L18: Acute coronary syndrome Flashcards
What is acute coronary syndrome?
Plaque ruptures leading to thrombus formation and varying degrees of occlusion to the arteries
Rarer pathologies–> coronary dissection and coronary spasm
What are non ST elevation ACS? How do we differentiate between them?
Non STEMI and unstable angina
No ST elevation of ECG, T wave inversion
Differentiate–> troponin
Produced in NSTEMI but not unstable angina
What are the different types of ST elevated ACS? How do we differentiate between?
STEMI and Absorted STEMI
Aborted STEMI–> no troponin produced
What is the actual definition of MI?
Cardiomyocyte necrosis in a clinical setting with acute myocardial ischaemia
Detection of increase/decrease in cardiac biomarker–> preferable troponin–> one value above 99th percentile of upper reference limit
At least one of the following:
1. Symptoms of ischaemia
2. New or presumed new significant ST-T wave change 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 thombus detected on angiography or autopsy
How many classification of MI are there? Which is the most important?
5 types
Type 1 most important–> atherosclerotic plaque rupture, ulceration, fissure, erosion or dissection with resulting intraluminal thrombus in one or more coronary arteries leading to decrease myocardial BF and/or distal embolisation and subsequent myocardial necrosis
How should patients be assessed?
History?
Examination?
Investigation?
What things should be asked in the history?
1–> Cardiac sounding? –> dull central pain, not localised (widespread)
2–> Radiation? –> radiating to left jaw and arm
3–> Relieved with GTN? How long?
- seconds to minutes–> cardiac
- >10 mins–> oesophageal spasm
4–> How long pain? - minutes, hours etc aortic dissection epigastric pain, worse pain ever, maximal onset, radiates onto back
5–> Is it getting worse?
6–> Pleuritic?
7–> Risk factors–> smoker (vaping), family history, cholesterol, hypertension, thrombophilia (people prone to blood clots)
What things should be examined? Why?
Haemodynamics
- BP–> systolic low <90mmHg -cardiogenic shock
- Tachycardia (sinus tachycardia (stress response for MI) or ventricular tachycardia (fast abnormal HR, 3+ heartbeats in a row at >100bpm (PVC))) or bradycardia (2:1 heart block or complete heart block)
- Jugular venous pressure–> pressure in the system
- Lungs–> clear or wet? crackling or crepidations? sign of oedema, potentially not lie down during procedure
- Heart sounds–> murmurs–> guide treatment (open heart surgery)
- Cool clammy peripheries –> fits in with shock response
What are the names of the coronary arteries? What are the major branches?
Right coronary artery–> right marginal artery and posterior interventricular artery
Left coronary artery–> LAD and circumflex artery
How can we tell which part of the heart is affected by looking at an ECG?
Anterior heart: defects in V1-V6 Lateral heart: defects in Lead I, aVL, V5 and V6 (high lateral Lead I and aVL) Inferior heart: defect in Lead II, III and aVF (Right heart: aVR) Septal: V1 and V2 Anterospetal: V1-V4 Anterolateral: V3-V6
What does ST elevation imply?
Sudden occlusion
Persist long term as a mark of LV aneurysm
Q wave usually present
What does ST depression imply?
Under supply of blood to myocardium
Not sudden coronary occlusion
(in anterior leads can sometimes be due to sudden occlusion of a vessel in posterior heart)
What does T wave inversion imply?
Under supply of blood to myocardium but not sudden
What would ventricular dysrhythmia imply?
Ventricular tachycardia, ventricular fibrillation or ectopics
What happens to ECG in STEMI?
ST elevation evoles with:
- Hyperacute T waves
- ST segment elevation
- T wave inversion
- Pathological Q waves –> complete infarct myocardium dead
What does the ECG for NSTEMI look like? What else is looked at for NSTEMI?
ECG can be normal
or T wave inversion and ST depression
Blood test
–> Heamoglobin –> all patients given anti-platelets need to consider if pt is anaemic
–> Renal function –> renal failure impact on cath lab and contrast used in coronary angiogram
–> Cholesterol –> young pt with ↑ cholesterol (10) consider familial hypercholesterolaemia
–> HbA1c–> Diabetes
–> Troponin –> last, if history is not complete it is used
What role does troponin normally play in cardiac muscle?
Involved in the troponin-tropomyosin complex which is involved in contraction
What happens to troponin levels during MI?
Increase
Raised within three hours of cardiac damage
Peak at 24-48 hrs
Remains elevated for 2+ weeks
Troponin T and I highly sensitive and specific to cardiac origin
Why are troponin levels used alongside history and ECG?
Troponin released from other tissues upon damage
Raised in many conditions
What other investigations would be done? Why?
Chest x-ray
Check for pulmonary oedema–> pt severely unwell, large amount of infarction
Widened mediastinum–> suggest aortic dissection
Echocardiogram
Ultrasound of the heart–> useful for showing where lesion in coronary architecture is
What can echocardiograms show?
Lesion in coronary artery–> show which one needs fixing
LV function–> normal vs impaired
Wall motion–> regional vs global abnormality
Valvular disease–> mitral regurgitation
Complications from MI–> VSD
How are STEMI managed?
- Aspirin 300mg inhibit platelet activation
- Second antiplatelet–> Ticagrelor 180mg or Prasugrel 60mg (wt>60kg and <75 yrs)
- Morphine 5-10mg IV with metoclopromide 10mg IV–> pain relief and antisickness (morphine makes you feel sick)
- Nitrate 2 puffs under tongue SBP>110mmHg–> vasodilator, if BP lower will cause pt to collapse
- Oxygen if sat <92%–> only given if low now
- Transfer to cardiac catheter lab for PCI (percutaneous coronary intervention)
What is percutanous coronary intervention?
Insertion of a catheter with a stent attached to a balloon to open up BV in the heart that have been narrowed by plaques (atherosclerosis)
How are NSTEMI managed?
Antiplatelets and antithrombotics–> aspirin and clopidogrel/ ticagrelor, Enoxaparin SC injection (antithrombotic)
Anti-ischaemics–> bisopolol (beta blocker- Lower HR, improve ventricle filling), GTN infusion –> vasodilators
Secondary prevention–> Statin, ACE inhibitors
In which cases would you send a patient with NSTEMI to the catheter lab?
Dynamic ECG changes with ongoing chest pain
or
Patient develops arrythmias with compromise
What is an invasive coronary angiogram? How is it done?
Use X-ray dye to opacify (make opaques) the coronary arteries
Establishes the type of lesion and the location of the lesion
Done under local anaesthetic
–> Radial artery (wrist) or femoral artery (groin) acessed
–> Catheter used to inject dye
Take pictures of the narrowed vessel
How is invasive coronary angioplasty done? What does it allow?
Following an invasive coronary angiogram
- -> 30 minute procedure
- -> Detect narrowing
- -> Wire the occluded vessel
- -> Predilate narrowed sections with balloons
- -> Stent with metal scaffold to keep vessel patent
- -> Options to include intravascular ultrasound or optical coherence tomography
How is STEMI and NSTEMI managed in the long term?
Lifestyle changes–> regular exercise, low fat diet, low salt intake
Dual antiplatelets for 12 months –> aspirin for life
Statin–> reduce cholesterol <4mmol/L LDL-C<2mmol/L
Bisoprolol–> reduce HR - 70bpm
ACE inhibitor BP<140/80
If ejection fraction<40%-> Eplerenon (mineralocorticol antagonist–> works on kidney to reduce Na+ reasorption to decrease BP)
If Echo at 3 month shows EF<35% implantable cardiac defibrillator necessary
