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

Acute coronary syndrome and acute myocardial infarction Flashcards

(62 cards)

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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
Proximal occlusion causes greater damage, however what significant problems can arise due to occlusion of distal or branch vessel to critical structures?
Rupture of papillary muscle Acute mitral regurgitation Occlusion of AV nodal artery
26
What are the two methods of opening the infarct related artery?
Primary percutaneous coronary intervention | Fibrinolysis
27
When is primary PCI best?
``` 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
When is thrombolysis best?
Door to balloon time is more than 90 minutes | Less than 3 hour symptom onset
29
Is primary PCI or thrombolysis better?
Primary PCI as reduced mortality, recued risk of recurrent MI or stroke
30
What secondary prevention can be done to reduce risk of recurrent STEMI?
``` General measures - stop smoking, diet, exercise Control co-morbidities Aspirin and clopidogrel (1 year only) Beta blockers Statins ACE inhibitors ```
31
If someone has had a STEMI, what in-patient investigation should be done?
Echo
32
What is sudden cardiac death?
When the atherothrombotic event causes acute myocardial ischaemia and subsequent sufficient electrical disturbance to cause ventricular arrhythmia
33
Treatment of sudden cardiac death (ventricular fibrillation)
Defibrillation
34
What are the two main groups of immediately life threatening complications of acute MI
Mechanical complications | Ventricular arrhythmic complications
35
What are the three main mechanical complications from an MI
Free wall rupture Papillary muscle rupture Rupture of IVS
36
What can be a later complication, which is less threatening but still needs treatment
Left ventricular thrombus
37
Which MI (STEMI or NSTEMI) or more likely to have complications
STEMI
38
Where abouts in the coronary arteries is a free wall rupture most likely to happen?
Left anterior descending
39
What does a free wall rupture lead to?
Haemopericardium | Acute tamponade
40
How may a free wall rupture be contained if it doesn't result in death?
Adhesions | False aneurysm
41
What patients are more likely to have a free wall rupture?
Elderly Females Hypertension Anterior MI
42
Management of free wall rupture
Urgent echo Pericardiocentesis - fluid aspirated from pericardium Drainage with pigtail catheter Immediate surgery - if survives first episode
43
What do most patients who have a septal wall rupture have?
Multi-vessel coronary artery disease
44
What percentage of people survive a papillary muscle rupture
6%
45
Symptoms of papillary muscle rupture and VSD
``` Sudden severe breathlessness Sweating Nausea Vomiting Chest pain ```
46
Signs of papillary muscle rupture and VSD
``` Shock Tachycardia Pulmonary oedema New harsh systolic murmur Right parasternal heave Palpable thrill Elevated JVP ```
47
Investigation for papillary muscle rupture
Echo Cath lab: Right heart cath - oxygen sats with VSD, confirm defect Left heart cath - establish coronary anatomy
48
Management of papillary muscle rupture (although generally only temporary as most die)
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
When does ventricular tachycardia occur
Any time following MI
50
What else can cause acute coronary syndromes (other than atherosclerosis)
Superimposed platelet aggregation and thrombosis | Vasospasm and vasoconstriction
51
What is the time frame for doing percutaneous intervention for a STEMI
within 2 hours ideally
52
How do thrombolytics work
They convert plasminogen into the natural fibrinolytic agent, plasmin. Plasmin lyses clot by breaking down fibrinogen and fibrin, contained within it.
53
What are serine proteases
thrombolysis agents
54
What two categories are thrombolytic agents divided into
1. Fibrin-specific agents (plasminogen to plasmin) | 2. Non-fibrin-specific agents (catalyse systemic fibrinolysis)
55
Examples of fibrin-specific thrombolytic agents
Alteplase Reteplase Tenecteplase
56
Example of non-fibrin-specific agent
streptokinase
57
What can streptokinase cause
Anaphalaxis
58
When should you not use thrombolytics
If patient has had recent bleeding as they could die
59
Other contraindications for thrombolytics
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
In no evidence of STEMI, then ACS medical treatment protocol, which is:
``` Aspirin Ticagrelor/Clopidogrel Fondaparinux/ LMW heparin Intravenous nitrate Analgesia Beta blockers ```
61
Why is ticagrelor slightly more effective than clopidogrel
Clopidogrel is a prodrug so does not metabolise as easily as ticagrelor
62
What analgesia would be appropriate
Morphine / opiates

Cardiovascular - exam style qs (20 decks)

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