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Yr 4 - ACC > Cardiology: ACS > Flashcards

Cardiology: ACS Flashcards

1
Q

How can ACS be categorised?

A

1) STEMI

2) NSTEMI

3) Unstable angina

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2
Q

What does a new left bundle branch block on an ECG indicate?

A

Always pathological:

1) MI

2) HTN

3) aortic stenosis

4) cardiomyopathy

5) rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia

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3
Q

A new LBBB due to ischaemia is the result of the occlusion of what artery?

A

Proximal left anterior descending (LAD) or left main stem artery.

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4
Q

Why is a new LBBB indicate a worse prognosis in MI?

A

A large amount of myocardium and conductive tissue needs to be affected to cause this ECG appearance and these patients are usually acutely unwell.

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5
Q

What ECG changes may be seen in an MI?

A

1) hyperacute T waves (often the first sign of MI but often only persists for a few minutes)

2) ST elevation

3) T wave inversion

4) pathological Q waves

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6
Q

What is often the first ECG sign of an MI?

A

Hyperacute T waves

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7
Q

When does T wave inversion on an ECG typically appear in an MI?

How long do they last?

A

The T waves typically become inverted within the first 24 hours.

The inversion of the T waves can last for days to months.

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8
Q

When do pathological Q waves on an ECG in an MI typically appear?

How long do they last?

A

Pathological Q waves develop after several hours to days.

This change usually persists indefinitely.

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9
Q

What does the Q wave reflect?

A

Septal depolarisation.

This is usually hidden behind the much more forceful and electrically active ventricular wall depolarisation.

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10
Q

How does an MI lead to the development of Q waves on an ECG?

A

The Q wave reflects septal depolarisation. This is usually hidden behind the much more forceful and electrically active ventricular wall depolarisation.

If the ventricular wall is dead, a ‘window’ is created that allows the septal depolarisation to show up on the surface ECG.

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11
Q

The sequence of changes and signs of ischaemia (the ischaemic cascade) in an MI

A

1) Flow disruption (start of the MI)

2) Hypoperfusion (detectable on sensitive scanning but not particularly clinically relevant)

3) Diastolic dysfunction

4) Systolic dysfunction

5) ECG changes

6) Angina

7) Identification of intracoronary thrombus by angiography or at autopsy

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12
Q

Give some causes of a raised troponin

A

1) MI

2) Tachy/bradyarrhythmias

3) Aortic dissection

4) Severe aortic valve disease

5) Hypertrophic cardiomyopathy

6) Severe respiratory failure

7) Severe anaemia

8) Coronary spasm

9) Heart failure

10) Takotsubo cardiomyopathy

11) Sepsis

12) Renal failure

13) Stroke

14) Subarachnoid haemorrhage

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13
Q

What are the 5 classifications of MI?

A

1) Spontaneous MI

2) MI 2ary to ischaemia

3) MI diagnosed post-mortem

4a) MI related to percutaneous coronary intervention

4b) MI related to stent thrombosis

5) MI related to bypass (CABG) operation

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14
Q

What occur in a spontaneous (type 1) MI?

A

This is your ‘typical’ myocardial infarction.

1) Atherosclerosis originates from damage to the endothelium and a build-up of cholesterol.

2) The inflammatory reaction to atherosclerosis by macrophages causes a plaque of foam cells, lipids, cellular debris and (eventually) calcium to build up with a fibrous cap on top.

3) When this cap cracks, the exposed debris triggers thrombus formation in the confines of the affected coronary artery (which are only typically between 2 and 5mm in diameter)

4) This causes partial or total occlusion of the artery.

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15
Q

What is an MI 2ary to ischaemia (type 2)?

A

A common event in hospitals where patients with stable coronary artery disease +/ previous coronary intervention (PCI or CABG) are unwell and put additional stress on their heart that would not normally be present.

The myocardium can become ischaemic without a plaque rupture event.

