IHD Flashcards

1
Q

Describe stable angina

A

induced by effort, relieved by rest

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2
Q

What type of angina is described by “Occurs at rest or recent onset, increases in severity, high risk of MI”

A

Unstable angina

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3
Q

When does decubitus angina occur?

A

When lying down

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4
Q

Angina is mostly caused by atheroma, what are its other causes?

A
Anaemia
Aortic stenosis (AS)
Tachyarrhymias
Hypertrophic cardiomyopathy (HCM)
Arteritis/small vessel disease (microvascular angina/cardiac syndrome X)
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5
Q

Describe the typical chest pain experienced by a patient with angina

A

Central crushing retrosternal chest pain
Comes on with exertion and relieved upon rest
Radiates to arms and neck
Exacerbated by: cold weather, anger, excitement, heavy meals

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6
Q

Other than chest pain what other symptoms are associated with angina?

A

sweatiness, dyspnoea, faintness and nausea

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7
Q

What are the different causes of chest pain?

A
Angina 
MI
Pericarditis
Acute coronary syndrome 
MSK 
GORD
Pulmonary embolism 
Myocarditis 
Aortic dissection
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8
Q

An ECG in a patient with angina is usually normal, however when a patient is experiencing an acute attack it will show signs of ischaemia. What are these signs?

A

ST depression

T wave inversion

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9
Q

If a patient is suffering asymptomatic pain and has no risk factors for angina, further testing is required. What tests are these?

A

Exercise ECG and functional imaging (coronary angiography

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10
Q

What ECG signs in an exercise test indicate a positive result? A positive test is an indication for further angiography

A

ST depression at low workload

Paradoxical fall in blood pressure with increased work load.

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11
Q

If a patient is unable to do an exercise test what alternative is often undertaken?

A

Drug induced stress test

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12
Q

What secondary preventative measures are taken in patients with angina, to prevent MI, stroke ect.

A

Risk factor modification
Low dose aspirin (75mg daily)
Clopidogrel is an aspirin alternative
Lipid-lowering agents – statins, fibrates

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13
Q

How does aspirin work as an anti-platelet

A

inhibits COX2 and formation of thromboxane A2 (platelet aggregating agent)

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14
Q

Clopidogrel is alternative to aspirin, how does it work?

A

P2Y12 receptor inhibitor

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15
Q

What symptomatic treatment is offered to patients with angina?

A

Sublingual GTN spray for acute attacks
β-blockers – e.g. atenolol, metroprolol.
Calcium channel blockers (calcium antagonists) e.g. diltiazem, amlodipine
Nitrates e.g. isosorbide mononitrate, slow release preparations may be given for prophylaxis

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16
Q

What is a common side effect of GTN spray

A

severe headache

17
Q

What are contraindications to B Blocker usage

A

ASTHMA, COPD, LVF, bradycardia, coronary artery spasm.

18
Q

What is effect of Calcium channel blockers

A

Relaxes the coronary arteries and reduces force of LV contraction, thus reducing oxygen demand.

19
Q

What is a Percutaneous coronary intervention (PCI)?

A

catheter inserted, balloons used to dilate atheromatous areas of arteries. Stents can be placed.

20
Q

When preforming a PCI what drugs should be given to reduce risk of a) clotting b) procedure related ischaemic events?

A

a) clopidogrel (anti-platelet)

b) IV glycoproteins IIb/IIIa inhibtiors (e.g. eptifibatide)

21
Q

What disease does acute coronary syndrome cover?

A

Unstable angina
NSTEMI
STEMI

22
Q

Describe the common pathology to acute coronary syndrome caused by atheroma (main cause)

A

Rupture/ erosion of fibrin rich cap on a coronary artery atheromatous plaque. (Rupture more likely with a lipid rich core)
Formation of a platelet rich clot
Vasoconstriction produced by platelets releasing thromboxane A2 and serotonin

23
Q

How is an unstable angina differentiated from NSTEMI

A

NSTEMI will show rise in Troponin and creatine kinase

24
Q

What are non modifiable risk factors for ACS?

A

Age
Male
FHx of IHD (MI in 1st degree relative <55yrs)

25
Q

Describe the clinical presentation of acute coronary syndrome

A

Acute central chest pain >20mins
Dyspnoea
Palpitations
Pallor, sweatiness

Signs: Pulse may be high or low
BP high or low
4th heart sound

26
Q

What test should be done on a patient experiencing acute coronary syndrome?

A

Bloods- FBC, U&E, glucose, lipids
ECG
Cardiac enzyme test

27
Q

What ECG changes are expected in a patient with acute coronary syndrome?

A

Hyperacute (tall) T waves
ST elevation (if STEMI)
ST depression in NSTEMI/unstable angina
New LBBB (S shape in V1 and V2 , M in V5 and V6 and broad QRS)
Over the next hrs-days = T wave inversion, pathological Q waves

28
Q

What enzymes are measured to assess cardiac damage ?

A

Troponin (T and I) (specific)
Creatine kinase (non specific)
Myoglobin

29
Q

What does MONA(T) stand for with regard to the treatment of acute coronary syndrome

A
Morphine
Oxygen 
Nitrates 
Aspirin 
(T)- if severe ticragelor or clopidogrel
30
Q

Metoclopramide is often given with morphine or diamorphine, what is its purpose?

A

Anti- emetic

31
Q

Anti- anginal therapy is important in the long term management of acute coronary system, what does this include?

A

beta blocker, nitrates, calcium antagonist

32
Q

What is fondaparinux?

A

anti coagulant- factor 10a inhibitor, interferes with thrombus formation at the site or Heparin

33
Q

Describe clinical presentation of an acute stemi

A

Central crushing chest pain, similar to angina
Differs from angina as: occurs at rest, is more severe, lasts up to several hours
Sweating, breathlessness, nausea, vomiting, restlessness
Patient appears pale and grey

34
Q

Diagnostic tests and results for acute STEMI

A

Take brief history to ID risk factors

ECG- will show: Tall, peaked T waves
ST elevation 
After a few hours T waves invert 
Pathological Q waves develop
Will return to normal eventually, although Q waves remain – may take months for T waves to return to upright

Bloods- cardiac enzymes
Xray if there is time

35
Q

Changes are typically confined to leads that are “looking at” the infarcted area and opposite leads show reciprocal change.
What leads would demonstrate an inferior infarct

A

2, 3 and aVF= inferior infarct

36
Q

Changes are typically confined to leads that are “looking at” the infarcted area and opposite leads show reciprocal change.
What leads would demonstrate an anterior infarct?

37
Q

Changes are typically confined to leads that are “looking at” the infarcted area and opposite leads show reciprocal change.
What leads would show a lateral infarct

A

1, 2 and aVL show lateral infarct

38
Q

From hospital admission, how would you manage an acute STEMI

A

1) attach ECG and record
2) Establish IV access, bloods for- FBC,U&E, glucose, lipids, cardiac enzymes
3) Brief assessment: risk factors for CVS disease. Assessment of pulse BP ect. Check for contraindications for PCI or fibrinolysis
4) Aspirin 300mg (unless already given by paramedics)
5) Morphine + metoclopramide IV
6) If STEMI on ECG and PCI available within 120mins—> PCI . If not—> Fibrinolysis, then transfer to PCI centre.

39
Q

When managing an acute STEMI, what should you do to prevent hyperglycaemia (glucose >11mmol/L)?
Hypoxia?
Tachycardia

A

insulin infusion
Oxygen
B blocker