Lecture 17- Acute coronary syndrome Flashcards

1
Q

pathology of acute coronary syndrome

A
  • Atheromatous plaque rupture
  • Coronary dissection (rarer)
  • Coronary spasm (rarer)
  • Not all that causes myocardial damage is coronary
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2
Q

Sub-occlusive=

A

NON-STEMI

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3
Q

Occlusive

A

= STEMI

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4
Q

categories of acute coronary syndrome: ST elevation ACS positive

A

STEMI

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5
Q

categories of acute coronary syndrome: ST elevation ACS without signs of myocardial damage (troponin)

A

aborted STEMI

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6
Q

categories of acute coronary syndrome: Non-ST elevation ACS with signs of myocardial damage (troponin)

A

NSTEMI

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7
Q

categories of acute coronary syndrome: Non-ST elevation ACS without signs of myocardial damage (troponin)

A

unstable angina

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8
Q

Myocardial infarction

A

Acute myocardial infarction (MI) defines cardiomyocyte necrosis in a clinical setting consistent with acute myocardial ischaemia.

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9
Q

A combination of criteria is required to meet the diagnosis of acute MI:

A
  • increase and/or decrease of a cardiac biomarker (troponin)
  • Symptoms of ischaemia.
  • New or presumed new significant ST-T wave changes or left bundle branch block on 12-lead ECG.
  • Imaging evidence of new or presumed new loss of viable myocardium or regional wall motion abnormality.
  • Intracoronary thrombus detected on angiography or autopsy.
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10
Q

Type 1 MI

A
  • is caused by an acute atherothrombotic coronary event- thrombus in coronary artery leading to decreased myocardial blood flow- myocardial necrosis
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11
Q

Type 2- MI

A

is a more heterogeneous entity, where a condition other than coronary artery disease (CAD) contributes to an acute imbalance between oxygen supply (e.g., hypoxemia, anemia, hypotension) and demand (e.g., tachycardia, hypertension).

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12
Q

Assessment of the patient: History

A
  • Cardiac sounding?
    • DULL?
    • Central?
    • Radiating?
  • Relieved with GTN? How long did it take to work?
  • How long have you had the pain?
  • Is the pain getting worse?
    • Cardiac dissection
  • Pain worse on inspiration? Pleuritic?
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13
Q

Risk factors for MI

A
  • Smoker
  • Family history
  • High cholesterol
  • Hypertension
  • Thrombophilia
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14
Q

Assessment of the patient: Examination

A
  • BP (if systolic <90mmHg- cardiac shock)
  • Tachy or bradycardia?
  • Jugular venous pressure
  • Lungs- crackles? Pulmonary oedema?
  • Heart sounds- missing a murmur could be costly
  • Cool peripheries
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15
Q

coronary artery anatomy

A
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16
Q

ECG territories

A
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17
Q

leads showing abnormal compelxes- septal

A

Septal= V1 and V2

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18
Q

leads showing abnormal complexes- anterior

A

Anterior: V1 and V6

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19
Q

leads showing abnormal complexes: lateral

A

Lateral: V5 and V6

20
Q

leads showing abnormal complexes

A

Anteroseptal: V1- V4 (LAD)

21
Q

leads showing abnormal complexes: anterolateral

A

V3-V6

22
Q

leads showing abnormal complexes: inferior

A

Inferior: II, III, aVF

23
Q

leads showing abnormal complexes: high lateral

A

High lateral: I, aVL

24
Q

MI ECG: ST elevation

A

Implies sudden occlusion. Can persit long term as a mark of LV aneursysm (Q wave usually present)

25
Q

MI ECG: ST depression

A

Under supply of blood to myocardium but not sudden coronary occlusion.

