R shunt, R sided heart overload
Mural thrombosis – risk of peripheralembolisation
Papillary muscle infarction – mitral valveincompetence
Pericarditis – fibrinous-to-hemorrhagic
Repetitive infarction