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16
Q

What is a type 4a MI?

A

This is related to percutaneous coronary intervention (i.e. caused by an angioplasty procedure blocking a side branch or damaging the main coronary artery causing ischaemia)

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17
Q

What is a type 4b MI?

A

This is related to stent thrombosis.

If patients stop anti-platelets early post-angioplasty or continue to smoke, stents can occlude (this usually results in a STEMI if complete sudden thrombosis or NSTEMI if gradual re-stenosis over time).

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18
Q

Clinical features of ACS?

A

1) chest pain:
- classically on the left side of the chest
- pressure, tightness, or crushing sensation
- may radiate to the left arm or neck

2) dyspnoea

3) N&V:
- due to vagal activation or gastric distension

4) sweating (poor indicator as signifies sympathetic activation)

5) palpitations

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19
Q

In which patients may chest pain not be present in ACS?

A

Diabetics & elderly

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20
Q

What are 3 atypical symptoms that may be seen in ACS?

A

1) epigastric pain

2) fatigue

3) syncope or presyncope

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21
Q

Who may epigastric pain in an MI be seen in?

A

Diabetics, elderly, & women

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22
Q

Who may fatigue in an MI be seen in?

A

Generalised fatigue without chest pain can sometimes be the sole symptom, particularly in older adults.

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23
Q

What may syncope or presyncope indicate in MI?

A

may indicate arrhythmias or severe ischemia affecting cardiac output.

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24
Q

An MI can cause hypotension or hypertension.

What may each indicate?

A

Hypotension: cardiogenic shock

HTN: stress response

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25
MI can cause tachycardia or bradycardia. What type of MI would bradycardia indicate?
inferior myocardial infarction due to vagal activation.
26
What causes a STEMI?
Complete occlusion of an epicardial coronary artery by thrombus causing immediate myocardial death relating to the territory affected.
27
What criteria is required for a STEMI diagnosis
Clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of: 1) 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years 2) 1.5 mm ST elevation in V2-3 in women 3) 1 mm ST elevation in other leads 4) new LBBB (LBBB should be considered new unless there is evidence otherwise)
28
Give the artery affected & ECG leads affected in the following MIs: 1) Anterior 2) Inferior 3) Lateral 4) Posterior 5) Anterolateral
1) Anterior: - left anterior descending artery - V1-V4 2) Inferior: - right coronary artery - II, III, aVF 3) Lateral: - left circumflex artery - I, aVL +/- V5-V6 4) Posterior: - usually left circumflex, also right coronary artery - Tall R waves V1-2 5) Anterolateral: - left anterior descending or left circumflex - V4-6, I, aVL
29
What is the initial management when ACS is suspected?
1) 12 lead ECG 2) Morphine 3) Oxygen; only if low O2 4) Nitrates (e.g. GTN) 5) Aspirin (300mg) and a second rapid-acting antiplatelet such as Ticagrelor or Prasugrel
30
Define a STEMI
ST-segment elevation + elevated biomarkers of myocardial damage
31
Define an NSTEMI
ECG changes but no ST-segment elevation + elevated biomarkers of myocardial damage
32
What is the common management of all patients with ACS?
1) aspirin 300mg 2) O2 (only if sats <94%) 3) morphine: only if in severe pain 4) nitrates: - sublingually or IV - useful if the patient has ongoing chest or HTN - caution if patient hypotensive Then determine whether they meet the ECG criteria for STEMI.
33
Is morphine given routinely in ACS?
No, only in severe pain. Evidence suggests that giving IV morphine routinely may be associated with adverse outcomes
34
Once a STEMI has been confirmed, what is the next step?
Assess elegibility for coronary reperfusion therapy.
35
What are the 2 types of coronary reperfusion therapy?
1) primary coronary intervention (PCI) 2) thromboylsis
36
Who should PCI be offered to in STEMI patients?
1) if the presentation is within 12 hours of onset of symptoms AND 2) PCI can be delivered within 120 minutes of the time when thrombolysis could have been given Also, if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered.
37
If patients with STEMI present after 12 hours but still have evidence of ongoing ischaemia, can they be considered for PCI?
Yes
38
Who should thrombolyis be offered to in patients having a STEMI?
Should be offered within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120 minutes.
39
If the patient's ECG taken 90 minutes after thrombolysis failed to show resolution of the ST elevation, what is next step?
Transfer for PCI.
40
What should all STEMI patients be given prior to PCI?
Dual antiplatelet therapy i.e. aspirin + another drug
41
How is the 2nd antiplatelet drug given prior to PCI determined?
Is the patient taking an oral anticoagulant?
42
If the patient is taking an oral anticoagulant, what is the 2nd antiplatelet given prior to PCI?
Clopidogrel
43
If the patient is NOT taking an oral anticoagulant, what is the 2nd antiplatelet given prior to PCI?
Prasugrel
44
What is the site of choice in PCI?
Radial artery
45
What drug therapy is required DURING PCI in STEMI patients?
Patients undergoing PCI with radial access: - unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) Patients undergoing PCI with femoral access: - bivalirudin with bailout GPI
46
What do thrombolysis involve?
Fibrinolytic drugs that: 1) activate plasminogen to form plasmin 2) this degrades fibrin and helps break up thrombi
47
Give 3 examples of thrombolytic drugs
1) alteplase 2) tenecteplase 3) streptokinase
48
What are some contraindications to thrombolysis?
1) active internal bleeding 2) recent haemorrhage, trauma or surgery (including dental extraction) 3) coagulation and bleeding disorders 4) intracranial neoplasm 5) stroke < 3 months 6) aortic dissection 7) recent head injury 8) severe HTN
49
What are 3 indications for thrombolysis?
1) STEMI 2) ischaemic stroke (criteria must be met) 3) massive PE with haemodynamic instability
50
Side effects of thrombolysis?
1) haemorrhage 2) hypotension (more common with streptokinase) 3) allergic reactions (may occur with streptokinase)
51
What ECG changes does a posterior MI cause?
A posterior MI causes ST depression not elevation on a 12-lead ECG.
52
What should all STEMI patients undergoing thrombolysis be given?
Antithrombin drug e.g. fondaparinux, UH
53
Which type of MI is associated with worse long-term outcomes?
NSTEMIs
54
Which type of MI is associated with a high risk of death in the short-term?
STEMI
55
What does a diagnosis of an NSTEMI involve?
1) Clinical assessment 2) Troponin 3) ECG
56
In patients diagnosed with an NSTEMI, what further treatment should they be given?
Antithrombin treatment: - fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately - if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given (regardless of whether the patient has had fondaparinux or not)
57
What is the decision about angiography in NSTEMI based on?
GRACE score
58
Which NSTEMI patients should be considered for angiography?
Unstable patients are considered for immediate angiography.
59
What does the GRACE score predict?
Gives the 6 month probability of death after having an NSTEMI.
60
What GRACE score indicates a low risk of death after an NSTEMI?
3% or less
61
What GRACE score indicates a medium to high risk of death after an NSTEMI?
>3%
62
What GRACE score indicates the need for consideration for early angiography with PCI (within 72 hours)?
Patients at medium or high risk (>3%)
63
How is the type of antithrombin treatment given in NSTEMI decided?
1) patients who are not at a high risk of bleeding and who are not having angiography immediately --> fondaparinux 2) if immediate angiography is planned or a patients creatinine is > 265 µmol/L --> unfractionated heparin
64
What are the 3 categories of NSTEMIangina patients that should have coronary angiography?
1) immediate: patient who are clinically unstable (e.g. hypotensive) 2) within 72 hours: patients with a GRACE score > 3% i.e. those at immediate, high or highest risk 3) considered for patients is ischaemia is subsequently experienced after admission
65
What further drug therapy is indicated in patients with NSTEMI/unstable angina prior to 1ary coronary invention?
1) UH: should be given regardless of whether the patient has had fondaparinux or not 2) further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) prior to PCI - if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor - if taking an oral anticoagulant: clopidogrel
66
What further drug therapy is indicated for conservative management for patients with NSTEMI
Further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) 1) if the patient is not at a high-risk of bleeding: ticagrelor 2) if the patient is at a high-risk of bleeding: clopidogrel
67
What defines unstable angina?
Defined by the absence of biochemical evidence of myocardial damage. It is characterised by specific clinical findings of: 1) prolonged (>20 minutes) angina at rest 2) new onset of severe angina 3) angina that is increasing in frequency, longer in duration, or lower in threshold 4) angina that occurs after a recent episode of myocardial infarction
68
Management of unstable angina?
Same as NSTEMI
69
How can LBBB be seen on an ECG?
There is a 'W' in V1 and a 'M' in V6 ('WILLIAM')
70
How can RBBB be seen on an ECG?
There is a 'M' in V1 and a 'W' in V6 ('MARROW')
71
When is UH indicated in NSTEMI?
1) if immediate angiography is planned or 2) a patients creatinine is > 265 µmol/L
72
What would decide whether NSTEMI patient would receive immediate angiography or delayed (within 72 hours)?
If patient is unstable (e.g. hypotensive) --> immediate
73
What are some complications of an MI?
1) Cardiac arrest 2) Cardiogenic shock 3) Chronic HF 4) Tachyarrhythmias 5) Bradyarrythmias 6) Pericarditis 7) Left ventricular aneurysm 8) Left ventricular free wall rupture 9) Ventricular septal defect 10) Acute mitral regurgitation
74
What is the most common cause of death following an MI?
Ventricular fibrillation resulting in cardiac arrest.
75
How can an MI result in cardiogenic shock?
If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock.
76
What 2 medications have been shown to improve the long-term prognosis of patients with chronic heart failure?
1) ACEi 2) Beta blockers N.B. Loop diuretics such as furosemide will decrease fluid overload but do NOT improve prognosis.
77
Bradyarrhythmias can occur post-MI. AV block is more common after what type of MI?
Inferior MI
78
Pericarditis in the first 48 hours is common following what type of MI?
Transmural
79
Features of pericarditis post-MI?
- pain worse on lying flat - pericardial rub - pericardial effusion may be demonstrated with an echocardiogram.
80
What is Dressler's syndrome?
Dressler's syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers.
81
How does Dressler's syndrome present?
- fever - pleuritic pain - pericardial effusion - raised ESR
82
Management of Dressler's syndrome?
NSAIDs
83
How can an MI lead to LV aneurysm?
The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation.
84
What is LV aneurysm post-MI typically associated with?
1) persistent ST elevation 2) LV failure
85
What does LV aneurysm post-MI increase the risks of?
Thrombus may form within the aneurysm increasing the risk of stroke. Patients are anticoagulated.
86
When does LV free wall rupture typically occur post-MI?
1-2 weeks after
87
How do patients with LV free wall rupture post-MI typically present?
Acute HF 2ary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds.
88
Management of LV free wall rupture?
Urgent pericardiocentesis and thoracotomy are required.
89
Features of ventricular septal defect post-MI?
Acute heart failure associated with a pan-systolic murmur. N.B. acute mitral regurgitation presents in a similar fashion --> get an echo!
90
Acute mitral regurgitation post-MI is more typical with what type of MI?
Infero-posterior infarction.
91
What causes acute mitral regurgitation post-MI?
Ischaemia or rupture of the papillary muscle.
92
Fetures of acute mitral regurg post-MI?
1) Acute hypotension 2) pulmonary oedema may occur 3) early-to-mid systolic murmur is typically heard.
93

Yr 4 - ACC (73 decks)

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