Seminar iHD

8/13/2019 Seminar iHD

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ACUTE CORONARY SYNDROME (ACS)

INTAN NADRAH BINTI IDRIS



ACUTE CORONARY SYNDROME (ACS)

unstable angina (UA) Myocardial infarction

NSTEMI

STEMI

Share a common underlying pathology – plaquerupture, thrombosis, and inflammation



RISK FACTORS

NON-MODIFIABLE

Age, male, family history of IHD (MI in 1st degreerelative <55yrs)

MODIFIABLE

Smoking, hypertension, DM, hyperlipidemia,obesity, sedentary lifestyle



PATHOPHYSIOLOGY



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

5



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

6



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



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)



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

9

DIAGNOSIS of MI



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



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



INVESTIGATION ACS

12

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







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

15





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.



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



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



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

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