CVS S10 - Chest pain and IHD Flashcards

1
Q

List the 4 general types of chest pain

A

Cardiovascular, Respiratory, GI, Musculoskeletal

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2
Q

List the different causes of cardiovascular chest pain and how the pain would feel

A

MI - Tightening

Pericarditis - Sharp

Aortic dissection - Tearing

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3
Q

Give an example for each of the other types of pain (GI/ Musculoskeletal/ Respiratory)

A

Respiratory - Infection, pneumothorax

GI - reflux oesophagitis, pancreatic disease

MSK - trauma, bone metastases, muscle pain

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4
Q

List the modifiable and non-modifiable risk factors for CAD

A

M- hyperlipidaemia, diabetes, smoking, hypertension

NM- increasing age, male gender, family history

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5
Q

What is the cause of stable angina?

A

Stable plaque- small necrotic core, thick fibrous cap, cap less likely to fissure

Moderate reduction in blood flow results in transient ischaemic attacks during periods of high oxygen demand

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6
Q

How would the chest pain present in a patient with stable angina?

A
  • Central tightening pain
  • Brief episodes with radiation to left/right/both arms or shoulders and neck, jaw or back
  • Brought on by exertion and relieved by rest or nitrates
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7
Q

How would a diagnosis of stable angina be made?

A
  • Based on history
  • No specific signs on examination but may have signs related to risk factors e.g. increased BP, corneal arcus, signs of atheroma elsewhere due to absent pulses
  • Resting ECG usually normal
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8
Q

What can be done if the diagnoses of stable angina is uncertain?

A
  • Exercise stress ECG Test
  • Patient connected to ECG and undertakes graded exercise on a treadmill until target heart rate reached or chest pain occurs/
  • ECG changes/ other problems such as fall in BP
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9
Q

What would be the results of an exercise stress test in a patient with stable angina?

A
  • Transient sub-endocardial ischaemia with exercise- ST depression of more than 1mm
  • With rest ST segment goes back to baseline
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10
Q

What does a strongly positive exercise test indicate?

A

Critical stenosis

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11
Q

What are the aims of treatment for stable angina?

A
  • Reduce myocardial oxygen demand
  • Increase blood flow by revascularisation
  • Prevent progression of atheroma, stabilise plaque, prevent thrombosis
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12
Q

What factors does myocardial oxygen supply depend on?

A

O2 carrying capacity of blood and coronary blood flow (depends on perfusion pressure (DBP) and coronary artery resistance)

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13
Q

What factors must be altered to reduce myocardial oxygen demand?

A

Wall tension, heart rate, contractility

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14
Q

What drugs can be given to reduce myocardial oxygen demand?

A

Nitrates, calcium channel blockers, beta blockers

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15
Q

What are the two potential methods of revascularisation?

A

Percutaneous Coronary Intervention and stenting (PCI)

Coronary Artery Bypass Grafting (CABG)

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16
Q

What are the two different types of Acute Coronary syndrome?

A

STEMI- occlusion complete, persistent, no collaterals, severe ischaemia and necrosis

NSTEMI/Unstable Angina- non occlusive thrombus, brief, collaterals present, less severe ischaemia

17
Q

How does unstable angina differ from NSTEMI?

A

NSTEMI is a non ST segment elevation MI with necrosis and biomarkers present

Unstable angina is ischaemia but no infarction so no necrosis and no biomarkers present

18
Q

How would a patient with unstable angina present?

A
  • Acute worsening of stable angina- more frequent, more severe and longer duration
  • Angina at rest
  • Recent onset of new, effort limiting angina
  • Presence of risk factors
19
Q

How would patient with MI present?

A
  • Severe central crushing chest pain with typical radiation
  • Persistent and continues at rest
  • Not relieved by rest/ nitrate spray
  • Autonomic features present e.g. sweating/pallor
  • Nausea/ vomiting/ breathlessness/ faint
20
Q

What would you find on examination of a patient with an MI?

A
  • Sweating, pallor
  • Cold, clammy skin
  • Tachycardia/ Arrythmias
  • Low BP
  • Signs of heart failure- S3/S4, crackles in lung bases
21
Q

What are the main biochemical markers of myocyte damage?

A

Cardiac Troponin I and Cardiac Troponin T

Rise 4 hours after onset of pain, peak 18-36 hours, decline slowly up to 10-14 days

22
Q

What other biochemical marker can be used to detect myocyte damage?

A

Creatine Kinase (CK-MB)

Rise 3-8 hours after onset, peak at 24 hours, back to normal 48-72 hours

23
Q

How would a STEMI be treated?

A

Emergency Percutaneous coronary intervention (PCI) within 90-120 minutes

If not available then fibrinolytic therapy

24
Q

How would an NSTEMI be treated?

A

Prevent extension of thrombus with anti-thrombotic therapy

Possible PCI/CABG but not emergency

25
Q

What are the long term treatments given after an MI and why?

A

Aspirin- decrease mortality and re infarction

Beta Blocker- decrease mortality and re infarction

ACE Inhibitors- improved survival

Statins- decrease mortality and re infarction

Manage risk factors via lifestyle modifications

26
Q

List some potential complications of MI

A
  • Sudden cardiac death
  • Arrhythmias- tachycardia/ bradycardia
  • Heart block- primary/ secondary/ tertiary
  • Ventricular tachycardia/ fibrillation
  • Atrial fibrillation
  • Heart failure
  • Cardiogenic shock
27
Q

How can MI lead to bradycardia?

A

SA node ischemia

28
Q

How can MI lead to ventricular tachycardia?

A

Ventricular ishaemia causes re-entry circuits or increased automatic firing

29
Q

How can MI lead to heart failure?

A

Loss of myocardium causes decreased myocardial contractility

30
Q

How can MI lead to cardiogenic shock?

A
  • > 40% myocardium infarcted
  • Severely decreased CO
  • Systolic BP