Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Year 5 - GIM > Acute coronary syndrome > Flashcards

Acute coronary syndrome Flashcards

(39 cards)

Start Studying
1
Q

Define acute coronary syndrome

A

spectrum of acute myocardial ischaemia and/or infarction

i.e.

“umbrella term for situations where the blood supplied to the heart muscle is suddenly blocked”

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

Define unstable angina

A

Unstable angina (UA) is defined as myocardial ischaemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury/necrosis

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

What are the clinical features of unstable angina

A

prolonged (>20
minutes) angina at rest
new onset of severe angina; angina that is increasing in frequency, longer in
duration, or lower in threshold
or angina that occurs after a recent episode of myocardial infarction
- NO ST ELEVATION
- NO TROPONIN RISE

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

Outline the main risk factors for coronary artery disease (13)

A
  • Diabetes mellitus
  • Hyperlipidaemia
  • Hypertension
  • Metabolic syndrome
  • Renal impairment
  • Peripheral arterial disease
  • Obesity
  • Advanced age
  • Smoking
  • Cocaine use
  • Physical inactivity
  • FH of premature coronary artery disease
  • history of ischaemic heart disease and any previous treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the aetiology of unstable angina?

A
  1. Most common –> non-occlusive coronary artery narrowing 2ndary to thrombus
  2. Coronary spasms (Prinzmetal’s angina)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the pathophysiology of ACS

A
  1. Plaque fissures (more common in thin fibrous cap plaques –> high lipid content, few smooth muscle cells, and a high proportion of
    macrophages and monocytes)
  2. Subendothelial matrix elements (e.g. collagen) exposed to blood
  3. Release of tissue factor activates coagulation cascade and promotes the formation of fibrin
  4. Thrombus is formed (occlusive or non-occlusive)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which subdivisions of ACS are associated with
1. Occlusive thrombus
2. Non-occlusive thrombus

A
  1. STEMI
  2. NSTEMI or unstable angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Potential causes of ischaemia unrelated to CAD

A
  1. Increased myocardial oxygen requirements such as fever, tachycardia, thyrotoxicosis
  2. Reduced coronary blood flow: for example, hypotension
  3. Reduced myocardial oxygen delivery such as anaemia or hypoxaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How to classify ACS

A

Based on ECG finding:
1. Chest pain + persistent ST-segment elevation on ECG –> STEMI
2. Chest pain + ST-segment depression, or T-wave changes OR no ECG changes at presentation –> Non-ST-elevation ACS

Further categorisation of non-ST-elevation ACS is by measurement of cardiac biomarkers:
* Elevated: non-STEMI
* Non-elevated: UA.

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

What are the clinical subdivisions of ACS

A
  1. STEMI
  2. NSTEMI
  3. Unstable angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Key features of unstable angina
1. Clinical features
2. Biochemically
3. ECG

A
  1. Chest pain
    a. prolonged (>15 minutes) angina at rest
    b. new onset of severe angina; angina that is increasing in frequency, longer in
    duration, or lower in threshold;
    c. or angina that occurs after a recent episode of myocardial infarction

+/- radiating to arms/back/jaw;
Nausea & vomiting, sweating, breathlessness

  1. No no dynamic rise above the 99th percentile for cardiac troponin
  2. No ST elevation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Aetiology of unstable angina

A

Non-occlusive thrombus narrowing coronary artery
(Less common -> vasospams aka Prinzmetal’s angina)

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

How is a diagnosis of unstable angina confimed?

A

diagnostic imaging, which includes invasive coronary
angiography, functional (stress) testing, or coronary computed tomography angiography.

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

Describe some atypical presentations of ACS

A
  1. epigastric pain
  2. indigestion-like symptoms, 3. isolated dyspnoea,
  3. syncope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In what patient population is an atypical presentation of ACS more common?

A

Older patients, women, and patients with diabetes, chronic kidney disease, or dementia.

