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Heart Attack Flashcards

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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
Which ECG leads show changes in an inferior MI?
Leads II, III and aVF
26
Which ECG leads show changes in an anterior MI (anteroseptal and anterolateral)?
Anterior leads are V1-V6 Anteroseptal leads - V1-V4 Anterolateral leads - I, aVL and V1-V6
27
Main protein marker for MI diagnosis?
Troponin - preferably, TnT or TnI
28
Usefulness of Troponin?
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
How do aspirin and Clopidogrel act on the clotting cascade?
Clopidogrel - blocks receptors for ADP | Aspirin - switch off COX system
30
Acute treatment for patients with ACS?
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
Thrombolysis meaning?
Breaks up clot, restoring blood flow
32
When is thrombolysis most useful?
Best effects within 1-2 hours and can be delivered pre-hospital thrombolysis
33
Indications for reperfusion therapy?
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
Risks of thrombolytic therapy?
Failure to reperfuse Haemorrhage - can lead to disability Hypersensitivy
35
Success rate of thrombolysis?
50%
36
Risks of thrombolysis?
Long-term mortality risk double in patients with failed thrombolysis or acute reocclusion
37
Time till optimal reperfusion for STEMI?
When patients are unlikely to receive angioplasty within 90 mins (40 mins) of diagnosis, they should receive immediate thrombolytic therapy
38
Early treatment of STEMI?
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
Complications of Acute MI?
Death Arrhythmic complications - infarcting cells are potent arrhythmic substances Structural complications Functional complications
40
Common arrhythmic complications and treatment?
Ventricular fibrillation (chaotic, rapid and disorganised ventricular activity and decreased CO) Only treatment if DEFIBRILLATION
41
Types of structural complications?
``` 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
Functional complications of MI?
Ventricular dysfunction leading to acute heart failure or chronic heart failure Cardiogenic shock - despite treatment, pump fails
43
Types of MI in Killip classification of in-hospital mortality?
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
Role of intravascular thrombolysis in an NSTEMI?
Unlike in a STEMI, there is no acute occlusion of the coronary artery as tPA leads to plasmin breaking down the clot
45
Describe the clot in an NSTEMI
Waxing and waning of atherothrombosis - builds and breaks down
46
Comparison of mortality in different ACS, according to ECG changes?
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
Challenge in NSTEMI treatment if unsure of diagnosis?
Identify those patients who would benefit from new therapies but avoid potentially harmful therapies in patients without prognostically significant disease
48
ECG in acute NSTEMI?
ECG MAY BE NORMAL | If ECG changes are present, this is a marker of a bad outcome
49
Other than in MI, when is troponin elevated?
``` CCF Hypertensive crisis Renal failure PE Sepsis Stroke/TIA Pericarditis/myocarditis Post-arrhythmia ```
50
Clinical classification of MI?
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
In the blood coagulation cascade, where do the intrinsic and extrinsic pathways meet?
At factor Xa (target to prevent clotting and so can prevent an NSTEMI from becoming a STEMI)
52
What are the ADP antagonist anti-platelet drugs?
Ticagrelor Clopidrogrel Prasugrel
53
What is a COX inhibitor anti-platelet drug?
Aspirin
54
What are the GP IIb/IIIa inhibitors?
Tirofiban Eptifibatide Abciximab
55
Role of GP IIb/IIIa receptors in platelet activation and aggregation?
Expressed on platelets and allow fibrinogen to aggregate platelets together
56
Role of GP IIb/IIIa inhibitors?
Decrease platelet aggregation and reduce changes of NSTEMI
57
Which patients should undergo early coronary angiography and revacularisation?
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
Process of coronary revascularisation/primary coronary angioplasty/PCI?
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
Types of stents?
Bare metal stents | Drug-eluting stents
60
Clopidogrel use in different scenarios?
``` 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
4 phases of cardiac rehabilitations?
* 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

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