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Clinical > Heart Attack > Flashcards

Heart Attack Flashcards

1
Q

Effect of plaque on blood flow?

A

Narrows luminal space, reducing blood flow and leading to symptoms

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2
Q

What is chronic stable angina?

A

There is FIXED stenosis and DEMAND-LED ischaemia

It is predictable and “safe”

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3
Q

When do cardiac requirements increase?

A

Exercise
After a meal - for digestion
With sympathetic stimulation
In cold weather

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4
Q

Typical cardiac chest pain descriptions?

A

Heavy weight on chest, pressure, tightness, etc

Hand gestures are often made

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5
Q

Acute Coronary Syndrome (ACS) definition?

A

Any ACUTE presentation of coronary artery disease, due to the coronary artery undergoing a rapid decrease in luminal space

This covers a spectrum of conditions, one of which must be diagnosed; essentially, these are unstable angina and MI

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6
Q

What are the Acute Coronary Syndromes?

A

Proceed as follows:
Asymptomatic
Stable angina

And then to the Acute Coronary Syndromes, which are:
Unstable angina
Acute NSTEMI
STEMI

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7
Q

Pathogenesis of ACS?

A 
Normal artery proceeds to:
Fatty streak
Atherosclerotic plaque
Fibrous plaque
Plaque rupture/fissure and thrombosis
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8
Q

In the pathogensis, when does ACS occur?

A

At the point of plaque rupture, unstable angina, MI and sudden cardiac death occur

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9
Q

What is ACS, in the same way as chronic stable angina was described?

A

Dynamic stenosis (subtotal/complete ischaemia) and there is SUPPLY-LED ischaemia

This is unpredictable and dangerous

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10
Q

In the context of a heart attack, what event commonly causes initiation of the platelet cascade?

A

Spontaneous PLAQUE RUPTURE

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11
Q

Factors affecting plaque rupture/fissure?

A

Lipid content of plaque
Thickness of fibrous cap

Sudden changes in intra-luminal P or tone
Plaque shape
Mechanical injury

Newer plaques can be be more prone to rupture than older, calcified plaques

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12
Q

Initiation of platelet cascade events?

A

Vascular damage exposes sub-endothelial amtrix containing collagen and vWF

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13
Q

Describe the adhesion and activation stages of the platelet cascade

A

At the site of injury, platelet recruitment and adhesion forms a monolayer

Adhesion leads to activation - changes in platelet conformation to form pseudopodia, allowing platelets to stick to one another

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14
Q

Release of activators from platelets and their function?

A

ADP and other activators are released via degranulation of the platelets

Thromboxane A2 is generated via COX

All bind to platelet receptors to cause the conformation change of pseudopodia

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15
Q

Amplification of platelets activation?

A

Platelet activation accelerates, resulting in platelet aggregation

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16
Q

What does platelet activation trigger and what does this involve?

A

Activated platelets express adhesion receptors for leucocytes , forming platelet-leukocyte conjugates

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17
Q

End result of clotting cascade?

A

Formation of an organised, fibrin-rich THROMBUS

There is vascular blockage, leading to MI, stroke,death, etc

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18
Q

How can occlusion of LAD lead to heart failure?

A

Tissue downstream infarcts, so there is scarring and a loss of ventricular function leads to dilatation and decreased ventricular blood flow

Left-sided HF results

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19
Q

Symptoms of left-sided HF?

A 
PND
Pink, frothy sputum
Cough
Orthopnea
Exertional-dyspnea
Cyanosis
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20
Q

Typical features of MI chest pain?

A

Severe, crushing, central chest pain that can radiates to jaw and arms, esp. the left

Similar to angina but more severe, prolonged and not relieved by GTN

Assoc. with sweating, nausea and often vomiting

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21
Q

Differentiating angina from an acute MI?

A 
Angina:
Duration - 10 mins
Onset - on exertion
Severity - usual pain
GTN - relief
Assoc. symptoms - usually none
MI:
Duration - 30 mins or longer
Onset - at rest
Severity - more severe
GTN - no effect
Assoc. symptoms - sweating, nausea, vomiting
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22
Q

Difference between STEMI and NSTEMI?

