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1st year systems ADAM > Acute Coronary Syndromes and Acute myocardial Infarction - Presentation And Investigation > Flashcards

Acute Coronary Syndromes and Acute myocardial Infarction - Presentation And Investigation Flashcards

1
Q

What are the different incidences of caridac chest pain?

New excertional angina?

Unstable angina?

Acute MI?

Sudden Cardiac Death?

A

New exertional angina - 52%

Unstable angina - 13%

Acute MI - 22%

Sudden cardiac death - 13%

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2
Q

What is Stable Angina defined as?

A

Myocardial blood flow does not meet demand - ischaemia

Central chest tightness, often radiation to neck and/ or arms.

Aggravated by exertion & stress.

Relief by stopping activity & rapid improvement with sublingual nitrate.

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3
Q

What are the different acute coronary syndromes?

A

Unstable angina

NSTEMI- Non-ST-segment elevation MI

STEMI

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4
Q

How does atherothrombosis formation (the pathogenesis of all acute coronary syndromes) occur?

A

Plaque disruption

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5
Q

Why do plaques rupture?

A

Inflammation and sheer stress

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6
Q

What is the main difference between acute coronary syndromes and ACS?

A

ACS symptoms will almost always give symptoms at rest in contrast to stable angina which is only on exertion.

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7
Q

What are the non-modifiable risk factors for Acute Coronary Syndromes?

A

Age, gender, creed, family history & genetic factors.

Previous angina, cardiac events or interventions.

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8
Q

What are the modifiable risk factors for Acute Coronary Syndromes?

A

Smoking

Diabetes mellitus

Hyperlipidaemia

Hypertension

Lifestyle- exercise & diet

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9
Q

What is a typical history of unstable angina Pectoris (UAP)?

A

Angina on effort

Progressive increasing severity and frequency

Often provoked by less exertion and/or then at rest

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10
Q

What is a typical history for those with NSTEMI?

A

More often start with myocardial ischaemic symptoms occurring at rest.

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11
Q

What is the pain like in acute coronary syndromes?

A

Site - retrosternal

Character - often tight band/pressure/heaviness

Radiation - neck and/or into jaw, down arms

Aggravating factors - with exertion, emotional stress

Relieving factors: relieving factors e.g. incomplete improvement with GTN, or physical rest; and/or ongoing

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12
Q

What must you ensure to check for on examination for unstable angina and NSTEMI?

A

HR, BP

Listen for murmurs, crackles in chest

May look very unwell

May look completely fine

Often no specific features to find

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13
Q

What are the possible investigations for unstable angina and NSTEMI?

A

Electrocardiogram and Biomarkers

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14
Q

What are common results of ECG in UAP and NSTEMI?

A

Often normal ECG results

Commonly ST-segment depression, transient ST-segment elevation and/or T-wave inversion

More often in UAP changes resolve after pain, and in NSTEMI they tend to persist (but not always);

serial ECGs to detect delayed changes essential

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15
Q

Why is the difference in infarction between STEMI and NSTEMI?

A

STEMI - transmural

NSTEMI - sub endocardial infarct

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16
Q

How do you differentiate between NSTEMI and unstable angina?

A

Biomarkers - troponin and CKMB

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17
Q

Here is why there is a rise in ST segment in STEMI

A

Rise in ST segment because:

Infarcted tissue loses the ability to maintain resting potential of -90mv. Sodium potassium pumps no longer work, so it is partially depolarised. Normally true baseline of an ECG is zero because there is no difference in voltage. However the positve vector of depolarisation travels away from the electrode - negative deflection of baseline – so it shifts lower. ST segment now appears elevated because the ST segment is where there is complete depolarisation – so the ST segment is on the true baseline. In comparison to original baseline, ST segment is higher up.

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18
Q

Here is why there is ST depression in NSTEMI

A

NSTEMI – depolarisation vector travels towards the detector, shift of baseline upwards. ST segment refers to the point where there is complete depolarisation. ST segment now appears lower. ST segment returns to normal because of fibrosis. Fibrotic tissue doesn’t have the ionic leakage of necrotic tissue.

