Acute Coronary Syndrome Flashcards

1
Q

Define acute coronary syndrome

A

Spectrum of acute myocardial ischaemia and/or infarction, including:
- STEMI
- NSTEMI
- Unstable angina.

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2
Q

Aetiology of acute coronary syndrome

A

Coronary artery disease.
Atherosclerosis with plaque fissuring or rupture and thrombus formation
Coronary spasm → reduced myocardial perfusion
Chest trauma or spontaneous coronary or aortic dissection or emboli

  1. Artery occlusion
    - Sudden change of plaque (e.g. rupture) → superimposed platelet activation and aggregation
    - vasospasm, coagulation and thrombosis
    - Occlusive intracoronary thrombus overlying disrupted plaque
  2. Myocardial infarction
    - compromised myocardial supply → ischaemia
    - Contractility loss within 60s (HF may precede)
    - Necrosis, myocyte death

Ischaemia >20-40mins → irreversible injury and myocyte death

4H’s and 4T’s: hypoxia, hypo/hyperkalaemia/hypoglycaemia, hypothermia, hypovolaemia | thrombosis, tamponade, toxins, tension pneumothorax

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3
Q

Risk factors for acute coronary syndrome

A

Non-modifiable:
Age
Male gender
Family history of IHD

Modifiable:
Smoking
Hypertension
DM
Hyperlipidaemia
Obesity
Sedentary lifestyle
Cocaine use

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4
Q

Symptoms of acute coronary syndrome

A

Acute central chest pain
- Lasts >20 minutes
- Radiates to the jaw, arm or neck
- Increasing in severity and frequency
+ nausea
+ sweatiness
+ dyspnoea
+palpitation

ACS without chest pain (30%) -> “silent”, mostly seen in elderly and diabetics (+women). Presents with:
- Syncope
- Pulmonary oedema
- Epigastric pain
- Vomiting
- Post-op hypotension
- Oligouria
- Acute confusional state
- Stroke
- Diabetic hyperglycaemic states

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5
Q

Signs of acute coronary syndrome on examination

A

Distress
Anxiety
Pallor
Sweatiness
Pulse raised or depressed
BP raised or depressed
4th heart sound
Signs of heart failure (Raised JVP, 3rd heart sound, basal crepitations)
Pansystolic murmur
Low-grade fever
Pericardial

Signs of risk factors:
Tar staining
Acanthosis nigricans
Xanthoma

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6
Q

Investigations for acute coronary syndrome

A

ECG: diagnose

Troponin/cardiac enzymes: elevated/20% increase in STEMI/NSTEMI (NOT in angina) (if negative and <4-6 hrs since onset, measure again in 4 hrs)
FBC
U&Es
LFTs
Glucose
Lipids
Clotting screen

CXR: pulmonary oedema, cardiomegaly (HF), widened mediastinum (dissection)
echo: assess LV function
Coronary angiography: can show stenosis or presence thrombus in a coronary artery

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7
Q

What is seen on ECG in STEMI

A

First sign: Hyperacute T waves
ST elevation
New LBBB
ST depression V1-V4 -> posterior STEMI
T wave inversion

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8
Q

What is seen on ECG in NSTEMI

A

NO ST elevation, may be ST depression
T wave inversion

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9
Q

What is seen on ECG in unstable angina

A

NO ST elevation
May have ST depression and T wave inversion

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10
Q

How does the location of myocardial infarction relate to the ECG

A

Anteroseptal (left anterior descending): V1-V4
Anterolateral (left anterior descending/left circumflex): V4-6, aVL
Inferior (right coronary): II, III, aVF
Lateral (left circumflex): I, aVL ± V5-6
Posterior (left circumflex or right coronary): tall R waves V1-2, ST depression