Women can also present more commonly with middle/upper back pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Key aspects of unstable angina history

Study These Flashcards
A
  • Whether the patient has experienced this type of pain before
  • SOCRATES
  • If symptoms are intermittent, it is important to ask when the last episode of pain
    occurred
  • Previous investigations for chest pain

Ask the patient about other important points:
* Current medications that may affect treatment of unstable angina:
- Anticoagulants
- Antiplatelet drugs
- Recent use of phosphodiesterase inhibitors (sildenafil, vardenafil, or tadalafil)
* Allergies (ASPIRIN)

17
Q

What to expect in physical examination of unstable angina

Study These Flashcards
A
  • Unremarkable
  • Sympathetic drive - sweaty, pallor, n&v
18
Q

Investigations for ACS

Study These Flashcards
A

Within 10min of contact
- ECG

Within 60min
- High-sensitivity cardiac Troponin (hs-cTn)

  • CXR (after ECG recorded + interpreted i.e. if STEMI, then patient should be referred for PCI immediately, not wait for CXR)

Bloods

  • FBC
    • thrombocytopenia (risk of bleeding -> management of unstable angina increases risk of bleed)
    • anaemia is a 2ndary cause of unstable angina
  • U&Es
    • choice of anticoagulant
    • prevent contrast-induced nephropathy
  • LFTs - bleeding risk before anticoagulation
  • Blood glucose - in diabetics
  • CRP (to rule out other causes e.g. pneumonia)
19
Q

What are other causes of a raised troponin

Study These Flashcards
A

Acute - myocarditis, aortic dissection, or
acute PE
Chronic - CKD and heart failure

20
Q

What imaging would you consider in unstable angina?

Study These Flashcards
A

Echocardiography - assess left ventricular systolic function

Invasive coronary angiography (not that beneficial when compared to nSTEMI or STEMI)

Functional (stress) testing (e.g., stress echocardiography, perfusion/stress cardiac magnetic resonance
imaging, myocardial perfusion scan) if no ischaemic changes in ECG + pain-free for several hours

Coronary computed tomography angiography - if no ischaemic changes on ECG and has been pain-free for several hours.[1]

21
Q

What screening is done in asymptomatic population for CAD?

Study These Flashcards
A

None, no evidence

22
Q

When to refer patients in the community to hospital?

Study These Flashcards
A
  1. Currently have chest pain
  2. Are currently pain-free, but have had chest pain within the last 12 hours and a resting 12-lead ECG
    is abnormal or unavailable
  3. Have had a recent ACS (confirmed or suspected) and develop further chest pain.
23
Q

Key considerations in management of UA/NSTEMI (NICE guidelines)

Study These Flashcards
A

Initial drug therapy
- Antiplatelet: aspirin 300mg loading dose + 75mg OD
- Antithrombin: fondaparinux (unless immediate pCI)

If low GRACE score (</=3%)
- Consider conservative management
- Dual antiplatelet: ticagrelor + aspirin (if high bleed risk, clopidogrel + aspirin, or just aspirin)
- Consider ischaemia testing

If high GRACE (>3%)
- If unstable: immediate ICA with pCI. If stable, consider within 72hr
- Dual antiplatelet: ticagrelor + aspirin (if high bleed risk or different indication for anticoagulation –> clopidogrel + aspirin)
- Only give prasugrel once PCI intended
- Offer systemic unfractionated heparin in catheter laboratory if having PCI
- Drug-eluting stent if stenting indicated

https://www.nice.org.uk/guidance/ng185/chapter/Recommendations#nstemi-and-unstable-angina-early-management

