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Study Notes - Cardiology > *Ischaemic heart disease (2) - MI > Flashcards

*Ischaemic heart disease (2) - MI Flashcards

(71 cards)

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1
Q

What are the 4 main progressive steps involved in atherogenesis?

A

Normal -> fatty streak -> atheromatous plaque -> atherosclerotic plaque

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2
Q

What is atherosclerosis?

A

A disease of the arteries characterized by the deposition of fatty material on their inner walls causing progressive narrowing and hardening

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3
Q

What is an atheroma?

A

A fatty deposit in the intima

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4
Q

Risk factors for coronary heart disease?

A 
Gender 
Age
Drug abuse
alcohol
Smoking
Stress
Hypertension
High cholesterol
Obesity
Family history
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5
Q

What is chronic stable angina?

A

Chest pain caused by demand led ischaemia due to fixed stenosis which occurs in a predictable manner

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6
Q

What is the immediate treatment of chest pain due to chronic stable angina?

A

Stop
Sit
Spray

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7
Q

What is an acute coronary syndrome in general?

A

Any acute presentation of coronary artery disease
Only a provisional diagnosis that covers a spectrum of conditions
Like stable angina it is caused by ischaemia caused by atherosclerosis

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8
Q

What conditions are classified as acute coronary syndromes?

A

Unstable angina
NSTEMI
STEMI

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9
Q

What are 2 older alternative names for a NSTEMI?

A

Non-Q wave

Sub-endocardial MI

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10
Q

What are 2 older alternative names for a STEMI?

A 
Acute MI (not called this anymore)
Q wave MI
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11
Q

What are the 2 types of MI?

A

ST elevation MI

Non ST elevation MI

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12
Q

Does a fatty streak cause symptoms?

A

No - it is clinically silent

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13
Q

What is the pathogenesis surrounding unstable coronary syndrome?

A

Plaque rupture/ fissure and thrombosis

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14
Q

What can happen to the plaque which bridges between an atherosclerotic plaque and plaque rupture/ fissure and thrombosis?

A

Fibrous cap forms over the fatty core

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15
Q

What type of stenosis does acute coronary syndrome have?

Type of ischaemia?

A 
Dynamic stenosis (subtotal or complete occlusion)
Supply led ischaemia
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16
Q

What are the stages of the platelet cascade?

A

Initiation
Adhesion
Activation

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17
Q

What causes initiation of the platelet cascade?

A

Spontaneous plaque rupture which leads to exposed tissue elements (sub endothelial collagen and Von Willebrand factor)

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18
Q

What are factors affecting plaque rupture/ fissure? (6)

A

Lipid content of plaque
Thickness of fibrous cap
Sudden changes in intraluminal pressure or tone
Bending and twisting of an artery during each heart contraction
Plaque shape
Mechanical injury

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19
Q

What is von willebrand factor?

A

A glycoprotein that plays an important role in stopping the escape of blood from vessels

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20
Q

What is involved in adhesion (platelet cascade)?

A

Platelet recruitment and adhesion at the site of injury forming a monolayer

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21
Q

What is involved in activation (platelet cascade)?

A

Activators are released (ADP and Thromboxane A2)
They bind to surface receptors on platelets
Platelet activation accelerates resulting in platelet aggregation
Activated platelets express adhesion receptors for leukocytes (P-selectin and CD40 ligand) = inflammation
Organised fibrin-rich thrombus forms
(This leads to vascular blockage = acute MI/ stroke)

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22
Q

How is ADP and other activators released during platelet cascade?

A

Through degranulation

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23
Q

How is thromboxane A2 generated?

A

Via cycloxygenase

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24
Q

What adhesion receptors for leukocytes do activated platelets express (2)?

