Acute Coronary Syndromes Flashcards

1
Q

acute coronary syndromes

A

umbrella term for any acute presentation of coronary artery disease covers unstable angina, NSTEMI and STEMI

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2
Q

aetiology

A

usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery

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3
Q

pathophysiology 1

A

The mechanism that is common to all ACSs is rupture or erosion of the fibrous cap of a coronary artery plaque

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4
Q

pathophysiology 2

A

This leads to platelet aggregation and adhesion, localized thrombosis, vasoconstriction and distal thrombus embolization

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5
Q

pathophysiology 3

A

Thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2 result in myocardial ischaemia due to reduction of coronary blood flow

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6
Q

what can acute coronary syndromes lead to

A

can lead to cardiac arrest
Ischaemia of the heart causes myocytes to be replaced with scar tissue, decreasing the hearts ability to pump blood, potentially leading to left-sided heart failure

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7
Q

unstable angina

A

subtotal occlusion, supply led ischaemia without infarction, high (50%) risk of MI in subsequent 30 days

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8
Q

NSTEMI

A

subtotal occlusion

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9
Q

STEMI

A

complete occlusion

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10
Q

MI

A

myocardial necrosis with a raised troponin and at least one other symptom suggestive of an mi

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11
Q

type 1 MI

A

Traditional MI due to an acute coronary event

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12
Q

type 2 MI

A

Ischaemia secondary to increased demand or reduced supply of oxygen

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13
Q

type 3 MI

A

Sudden cardiac death or cardiac arrest suggestive of an ischaemic event

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14
Q

type 4 MI

A

MI associated with PCI / coronary stunting / CABG

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15
Q

non ischaemic myocardial injury with necrosis

A
  • Not technically a type II MI
    • Can be caused by cardiac contusion, ablation, pacing, cardiotoxic chemotherapy
    • Can raise Troponin even though it is not an atherosclerotic MI
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16
Q

symptoms

A
  • Severe crushing central chest pain at rest
    • Pain radiates to jaw and arms
    • Similar to angina but more prolonged and not relieved by GTN
    • Associated with sweating, nausea, and often vomiting
    • Can occur at rest, as opposed to stable angina
    • 30 mins or longer
17
Q

atypical presentation - silent MI

A
  • Particularly important in women, the elderly and patients with diabetes
  • Milder symptoms (without chest pain) especially in younger women
  • Shortness of breath, fatigue, body aches, overall feeling of illness
  • Unusual feeling/mild discomfort in the back, chest, arm, neck or jaw (without chest pain)
  • Heartburn, nausea/vomiting, abdominal pain
  • Symptoms may occur up to a month before MI: fatigue, sleep disturbance, SOB, anxiety, indigestion, palpitations
18
Q

signs

A

xanthelasma - sign of atherosclerosis

19
Q

what do to when a suspected acute coronary syndrome 1

A
  • 12 lead electrocardiogram
  • ST elevation acute coronary syndrome
  • troponin positive
  • ST elevation MI
20
Q

what do to when a suspected acute coronary syndrome 2

A
  • 12 lead electrocardiogram
  • Non ST elevation acute coronary syndrome
  • troponin positive
  • non ST elevation MI
21
Q

what do to when a suspected acute coronary syndrome 3

A
  • 12 lead electrocardiogram
  • Non ST/ ST elevation acute coronary syndrome
  • troponin negative
  • unstable angina
22
Q

STEMI ECG

A
  • ST segment elevationin leads consistent with an area of ischaemia
  • T wave inversion
  • Q waves
23
Q

evolution of abnormal ECG in a STEMI

A
  • ST elevation - first few hours
  • Q wave formation and T wave inversion - first day
  • Old MI (previous heart attack) - Q waves with out without inverted T waves
24
Q

NSTEMI ECG

A
  • May be normal
  • ST segment depressionin a region
  • Deep T Wave Inversion
  • Pathological Q Waves(suggesting a deep infarct - a late sign)
25
Q

unstable angina ECG

A
  • May be normal
  • May include non-specific changes, abnormal T waves or ST depression
26
Q

initial management

A
  • Analgesia → DiaMorphine IV
  • Anti-emetic - IV
  • Oxygen if hypoxic (i.e <94%)
  • Nitrates if patient hypertensive or in acute LVF
  • Aspirin → 300mg aspirin loading dose to chew on
  • Ticagreor (180mg) /clopidogrel (600mg)
27
Q

definitive management

A

If a patient has a stent, dual antiplatelet therapy should never be stopped without consulting with a cardiologist

28
Q

STEMI - management

A
  • Primary PCI (if available within 2 hours of ECG diagnosis )
  • Thrombolysis (if PCI not available within 2 hours)
29
Q

NSTEMI - management

A
  • All receive continuing aspirin and fondaparinux
  • Consider IV nitrate
  • High risk - consider PCI, may give tirofiban (antiplatelet)
  • Low risk patients may be discharged after repeat negative troponin and followed up
  • Beta-blockers may be considered in patients with no evidence of bradycardia, hypotension or cardiogenic shock
  • GPIIB/IIIA inhibitors may be considered in very high risk patients
30
Q

secondary prevention

A

life style mod
medication - DABS

31
Q

DABS

A

dual antiplatelet
ACEi
Beta blockers
Statin

32
Q

complications

A
  • death
  • arrythmias
  • heart failure
  • structural damage
  • functional complications
  • pericarditis
33
Q

management of complications

A
  • Cardiac monitoring (rythym)
  • ask patient how they feel
  • Pulse and BP
  • heart sounds (especially added sounds)
  • murmurs
  • pulmonary crepitations
  • fluid balance