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Semester 2 Cardiovascular System > L18: Acute coronary syndrome > Flashcards

L18: Acute coronary syndrome Flashcards

1
Q

What is acute coronary syndrome?

A

Plaque ruptures leading to thrombus formation and varying degrees of occlusion to the arteries
Rarer pathologies–> coronary dissection and coronary spasm

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2
Q

What are non ST elevation ACS? How do we differentiate between them?

A

Non STEMI and unstable angina
No ST elevation of ECG, T wave inversion
Differentiate–> troponin
Produced in NSTEMI but not unstable angina

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3
Q

What are the different types of ST elevated ACS? How do we differentiate between?

A

STEMI and Absorted STEMI

Aborted STEMI–> no troponin produced

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4
Q

What is the actual definition of MI?

A

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

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5
Q

How many classification of MI are there? Which is the most important?

A

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

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6
Q

How should patients be assessed?

A

History?
Examination?
Investigation?

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7
Q

What things should be asked in the history?

A

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)

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8
Q

What things should be examined? Why?

A

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
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9
Q

What are the names of the coronary arteries? What are the major branches?

A

Right coronary artery–> right marginal artery and posterior interventricular artery
Left coronary artery–> LAD and circumflex artery

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10
Q

How can we tell which part of the heart is affected by looking at an ECG?

A 
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
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11
Q

What does ST elevation imply?

A

Sudden occlusion
Persist long term as a mark of LV aneurysm
Q wave usually present

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12
Q

What does ST depression imply?

A

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)

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13
Q

What does T wave inversion imply?

A

Under supply of blood to myocardium but not sudden

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14
Q

What would ventricular dysrhythmia imply?

A

Ventricular tachycardia, ventricular fibrillation or ectopics

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15
Q

What happens to ECG in STEMI?

A

ST elevation evoles with:

  • Hyperacute T waves
  • ST segment elevation
  • T wave inversion
  • Pathological Q waves –> complete infarct myocardium dead
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16
Q

What does the ECG for NSTEMI look like? What else is looked at for NSTEMI?

A

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

17
Q

What role does troponin normally play in cardiac muscle?

A

Involved in the troponin-tropomyosin complex which is involved in contraction

18
Q

What happens to troponin levels during MI?

A

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

19
Q

Why are troponin levels used alongside history and ECG?

A

Troponin released from other tissues upon damage

Raised in many conditions

20
Q

What other investigations would be done? Why?

A

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

21
Q

What can echocardiograms show?

A

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

22
Q

How are STEMI managed?

A
  1. Aspirin 300mg inhibit platelet activation
  2. Second antiplatelet–> Ticagrelor 180mg or Prasugrel 60mg (wt>60kg and <75 yrs)
  3. Morphine 5-10mg IV with metoclopromide 10mg IV–> pain relief and antisickness (morphine makes you feel sick)
  4. Nitrate 2 puffs under tongue SBP>110mmHg–> vasodilator, if BP lower will cause pt to collapse
  5. Oxygen if sat <92%–> only given if low now
  6. Transfer to cardiac catheter lab for PCI (percutaneous coronary intervention)
23
Q

What is percutanous coronary intervention?

A

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)

24
Q

How are NSTEMI managed?

A

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

25
Q

In which cases would you send a patient with NSTEMI to the catheter lab?

A

Dynamic ECG changes with ongoing chest pain
or
Patient develops arrythmias with compromise

26
Q

What is an invasive coronary angiogram? How is it done?

A

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

27
Q

How is invasive coronary angioplasty done? What does it allow?

A

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
28
Q

How is STEMI and NSTEMI managed in the long term?

A

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

Semester 2 Cardiovascular System (21 decks)

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