A

STEMI - transmural infarction of myocardium (so entire thickness or myocardium undergoes infarction) usually due to complete clock of a coronary artery

NSTEMI - partial dynamic block to coronary arteries (non-occlusive thrombus)

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23
Q

What changes will be seen on the ECG in STEMI?

A

ST elevation is an early sign and this proceeds to:
T wave inversion
Pathological Q waves

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24
Q

What requirements must ST elevation meet to be considered as due to STEMI?

A

Greater than or equal to 1 mm ST elevation in 2 adjacent limb leads

Greater than or equal to 2 mm ST elevation in at least 2 contiguous (next to each other on the on ECG) precordial leads

New onset left bundle branch block is always pathological and can be a sign of an MI

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25
Q

Which ECG leads show changes in an inferior MI?

A

Leads II, III and aVF

26
Q

Which ECG leads show changes in an anterior MI (anteroseptal and anterolateral)?

A

Anterior leads are V1-V6

Anteroseptal leads - V1-V4
Anterolateral leads - I, aVL and V1-V6

27
Q

Main protein marker for MI diagnosis?

A

Troponin - preferably, TnT or TnI

28
Q

Usefulness of Troponin?

A

Highly specific for cardiac muscle damage and can detect tiny amounts of myocardial necrosis

Clots can break down and embolise to microvasculature causing infarcts downstream; so, even microscopic damage can be detected using Tn

29
Q

How do aspirin and Clopidogrel act on the clotting cascade?

A

Clopidogrel - blocks receptors for ADP

Aspirin - switch off COX system

30
Q

Acute treatment for patients with ACS?

A

Treated immediately with aspirin (300 mg)

In the presence of ischaemic ECG changes or elevation of cardiac markers, patients with an ACS should be treated immediately with combo aspitin (300 mg) + Clopidogrel (300 mg)

31
Q

Thrombolysis meaning?

A

Breaks up clot, restoring blood flow

32
Q

When is thrombolysis most useful?

A

Best effects within 1-2 hours and can be delivered pre-hospital thrombolysis

33
Q

Indications for reperfusion therapy?

A
  1. Chest pain suggestive of acute MI - more than 20 mins, less than 12 hours
  2. ECG changes - acute ST elevation or NEW left bundle branch block (LBBB)
  3. No contraindications
34
Q

Risks of thrombolytic therapy?

A

Failure to reperfuse

Haemorrhage - can lead to disability

Hypersensitivy

35
Q

Success rate of thrombolysis?

A

50%

36
Q

Risks of thrombolysis?

A

Long-term mortality risk double in patients with failed thrombolysis or acute reocclusion

37
Q

Time till optimal reperfusion for STEMI?

A

When patients are unlikely to receive angioplasty within 90 mins (40 mins) of diagnosis, they should receive immediate thrombolytic therapy

38
Q

Early treatment of STEMI?

A

Analgesia - diamorphine iv
Anti-emetic (for nausea) - iv
GTN - if BP is greater than 90 mmHg
Oxygen if hypoxic

Primary angioplasty or thrombolysis (if angioplasty is unavailable within 90 mins)

39
Q

Complications of Acute MI?

A

Death
Arrhythmic complications - infarcting cells are potent arrhythmic substances
Structural complications
Functional complications

40
Q

Common arrhythmic complications and treatment?

A

Ventricular fibrillation (chaotic, rapid and disorganised ventricular activity and decreased CO)

Only treatment if DEFIBRILLATION

41
Q

Types of structural complications?

A 
Cardiac rupture
Ventricular septal defects
Mitral valve regurgitation
Left ventricular aneurysm formation
Mural thrombus +/- systemic emboli
Inflammation
Acute pericarditis
Dressler's syndrome (autoimmune condition causing pain post-MI)
42
Q

Functional complications of MI?

A

Ventricular dysfunction leading to acute heart failure or chronic heart failure

Cardiogenic shock - despite treatment, pump fails

43
Q

Types of MI in Killip classification of in-hospital mortality?

