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ESA 2 > CVS 10.1 - Ischaemic Heart Disease > Flashcards

CVS 10.1 - Ischaemic Heart Disease Flashcards

1
Q

What are some potential causes of chest pain?

A
  • Rib/muscle pain (localised)
  • Pneumonia
  • MI/Angina
  • Cholesystitis
  • Gastroesophogeal Reflux Disease (burning pain)
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2
Q

Give some causes of central chest pain and the type of pain they produce

A
  • Myocardial ischaemia = tightening pain
  • Pericarditis = Sharp pain
  • Aortic dissection = tearing pain
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3
Q

What is pericarditis?

A

Inflammation of the pericardium which causes swelling

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4
Q

How can pericarditis be tested for/diagnosis be confirmed?

A
  • Friction rub heard when using a stethoscope

- Sounds like squeaky leather/ scratching

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5
Q

What is Beck’s Triad?

A
  • Signs of pericarditis
  • Low arterial blood pressure
  • Distended neck veins (increased venous blood pressure)
  • Muffled heart sounds (due to fluid)
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6
Q

Why is arterial blood pressure lowered due to pericarditis?

A
  • Accumulation of pericardium = Increased pressure

- Limits pre-load and decreases end diastolic volume & stroke volume

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7
Q

What can pericarditis lead to?

A
  • Cardiac tamponade

- Limits ability of the heart to adequately pump blood

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8
Q

What is aortic dissection?

A
  • Tear in the tunica intima of the aorta
  • Increases space between layers as blood can flow through
  • Leads to a murmur
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9
Q

What can aortic dissection lead to?

A
  • Decreased blood supply to other organs common with hypertension
  • Can get pseudohypotension (false low measure due to brachiocephalic subclavian arteries)
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10
Q

Describe respiratory pain

A
  • Lateral chest pain

- Pleuritic i.e. becomes worse with inspiration/coughing

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11
Q

In what direction is coronary blood flow? What does this result in?

A
  • Epicardium to endocardium

- Leaves subendocardial surface as most vulnerable place to ischaemia

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12
Q

When does filling occur? How can ischaemia be caused by interrupted filling?

A
  • Occurs during diastole
  • ↑ heart rate = ↓ time of diastole
  • ↓ filling = ↓ coronary blood flow
  • Leads to ischaemia
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13
Q

What are the non-modifiable risk factors for coronary atheroma?

A
  • Age
  • Male sex (up to menopause)
  • Family history
  • Ethnicity
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14
Q

What are the modifiable risk factors for coronary atheroma?

A
  • Hyperlipidaemia
  • Cigarette smoking
  • Hypertension
  • Diabetes type 2
  • Lifestyle i.e. obesity
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15
Q

What does coronary atheroma lead to?

A
  • ↓ lumen diameter
  • ↑ risk of thrombosis
  • ↑ risk of MI
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16
Q

Descibe stable plaque

A
  • Small necrotic core
  • Thick fibrous cap
  • Not likely to rupture
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17
Q

Describe vulnerable plaque

A
  • Large necrotic core
  • Thin fibrous cap
  • More likely to rupture
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18
Q

What causes rupturing of vulnerable plaque?

What does this lead to?

A
  • High sheering forces e.g. hypertension
  • Erosion/fissuring (splits)
  • Exposes blood to thrombogenic core causing formation of a clot
  • Causes variable obstruction to flow in lumen and downstream ischaemic myocardial injury
  • Complete obstruction = STEMI
  • Incomplete obstruction = NSTEMI and/or unstable angina
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19
Q

What is stable angina?

A
  • Chest pain/discomfort due to activity or emotional stress
  • 70-80% occlusion = limited blood flow during exertion
  • Has stable, fixed plaque
20
Q

How can stable angina be tested for?

A
  • Do an exercise stress test
  • ECG on a treadmill with continuous monitoring whilst increasing difficulty
  • ECG changes = positive result
  • No pain at rest
21
Q

What ECG changes would be seen during stable angina?

A
  • Like a left bundle branch block
  • Inverted S-T elevation (more than 1mm)
  • DURING EXERTION
22
Q

How can stable angina be treated?

A
  • Sublingual nitrates (immediate effect)
  • Lifestyle changes
  • Revascularisation
23
Q

What is acute coronary syndrome?

