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Acute Coronary Syndromes Flashcards

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1
Q

What is chronic stable angina? (Not an acute coronary syndrome)

A

Fixed stenosis within the coronary artery
Demand lead ischaemia - ischaemia only comes on when demand is on the heart
This makes it predictable
Safe symptoms

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2
Q

How to relieve symptoms of chronic stable angina? (Not an acute coronary syndrome)

A

Ask patients to stop and sit down = reduce work rate of heart
Take GTN spray - decreases blood pressure, reduces afterload on the heart, may cause coronary vasodilation to bring about sensation to chest pain

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3
Q

How can cardiac chest pain be described?

A

Heavy feeling
Weight on chest
Pressure, tightness

Usually in centre of chest and radiating to jaw and arms

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4
Q

What is an acute coronary syndrome?

A

Any acute presentation of coronary artery disease
Only a provision of diagnosis that covers a spectrum of conditions

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5
Q

Why are the Acute coronary syndromes?

A

Unstable angina > acute non-STEMI (ST elevation MI), non-Q wave, sub-endocardial MI > STEMI, AMI, Q wave MI

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6
Q

What is the pathogenic trigger for coronary syndromes

A

Atherosclerotic plaque develops until spontaneous plaque rupture/fissure and thrombosis and acute occlusion of a vessel

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7
Q

What is unstable angina/MI?

A

Dynamic stenosis (subtotal or complete occlusion)
It is supply led ischaemia
It is very unpredictable (can happen at rest)
Dangerous

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8
Q

What causes plaque rupture?

A

Cause still debatable but:
Lipid content and thickness - Young fatty plaques more at risk of rupturing
Sudden changes in pressure/tone or bending in vessel
Plaque shape
Mechanical injury

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9
Q

How is a blood clot formed?

A

Damage to vessel wall or spontaneous plaque rupture - sub-endothelial tissue to blood
Platelet = initiator
Platelet forms a monolayer over the site of vascular injury (recruitment and adhesion of platelets at injury)
Monolayer develops and leads to adhesion of circulating platelets

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10
Q

How is left sided heart failure caused? (This is associated with mortality)

A

Patents that survive MI of left coronary artery-
Muscle in left ventricle damaged and is replaced with scar tissue
Volume in left ventricular cavity increases and heart function decreases as volume decreases
Loss of muscle function

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11
Q

What is the first step in diagnosing an ST elevation MI (highest risk ACS)?

A

History:
Severe crushing central chest pain (similar to angina if they previously had it but is more severe and prolonged)
Radiating to jaw and arms (especially left)
Not relieved by GTN
Sweating nausea and sometimes vomiting

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12
Q

Differentiation of angina vs acute MI

A

Angina:
Lasts 10 mins
Occurs on exertion
Severity: usual pain
GTN:relief
Usually no associated symptoms

MI:
Lasts 30+mins
Occurs at rest
Severe pain
GTN: no effect
Sweating, nausea, vomiting associated symptoms

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13
Q

What is the next step in diagnosing an ST elevation MI?

A

An ECG
Looking for:
ST elevation
- >1mm ST elevation in 2 adjacent limb leads
-> 2mm ST elevation in at least 2 contiguous pericardial leads
- new onset bundle branch block
T wave inversion
Q waves

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14
Q

How to tel the difference from an acute MI (happening now) to an “old MI”

A

Acute - ST elevation = first few hours
Old MI - Q waves +/- nerve that T waves

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15
Q

Diagnosis using cardiac enzymes and protein markers

A

Markers may be normal at presentation and we dont have time to wait for results in STEMI
We use protein marker - Tn - troponin
> highly specific for cardiac muscle damage
> can detect tiny amounts of myocardial necrosis

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16
Q

What is the criteria to determine MI

A

A rise and/or fall of a cardiac biomarker values (preferably cardiac troponin) with at least on value above the 99* percentile upper reference limit, and at least ONE of the following:
- Symptoms of ischaemia
- New significant ST-segment T-wave (ST-T) changes or new left bundle branch block
- Development of pathological Q waves in the ECG
- Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
- Identification of an interacoronary thrombus by angiography or autopsy

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17
Q

What is early treatment of ST elevation MI?