A

I - no signs of heart failure
II - crepitations in less than 50% of lung fields
III - crepitations in greater than 50% of lung fields
IV - cardiogenic shock

Mortality increases with number

44
Q

Role of intravascular thrombolysis in an NSTEMI?

A

Unlike in a STEMI, there is no acute occlusion of the coronary artery as tPA leads to plasmin breaking down the clot

45
Q

Describe the clot in an NSTEMI

A

Waxing and waning of atherothrombosis - builds and breaks down

46
Q

Comparison of mortality in different ACS, according to ECG changes?

A

ST depression has a worse outcome in ACS

STEMI with fibrinolytics has a better outcome

T-wave inversion ACS has an even better outcome

47
Q

Challenge in NSTEMI treatment if unsure of diagnosis?

A

Identify those patients who would benefit from new therapies but avoid potentially harmful therapies in patients without prognostically significant disease

48
Q

ECG in acute NSTEMI?

A

ECG MAY BE NORMAL

If ECG changes are present, this is a marker of a bad outcome

49
Q

Other than in MI, when is troponin elevated?

A 
CCF
Hypertensive crisis
Renal failure
PE
Sepsis
Stroke/TIA
Pericarditis/myocarditis
Post-arrhythmia
50
Q

Clinical classification of MI?

A

1 - Spontaneous MI related to ischaemia due to a primary coronary event, such as plaque erosion and/or rupture, fissuring or dissection

2 - MI secondary to ischaemia due to an imbalance of O2 supply and demand, as from coronary spasm/embolism, anaemia, arrhythmias, hypertension or hypotension

3 - Sudden unexpected cardiac death, inc. cardiac arrest, often with symptoms suggesting ischaemia with new ST-segment elevation; new LBBB; or pathologic/angiographic evidence of fresh coronary thrombus - in the absence of reliable biomarker findings

4a - MI assoc. with PCI

4b - MI assoc. with documented in-stent thrombosis

5 - MI assoc. with CABG surgery

51
Q

In the blood coagulation cascade, where do the intrinsic and extrinsic pathways meet?

A

At factor Xa (target to prevent clotting and so can prevent an NSTEMI from becoming a STEMI)

52
Q

What are the ADP antagonist anti-platelet drugs?

A

Ticagrelor
Clopidrogrel
Prasugrel

53
Q

What is a COX inhibitor anti-platelet drug?

A

Aspirin

54
Q

What are the GP IIb/IIIa inhibitors?

A

Tirofiban
Eptifibatide
Abciximab

55
Q

Role of GP IIb/IIIa receptors in platelet activation and aggregation?

A

Expressed on platelets and allow fibrinogen to aggregate platelets together

56
Q

Role of GP IIb/IIIa inhibitors?

A

Decrease platelet aggregation and reduce changes of NSTEMI

57
Q

Which patients should undergo early coronary angiography and revacularisation?

A

Patients with NSTEMI at medium/high risk (identifiable Tn) of early recurrent CV events should

Patients with STEMI treated with thrombolytic therapy should be considered

58
Q

Process of coronary revascularisation/primary coronary angioplasty/PCI?

A

Balloon catheter with uninflated balloon approaches obstructed area in the artery

When balloon is inflated, it breaks up atherosclerotic plaque

After lumen widened, balloon catheter with deflated balloon is withdrawn

59
Q

Types of stents?

A

Bare metal stents

Drug-eluting stents

60
Q

Clopidogrel use in different scenarios?

A 
Any drug-eluting stent - 1 year
ACS medical treatment - 3 months 
ACS bare metal stent - 3 months 
Elective PCI (bare metal) - 3 months
STEMI and no PCI - 4 weeks
Aspirin intolerant - monotherapy with clopidogrel indefinitely

All are in addition to aspirin

61
Q

4 phases of cardiac rehabilitations?

A
  • Phase 1 in-patient
  • Phase 2 early post discharge period

• Phase 3 structured exercise
programme – usually hospital based

• Phase 4 long term maintenance of
physical activity and lifestyle change – usually community based

Clinical (54 decks)

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