24
Q

Acute considerations in UA management

Study These Flashcards
A
  1. Dual antiplatelet therapy: aspirin + P2Y12 inhibitor - e.g. ticagrelor
    -consider glyceryl trinitrate
    -consider morphine
    -consider anti-emetic
    - consider anticoagulation
    -consider referral for invasive coronary angiography
    ± revascularisation
  2. manage hyperglycaemia
25
Ongoing - post-stabilisation considerations in UA
1. anti-anginal medication - beta blocker (bisoprolor or carvedilol) or CCB (verapamil) 2. glyceryl trinitrate 3. continue dual antiplatelet therapy -consider ACE inhibitor or angiotensin-II receptor antagonist - heart failure with reduced left ventricular ejection fraction, diabetes, or chronic kidney disease. - consider statin - consider aldosterone antagonist - heart failure with reduced left ventricular ejection fraction (<40%). 4. plus discuss cardiovascular disease risk factor modification
26
Important primary prevention points for ACS
healthy diet, physical activity smoking cessation maintenance of ideal body weight - avoid strenuous exercise until noninvasive risk stratification (using either exercise or pharmacological stress, and echo or nuclear imaging modalities) is performed in the outpatient setting. - blood pressure and diabetes management must be tightly controlled as appropriate.
27
Complications of UA
- Treatment complications - bleeding and thrombocytopenia - Ventricular arrhythmias - Congestive heart failure
28
How to explain unstable angina to patient?
Unstable angina is a medical emergency. It's a severe pain in your chest that happens if your heart is not getting enough oxygen. This is because the blood flow in your coronary arteries is partly blocked (the coronary arteries carry blood of your heart muscle). There are good treatments for unstable angina, but if it happens it's important to go to hospital straight away, as it can lead to a heart attack. Most people get unstable angina because they have coronary artery disease. The coronary arteries carry blood and oxygen to the heart muscle. Coronary artery disease happens when clumps of fat build up on the lining of a coronary artery. Over time, they make the artery narrower. If you have unstable angina, a clump of fat in one of your coronary arteries tears open. A blood clot forms over the tear to try to patch it up and partly blocks the artery. Not enough oxygen gets to your heart. This is what causes the pain.
29
Define NSTEMI
Non-ST-elevation myocardial infarction (NSTEMI) is an acute ischaemic event causing myocyte necrosis.
30
Risk factors for NSTEMI
Modifiable - Smoking - Obesity - Cocaine use - Physical inactivity Non-modifiable - Atherosclerosis (Hx of angina, myocardial infarction, stroke, transient ischaemic attack, peripheral vascular disease) - Age>65yo - Diabetes - FH of CAD - Metabolic syndrome - Depression - Stent thrombosis or restenosis - CKD - Surgical procedures - Sleep apnoea
31
Aetiology of NSTEMI
- transient or near complete occlusion of a coronary artery or acute factor that deprives myocardium of oxygen.
32
Types of MI (4)
Type 1: Traditional MI due to an acute coronary event Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension) Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event Type 4: MI associated with PCI / coronary stunting / CABG
33
Key points in NSTEMI history
- SOCRATES - Typical cardiac chest pain is a retrosternal sensation of pain, pressure, or heaviness radiating to the left arm, both arms, right arm, neck, or jaw, which may be intermittent or persistent - Assoc symptms - RFs Previous invx for chest pain? - DH - Hypersensitivity to aspirin
34
Important signs in physical examination
1. May be normal 2. Excessive sweating (sympathetic drive) 3. New murmur - systolic murmur may be present due to ischaemic mitral regurgitation (poor prognosis) OR mechanical complication e.g. papillary muscle rupture or VSD 4. URGENT - if LVHF, haem unstable or LT arrhythmia --> SENIOR
35
Acute management of NSTEMI
1. Dual antiplatelet: aspirin + P2Y12 inhib (ticagrelor) -consider oxygen -consider glyceryl trinitrate -consider morphine -consider anti-emetic 2. anticoagulation e.g. fondaparinux -consider beta-blocker 3. ACE inhibitor or angiotensin-II receptor antagonist (-sartan) -consider referral for invasive coronary angiography ± revascularisation 4. plus manage hyperglycaemia If unstable --> get senior input for ICA+pCI immediately (UNFRACTIONED HEPARIN)
36
Post-stabilisation management of NSTEMI
1. continue dual antiplatelet therapy 2. start or continue beta-blocker 3. start or continue ACE inhibitor or angiotensin-II receptor antagonist 4. statin - consider aldosterone antagonist - LVEF <40% 5. plus cardiac rehabilitation
37
Secondary prevention: ACS
1. cardiac rehabilitation 2. Advice on * Changes to diet * Reduction of alcohol consumption * Smoking cessation * Weight management * Physical exercise.
38
When should follow-up be arranged for NSTEMI.STEMI
1/2 weeks
39
Management of STEMI
1. MONA +/- antiemetic 2. Coronary reperfusion therapy a. PCI - within 12hr of onset - within 120min from time fibrinolysis could have been given - radial > femoral access - drug-eluting stents used instead of bare metal stents b. Fibrinolysis - offered within 12hrs of onset if PCI not available within 120min - ECG WITHIN 60-90MIN 3. Antiplatelet a. Prior to PCI - No prior anticoagulant: prasugrel - If on AC: clopidogrel b. During PCI - radial access: unfractioned heparin + bailout GPI (e.g. eptifibatide) - bivalirudin + bailout GPI *bailout - not expected to use from outset

Year 5 - GIM (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions