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Cardiovascular - exam style qs > Acute coronary syndrome and acute myocardial infarction > Flashcards

Acute coronary syndrome and acute myocardial infarction Flashcards

1
Q

What is the pathology of an acute coronary syndrome

A

Spontaneous plaque rupture
Local thrombosis
Occlusion

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2
Q

What are the four types of acute coronary syndrome

A

Unstable angina
NSTEMI
STEMI
Sudden cardiac death

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3
Q

Why do plaques rupture?

A

Inflammation and stress

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4
Q

Important differentiation between angina and acute coronary syndromes

A

Symptoms at rest in ACS

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5
Q

Characteristics of pain

A

Site: retrosternal
Character: tight band, pressure, heaviness
Radiation to neck, jaw, down arms
Aggravation with exertion, emotional stress
GTN or physical rest DOES NOT relieve

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6
Q

Non-modifiable risk factors

A

Age, gender, creed, family history, genetics

Previous angina, cardiac events or interventions

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7
Q

Modifiable risk factors

A 
Smoking
Diabetes mellitus
Hyperlipidaemia
Hypertension
Lifestyle - exercise and diet
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8
Q

What is unstable angina pectoris (UAP)

A

Angina on effort, but of progressive increasing frequency and severity, often provoked by less exertion and/or then at rest

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9
Q

What is NSTEMI

A

Non ST elevated myocardial infarction

often starting with myocardial ischaemic symptoms at rest

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10
Q

Findings in examination for UAP or NSTEMI

A

Patient may look very unwell or completely fine

Often no specific features

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11
Q

What would an ECG show for UAP and NSTEMI

A

Commonly ST-segment depression
T-wave inversion
Transient ST elevation

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12
Q

Why are serial ECGs essential in UAP and NSTEMI

A

To detect delayed changes

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13
Q

Who may present atypically or have a silent ACS due to reduced pain sensation

A

The elderly, diabetics or women

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14
Q

Typical symptoms of UAP and NSTEMI

A

breathlessness (may have signs of heart failure)
Nausea and vomiting
Epigastric pain

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15
Q

What cardiac biomarker is helpful in diagnosis and suggests high risk of adverse events

A

Cardiac troponin

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16
Q

After ABCDE when UAP/NSTEMI patient initially comes in, what is the next approach in terms of treatment (MONA)

A

Morphine
Oxygen
Nitroglycerine (GTN spray or tablet)
Aspirin 300mg orally

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17
Q

What anti-platelet therapy should the UAP/NSTEMI patient now receive?

A

Both aspirin and a ADP receptor blocker

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18
Q

Give 2 examples of an ADP receptor blocker (anti-platelet)

A

Clopidogrel
Ticagrelor
Prasugrel

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19
Q

What dosage of Clopidogrel

A

Bolus 300mg and 75mg daily

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20
Q

How long should patient be on dual anti-platelet therapy following ACS event

A

1 year

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21
Q

What anti-thrombotic therapy for UAP/NSTEMI patient to try and thrombolyse the clot

A

Low weight molecular heparin

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22
Q

What other medical therapy may you consider for patient as prevention measures

A

Beta blockers
Statins
ACE inhibitors

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23
Q

If you can’t control the unstable angina or NSTEMI with medication or high risk patient, what further treatment would you consider

A

Coronary angiography and revascularisation by PCI

CABG

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24
Q

What is STEMI

A

ST elevated myocardial infarction caused by complete/more complete thrombotic occlusion of coronary lumen

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25
Q

Proximal occlusion causes greater damage, however what significant problems can arise due to occlusion of distal or branch vessel to critical structures?

A

Rupture of papillary muscle
Acute mitral regurgitation
Occlusion of AV nodal artery

26
Q

What are the two methods of opening the infarct related artery?

A

Primary percutaneous coronary intervention

Fibrinolysis

27
Q

When is primary PCI best?

A 
If door to balloon time is under 90 minutes
If greater than 3 hour symptom onset
Cardiogenic shock, HF
High bleeding risk
Diagnosis uncertain
28
Q

When is thrombolysis best?

A

Door to balloon time is more than 90 minutes

Less than 3 hour symptom onset

29
Q

Is primary PCI or thrombolysis better?

A

Primary PCI as reduced mortality, recued risk of recurrent MI or stroke

30
Q

What secondary prevention can be done to reduce risk of recurrent STEMI?

A 
General measures - stop smoking, diet, exercise
Control co-morbidities
Aspirin and clopidogrel (1 year only)
Beta blockers
Statins
ACE inhibitors
31
Q

If someone has had a STEMI, what in-patient investigation should be done?

A

Echo

32
Q

What is sudden cardiac death?

A

When the atherothrombotic event causes acute myocardial ischaemia and subsequent sufficient electrical disturbance to cause ventricular arrhythmia

33
Q

Treatment of sudden cardiac death (ventricular fibrillation)

A

Defibrillation

34
Q

What are the two main groups of immediately life threatening complications of acute MI

A

Mechanical complications

Ventricular arrhythmic complications

35
Q

What are the three main mechanical complications from an MI

A

Free wall rupture
Papillary muscle rupture
Rupture of IVS

36
Q

What can be a later complication, which is less threatening but still needs treatment

A

Left ventricular thrombus

37
Q

Which MI (STEMI or NSTEMI) or more likely to have complications

A

STEMI

38
Q

Where abouts in the coronary arteries is a free wall rupture most likely to happen?

A

Left anterior descending

39
Q

What does a free wall rupture lead to?

A

Haemopericardium

Acute tamponade

40
Q

How may a free wall rupture be contained if it doesn’t result in death?

A

Adhesions

False aneurysm

41
Q

What patients are more likely to have a free wall rupture?

A

Elderly
Females
Hypertension
Anterior MI

42
Q

Management of free wall rupture

A

Urgent echo
Pericardiocentesis - fluid aspirated from pericardium
Drainage with pigtail catheter
Immediate surgery - if survives first episode

43
Q

What do most patients who have a septal wall rupture have?

A

Multi-vessel coronary artery disease

44
Q

What percentage of people survive a papillary muscle rupture

A

6%

45
Q

Symptoms of papillary muscle rupture and VSD

A 
Sudden severe breathlessness
Sweating 
Nausea 
Vomiting
Chest pain
46
Q

Signs of papillary muscle rupture and VSD

A 
Shock
Tachycardia
Pulmonary oedema
New harsh systolic murmur
Right parasternal heave
Palpable thrill
Elevated JVP
47
Q

Investigation for papillary muscle rupture

A

Echo
Cath lab:
Right heart cath - oxygen sats with VSD, confirm defect
Left heart cath - establish coronary anatomy

48
Q

Management of papillary muscle rupture (although generally only temporary as most die)

A

IV nitrates if systolic blood pressure > 90mmHg
Inotropes if SBP < 90mmHg
IABP (balloon pump)
Cardiac surgeons - mitral valve replaced, VSD repair, coronary artery bypass if needed

49
Q

When does ventricular tachycardia occur

A

Any time following MI

50
Q

What else can cause acute coronary syndromes (other than atherosclerosis)

A

Superimposed platelet aggregation and thrombosis

Vasospasm and vasoconstriction

51
Q

What is the time frame for doing percutaneous intervention for a STEMI

A

within 2 hours ideally

52
Q

How do thrombolytics work

A

They convert plasminogen into the natural fibrinolytic agent, plasmin.
Plasmin lyses clot by breaking down fibrinogen and fibrin, contained within it.

53
Q

What are serine proteases

A

thrombolysis agents

54
Q

What two categories are thrombolytic agents divided into

A
  1. Fibrin-specific agents (plasminogen to plasmin)

2. Non-fibrin-specific agents (catalyse systemic fibrinolysis)

55
Q

Examples of fibrin-specific thrombolytic agents

A

Alteplase
Reteplase
Tenecteplase

56
Q

Example of non-fibrin-specific agent

A

streptokinase

57
Q

What can streptokinase cause

A

Anaphalaxis

58
Q

When should you not use thrombolytics

A

If patient has had recent bleeding as they could die

59
Q

Other contraindications for thrombolytics

A

Prior intracranial haemorrhage
Known structural cerebral vascular lesions
Known malignant intracranial neoplasm
Ischaemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis
Significant closed-head trauma or facial trauma within 3 months

60
Q

In no evidence of STEMI, then ACS medical treatment protocol, which is:

A 
Aspirin
Ticagrelor/Clopidogrel
Fondaparinux/ LMW heparin
Intravenous nitrate
Analgesia
Beta blockers
61
Q

Why is ticagrelor slightly more effective than clopidogrel

A

Clopidogrel is a prodrug so does not metabolise as easily as ticagrelor

62
Q

What analgesia would be appropriate

A

Morphine / opiates

Cardiovascular - exam style qs (20 decks)

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