A

Conditions due to a decrease in blood flow to coronary arteries, usually caused by thrombus, plaque rupture or platelet aggregation

24
Q

How do acute coronary syndromes present?

A
  • Pain at rest
  • Becomes more severe upon exertion
  • No relief with nitrates
  • Lasts a while
25
Q

What is unstable angina?

A

Angina caused by the disruption of atheroslerotic plaque with partial thrombosis

26
Q

What are the signs of unstable angina?

A
  • Long lasting pain at rest/with minor exercise
  • Pain is severe and new in onset
  • Has a crescendo pattern of occurrence i.e. becomes longer, more frequent and more severe
  • Has no biomarkers of necrosis
  • ST depression/ T wave inversion/ normal ECG
27
Q

How can unstable angina be treated?

A
  • Antithrombin therapy
  • Aspirin (↓ platelet clotting so ↓ thrombus)
  • Coronary Angiography
  • Revascularisation
28
Q

What is revascularisation?

A
  • Angioplasty and stenting
  • Catheter is inserted and guided to blocked area via wrist/groin
  • Small balloon is attached that then inflates so holds artery open
  • Stent is inserted and balloon is removed so keeps artery open
29
Q

What is bypass grafting?

A
  • Anastamose internal mammary artery
  • Sew it to LAD at a site that is distal to the occlusion
  • Can use radial artery/ reversed saphenous vein (so valves are down)
30
Q

What is a STEMI

A
  • Myocardial death due to stoppage of blood flow

- ST segment elevation in leads facing the injured area

31
Q

What are the different levels of occlusion in a STEMI?

A
  • Total occlusion (>90%) = injury to full thickness of ventricular wall/is transmural
  • Partial occlusion = subendocardial area is affected
32
Q

How is an ECG changed during a STEMI?

A
  • Acute T wave elevation
  • ST elevation (0-12 hours after)
  • Q wave develops over 1-12 hours
  • ST elevation with T wave inversion = 2-5 days
33
Q

What is an NSTEMI?

A
  • Non ST segment elevation MI
  • ST depression/ T inversion/ normal
  • Troponins are released
  • Pain like MI
34
Q

What is a myocardial infarction?

A
  • Irreversible damage to heart muscle due to a lack of blood flow (prolonged ischaemia and hypoxia)
35
Q

Describe the pain felt during an MI

A
  • Severe
  • Crushing
  • Persistent
  • Central
  • Radiating chest pain that isn’t relieved by rest/nitrates
36
Q

Why would a patient become pale and sweaty during an MI?

A
  • Increased sympathetic stimulation
  • Increased by baroreceptor reflex due to ↓ blood pressure
  • ↑ circulating catecholamines
37
Q

Why would a patient suffer from nausea and vomiting during an MI?

A

Decreased parasympathetic stimulation

38
Q

What are the most commonly used biochemical markers of myocyte damage? Why are they used?

A
  • Cardiac troponin I or cardiac troponin T
  • Released during myocyte death/damage = ↑ levels during STEMI/NSTEMI
  • Are more sensitive and more specific
  • Levels are raised for 7 days
39
Q

Give another biomarker of myocyte damage, when would it be used?

A
  • Creatinine kinase
  • Specific as long as skeletal muscle isn’t damaged too
  • Levels return to normal within 2-3 days
40
Q

Which artery would be occluded if the area of infarction was inferior? Which leads would this show in?

A
  • Right coronary artery

- Leads: 2, 3 and AvF

41
Q

Which artery would be occluded if the area of infarction was antero-septal? Which leads would this show in?

A
  • Left anterior descending artery

- V1 - V2

42
Q

Which artery would be occluded if the area of infarction was antero-apical? Which leads would this show in?

A
  • Left anterior descending artery (distal)

- V3 - V4

43
Q

Which artery would be occluded if the area of infarction was anterolateral? Which leads would this show in?

A
  • Circumflex artery

- 1, AvL, V5 - V6

44
Q

Which artery would be occluded if the area of infarction was extensive anterior? Which leads would this show in?

A
  • Proximal left coronary artery

- 1, AvL, V2 - V6

45
Q

Which artery would be occluded if the area of infarction was true posterior? Which leads would this show in?

A
  • Right coronary artery

- Tall R wave in V1

ESA 2 (63 decks)

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