Acute coronary syndromes (ACS) Flashcards

1
Q

What is a typical history of a patient with acute coronary syndrome?

(symptoms)

A
  • Sever crushing, gripping or heavy chest pain lasting longer than 20 minutes
    • Not relieved by 3x GTN sprays at 5 minute intervals
  • Radiates to the left arm, neck or jaw
  • Associated dyspnoea, nausea, fatigue, sweatiness and palpitations in the elderly or diabetics, who can present later with a variety of symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the clinical features of ACS?

(on examination)

A

Can be variable

  • Sympathetic activation: tachycardia, hypertension, pallor, sweatiness
  • Vagal stimulation: bradycardia, vomiting
  • Myocardial impairment: hypotension, narrow pulse pressure, raised JVP, basal crepitations, 3rd heart sound
  • Tissue damage: low grade pyrexia

Later a pericardial rub and peripheral oedema may develop, or pansystolic murmer due to papillary muscle rupture/ventriculo-septal defect

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

What are differential diagnosis of central chest pain from ACS?

(not an objective)

A

Cardiac:

  • Coronary artery spasm
  • Pericarditis/myocarditis
  • Aortic dissection

Non-cardiac:

  • PE
  • Pneumothorax
  • Oesophageal disease
  • Mediastinitis
  • Costochondritis
  • Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does the spectrum of acute coronary syndromes cover?

A

ST-segment elevation myocardial infarction (STEMI)

Non-ST-segment elevation myocardial infarction (non-STEMI)

Unstable angina (UA)

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

What pathology do all acute coronary syndromes share?

A
  • Atheromatous plaque formation in the coronary arteries
  • Fissuring/ulceration of the plaque leading to platelet aggregation
  • Localised thrombosis, vasocontriction and distal thromboembolism
  • Myocardial ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is unstable angina?

A

(aka crescendo angina)

  • Angina occuring at rest, or sudden increased frequency/severity of existing angina
  • Pathologically caused by fissuring of plaques, thus there is a risk of subseuent total vessel occlusion and progression to acute MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the an acute myocardial infarction?

What are the two different types?

A
  • Occurs followinf full arterial occulsion, with different patterns
  • The diagnosis of MI requires elevations in serum cardiac troponin levels, with additional categorisation based on ECG changes:
    • ST elevation = STEMI
    • No ST elevation = NSTEMI (ECG often shows T wave inversion or ST depression)

NSTEMI occurs by developing a complete occlusion of a minor coronary artery or a partial occlusion of a major coronary artery previously affected by atherosclerosis.

STEMI occurs by developing a complete occlusion of a major coronary artery previously affected by atherosclerosis. This causes a full thickness damage of heart muscle.

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

What is the time course of an MI?

(not an objective)

0-12 hours

12-24 hours

24-72 hours

3-10 days

10 days - months

A
  • 0-12 hours: infarct not visible, loss of oxidative enzymes
  • 12-24 hours: infarct pale and blotchy , intercellular oedema
  • 24-72 hours: infarcted area excites acute inflammatory response, with dead area soft and yellow with neutophilic infiltration
  • 3-10 days: organisation of infarcted area by vascular granulation tissue
  • 10 days-several months: collagen deposition, infarct replaced by collagenous scar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does an ECG and serum troponin establish the diagnosis of an ACS?

A

STEMI:

  • ST segment elevation, troponin elevated.
  • Troponin is released at 4-8 hours and peaks at around 24 hours. dectectable for 10 days
  • A release of CK-MB may be an earlier enzyme sign.

NSTEMI:

  • No ST segment elevation, troponin elevated.

Unstable angina:

  • No ST segment elevation, troponin normal.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the management of unstable angina and NSTEMI?

A

(normal A-E)

(asses patient using GRACE score)

BROMANCE

  • Beta-blocker
  • Reassurance
  • Oxygen
  • Morphine
  • Aspirin
  • Nitrates/GTN spray
  • Clopidigrel
  • Enoxaparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the management of STEMI?

A

MONA

  • Morphine
  • Oxygen
  • Nitrates (GTN spray)
  • Aspirin

Percutaneous coronary intervention (PCI) is gold standard treatment if available in a timely fashion: door to ballon in 90 minutes, patient transfer advised if intervention can occur within this window

GRACE score as well

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

What if PCI are contra-indicated for a STEMI?

What are the conta-indications?

A

Thrombolysis is indicated if PCI not available or there are significant co-morbidities

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

What are contra-indications for thrombolysis?