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19
Q

When is there likely going to be an atypical ACS presentation?

A

In women; the elderly or diabetics, influenced by reduced pain sensation.

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20
Q

What are the symptoms of angina and NSTEMI?

A

Breathlessness alone +/- signs of heart failure

Nausea & vomiting +/- other autonomic symptoms

Epigastric pain +/- recent onset indigestion

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21
Q

What does elevated cTn (cardiac troponin) suggest?

A

High risk of adverse events

Beware, not all troponin elevations are a ACS and caused by atherothrombosis

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22
Q

What does elevation of cardiac troponin indicate?

A

Elevated with compromise of myocyte integrity.

Sensitive and specific marker of cardiac myocyte damage

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23
Q

What do the levels of biomarkers indicate?

A

Characteristic rise and fall of cTn with ischaemic damage

Different pattern for acute myocardial infarction to unstable angina pectoris

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24
Q

What is the immediate treatment for UAP and NSTEMI?

A

First ABCDE approach, then MONA

Morphine (or diamorphine)

Oxygen

Nitroglycerine (GTN spray or tablet)

Aspirin 300 mg orally (crush/chew)

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25
Q

What does antiplatelet therapy for UAP and NSTEMI event consist of?

A

Usually dual anti-platelet therapy (Aspirin & ADP receptor blocker) for one year following ACS event (look at McClays pharmacology treatment of ACS and AMI for further details)

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26
Q

What does antithrombotic therapy for UAP and NSTEMI consist of?

A

Intravenous unfractionated heparin (UFH) or s/c low molecular weight heparin (LMWH)

27
Q

What is other medical therapy for unstable angina and NSTEMI that isn’t anti-platelet therapy or antithrombotic therapy?

A

β-blockers are recommended in ACS in the absence of contraindications (asthma, acute left ventricular dysfunction, impaired AV nodal conduction); target heart rate should be between 50 and 60 bpm.

Statins both acutely & chronically reduce further events.

Angiotensin converting enzyme inhibitors: always if left ventricular dysfunction, controversial if normal function

28
Q

Which UA/NSTEMI patients benefit from invasive strategy? (coronary revascularisation)

A

High risk patients

29
Q

Give examples of invasive strategy/ coronary revascularisation

A

Coronary angiography and revascularisation by PCI

CABG

30
Q

Typical Treatment Path for

Unstable angina & Non-ST elevation MI

Treatment path? (Not really in learning outcomes)

A

Most patients stay in hospital for 2-7 days.

Not all patients will have angiography, and not all who an angio. will need or have revascularisation.

Decisions more difficult in the elderly and/or those with important co-morbidities.

Many not reviewed after hospital discharge, some are for further decision making.

31
Q

What is the result of coronary plaque rupture?

A

More complete, or complete thrombotic occlusion of coronary lumen and infarction of distal myocardium

Proximal occlusion of main artery causes greater damage

32
Q

What can be the occlusion of distal or branch vessel cause?

A

if it supplies a critical structure - significant problems - rupture of papillary muscle, acute mitral regurgitation, occlusion of AV nodal artery – CHB (complete heart block)

33
Q

What are the two forms of treatment for STEMI?

A

Fibrinolysis or primary PCI

34
Q

What is the effect of removing an occlusive thrombus early?

A

nsooner occlusive thrombus is dissolved/removed, and vessel opened, the more myocardium will be salvaged.

Less LV damage results in better survival.

35
Q

Why is PCI better than fibrinolytic therapy?

A

Superiority in terms of all-cause and cardiac mortality, recurrent MI; and, reduced risk of haemorrhagic stroke.

36
Q

When is PCI most effective?

A

If delivered within 120-150 mins of the patient’s call for help (call to balloon time)

If door to balloon time is less than 90 minutes

If it has been over 3 hours of symptom onset

If there is cardiogenic shock, HF

High bleeding risk

If the diagnosis is uncertain

37
Q

When is fibrinolysis the choice of treatment?

