Acute Coronary Syndrome (ACS) and Acute Myocardial Infarction (AMI) Flashcards

(31 cards)

1
Q

Describe the EPIDEMIOLOGY of Coronary Heart Disease (CHD) in the community:

A

Presentation:

> 50% Stable Angina
20% Myocardial Infarction (MI)
10% Unstable Angina
10% Sudden Cardiac Death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What conditions ENCOMPASS ACS?

A

1) Unstable Angina (UA)
* Evolving to MI

2) Non ST Elevated MI (NSTEMI)
3) ST Elevated MI (STEMI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the PROGRESSIVE PATHOGENESIS of ACS to AMI:

A

1) Inflammation Leads to Rupture of Fibrous Plaque
2) Thrombus Formation
3) > Occlusion of Coronary Artery Lumen
4) > Ischaemia and > Need for Blood Supply (O2 to Tissues)

  • Leading to MI
    5) Complete Occlusion of Vessel Ensues
    6) Blood Cannot Supply Tissues
    7) Tissue Necroses and Infarcts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a CARDINAL CLINICAL FEATURE of ACS?

A

Symptoms Always Occur at Rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the NON-MODIFIABLE RISK FACTORS for ACS?

A

1) Gender
2) Race
3) Age
4) Genetics
5) Family History
6) Previous Angina, Cardiac Events or Interventions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the MODIFIABLE RISK FACTORS for ACS?

A

1) Lifestyle, i.e. Diet and Weight; Exercise
2) Smoking
3) Hyperlipidaemia (Cholesterol Control)
4) Hypertension (BP Control)
5) Diabetes Mellitus (Glycaemic Control)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the CHARACTERISTICS of ACS CHEST PAIN?

A

Site - Retrosternal
Onset - Sudden
Character - Tight Band/Heaviness/Pressure
Radiation - Jaw and/or Neck; Down Arms
Exacerbating/Alleviating - No Relief with GTN Spray; At Rest; is Ongoing
Severity - > Pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How might a patient with UA or NSTEMI PRESENT?

A

1) May Look Very Unwell
2) May Look Completely Fine
* Often No Specific Features to Find

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some of the SIGNS of ACS?

A

1) Distress
2) Diaphoresis
3) Pallor
4) > or < BP
5) > or < Pulse Rate
6) Distended JVP (If HF)
7) 3rd Heart Sound (If HF)
8) Chest Crepitations (If HF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some of the SYMPTOMS of ACS?

A

Can be Asymptomatic

OR

1) Dyspnoea
2) Nausea and Vomiting
3) Palpitations
4) Anxiety
5) Epigastric Pain
6) Chest Pain

< Pain Sensation in Women, Elderly and Diabetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the MAIN INVESTIGATIONS for a patient suspected of having ACS?

A

1) Serial ECGs
2) FBCs - Cardiac Troponin (cTn) and Creatine Kinase-MB (CK-MB)
3) CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What would be the EXPECTED FINDINGS on ECG from a patient with UA or NSTEMI?

A

*May be Normal

Commonly:

1) ST-Segment Depression
2) Transient ST Elevation and/or T-Wave Inversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What would be the EXPECTED FINDINGS from CARDIAC TROPONIN in a patient with UA?

A

No Elevation in Troponin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What would be the EXPECTED FINDINGS from CARDIAC TROPONIN in a patient with NSTEMI?

A

Elevated Troponin

*Not all > in Troponin are Triggered by ACS and Caused by Atherothrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What would be the IMMEDIATE TREATMENT for a patient with UA or NSTEMI?

A

1) ABCDE Approach

  • MONA
    2) Morphine
    3) O2 Therapy
    4) Nitrates - GTN
    5) Aspirin (300mg; Chewed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the GOALS of PHARMACOTHERAPY for ACS and AMI?

A

1) > Myocardial O2 Supply
- Coronary Vasodilation
2) < Myocardial O2 Demand
- < HR
- < BP
- < Preload and Contractility

17
Q

What are the LONG-TERM TREATMENTS for UA/NSTEMI according to ACS PROTOCOL?

A

1) Dual Anti-Platelet Therapy
- Aspirin (< Dose) and Clopidogrel/Ticagrelor
2) Anti-Thrombotic Therapy
- LMWH (Fondaparinux)
3) Statins (i.e. Simvastatin)
4) ACEIs (i.e. Ramipril; particularly if in HF)
5) Analgesia
6) Nitrates (i.e. GTN)
7) Beta-Blockers (i.e. Bisoprolol)

18
Q

In what INSTANCES would you use a DIFFERENT ANTI-PLATELET drug to clopidogrel?

A

Patients With < CYP2C19 Levels - Resistant to Clopidogrel

*Consider Ticagrelor or Prasugrel as Alternatives

19
Q

What is a COMMON SIDE EFFECT of ASPIRIN use?

A

GI Bleeds

  • Low Doses (75-150mg) should be used for 1 year Post-ACS Event
  • Proton Pump Inhibitors (PPIs) could be used In Conjunction to Prevent Bleed; < Efficacy of Anti-Platelet Therapy
20
Q

What TREATMENT would be adopted in “HIGH RISK” patients with UA/NSTEMI instead of medical therapy alone?

A

Percutaneous Coronary Intervention (PCI) and Stenting

or

Coronary Artery Bypass Grafting (CABG)

21
Q

What are the STRENGTHS and WEAKNESSES of using BETA-BLOCKERS POST-MI?

A

Strength - Secondary Prevention; < Mortality Rate

Weakness - > Risk of Cardiogenic Shock

22
Q

What are the ADVANTAGES of using ASPIRIN for ACS or in AMI?

A

> Mortality Rate

< Reinfarction Rate

23
Q

What PROPORTION of the MYOCARDIUM is DAMAGED during NSTEMI?

A

Subendocardium (Partial Thickness of the Muscle)

24
Q

What PROPORTION of the MYOCARDIUM is DAMAGED during STEMI?

A

Transmural (Full Thickness of the Muscle)

25
What would be the EXPECTED FINDINGS on ECG from a patient with STEMI?
1) ST-Segment Elevation 2) Pathological Q Waves After 3 Days 3) Hyperacute T Waves
26
Following AMI, what is CRUCIAL FACTOR for patient SURVIVAL?
Time * Necrosis of Myocardial Tissue Happens in Time-Dependent Manner * Early Intervention is Key to Preserving Tissue Integrity
27
What is FIRST-LINE TREATMENT for a patient with STEMI?
Primary PCI
28
HOW LONG AFTER the incidence of STEMI MUST REVASCULARISATION occur?
Within 90 Minutes
29
In the event that revascularisation cannot be given in time following STEMI, what is the NEXT COURSE of ACTION?
Thrombolysis Via Tissue Plasminogen Activators (t-PA), i.e. Alteplase
30
What is the MECHANISM of ACTION of THROMBOLYSIS?
1) Serine Proteases Convert Plasminogen to Plasmin | 2) Plasmin Lyses the Blood Clot by Breaking Down Fibrinogen and Fibrin Mesh
31
What are some of the CONTRAINDICATIONS for THROMBOLYSIS?
1) Previous Intracranial Haemorrhage 2) Recent Ischaemic Stoke 3) Suspected Aortic Dissection 4) Known Malignant Intracranial Neoplasm 5) Recent Significant Closed Head-Trauma