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Block 2 > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

What is the site of ischaemic chest pain? Where can it radiate to?

A

Central (usually) radiating down inner left arm, neck + abdomen

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2
Q

What does ischaemic chest pain feel like?

A

Crushing
Band-like
Heavy

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3
Q

How long does ischaemic chest pain last?

A

Remits in several minutes with rest, if its effort related

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4
Q

What are the exacerbating and relieving factors of ischaemic chest pain?

A

Exacerbating: exercise, effort, stress + tachycardia

Relieving: rest + sublingual nitrate (GTN)

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5
Q

What conditions can be confused with ischaemic chest pain? How can you tell the difference?

A

MSK pain + chrondritis: localised, reproducible on palpation/movement

Reflux oesophagitis: not effort related, nausea, odynophagia + dysphagia

Gastritis: epigastric modified by antacids

Pericarditis: sharp, better on sitting, pericardial rub + ECG

Mediastinitis: septic + ill, febrile, constant pain + inflammatory markers raised

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6
Q

What may you notice on examination of ischaemic chest pain?

A 
Pallor
Hypotension
Tachycardia
Diaphoresis
Cold/clammy 
Distressed/impending doom (due to chest discomfort, dyspnoea, weakness or dizziness)
Central/peripheral cyanosis
Low SpO2
Bilateral crackles 
Raised JVP
Hepatomegaly 
Pedal, lower limb + sacral oedema 
Mitral regurg, 3/4 sound gallop rhythm, AF or extrasystoles
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7
Q

When could a examination be completely normal regarding ischaemic chest pain?

A

If the pain has settled

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8
Q

What is unstable angina?

A

Clinical entity which is the first episode of pain at rest or with minimal exertion with sudden worsening of intensity of frequency of episodes

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9
Q

What is NSTEMI?

A

Clinico-pathological entity where there is evidence of myocardial damage w/o ST segment changes but many have non-specific ECG changes

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10
Q

What will the history of a NSTEMI look like?

A

Similar to unstable angina or STEMI

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11
Q

How would you investigate acute coronary syndromes?

A
  1. Patient comes in with chest pain
  2. Working diagnosis is ACS
  3. ECG
  4. Biochemistry (e.g. troponin)
  5. Diagnosis
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12
Q

What are some complications of acute coronary syndrome?

A 
Hypotension
Cardiogenic shock
AKI
Right ventricular infarction
Tachy/brady arrhythmias
Conduction defects
Papillary muscle rupture
Pericarditis
Ventricular aneurysm
Cardiac rupture
Recurrent ischaemia
Mural thrombosis
Post MI (Dressler's) syndrome
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13
Q

What are the 3 main signs of unstable angina?

A
  1. Non-occlusive thrombus
  2. Normal or non-specific ECG
  3. Normal cardiac enzymes e.g. troponin T
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14
Q

What are the 3 main signs of NSTEMI?

A
  1. Non-occlusive thrombus sufficient to cause tissue damage + mild myocardial necrosis
  2. ST depression/T wave inversion on ECG
  3. Elevated troponin T by 6 hrs after symptoms commence
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15
Q

What are the 4 main signs of STEMI?

A
  1. Complete thrombus occlusion
  2. ST elevation >1mm in 2 contiguous leads or new LBBB
  3. Elevated troponin T by 6 hrs after symptoms commence
  4. Most severe symptoms
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16
Q

Why else can troponin be raised other than for cardiac reasons?

A

Renal failure

17
Q

How does vascular injury result in a platelet-fibrin thrombus?

A

Exposure of collagen + vWF -> platelet adhesion + release -> platelet recruitment + activation -> platelet aggregation

TF exposure -> activation of coagulation -> thrombin generation -> fibrin formation

18
Q

What types of clots do unstable angina and NSTEMI’s tend to be associated with?

A

White, platelet-rich + partially occlusive -> microemboli can detach + embolise downstream casing myocardial ischaemia/infarction

19
Q

What types of clots do STEMI’s tend to be associated with?

A

Red, fibrin rich + more stable thrombus

20
Q

What is the pathophysiology of ischaemic heart disease?

A
  1. Atherosclerotic plaque causes a fixed coronary obstruction
  2. Severe fixed coronary obstruction may ensue causing chronic IHD
  3. Plaque disruption may occur
  4. Occlusive thrombus may cause acute transmural MI/sudden death
  5. Mural thrombus with variable obstruction/emboli may cause unstable agina or acute subendocardial MI/sudden death
21
Q

Explain the phases of a myocardial infarction.

A
  1. Ischaemic: survives on anaerobic metabolism initially for several minutes
  2. Infarction: anaerobic metabolism cannot keep up with metabolic needs causing irreversible damage + cell death

-> affected area contributes less to depolarization

22
Q

What is an indicative ECG change of ischaemia?

A

Inverted T waves

ST segment depression

23
Q

What is an indicative ECG change of injury?

A

ST segment elevation

24
Q

What is an indicative ECG change of infarct/scar?

A

Pathological Q wave formation (old injury)

25
Q

What ECG change would you see in a inferior wall MI?

A

ST elevation in lead II, III + AVF

26
Q

What ECG change would you see in a anterior wall MI?

A

ST elevation in V1-V6

27
Q

Define acute coronary syndrome.

A

Spectrum of clinical presentations ranging from those for STEMI to presentations found in STEMI or in UA. It almost always associated with rupture of an atherosclerotic plaque + partial/complete thrombosis of the infarct-related artery.

28
Q

What drugs are involved in the primary or secondary prevention?

A 
Statins
B-blockage
ACE inhibitors
Aspirin
Clopidogrel
Exercise
Diet 
Smoking cessation
29
Q

What drugs are used to treat acute coronary syndromes?

A 
O2
Coronary care unit
Aspirin
Clopidogrel
Opiates
Low MW heparin
GRP IIb IIIa inhibitors
Nitrates
Thrombolytics
Statins
B-blockade
ACE inhibition
Percutaneous coronary intervention with angioplasty
Suction/stenting
CABG
30
Q

What can be used to treat the complications of acute coronary syndromes?

A 
Anti-arrhythmics
Mg sulphate
Percutaneous, temporary + permanent pacemakers
Ionotropes
Diuretics
Intra-aortic balloon pump
Adrenaline
Atropine
Cardio-pulmonary resuscitation
DC cardioversion
CPAP
Mechanical ventilation
31
Q

What other treatments can be used to treat acute coronary syndromes?

A

Heart transplant
Cardiac rehabilitation
Palliative care

Block 2 (45 decks)

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