Transcript
Acute Coronary Syndromes
dr. Murthado Sani dr. Murthado Sani Sp.Jp (K), FIHASp.Jp (K), FIHA
Introduction The term of ACS has been developed to describe
the collection of ischaemic conditions which occur through Coronary Plaque Rupture
ACS includes:
[1] STEMI
[2] NSTEMI & Unstable angina
NSTEMI & Unstable Angina UA/NSTEMI defines a syndrome in which the symptoms of CAD and
ISHD increase in frequency, occur with less physical activity (later at rest), last longer or become more severe.
Clinically, it is difficult to distinguish between UA and NSTEMI based on symptoms alone. The differentiating feature is that patients with NSTEMI have abnormal blood enzymes (Troponin) proving that a heart attack has occurred. For many patients, it takes 6-12 hours to complete a series of blood enzyme tests to make this determination.
It is not necessary for an artery to be severely blocked in order for unstable angina to occur.
Etiology
Key stages in the development of ACS
[1] Ischaemic cascade
[2] Plaque formation and rupture
[3] Coronary occlusion and MI
[4] Ventricular remodelling
[1] Ischaemic CascadeA cascade of ischaemic events is triggered as
shown in the diagram
Perfusion Deficit Diastolic Dysfunction
Systolic Dysfunction TIME
ECG Changes
MI Unstable Angina
[2] Plaque Formation and Rupture Plaques composed of fibrous and fatty tissues formed
within the arterial wall.
The atheromatous plaques usually grow slowly as they have a Fibrous Cap on their luminal surface.
Sometimes, the cap is breached and the softer plaque tissues become exposed to the thrombotic factors in the blood.
The plaque suddenly increase in size, causing a critical reduction in myocardial blood flow.
Plaque Rupture
Plaque Rupture & Thrombus Formation
Plaque
Plaque
Rupture &
Thrombus
Formation
[3] Coronary Artery Occlusion and MI
Sudden Plaque Rupture and thrombus formation to the extent where the coronary artery becomes totally occluded causing MI.
If blood flow is not restored rapidly (within 6 hr.), the muscle dies and becomes scar tissue.
[4] Ventricular Remodelling Once an area of the heart becomes scar tissue, the
myocardium becomes this, fibrosed and functionless
The remaining healthy myocardium hypertrophies and becomes hyperdynamic in function in an attempt to compensate for the dead area.
This increased activity ultimately leads to worsening cardiac function and development of a dilated poorly functioning ventricle.
Clinical Features Central chest pain Dyspnoea Nausea/vomiting Sweating
Beware of Atypical Presentation without classic chest pain (pulmonary oedema, acute confusion) in diabetics and elderly patients.
Investigate ACS case
[1] Immediate assessment [ECG].
[2] Admission tests
• Cardiac markers.
• Chest x-ray.
[3] Urgent coronary angiography (if indicated and available).
[1] Immediate Assessment (ECG)
12-lead ECG is the most urgent investigation in a patient with a suspected ACS.
ECG changes and in particular ST elevation or new onset LBBB mandates immediate action.
[2] Admission Tests 1- Cardiac Markers
Cardiac markers are measured at an appropriate time interval. Commonly measured markers of myocardial damage include:
Troponin I
Creatine kinase (CK)
Lactate dehydrogenase (LDH)
Aspartate transaminase (AST)
Cardiac markers are of no value in making a decision regarding thrombolysis, as even the earliest markers may be undetectable for the first 6-12 hours after the infarction.
Cardiac Markers
[2] Admission Tests 2- Chest x-ray Chest x-ray is often normal in patients with ACS.
However it may show evidence of: • Aortic Dissection • Cardiomegaly • Pulmonary oedema
In case of STEMI, thrombolysis should not be delayed while awaiting a CXR unless an Aortic Dissection is suspected.
[3] Urgent Coronary Angiography Cardiac catheterisation allows invasive assessment
of:
• Coronary arteries. • Left ventricle.
• Cardiac output. • Oxygen saturations.
• Aorta. • Bypass grafts.
• Intracardiac pressures.
With coronary angiography there is a possibility to proceed into Primary Angioplasty
Coronary Angiography
Diagnostic Coronary Angiography with proceeding
Stent implantation into the proximal RCA
(Primary Angioplasty)
Occluded
Proximal
RCA
Stent implantation
& patent RCA
Diagnosis of STEMI ECG … ST segment elevation
New onset LBBB
Cardiac markers … Troponin I
CK
Management of STEMI On Admission IV access Oxygen Aspirin 300 mg (and 75 mg daily thereafter) Pain relief (opiate) Sublingual GTN Urgent Thrombolysis (unless contraindicated) Primary Angioplasty blockers Insulin/glucose regimen if plasma glucose 11 mmol/L
Thrombolysis The decision to consider thrombolysis depends upon:
• A Good Clinical History for MI with an onset
within the last 12 hours.
• ECG that shows evidence of acute STEMI or
new onset LBBB.
Where thrombolysis is indicated, aim to initiate treatment within 20 min of presentation to hospital.
Thrombolytic Agents Available Thrombolytic Agents
[1] Streptokinase
[2] tissue Plasminogen Activator (tPA) • Reteplase • Tenecteplase • Alteplase
Tissue Plasminogen Activator (tPA)
Indications for tPA Administration
(1) Streptokinase allergy
(2) Previous streptokinase treatment (5 days to 2 years)
(3) Hypotension
(4) Large anterior wall damage.
(5) New thrombus after streptokinase therapy (in 10 to 15% of patients, usually within a few hours to days after thrombolysis).
Contraindications to Thrombolysis
Recent stroke (2 months) Previous haemorrhagic stroke (ever) Recent head trauma (4 weeks) Recent surgery – including dental extraction (2 weeks) Lumbar puncture (within 4 weeks) Active peptic ulceration or other GI blood loss Concurrent anticoagulation (unless INR <2.0)
Cont…
Contraindications to Thrombolysis (Cont.)
Severe liver disease or clotting disorder Pregnancy or <18 weeks postnatal Acute pancreatitis Aortic dissection Active pulmonary disease with cavitation Oesophageal varices Cerebral neoplasm Uncontrolled hypertension (BP >200/120)
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