A
  • haemorrhagic stroke at any time
  • ischaemic stroke within 6 months
  • CNS damage or neoplasm
  • recent trauma (3 weeks)
  • GI bleed within last month
  • known bleeding disorder or aortic dissection.
  • Relative contraindications include pregnancy, liver disease, endocarditis, traumatic CPR, oral anticoagulant therapy, refractory hypertension.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the difference in prognosis between STEMI, non-STEMI and unstable angina with respect to mortality and morbidity

A

6 month mortality in the GRACE registry was 13% for NSTEMI and 8% for UA.

1 month mortality in a community STEMI may be as high as 50%, with 50% of these deaths occurring within 2 hours. Early death may be due to arrhythmia. Of those who reach hospital, 80% survive up to 28 days. Prognosis is worse for anterior infarcts than inferior. Morbidity is likely to be related to the level of ischaemia and myocardial damage sustained.

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

What is the GRACE score for ACS?

A

Takes into account age, heart rate, blood pressure, class of CHF, renal function, ST segment changes, troponin elevation and whether there was an arrest at admission to give a mortaily risk at various time intervals (usually one for 6 months)

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

What are the potenital short term complications of ACS?

(think about the symptoms and signs that present)

A

Pulmonary oedema:

  • Left heart fails to pump effectively, with poor systolic emptying leading to dilation: ‘a dilated chamber is a failing chamber’
  • The backpressure in the pulmonary veins is reflected into the capillaries, leading to extravasation of low-protein fluid into the alveolar sacs
  • This is a life-threatening emergency, characterised by extreme breathlessness, with sweating and anxiety
  • There may be a cough producing frothy, blood-stained sputum
  • On examination there are signs of acute heart failure with crackles
  • Arterial PO2 falls, and initially PCO2 falls also due to overbreathing, but later the PCO2 rises due to impaired gas exchange

Cardiogenic shock:

  • Carries a high mortality due to the vicious cycle of hypotension causing further reduction in coronary flow, and thus further pump failure ect.

Thromboembolism:

  • Mural thrombus formation over the inflamed area of endocardium can cause emboli to the brain, kidney, gut, lower limbs ect. causing infection

Venticulo-septal defect:

  • Intracardiac rupture may occur through the septum, causing left-right shunt and development of severe LVF if severe

Ruptured chordae tendiae:

  • Leads to mitral valve incompetence

Rupture of ventricular wall:

  • Usually occurs 2-10 days after the infarct, due to re-organisation and softening of the wall
  • This leads to haemopericardium (blood in pericardial sac), cardiac tamponade (compression of the heart due to fluid in pericardium) and rapid death
17
Q

What are the potential long term complications of ACS?

A

Heart failure:

  • IHD is the most common cause of left heart failure
  • Often leads to right heart failure

Dressler’s syndrome

  • Immune-mediated pericarditis, associated with a high ESR and sometimes anti-myocardial antibodies
  • Rare, develops 2-10 months after infarction
  • Pericarditis gives a sharp chest pain, exacerbated by movement and lying down - relieved by sitting forward
  • May be a pericardial effusion, leading to dyspnoea if it compresses adjacent bronchi

Ventricular aneurysm formation:

  • Gradual distension of the infarcted part of the ventricular wall, which has been replaced by a collagen scar
  • Aneurysmal rupture will lead to cardiac tamponade and death
18
Q

Describe the pathway of care developed within the hospital for STEMI/non-STEMI and unstable angina

A
  • Aspirin 300mg + Clopidogrel 300mg.
  • Sublingual GTN.
  • Oxygen (*if <94%, check NICE guideline).
  • Brief history.
  • IV access and bloods (troponin, FBC, lipids, biochemistry, glucose).
  • 12-lead ECG.
  • IV opiate and antiemetic.
  • Beta-blocker if not contraindicated.
  • GPIIb/IIIa inhibitor if PCI available.

STEMI - “MONA” = Morphine, Oxygen, Nitrates, Aspirin NSTEMI/UA - “BROMANCE” = Beta-blocker, Reassurance, Oxygen, Morphine, Aspirin, Nitrates (GTN), Clopidogrel and Enoxoparin

19
Q

What is the TIMI scoring system?

A

In patients with UA/NSTEMI, the TIMI risk score is a simple prognostication scheme that categorizes a patient’s risk of death and ischemic events and provides a basis for therapeutic decision making.

  • age>65
  • >3 Cornary artery disease risk factors
  • known CAD (stenosis>50%)
  • aspirin use in last 7 days
  • severe angina
  • ST deviation
  • elevated cardiac markers.