A

1st line aspirin and clopidogrel (antiplatelet)

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18
Q

In the presence of ischaemic electrocardiograph if changes or elevation of cardiac troponin, patients with acute coronary syndrome should be treated immediately with what?

A

Aspirin (300mg loading dose) AND ticagrelor (180mg loading dose)

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19
Q

For patients with acute coronary syndrome undergoing percutaneous coronary innervation, what drugs/treatment should be considered?

A

Aspirin and Prasugrel (60 mg loading dose)

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20
Q

For patients with acute coronary syndrome that have greater risks (bleeding) than the benefits (reduction in recurrent atherothrombotic events) when on ticagrelor or prasugrel should be considered for what drugs instead?

A

Aspirin (300mg loading dose) and clopidogrel (300mg loading dose)

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21
Q

What is the central pathway to platelet aggregation and therefore Acute MI, stroke or death?

A

Activation of platelet
Activator released, aggregation, inflammation
Vascular blockage
Acute MI, stroke or death

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22
Q

How should aspirin be taken and why?

A

In tablet form
Starts at a loading dose of 300mg
Patients asked to chew tablet to increase surface area to start immediate absorption

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23
Q

What is a thrombolysis drug?

Study These Flashcards
A

Potent drug that breaks up clot, lysis the thrombus in coronary artery

24
Q

Of how many of 100 patients being treated within the first hour of symptoms with the treatment of thrombolysis will be saved from a fatality? What is the trend as time goes on?

Study These Flashcards
A

6.5
As time increases, the effect of thrombolysis falls away. Come 12 hours after onset of symptoms, clot will not be effected by thrombolysis

