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[AMS] Cardiovascular System > S8) Ischaemic Heart Disease > Flashcards

S8) Ischaemic Heart Disease Flashcards

1
Q

Outline, in detail, the principles of history-taking

A

- Site: location of the pain and if it radiates

- Quality: how the pain feels (sharp, dull, etc)

- Intensity: severity score

- Timing: when it started (sudden/gradual onset)

- Aggravating factors: what makes pain worse?

- Relieving factors: what makes the pain better?

- Secondary symptoms: other symptoms

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2
Q

What are the two types of chest pain?

A
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3
Q

Describe the features of visceral pain

A

Cardiac ischaemic pain:

  • Dull, poorly localised
  • Worsened with exertion
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4
Q

Describe the features of somatic pain

A

Pleural/pericardial pain:

  • Sharp pain, often well localised
  • Worse with inspiration, coughing or positional movement
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5
Q

What are the different causes of chest pain?

A
  • Cardiac causes – ischaemia, infarction, inflammation (pericarditis)
  • Non-cardiac causes – upper GI, respiratory, MSK
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6
Q

What are the respiratory causes of chest pain?

A
  • Pneumonia
  • Pulmonary embolism
  • Pleurisy
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7
Q

What are the upper gastro-intestinal causes of chest pain?

A
  • Reflux
  • Peptic ulcer disease
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8
Q

What are the musculoskeletal causes of chest pain?

A
  • Rib fracture
  • Costochondritis (inflammation of the costal cartilages)
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9
Q

What is pericarditis?

A
  • Pericarditis is the inflammation of the pericardium often secondary to a viral illness
  • It commonly occurs in men and adults
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10
Q

How does the pain in pericarditis present?

A
  • Retrosternal, sharp
  • Localised to front of chest
  • Aggravated with inspiration, coughing, lying flat
  • Relieved with sitting up and leaning forward
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11
Q

What can be heard on the examination of pericarditis?

A

Pericardial rub may be heard on auscultation

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12
Q

Briefly, explain what cardiac ischaemic chest pain is and how it is managed

A
  • Pain secondary to pathology involving the heart (ischaemic heart disease)
  • Primary concern is to rule out urgent, potentially life-threatening causes of chest pain
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13
Q

When does heart tissue ischaemia occur?

A

Heart tissue ischaemia occurs only when metabolic demands of cardiac muscle are greater than what can be delivered via coronary arteries

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14
Q

Describe the pathophysiology of ischaemic heart disease

A
  • Ischaemic heart disease is a disease of the coronary arteries
  • Fatty deposits build up over time → lipid-laden core with a fibrous external cap (atherosclerosis)
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15
Q

Risk factors for atherosclerosis are the same as risk factors for ischaemic heart disease.

Identify 6 modifiable risk factors

A
  • Smoking
  • Hypertension
  • Hypercholesterolaemia
  • Diabetes
  • Obesity
  • Sedentary lifestyle
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16
Q

Risk factors for atherosclerosis are the same as risk factors for ischaemic heart disease.

Identify 3 non-modifiable risk factors

A
  • Age – advanced
  • Genetics – family history
  • Gender – males
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17
Q

In stable angina, the atherosclerotic plaque is ‘stable’.

Describe the clinical features

A
  • Dull, retrosternal chest pain
  • Triggered by exertion
  • Relieved completely by rest
18
Q

What are some causes of stable angina?

A
  • Coronary artery stenosis
  • Spasm
  • Anaemia
  • Severe aortic valve stenosis
19
Q

What are the investigations for stable angina?

A
  • Bloods: FBC, cholesterol, renal and thyroid function
  • ECG: rhythm disturbance, atrial fibrillation, pathological Q waves
  • Chest X Ray
20
Q

What can be used to treat stable angina?

A

GTN spray – relieve pains

21
Q

How does unstable angina differ from stable angina?

A
  • Pain occurs at rest
  • Pain may be more intense
  • Pain may last longer
  • Risk of deteriorating further (NSTEMI/STEMI)
22
Q

What is the cause of unstable angina?

