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Cardiovascular > ACS + MI > Flashcards

ACS + MI Flashcards

1
Q

What is Acute coronary syndrome (ACS)?

A

encompasses unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI).

typically manifests as sudden, new-onset angina, or an increase in the severity of an existing stable angina.

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1
Q

What is Acute coronary syndrome (ACS)?

A

encompasses unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI).

typically manifests as sudden, new-onset angina, or an increase in the severity of an existing stable angina.

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2
Q

Epidemiology of ACS

A
  • STEMI = 5/1000 per annum in UK
  • M>F
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3
Q

RFs for ACS

A
  • Age (>65 years of age)
  • Male
  • Family history of premature coronary heart disease
    Smoking
    Diabetes
    HT
    Obesity
    Drugs
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4
Q

Atherosclerotic plaque formation

A
  • Thefirst stageof atherosclerotic plaque formation involves the accumulation of low-density lipoprotein cholesterol in the inner layer of the blood vessel
  • Leukocytes adhere to the endotheliumand gain entry into theintima, where they combine with the lipids to becomefoam cells
  • Artery remodellingandcalcification, alongside the presence offoam cells, causes atherosclerotic plaques to form
  • Rupture of a plaquecauses platelet activation, thrombus formation and coronary artery occlusion. (The thrombus is mainly made up of platelets)
  • This results in ischaemia and infarction
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5
Q

What happens in unstable angina and NSTEMI

A

Occlusion is partial

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6
Q

What happens in STEMI

A

Occlusion is complete
STEMI, ischaemia is initially just subendocardial, but eventually becomes transmural.

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7
Q

Signs of ACS

A
  • Hypotension or hypertension
  • Reduced 4th heart sound
  • Signs of heart failure: e.g. increased JVP, oedema; **red flag symptom
  • Systolic murmur: if mitral regurgitation or a ventricular septal defect develops
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8
Q

Symptoms of ACS

A
  • Shortness of breath
  • Sweating and clamminess
  • Nausea and vomiting
  • Palpitations
  • Anxiety: often described as a ‘sense of impending doom’
    Chest pain
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9
Q

Primary investigations for ACS

A

First line: ECG - perform every 10 minutes

Troponin:for a STEMI and NSTEMI, troponin levels will begin to elevate 4-6 hours after injury and will remain elevated for roughly 10 days. In unstable angina, there isnoelevation in troponin.

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10
Q

ECGs for ACS

A

Thyroid function tests
HbA1C and fasting glucose
FBC
U&Es
LFTs
CXR

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11
Q

Immediate management for unstable angina + NSTEMI

A

Oxygen
Analgesia: Morphine & Sublingual glyceryl nitrate
Dual antiplatelets: Aspirin + Prasugrel, ticagrelor or clopidogrel
Anticoagulation: Fondaparinux + unfractionated heparin
BBs

MONA: Morphine oxygen nitrates aspirin

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12
Q

STEMI immediate management

A

Oxygen
Analgesia: Morphine & Sublingual glyceryl nitrate
Dual antiplatelets: Aspirin + Prasugrel, ticagrelor or clopidogrel

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13
Q

What is a PCI

A

first-line method of revascularisation; insertion of a catheter via the radial or femoral artery to open up the blocked vessels using an inflated balloon (angioplasty), and a stent may also be inserted

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14
Q

Symptom onset within 12 hours AND access to PCI within 2 hours for STEMI management

A

PCI
- Anticoagulation and further antiplatelet therapy
- Unfractionated heparinand aglycoprotein IIb/IIIa inhibitor
- Bivalirudinmay be used as an alternative to unfractionated heparin

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15
Q

Management for STEMI if ineligible for PCI

A
  • Thrombolysis e.g. alteplase or tenecteplase
    • IV administration of a fibrinolytic agent
    • Offered if symptom onset is greater than 12h OR PCI not available within 120 mins
  • Anticoagulation
    • An antithrombin agent such as unfractionated heparin is usually given alongside thrombolysis
  • ECG:if the ECG shows residual ST elevation after 60-90 minutes of thrombolysis, offer immediate angiography and PCI
16
Q

Early complications for ACS

A

Post - MI pericarditis
Cardiac arrest/ tachyarrhythmias
Cardiogenic Shock
MR
Ventricular septal defect

17
Q

Late complications of ACS

A
  • Dressler’s syndrome:presents similarly to post-MI pericarditis but occurs2-6 weekspost-MI, and reflects anautoimmuneprocess against neo-antigens formed by the heartDiagnosis:ECG(global ST elevationandT wave inversion),echocardiogram (pericardial effusion) and raisedinflammatory markers(CRPandESR).Management:NSAIDs(aspirin/ibuprofen) and in more severe cases steroids (prednisolone). May needpericardiocentesisto remove fluid around the heart.
  • Heart failure:ventricular dysfunction following extensive damage can lead to chronic heart failure
  • Left ventricular aneurysm: bulge or ballooning of a weakened area of the heart
18
Q

Prognosis of ACS

A

Unstable anginahas a better outcome than anNSTEMIorSTEMI.

NSTEMIs and STEMIs have similar long-term outcomes. 5-10% of patients with ACS are predisposed tore-infarction.

Poor prognostic factorsinclude: increasing age, the magnitude of troponin rise, arrhythmias, left ventricular dysfunction,renal impairment, diabetes, anaemia, cerebrovascular disease

19
Q

What is a myocardial infarction?

A

Death of heart muscle cells via necrosis due to lack of blood flow

20
Q

Pathophysiology of MI

A

MI happens when coronary circulation becomes blocked

Mostly due to endothelial cell dysfunction relating to inflammation of tunica intima - toxins from tobacco can cause this

Damage becomes site for atherosclerosis

21
Q

How does an atherosclerotic plaque form

A

Starts with fibrous cap

In core of atherosclerotic plaque T lymphocytes, smooth muscle cells, macrophages, lipids

22
Q

NSTEMI MI pathophysiology

A

LAD blocked > Inner 3rd of myocardium first area affected

Blockage suddenly breaks down + blood flow returns damage is limited to the inner 3rd

Called subendocardial infarct - ECG shows no ST elevation

23
Q

NSTEMI MI features

A

Causes of subendothelial infarct and hypotension

24
Q

Pathophysiology of STEMI MI

A

3-6 hours zone of necrosis extends through entire wall of thickness - transmural infarct

Shows ST segment elevation

25
Q

Complications of of STEMI MI

A

HF
Arrhythmias
Pericarditis
Cardiogenic shock
Granulation tissue

26
Q

Treatment for MI

A

Fibrinolytic therapy - medication to breakdown Fibrin in blood clots
Angioplasty - Deflated balloon inserted into blockage then inflated to open the artery
PCI - catheter used to place stent in coronary artery to open up blood vessels

27
Q

What is reperfusion injury

A

Tissue damaged by returning blood

28
Q

Medications for MI

A

Antiplatelets - Aspirin
Anticoagulatn - Heparin or LMWH
Nitrates - relax coronary arteries - lower preload
BB
Pain medication
Statins

29
Q

Symptoms of MI

A

Chest pain/ pressure
Diaphoresis
Dyspnoea
Nausea
Fatigue
Left arm/ jaw pain

30
Q

3 most commonly blocked arteries in MI

A

LAD: Anterior wall + interventricualr septum 40/50% of cases
RCA : Posterior wall, septum + Papilary muscles of LV - 30/40% of cases
LCA: Lateral wall of LV - 15/20% of cases

Cardiovascular (14 decks)

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