Investigation Of Acute Coronary Syndrome Flashcards
What is acute coronary syndrome?
• Classifications overlap and are far from
perfect • Pathology
• Atheromatous plaque rupture • Rarer other pathologies:
• Coronary dissection
• Coronary spasm • Not all that causes myocardial damage is
coronary
• Common – but incidence declined in
last 10 years
Classify acute coronary syndrome
Broad category - ACS
2 types
ST elevation ACS
- myocardial damage = STE MI
- no myocardial damage = aborted STEMI
Non ST elevation ACS
- Myocardial damage = NSTEMI
- no myocardial damage = unstable angina
What is teh universal definition of MI?
• Acute myocardial infarction (MI) defines cardiomyocyte necrosis in a clinical
setting consistent with acute myocardial ischaemia. A combination of criteria is
required to meet the diagnosis of acute MI, namely the detection of an increase
and/or decrease of a cardiac biomarker, preferably high-sensitivity cardiac
troponin, with at least one value above the 99th percentile of the upper
reference limit and at least one of the following:
1. Symptoms of ischaemia.
2. New or presumed new significant ST-T wave changes or left bundle branch block on 12-lead ECG.
3. Development of pathological Q waves on ECG.
4. Imaging evidence of new or presumed new loss of viable myocardium or regional wall motion abnormality.
5. Intracoronary thrombus detected on angiography or autopsy.
What are type 1 and type 2 MI?
-Type 1 MI
• Atherosclerotic plaque rupture, ulceration, fissure, erosion or dissection with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow and/or distal embolization and subsequent myocardial necrosis.
Type 2 MI
• A condition other than coronary plaque instability contributes to an imbalance between
myocardial oxygen supply and demand. Mechanisms include
• Coronary artery spasm
• Coronary endothelial dysfunction
• Tachyarrhythmias, bradyarrhythmias
• Anaemia
• Respiratory failure
• Hypotension
• Severe hypertension
• In critically ill patients and in patients undergoing major non-cardiac surgery, myocardial necrosis may be related to injurious effects of pharmacological agents and toxins.
What are type 3 4 and 5 MI?
Type 3
• MI resulting in death when biomarkers not available Type 4
• MI related to Percutaneous Coronary Intervention Type 5
• MI related to Coronary Artery Bypass Surgery
What should be investigated for ACS?
- What happened?
- Coronary occlusion?
- Coronary narrowing?
- When did it happen?
- In last few minutes? Hours? Days, weeks, months?
- Where did it happen?
- Right coronary, left, circumflex etc?
- How bad is it?
- Is there acute pulmonary oedema?
- Is there complete heart block or dangerous tachyarrhythmia?
- Has a post MI ventricular septal defect developed?
- Is there mitral regurgitation due to papillary muscle rupture or dysfunction?
- Effect on LV function.
- Left ventricular mural thrombus?
- Why did it happen?
- Plaque rupture?
- Dissection?
- Triggering factors – eg CHD risk factors
Describe investigations of ACS in terms of what happened
- What happened?
- ECG – ST elevation ST depression, T inverson
- Invasive Coronary Angiogram – occluded or stenosed
- Troponin level – raised or not (MI or not)
Describe investigations of ACS in terms of when it happened
When did it happen?
• ECG – ST changes follow a timeline, Q waves imply established MI (>6 hrs,
often > 1 day)
• Profile of serial cardiac enzyme – eg troponin rise and fall, CK rise and fall
Describe investigations of ACS in terms of where it happened
Where did it happen?
• ECG
• Inferior changes imply right coronary
• Anterior changes imply left anterior descending
• Lateral changes imply diagonal, obtuse marginal, or circumflex
• Invasive angiogram
• Identifies the stenosis / occlusion / dissection in the specific vessel
• Echocardiogram
• Regional wall motion abnormalities can correlate with the occlusion / stenosis territory
Describe investigations of ACS in terms ofhow bad it is
How bad is it? • Chest X-ray • Pulmonary oedema • Urea and Electrolytes • Acute kidney injury – eg cardiogenic shock • ECG and associated cardiac monitoring (bedside, telemetry) • AV conduction block (heart block) • VT, VF • Echocardiogram • Ventricular septal defect due to septal infarction • Mitral regurgitation • Left ventricular impairment
Describe investigations of ACS in terms of why it happened
Why did it happen?
• Invasive coronary angiogram
• Plaque rupture? Vs dissection etc
• CT aorta if worried about aortic dissection into RCA
• FBC – Anaemia? Polycythaemia? Sepsis?
• Lipid profile - Triggering factors – eg CHD risk factors
What are several ECH characteristics seen in ACS and what do they indicate?
• ST elevation implies sudden occlusion. It can also persist long term as mark of LV aneurysm (Q waves usually present).
• ST depression usually implies under-supply of blood to myocardium but not
sudden coronary occlusion. If in the anterior leads it can sometimes be due to sudden occlusion of a vessel at the back of the heart (“Posterior STEMI”).
Other non-ischaemia related causes exist too.
• T wave inversion often implies under-supply of blood to myocardium but not
sudden coronary occlusion. There are other non-ischaemia related causes.
• Heart block – various grades
• Ventricular dysrhythmia VT, VF, Ectoics
Where are the chest electrode placed?
C1 – Fourth right interspace, parasternal
C2 – Fourth left interspace, parasternal
C3 – Mid way between C2 and C4
C4 – Fifth left interspace, mid clavicular line
C5 – Fifth left interspace, anterior axillary line
C6 – Fifth left interspace, mid axillary line
What si seen in a typical blood test for ACS
Anterior ST elevation (see slide fo leads)
What blood tests are typically taken for ACS test?
- FBC
- U&E
- Lipids
- Troponin
- Others as needed according to rarer conditions
