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cardiovacular > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

What is atherosclerosis?

A

The build-up of fatty plaques in the walls of arteries.

It is the pathology responsible for acute coronary syndromes, peripheral arterial disease, AAA, and ischaemic strokes.

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2
Q

What are risk factors for atherosclerosis?

A

Smoking
Hypertension
Obesity
Hypercholesterolaemia
Male gender
Family history
Age
Diabetes
Alcohol (as this raises BP)

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3
Q

What are the pathological stages involved in atherosclerosis?

A
  1. Primary endothelial injury.
  2. LDL taken from the blood into the tunica intima of the artery - it is oxidised.
  3. Macrophages migrate to these oxidised LDL, forming foam cells, which in turn creates the fatty streak.
  4. Activated macrophages release cytokines and growth factors (e.g., PDGF) which cause proliferation of the smooth muscle layer and deposition of collagen
  5. Plaque enlarges, compromising blood flow (e.g. angina/PAD)
  6. Progresses further, where clot can now block entire arterial lumen, initiating a clotting cascade - patient has an MI.
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4
Q

What causes stable angina?

A

Narrowing of the coronary arteries, reducing blood flow to the myocardium.

Symptoms appear during times of exercise as there is insufficient blood flow to meet the demands of the heart.

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5
Q

How is stable angina diagnosed?

A

It is a clinical diagnosis.

May use ECG or CT angiography to aid this.

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6
Q

How is stable angina treated?

A

Lifestyle interventions
GTN spray (for symptomatic relief)
Beta-blocker or CCB

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7
Q

What conditions are classified as the acute coronary syndromes?

A

STEMI
NSTEMI
Unstable angina

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8
Q

What is the mechanism responsible for an ACS?

A

Rupture/Erosion of the fibrous cap covering an atherosclerotic lesion.

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9
Q

What is the risk of MI in the 30 days following onset of unstable angina?

A

Around 50%.

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10
Q

In which leads would an infarction of the LCA show elevation in a STEMI?

A

Leads I, aVL, and V3-V6.

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11
Q

In which leads would an infarction of the LAD show elevation in a STEMI?

A

Leads V1-V4.

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12
Q

Which artery is said to be anterolateral?

A

Left coronary artery (LCA).

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13
Q

Which artery is said to be anterior?

A

Left anterior descending (LAD).

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14
Q

In which leads would an infarction of the circumflex show elevation in a STEMI?

A

Leads I, aVL, and V5-V6.

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15
Q

What artery is said to be lateral?

A

Circumflex

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16
Q

What artery is said to be inferior?

A

Right coronary artery (RCA).

17
Q

In which leads would an infarction of the RCA show elevation in a STEMI?

A

Leads II, III and aVF.

18
Q

What is the first-line investigations in a suspected ACS?

A

ECG
Troponin

19
Q

If patient has raised ST segment and positive troponins, what is the diagnosis?

A

STEMI

20
Q

If patient has raised/non-raised ST segment and negative troponins, what is the diagnosis?

A

Unstable angina

Troponin level is crucial here.

21
Q

If patient has non-raised ST segment and positive troponins, what is the diagnosis?

A

NSTEMI

22
Q

How should an ACS be initially managed?

A

Think ‘MONA-T’

Morphine
Oxygen (if hypoxic)
Nitrates (if hypertensive or LVF present)
Aspirin
Ticagrelor/clopidogrel

23
Q

What is the definitive treatment of a STEMI, within 2 hours of symptomatic onset?

A

Percutaneous Coronary intervention (PCI).

24
Q

How should a STEMI patient be treated if PCI not available within first 2 hours of symptoms?

A

Thrombolysis

25
Q

How is a NSTEMI patient definitively managed?

A

Consider risk of progression - watch ECG, troponin and take history.
Provide aspirin and fondaparinoux.
Consider an IV nitrate
If high risk, consider PCI.
If low-risk and troponins remain low, discharge and follow-up.

26
Q

How is an ACS patient managed following the event?

A

Cardiac rehab

Think ‘DABS’:
Dual antiplatelet (aspirin for life and ticagrelor for 6-12 months).
ACE inhibitor
Beta-blocker (Start within 24 hours of ACS)
Statin

Additionally, can give GT for symptoms of angina, or an aldosterone antagonist for HF/LV dysfunction.

27
Q

What are complications of an ACS?

A

Arrhythmias
Heart failure
Structural damage
Pericarditis (inflammatory in nature - called Dressler’s syndrome)

28
Q

Where does PAD typically present?

A

The legs

29
Q

What is intermittent claudication?

A

Exertional discomfort of the calves which is relieved by rest. Caused by insufficient blood to the muscles during exercise as a result of atherosclerotic build-up.

30
Q

What is the normal range of ABPI?

A

0.9-1.2

31
Q

What is a claudication range of ABPI?

A

0.4-0.85

32
Q

What is a severe claudication range of ABPI?

A

0.0-0.4

33
Q

How does critical limb ischaemia present?

A

Ulceration, necrosis, absent pulses, a lack of hair, thick nails, and shiny skin.

34
Q

What are management options in PAD?

A

Smoking cessation
Exercise(under supervision)
Angioplasty/Bypass graft
Vasodilator therapy (if exercise and interventions not desired)
If critical limb ischaemia, then amputate

cardiovacular (13 decks)

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