  • If in anterior leads it can sometimes be due to sudden occculsion of vessel at the back of heart (posterior STEMI)
26
Q

MI ECG: T wave inversion

A

Often implies under-supply of blood to myocardium but not sudden coronary occlusion- other non-ischaemic related causes e.g. stable angina

27
Q

MI ECG: Heart block

A

various grades

28
Q

MI ECG: ventricular dysrhythmia

A
  • VT
  • VF
  • Ectopics
29
Q

if someones ECG shows a STEMI

A
  • ST Elevation needs to go straight to cath lab for emergency percutaneous coronary intervention (PCI)
30
Q

ST elevation involves:

A
  • Hyperacute T waves
  • ST segment elevation
  • T wave inversion
  • Pathological Q wave
31
Q

which part of the heart is showing ST elevation

A

St elevation in anterior à LAD (look at V4)

32
Q

which part of the hear it showing ST elevation

A

ST elevation in inferior (look at II, III, aVL and aVF)

33
Q

ECG of NSTEMI

A
  • Can be normal
  • Or may be ST depression
34
Q

Blood tests of NSTEMI

A
  • Haemoglobin (anaemia- if anaemic may need to think about antiplatelet)
  • Renal function (angiograms- need to make sure contrast wont further damage the kidney- may develop AKI- nephrotoxic)
  • Cholesterol
  • HbA1C
  • Troponin
35
Q

Troponin

A

Troponin complex important in skeletal and cardiac muscle contractility

36
Q

Cardiac troponin I and T

A
  • Highly sensitive to cardiac origin
  • Measured using immunoassays
  • Typically raised within 3 hrs of cardiac damage, peaks at 24 to 48 hours, remains elevated 2+ weeks
  • Note: raised in many conditions not just coronary syndrome
37
Q

further investigations

A

CXR and echocardiogram

38
Q

CXR- cardiac X-ray

A
  • Pulmonary oedema – alveolar shadowing
  • Widened mediastinum
39
Q

Echocardiogram

A

Uses ultrasound to image the heart.

  • Gives you an idea of which artery needs treating
  • LV function
  • wall motional
  • Valvular disease
  • complications from MI
40
Q

Management of STEMI (DO ECG first)

A

B B-blockers

R Reassure

O Oxygen

M Morphine

A Aspirin

N Nitrate (GTN- be careful because will cause vasodilation and decrease BP more)

C Clopidogrel

E Enoxaparin

(S) Statins

41
Q

Management of NSTEMI

A
  • Antiplatelets and antithrombotic
    • Aspirin and clopidogrel/ ticagrelor (antithrombotic)
    • Enoxaparin- anticoagulant
  • Anti-ischaemic
    • Bisopolol (B-blocker)–>improve diastolic filling and reduce work of the heart–>reducing metabolic demand for O2
    • GTN infusion (spray)- vasodilation
  • Secondary prevention
    • Statin
    • ACE inhibitors
42
Q

Bisopolol (B-blocker)

A

–>improve diastolic filling and reduce work of the heart–>reducing metabolic demand for O2

43
Q

GTN

A
44
Q

what is an ainvasive coornary angiogram used for

A

Establishes type of lesion and its location

45
Q

outline how one would carry out an invasve coronary angiogram

A
  1. Local anaesthetic
  2. Radial or femoral artery access
  3. 30 min procedure
  4. Wire the occluded vessel
  5. Predilate the narrowed sections with balloons
  6. Stent with metal scaffold to keep vessel patent
  7. Option to include intravascular ultrasound or optical coherence tomography
46
Q

Management of ACS

A
  • Lifestyle changes
    • Low fat diet
    • Regular exercise
    • Low salt
  • Dual antiplatelets (DAPT) for 12 months then aspirin for life
    • Aspirin and secondary anti-platelet
  • Statin aiming to control cholesterol
  • Bisprolol (b-blocker)- aiming for 70bpm
  • ACE inhibitors aiming for BP <140/80
    • Reverse cardiac remodelling
  • If Echo shows ejection fraction (EF) below <40% then eplerenone (MRA)
  • Each at 3 months shows EF <35% then for implantable cardiac defibrillator