25
What are the correlating ECG leads to the anatomical site of an MI?
Inferior - II, III, AVF Anterior - V1-V6 > anteroseptal V1-V4 > anterolateral I, avL, V1-V6
26
When do you give pre-hospital thrombolysis?
When the journey to hospital is too long
27
What are the indications for reperfusion therapy (Giving thrombolysis treatment or PCI)
1. Chest pain suggestive of acute MI 2. ECG changes - acute ST elevation, new left bundle branch block (LBBB) 3. No contraindications
28
Who doesnt get thrombolysis?
People with contraindications When there is fear of harm from use (risks with using thrombolytic therapy): - failure to re-perfuse -haemorrhage - hypersensitivity
29
Is (primary) angioplasty or thrombolysis better?
(Primary) angioplasty has a better outcome in terms of death, ongoing infarction or stroke than thrombolysis However, some areas are too far away for an angioplasty so early thrombolytic reperfusion In more depth: when primary per cutaneous coronary intervention cannot be provided wooing 120 mins of ECG diagnosis, patients with an ST-segment-elevation acute coronary syndrome should receive immediate (prehospital admission) thrombolytic therapy
30
What is early treatment of STEMI?
Analgesia - diamorphine IV (sore condition, morphine very important) - to reduce workload of heart and infarct size Anti-emetic IV Aspirin 300mg and ticagrelor 180mg (as loading doses) GTN - if BP >90mmHg Oxygen - if hypoxic Primary angioplasty Thrombolysis - if angioplasty not available within g 120 mins
31
What are complications of an acute MI?
Death Arrhythmic complications Structural and functional complications
32
What are arrhythmic complications?
Often cause of early death Cause emergence of ventricular fibrillation
33
What does ventricular fibrillation look like on an ECG?
Chaotic and rapid, uncoordinated muscle activity
34
How can ventricular fibrillation STEMI be treated? (As it is lethal)
Defibrillation
35
What are the structural complications of STEMI?
Cardiac rupture Ventricular septal defect Mitral valve regurgitation Left ventricular aneurysm formation - by damaged muscle and scar Mural thrombus +/- systematic emboli Inflammation Post infarct Acute pericarditis Dressers syndrome (autoimmune - rare)
36
What are the functional complications of STEMI? (How heart ventricles/pump are damaged)
Acute ventricular failure (clinically silent - echocardiogram) - left, right or both (biventricular failure) Chronic cardiac failure Cardiogenic shock
37
How to observe patients for the first 24-36 hours
Cardiac monitor - rhythm How does the patient feel? Pulse and blood pressure Heart sounds - especiallly added sounds Murmurs - especially new murmurs Pulmonary crepitations Fluid balance - especially urine output
38
What is a NSTEMI?
An unstable (haemorrhage into plaque and extending out, coronary spasm) coronary syndrome Caused by dynamic narrowing of lumen of arteries Symptoms at rest Unpredictable Potentially dangerous
39
Treatment for NSTEMI?
Aspirin, clopidogrel, ticergralor and prasugrel
40
What causes a NSTEMI?
Spontaneous plaque rupture
41
What is the most important thing t remember about the ECG in acute non ST elevation myocardial infarction?
The ECG may be normal
42
What happens if you detect the bio marker troponin (TnT or TnI) in a blood test?
A myocyte has been damaged (necrosis) Any amount of myocardial ischaemia should be labelled as MI We are looking for a change in troponin and the troponin to be greater than the 99th percentile
43
In the presence of ischaemic electrocardiographic changes or elevation of cardiac troponin, patients with an acute coronary syndrome should be treated immediately with what?
Both aspirin (300mg loading dose) and ticagrelor (180mg loading dose)
44
In the presence of ischaemic electrocadiographic changes or elevation of cardiac markers, patients should be treated immediately with what?
Fondaparinux or low molecular weight heparin
45
For trying to lower the workload of the heart where there is no sign of cardiac shock (absence of bradycardia or hypotension) for patients with acute coronary syndrome, what should you give?
Oral beta blockade (As well as the aspirin + other antiplatelet, heparin or fondaparinux - key pharmacological measures)
46
Who do you consider giving group IIb-IIIa inhibitors to?
For patients who are at high risk of adverse cardiovascular events with NSTEMI Those not adequately pretreated with dual antiplatelet therapy Patients during the time of angioplasty (PCI)
47
When do you give immediate angioplasty?
Patents with no ST elevation who are very high risk - ongoing pain and distress and ongoing ECG changes (dynamic ST changes)
48
What is coronary revascularisation (angioplasty and stunting)?
Guide wire down Coronary artery past blockage Over wire feed balloon Blow up under pressure (stent in balloon) Don’t remove wire Embed stent into vessel wall which plasters down vulnerable plaque Increases blood supply and flow Stasis and clotting less likely Reduces chance of MI Deflate ballon and remove wire
49
What is troponin-itis
Condition leading to the misdiagnosis of acute coronary syndrome based only on a troponin elevation
50
What other conditions can increase troponin levels
CCF Hypertensive crisis Renal failure Pulmonary embolism Sepsis Stroke/TIA (sub arachnoid haemorrhage) Pericarditis/myocarditis Post arrhythmias
51
What is a type 2 MI?
MI secondary to ischaemia due to O2 imbalance of supply and demand. Prognosis generally worse than those with an anther-thrombotic (type I) problem
52
What is causes of a type II MI?
Increase O2 demand: Stained tachycardia Hypertension LVH Hypertrophic cardiomyopathy Valvular disease Decrease O2/blood flow: Anemia Hypoxia, resp failure Bradycardia Hypotension Vasospasm Coronary embolism
53
Typical features of type I Vs type II
Type I: Sudden symptoms Major ECG changes No obvious cause Higher troponin Severe CAD on angiography Type II: Less chest pain Minor ECG changes Tach/low BP/ illness Smaller more static troponins Mild-moderate coronary artery disease
54
What is MINOCA
Myocardial infarction with non obstructive coronary arteries
55
What is non-ischaemic Myocardial injury with necrosis?
Not technically type II but thought as such Occurs in complex atienes with significant medical or surgical issues Seriously unwell either acutely or chronically but without evidence of coronary artery disease
56
Conditions associated with non-ischaemic myocardial injury with necrosis
Cardiac injury not related to myocardial ischaemia -stabbing, ablation, shock from pacemakers -myocarditis, cardio toxic chemotherapy Multifactorial or intermediate myocardial injury -severe sepsis or respiratory failure - Pulmonary empolus, Pulmonary hypertension, cor pulmonale - chronic severe heart failure, chronic renal failure - severe acute neurological diseases e.g stroke, subarachnoid -exercise, burns - stress cardiomyopathy

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