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11
Q

Management for STEMI

A
  1. A-E assessment
    - ECG and diagnose
    - IV access + bloods
    - Oxygen supplementation if low
  2. Dual antiplatelet therapy (DAPT)
    - Aspirin 300mg
    - Ticagrelor 180mg PO (esp. after thrombolysis)
    - PCI considered → Prasugrel
    - Taking an oral anticoagulant → clopidogrel
  3. Calculate GRACE score
  4. Plan intervention - PCI?
    <12 hours
    – PCI in <120 minutes possible → PCI within 12 hours
    – PCI in <120 minutes NOT possible → thrombolysis within 12 hours (tissue plasminogen activator (tPA) or tenecteplase AND antithrombin)
    → ECG after 60-90 minutes → if ST-elevation persisting, PCI
    >12 hours → specialist advice + anticoagulation (fondaparinux or enoxaparin/heparin)
  5. Anticoagulate
    - Angiography ± PCI <24 hours → (1) enoxaparin (LMWH) OR unfractionated heparin OR bivalirudin
    - Fibrinolysis → (1) enoxaparin (LMWH) OR unfractionated heparin OR fondaparinux
    - No intervention (low GRACE) → (1) fondaparinux (AKA always give in NSTEMI)
  6. Supportive:
    - Analgesia: morphine 5-10mg IV + metoclopramide 10mg IV
    - Nitrates: GTN spray or sublingual tablet PRN
  7. Beta-blockers (start early; CI: low BP/HR, HF, COPD/asthma, cardiogenic shock, heart block)
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12
Q

Management for NSTEMI

A
  1. A-E assessment
    - ECG and diagnose
    - IV access + bloods
    - Oxygen supplementation if low
  2. Dual antiplatelet therapy (DAPT)
    - Aspirin 300mg to start
    - PCI considered → prasugrel
    - no IMMEDIATE PCI → fondaparinux
    - if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given
    - Ticagrelor 180mg PO (esp. after thrombolysis)
  3. Calculate GRACE score (6 month mortality)
  4. Plan intervention - PCI?
    - Intermediate/high risk → PCI within 72 hours (immediately if unstable)
    - Low risk → conservative
  5. Anticoagulate
    - PCI done → unfractionated heparin
    - PCI not done → ticagrelor
  6. Supportive:
    - Analgesia: morphine 5-10mg IV + metoclopramide 10mg IV
    - Nitrates: GTN spray or sublingual tablet PRN
  7. Beta-blockers (start early; CI: low BP/HR, HF, COPD/asthma, cardiogenic shock, heart block)
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13
Q

Criteria for PCI in NSTEMI/unstable angina

A

immediate: patient who are clinically unstable (e.g. hypotensive)
within 72 hours: patients with a GRACE score > 3% i.e. those at intermediate, high or highest risk
coronary angiography should also be considered for patients if ischaemia is subsequently experienced after admission

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14
Q

What drug therapy is used during PCI

A

patients undergoing PCI with radial access: unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus

patients undergoing PCI with femoral access: bivalirudin with bailout GPI

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15
Q

Long-term management for patients who have had an acute coronary event

A

ACEis - prevents the heart from remodelling around dead tissue e.g. ramipril 2.5mg orally 2x daily for 3 days, increase according to response

Beta blockers - reduce the work of the heart e.g. bisoprolol 1.25mg orally once daily initially for 1 week, increase according to response

Conservative:
Mediterranean diet
Exercise 20-30 minutes/day until slightly breathless (sex after 4 weeks; no sildenafil until 6m)
Control HTN and DM
Lifestyle: Stop smoking, exercise, weight loss, reduce alcohol intake

Dual antiplatelet e.g. aspirin 75-100mg orally once daily + ticagrelor 90mg orally twice daily
Stop the second antiplatelet after 12 months
Prasugrel OR ticagrelor can be used if there was PCI management

Statins e.g. atorvastatin 40-80mg orally once daily

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16
Q

What are the complications of MI

A

0-24h: sudden death | arrhythmia (VF) | cardiogenic shock

1-3 days: fibrinous pericarditis | embolism

3-14 days: papillary muscle rupture (→ mitral regurgitation) | ventricular septal rupture | LV free wall rupture

weeks-months: atrial/ventricular aneurysms | Dressler’s | re-infarction | heart failure | Reperfusion injury (oxidative stress, calcium overload, inflammation)

17
Q

What is the prognosis for MI

A

Predict using Killip classification
In hospital death rate is 7%
Half of deaths occur within 1 hour of onset (most of these do not reach hospital)
Age, female, DM and previous MI = worse prognosis
Total mortality is 30% in one year but 3-4% after this due to complications

18
Q

What is Wellen’s syndrome

A

Critical LAD stenosis that can flip in to acute anterior STEMI

ECG shows T wave inversion in the anterior leads