A

P-selectin

CD40 ligand

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25
Difference between unstable angina and NSTEMI?
There is no elevation in cardiac enzymes in unstable angina where as there will be an elevation in cardiac enzymes in an NSTEMI (infarction does not occur- pre-MI which can lead to an MI)
26
Difference between a STEMI and NSTEMI?
There is only partial damage in heart muscle with an NSTEMI compared to full thickness damage to heart muscle with a STEMI - due to this full thickness damage ST elevation occurs on the ECG
27
What are ECG changes that are seen with a STEMI?
ST elevation T wave inversion Pathological Q waves
28
What must be present on an ECG to confirm a STEMI? (either one of 3 of)
Greater than or equal to 1mm ST elevation in 2 adjacent limb leads Greater than or equal to 2mm elevation in at least 2 adjacent precordial leads New onset bundle branch block (usually left bundle branch block)
29
What changes in Q waves indicate a problem?
> 40 ms (1 mm) wide > 2 mm deep > 25% of depth of QRS complex -Seen in leads V1-3
30
What changes in ECG are seen in the first few hours of a STEMI?
ST elevation
31
What changes in ECG are seen in the first day?
pathological Q wave formation and T wave inversion
32
What ECG changes are suggestive of an old MI?
Q waves +/- inverted T waves
33
What leads have pathologies that indicate an inferior MI?
II, III and aVF
34
What leads have pathologies which indicate an anteroseptal MI?
V1-V4
35
What leads have pathologies indicating an anterolateral MI?
I, aVL, V1-V6
36
What is the cardiac enzyme? When does its levels peak post-MI? Where is this also present?
CK (creatinine kinase) 24 hours In skeletal muscle and brain
37
What is the cardiac protein marker? Specific/ not specific? Sensitive/ not sensitive?
Troponin Highly specific Can detect tiny small amounts of myocardial necrosis
38
Is CK or Tn better?
Tn
39
Difference between NSTEMI and UA?
NSTEMI will cause an elevation in cardiac enzymes due to necrosis, which will not be present in UA (as the muscle is not dying)
40
Management of acute coronary syndrome pre-hospital?
Emergency ambulance 300mg aspirin GTN Morphine (e.g. 5-10mg morphine IV) Anti-emetics (e.g. 10mg IV metoclopramide) O2 if required If 45 minutes or longer road time to hospital, pre-hospital thrombolysis
41
Management of STEMI?
``` 300mg aspirin GTN (if BP greater than 90mmhg) Morphine (e.g. 5-10mg morphine IV) Anti-emetics (e.g. 10mg IV metoclopramide) O2 (if hypoxic) 300mg clopidogrel PCI Thrombolysis if angioplasty not available within 90 minutes ```
42
What are the indications for repercussion therapy (thrombolysis or PCI) for acute coronary syndrome?
Chest pain suggestive of acute MI (more than 20 minutes but less than 12 hours) Ecg changes (acute ST elevation/ new left bundle branch block) No contraindicaitons
43
When is thrombolysis performed instead of PCI?
Patients who can't undergo PCI in a timely fashion - diagnosis to angioplasty time is greater than 90 minutes
44
Risk of thrombolysis?
Failure to re-perfuse Haemorrhage Hypersensitivity
45
What are the 4 categories of complications from an MI?
Death Arrhythmic complicaitons Structural complications Functional complications
46
Arrhythmic complications from a MI?
Ventricular fibrillation
47
Structural complications from an MI?
``` Cardiac rupture Ventricular septal defect Mitral valve regurgitation Left ventricular aneurysm Mural thrombus +/- systemic emboli Inflammation Acute pericarditis Dressler's syndrome ```
48
What are the functional complications of an MI?
Acute ventricular failure (left, right, both) Chronic cardiac failure Cardiogenic shock
49
What classification system can be used to determine in-hospital mortality post-MI?
Killip Classification
50
Killip classification?
``` I = no signs of heart failure (6%) II = crepitations less than 50% of lung fields (17%) III = crepitations greater than 50% of lung fields (38%) IV = cardiogenic shock (81%) ```
51
Routine observations post-MI?
``` Cardiac monitor - rhythm? How does the patient feel? Pulse and blood pressure Heart sounds especially added sounds Murmurs especially new murmurs pulmonary crepitations Fluid balance especially uric output ```
52
What is extremely important to remember about the ECG of a patient with an NSTEMI?
It may be normal
53
What are the different isotopes of troponin present in the body and where are these present?
Troponin C = heart and skeletal muscle Troponin I = cardiac specific Troponin T = cardiac specific
54
What are the preferred isoforms of troponin used as a biomarker?
TnT or TnI (high cardiac specificity)
55
What happens to the TnT or TnI levels over time?
Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days
56
What other conditions can cause an elevation in TnT levels?
``` CCF Hypertensive crisis Renal failure PE Sepsis Stroke/ TIA Pericarditis/ myocarditis Post arrhythmia ```
57
How many different classifications of MI are there according to the new clinical classification of MI?
6 (1, 2, 3, 4a, 4b, 5)
58
What is a class 1 MI?
Spontaneous MI related to ischaemia due to a primary coronary event, such as plaque erosion and/or rupture, fissuring or dissection
59
What is a class 2 MI?
MI secondary to ischaemia due to an imbalance of O2 supply and demand, as from coronary spasm or embolic, anaemia, arrhythmias, hypertension or hypotension
60
What is a class 3 MI?
Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggesting ischaemia with new ST-segment elevation, ew left bundle branch block, or pathological or angiographic evidence of fresh coronary thrombus - in the absence of reliable biomarker findings
61
What is a class 4a MI?
MI associated with PCI
62
What is a class 4b MI?
MI associated with documented in-stent thrombosis
63
What is a class 5 MI?
MI associated with CABG surgery
64
Treatment of NSTEMI?
Long term aspirin Clopidogrel therapy (continued for 3 months) Patients should receive coronary angioplasty within 72 hours of admission
65
How should patients with STEMI treated with thrombolysis be further treated?
Early coronary angiography and revasculirisation
66
What are the 4 phases of cardiac rehabilitation?
Phase 1 = in-patietn 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
67
What is the aim of blood pressure post MI?
Less than 140/85mmHg unless diabetic, renal disease or target organ damage = less than 130/80 mmHg
68
4 examples of thrombolytic drugs?
Streptokinase Altepase Reteplase Tenectaplase
69
Apart from MONA-C, how is an NSTEMI treated?
Low weight heparin or fondaparinux given | Angiography within 72 hours to determine best next steps e.g. PCI, CABG
70
Management of UA once in hospital?
Aspirin and other anti-platlet agent e.g. clopidogrel Low weight heparin or factor Xa inhibitor e.g. fondaparinux Opiates and anti-emetics May need IV nitrates for pain Secondary prevention with statin, ACEI and beta blocker If high risk of reoccurrence, revascularisaiton
71
Medicaitons after an MI?
``` 75mg aspirin OD for life Additional anti-playlet agent for over 1 year e.g. clopidogrel Statins ACEI Beta blocker ```

Study Notes - Cardiology (25 decks)

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