A

When PCI cannot be performed

Or when door to balloon (of PCI) is longer than 90 minutes

If the symptoms have been present for less than 3 hours (PCI most effective between 120-150 minutes)

If the difference in time between door to balloon is one or two hours greater than door to needle

38
Q

When is the best time to initiate fibrinolysis?

A

Within 90 minutes of patient calling for help (call to needle) or within 30 minutes of hospital arrival

39
Q

How can call to needle be reduced?

A

Prehospital fibrinolysis

40
Q

What is the benefit of pre-hospital fibrinolysis?

A

Reduces early mortality by 15-20% in comparison to in-hospital fibrinolysis

41
Q

What are the risks of fibrinolytic therapy?

A

Increased risk of bleeding and intra-cranial haemorrhage in some patients

42
Q

Which patients have an increased risk of bleeding and intracranial haemorrhage?

A

Age > 75

Female sex

Previous stroke

Low body weight (F<65 kg, M<70 kg)

SBP > 160 mmHg

INR > 4 (international normalized ratio - tells you how fast the blood clots in patients receiving oral anticoagulant medication)

Chronic kidney disease & elevated creatinine

43
Q

Not really in learning outcomes for this lecture, seen later in James McLay’s lecture

A
44
Q

What investigation would you use for ST elevation myocardial infarction for in-patient investigations?

A

Echocardiography

45
Q

What will echocardiography be used to see when examining a ST elevation myocardial infarction?

A

Size of wall motion and nature of wall motion

Overal contractility

Presence and degree of mitral regurgitation

Presence of mural thrombus

46
Q

What are the most important determinants of MI survival?

A

Age and LV ejection fraction

47
Q

What percentage of sudden cardiac deaths are resuscitated and survive?

A

about 2%

48
Q

What is common in 80% of patients that are resuscitated & survive?

A

In resuscitated patients 80% had VT (ventricular tachcardia – life-threatening arrythmia) or VF (ventricular fibrillation)

49
Q

Why does ACS result in ventricular arrythmia?

A

The atherothrombotic event causes acute myocardial ischaemia and subsequent electrical disturbance

50
Q

Are all Sudden cardiac deaths ACS events?

A

NO

51
Q

What does sudden cardiac death look like on an ECG?

A
52
Q

What is the only effective treatment for VF arrest?

A

Defibrillation

53
Q

How does sudden cardiac arrest differ from a heart attack?

A

Heart attacks occur when there is a blockage in one or more of the coronary arteries, preventing the heart from receiving enough oxygen-rich blood

In contrast, sudden cardiac arrest occurs when the electrical system to the heart malfunctions and suddenly becomes very irregular. The heart beats dangerously fast. The ventricles may flutter or quiver (ventricular fibrillation), and blood is not delivered to the body.

54
Q

What does VF deteriorate into?

A

Asystole (a condition in which the heart ceases to beat.)

55
Q

What is often proven to change the outcome of sudden cardiac death?

A

Bystander CPR

56
Q

What are the mechanical complications of MI?

A

Free wall rupture

Septal Wall Rupture

Papillary Muscle Rupture

57
Q

What are the ventricular arrythmia complications with MI?

A

VF

VT

58
Q

Describe another complication associated with MI than isn’t a mechanical or an arrhythmic complication?

A

LV Thrombus

59
Q

What is surgery for papillary muscle rupture or VSD?

A

Urgent surgery usually indicated.

Mitral valves are usually replaced rather than repaired.

VSD repair with pericardial or synthetic patch

Coronary artery bypass if needed & possible.

If survive acute episode long term prognosis is good

60
Q

How do you diagnose VF from an ECG?

A
  • P-waves and QRS complexes are not present
  • Heart rhythm is highly irregular
  • The heart rate is not defined (without QRS complexes)
61
Q

When is LV thrombus usually found?

A

48 hours after infarction

62
Q

What is treatment for LV thrombus?

A

Anticoagulation for 6/12 with warfarin and repeat echo

63
Q
A

1st year systems ADAM (52 decks)

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