A

Coronary plaque rupture

23
Q

Describe the signs and symptoms of a myocardial infarction

A
  • Dull, retrosternal chest pain
  • Radiates to neck & shoulders
  • Severe chest pain at rest
  • Look unwell (sweaty, pallor)
  • Nausea
  • Dyspnoea
24
Q

How do you account for the pallor, nausea and vomiting that is accompanied with MI?

A
  • Increased autonomic output – SNS reduces functions of all non-essential parts of the body (immunity, GI)
  • Pain creates substance P which acts on vomiting centres in the brain
25
Q

What causes myocardial infarction?

A

Coronary Heart Disease is the leading cause of heart attacks

26
Q

What is Coronary Heart Disease?

A

CHD is a condition in which atherosclerotic plaques accumulate in the coronary arteries

27
Q

In 3 steps, explain how CHD leads to an MI

A

⇒ Atherosclerotic plaque ruptures

⇒ Blood clot develops at the site of the rupture

⇒ Clot block blood supply to heart, triggering a heart attack

28
Q

What is an acute coronary syndrome?

A
  • An acute coronary syndrome is a condition wherein acute myocardial ischaemia occurs due to atherosclerotic coronary artery disease
  • Atheromatous plaques rupture with thrombus formation causing an acute increased occlusion leading to ischaemia
29
Q

Identify some conditions which are considered as acute coronary syndromes

A
  • Unstable angina
  • Myocardial infarction
  • NSTEMI
  • STEMI
30
Q

In 3 steps, explain how acute coronary syndromes involve a spectrum of increased occlusion following a plaque rupture

A

⇒ Atherosclerotic plaque rupture

⇒ Platelet aggregation and formation of thrombus

⇒ Partially occlusive thrombus → completely occlusive thrombus

31
Q

Differentiate between ischaemia and infarction

A
  • Heart tissue ischaemia: reduced O2 supply without enzyme leak
  • Heart tissue infarction: cardiac enzymes leak from necrosed cardiac muscle cells
32
Q

Differentiate between the clinical examination findings of stable angina and acute coronary syndromes

A
  • Stable angina: normal clinical examination (chest pain free at rest)
  • Acute coronary syndromes: normal clinical examination but may appear sweaty, anxious, pale ± clinical signs secondary to complications of cardiac tissue death
33
Q

Identify and describe the investigations used in the diagnosis of MI

A
  • ECG – ST segments, T waves, ± pathological Q wave
  • Blood tests – Troponin
  • Other investigations – to exclude potential diagnoses & identify potential complications
34
Q

Describe the ECG changes in STEMI

A

Patterns of infarct:

  • ST segment elevation
  • Hyperacute T waves
35
Q

Describe the ECG changes in Unstable angina and NSTEMI

A

Patterns of ischaemia:

  • ST segment depression
  • T wave flattening or inversion
36
Q

How does one differentiate between NSTEMI and Unstable angina?

A

Blood tests – there is troponin release in NSTEMI due to cardiac myocyte death

37
Q

Describe the clinical use of Troponin

A
  • Troponin is a biomarker of myocardial damage
  • However, it released in almost any condition (specificity poor)
38
Q

Which cardiac conditions result in the release of Troponin?

A
  • Acute coronary occlusion / severe stenosis
  • Acute heart failure
  • Prolonged tachycardia
  • Cardiac trauma
39
Q

Which non-cardiac conditions call for the release of troponin?

A
  • Acute PE
  • Pulmonary hypertension
  • Severe anaemia
  • Rhabdomyolysis
  • Kidney failure
40
Q

Describe the pharmacological management of stable & unstable angina

A
  • Aspirin – prevent heart attack, prevent blood clots
  • Beta blocker – reduces blood pressure and slows heart rate
  • Statin – reduce LDL cholesterol
  • ACE inhibitor – lower BP
  • Oral nitrate – ease angina pains, includes GTN (stable angina only)
41
Q

Identify two surgical interventions in the management of stable & unstable angina

A

Repercussion:

  • Percutaneous coronary intervention
  • Coronary artery bypass graft
42
Q

Describe the general management of myocardial Infarction

A
  • Oxygen
  • Pain relief
  • GTN spray (sublingual)
  • Aspirin
  • Repercussion (PCI & CABG)

[AMS] Cardiovascular System (17 decks)

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