Acute Coronary Syndrome Flashcards

1
Q

Define angina:

A

A condition marked by severe pain in the chest, often also spreading to the shoulders, arms, and neck, owing to an inadequate blood supply to the heart.

  • exacerbated by exercise
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2
Q

Define acute coronary syndrome.

A

Acute coronary syndrome (ACS) is the umbrella term or a set of signs and symptoms due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies.

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3
Q

Define STEMI.

A

ST-Elevation Myocardial Infarction (STEMI) is a very serious type of heart attack during which one of the heart’s major arteries.

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4
Q

Define NSTEMI.

A

NSTEMI stands forNon-ST-elevation myocardial infarction - causes less damage to a persons heart than a STEMI.

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5
Q

IHD

A

Ischaemic heart disease - decreased blood supply to the heart muscle.

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6
Q

Myocardial Infarction

A

MI refers to cardiac muscle necrosis resulting from ischaemia.

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7
Q

What are the three broad manifestations of atherosclerosis?

A
  1. Coronary - ACS -MI, Angina, Sudden death.
  2. Cerebrovascular - TIA, CVA.
  3. Peripheral - intermittent claudication.
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8
Q

Progression seqence of atherosclerosis:

A
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9
Q

What is the common underlying pathology of ACS?

A

Disruption of an atherosclerotic plaque.

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10
Q

Troponin is a biomarker of what?

A

Cardiac myocyte necrosis

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11
Q

How can pain present in a myocardial infarct?

A

Central crushing/tight/squeezing chest pain.

Tooth/Jaw pain.

Pain radiating down left arm.

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12
Q

What are non-modifiable risk factors of MI?

A

Age

FH

Male

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13
Q

What are modifiable risk factors of MI?

A

Smoking

Hypertension

Diabetes

Hyperlipidaemia

Obesity

Sedentary lifestyle

Cocaine use

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14
Q

How is cocaine a risk factor for MI?

A

Cocaine use causes vasospasm hence ischaemia.

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15
Q

What are symptoms of an MI?

A

Acute crushing central chest pain lasting longer than 20minutes.

Chest pain can radiate to left arm, neck, jaw, epigastrium.

Assocaited nausea, sweatiness, breathlessness, palpitations.

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16
Q

In whom may a silent infarct present in?

A

Diabetic / elderly patients.

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17
Q

How do silent infarcts present?

A

Syncope

Pulmonary oedema

Epigastric pain / vomiting

Post-operative hypotension

Oliguria

Acute confusion

Stroke/Diabetic hypoglycaemic states

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18
Q

A localised / Sharp / pain that is worse on inhalation suggests what?

A

That it is not a heart problem.

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19
Q

How is ACS defined clincally?

A

• Defined as 2 out of 3:

  • Unstable, ischaemic, chest pain (history)
  • Ischaemic ECG changes (investigations)
  • Raised cardiac biomarkers (investigations)
20
Q

What investigations are done in ACS?

A
  • ECG
  • Cardiac enzymes
  • CXR, routine bloods
21
Q

Explain the changes shown in this ECG stemi:

A
22
Q

Coronary anatomy and infarction territory:

A

Watch and potentially attach slide.

23
Q

How can NSTEMI or unstable angina present on an ECG?

A

NSTEMI or Unstable angina– can present with ST depression, T wave inversion, nonspecific changes or normal ECG.

24
Q

What is meant by tombstoning in ECG’s?

A

Tombstoning ST-segment elevation is a type of ST-segment elevation with a specific morphology which is observed in the early period of acute myocardial infarction.

25
Q

Explain the cardiac troponin biomarkers measured.

A

Troponin T and I are the most sensitive and specific markers of myocardial necrosis.

26
Q

What do troponin levels peak in the blood?

A

24hours following MI.

27
Q

Hs-cTnT

A

High-sensitive cardiac troponin T

28
Q

What is CKMB used for?

A

CKMB (Creatine kinase-MB) is used to help identify re-infarction.

CKMB peaks at 24hours and is back at baseline by 48-72hours.

29
Q

What is meant by “Troponinitis”?

A

Elevations in cardiac biomarkers reflect myocardial necrosis, they do not indicate its mechanism.

Therefore not all patients with a raised troponin have an ACS, or benefit from antiplatelet agents.

30
Q

What is the acute management of ACS?

A

Pre-hospital:

300mg Asprin

GTN Spray

In-hospital:

Morphine and metoclopramide

Oxygen (if resting sats <95%)

GTN spray, or IV

Antiplatelet agents e.g asprin

31
Q

What is the chronic management of ACS??

A

Dual Antiplatelet Therapy (DAPT)

Statins

ACE Inhibitors

Betablockers

32
Q

Why are ACE inhibitors in ACS?

A

Ace I help remodel the left ventricle, and are given to anyone whom has had an MI.

33
Q

What is the mechanism of how asprin works?

A

Asprin blocks the production of TxA2 (Thromboxin A2) at the site of platelet COX-1.

  • the action of asprin on polatelet COX-1 is permanent lasting the life of the platelet (7-10days).
34
Q

What are examples of other antiplatelets used in conjunction with asprin in DAPT?

A

Clopidogrel

Prasugrel

Ticagrelor

35
Q

How do nitrates affect the CV system?

A

Nitrates have a direct relaxant effect on vascular smooth muscles. Dilation of coronary vessels improves oxygen supply to the myocardium.

Dilation of peripheral veins, and in higher doses peripheral arteries, reduces preload and afterload, and thereby lowers myocardial oxygen consumption.

36
Q

Explain the action of betablockers:

A

Decreased heart rate.

Decreased contractility.

Decreased systolic wall tension.

Increased perfusion time.

37
Q

Explain the action of the following receptors:

Alpha 1

Alpha 2

ß1

ß2

D1

A
38
Q

What are the general effects of statins?

A

Reduce cholesterol.

Pleiotropic effect - anti-inflammatory.

Reduces the amount of cholesterol laid down in the heart.

39
Q

Definitive treatment of a STEMI.

A

• PPCI – primary PCI

– Emergency cath lab PCI procedure

– Each region has infrastructure to transport patient to PPCI centre

– Coronary stent to reverse mechanical obstruction.

• Fibrinolytics (if PPCI not available within 120 mins).

40
Q

PCI

A

Percutaneous coronary intervention

41
Q

Conclusion regarding ACS

A

Conclusion

  • ACS describes a spectrum of presentations of acute disease of the coronary arteries.
  • Underlying pathophysiology is atherosclerosis of coronary circulation
  • Treatment is directed at strategies to improve blood flow.
  • Antiplatelet agents to mitigate thrombus.
  • PPCI to remove mechanical obstruction.
42
Q

What is unstable angina?

(understand how it is different from an MI)

A

Unstable angina symptoms occur in an unexpected and unpredictable manner. The symptoms are more severe and less responsive to nitroglycerin medication. This is a medical emergency as it may culminate in a heart attack.

43
Q

Syncope

A

Syncope is a temporary loss of consciousness usually related to insufficient blood flow to the brain.

It most often occurs in hypotension and the heart doesn’t pump enough oxygen to the brain.

44
Q

In cases where MI cannot be treated with PCI what is the next best treatment?

A

Thrombolyse with tissue plasminogen activator.

45
Q

What are the post MI complications?

A
46
Q

Dresslers syndrome

A