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CVS 2023 > Session 9 ILOS - Chest Pain and Acute Coronary Syndromes > Flashcards

Session 9 ILOS - Chest Pain and Acute Coronary Syndromes Flashcards

1
Q

What are the 2 types of chest pain?

A

Cardiac (ischaemic)

Pleuritic

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2
Q

Describe the anatomy of the thoracic cavity from superficial to deep that can result in chest pain (7)

A
  • Skin
  • Musculoskeletal (bone/muscle/cartilage)
  • Trachea
  • Lungs
  • Heart
  • GI Tract
  • Blood vessels - aorta
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3
Q

Identify the different systems that can cause chest pain (5)

A

Different systems can because chest pain:

  • Cardiac (heart muscle and pericardial sac)
  • Respiratory (lungs and pleura)
  • Musculoskeletal
  • GI
  • Vascular
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4
Q

Name 2 Musculoskeletal causes of chest pain

A
  • Costochodritis
  • Rib fracture
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5
Q

Name a vascular cause of chest pain

A

Aortic dissection

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6
Q

Name a skin cause of chest pain

A

Shingles

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7
Q

Name 2 GI causes of chest pain

A
  • Gastro-oesophageal reflux disease(GORD)
  • Peptic ulcer disease
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8
Q

Name a respiratory cause of chest pain

A

Pneumonia

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9
Q

What determines the features of the chest pain?

A

The type of nerve ie visceral or somatic the signals are being sent through to reach the spinal cord and the brain

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10
Q

Give 3 cardiac causes of chest pain and state the type of pain that it causes and the innervation

A
  • Pericarditis - pleuritic pain because pain signals pass from the pericardium through somatic afferent nerves to the brain and spinal cord
  • Stable angina - visceral pain because the pain signals pass from the cardiac muscle through visceral afferent nerves to reach the brain and spinal cord
  • Acute coronary syndromes - visceral pain because the pain signals pass from the cardiac muscle through visceral afferent nerves to reach the brain and spinal cord
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11
Q

What kind of pain do you get from the heart muscle due to ischaemic or infarct reason? Why do you get this pain?

A
  • Visceral pain
  • Because pain signals from the heart are transferred through visceral afferent nerve to the brain and spinal cord
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12
Q

What kind of pain do you get from lungs, pleura, pericardial sac or MSK features of the chest wall?

A
  • Somatic pain
  • Because pain signals from these places are transferred through somatic afferent nerves to the brain and spinal chord
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13
Q

Describe the features of cardiac (ischaemic) chest pain (4)

A
  • Dull, felt centrally (centre of chest)
  • Poorly localised
  • Pain can be referred (perceived to come from another location e.g. shoulder)
  • Worsened with exercise/exertion
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14
Q

Describe the features of pleuritic chest pain (5)

A
  • Sharp
  • Well localised
  • No radiation
  • Worsened with position ie pericarditis
  • Worsened with inspiration and coughing (ie Respiratory or MSK cause)
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15
Q

Why can cardiac chest pain be referred to other parts of the body? (4)

A
  • Visceral afferents send signals towards spinal cord and enter at segments T1-T4/T5
  • Sensory/somatic afferents from T1-T4/5 dermatomes enter at same level
  • Brain interprets signals as arising from skin instead of from the heart, confusingly
  • So patient describes feeling the pain in T1-T4/5 dermatomes, which correspond to the front of your chest and a little bit down your arm
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16
Q

Pericardium innervation vs cardiac muscle innervation

A
  • Pericardium - innervated by somatic afferents that run in peripheral nerves
  • Cardiac muscle - innervated by visceral afferents that run in sympathetic nerves
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17
Q

What is pericarditis?

A

Inflammation of the pericardial sac

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18
Q

What is the typical presentation history for pericarditis? (3)

A
  • Usually more common in males than females
  • Usually due to Infection - typically viral cause
  • May have a prior history of viral infection leading up to development of symptoms
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19
Q

Which nerve innervates the pericardium?

A

Phrenic nerve

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20
Q

Describe the pain presentation of acute pericarditis (6)

A
  • Pleuritic/somatic pain
  • Sharp
  • Well localised
  • Sitting forward or up relieves pain
  • Lying down flat makes it worse
  • Coughing makes it worse
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21
Q

Describe the signs and symptoms of acute pericarditis (8)

A
  • May be normal
  • Tachycardia
  • Pounding or racing heartbeat (heart palpitations)
  • Pericardial rub on auscultation (scratchy noise)
  • Fatigue or general feeling of weakness or being sick
  • Low-grade fever
  • Cough
  • Shortness of breath when lying down
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22
Q

Name some further investigations that you might do with a patient with suspected pericarditis and describe what you may find in someone with pericarditis (4)

A
  • ECG - widespread saddle-shaped ST elevation in all leads.
  • Series of blood tests - inflammatory markers may be elevated ie CRP

Other investigations to rule out other causes of chest pain :

  • chest x-ray
  • echocardiogram
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23
Q

Compare Pericarditis ST elevation to MI ST elevation

A

Pericarditis:
- Widespread
- Saddle-shaped

MI:
- Only in the leads looking at the bit of the heart that is affected
- Non-saddle-shaped

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24
Q

Name 4 acute coronary syndromes
Name something that is not

A
  • Unstable angina
  • Myocardial infarction:
  • Non-ST-elevation myocardial infarction (NSTEMI)
  • ST-elevation myocardial infarction (STEMI)

NOT STABLE ANGINA

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25
Q

Describe the risk factors for coronary atheroma (10)

A

Risk factors:

  • Hypertension
  • Hyperlipidaemia
  • Smoking
  • Diabetes
  • Obesity
  • Sedentary lifestyle
  • Gender (male)
  • Advancing age
  • Family history
  • Ethnicity
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26
Q

What are acute coronary syndromes? (5)

A
  • A spectrum of acute myocardial ischaemic events,
  • caused by atheromatous plaque rupture with thrombus formation
  • causing acute increased occlusion in an already partially occluded coronary artery lumen
  • Leading to ischaemia and potentially infarction (mocardial tissue necrosis)
  • Causes chest pain
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27
Q

What causes acute coronary syndromes?

A
  • Atheromatous plaque rupture with thrombus formation
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28
Q

What do acute coronary syndromes cause? (2)

A
  • Acute/sudden increased occlusion in an already partially occluded coronary artery lumen
  • Chest pain
29
Q

What can acute coronary syndromes lead to?

A
  • Leading to ischaemia and potentially infarction (mocardial tissue necrosis)
30
Q

What is ischaemic heart disease?
Give 4 examples

A

Insufficient blood supply to heart muscle due to atherosclerotic disease of coronary arteries

eg stable/unstable angina, NSTEMI, STEMI

31
Q

Describe the pathophysiology of stable angina

A

Stable angina:

  • Partial, chronic (stable) occlusion of a coronary artery with atherosclerotic plaque
  • Only pain on exercise, due to increased metabolic demands and insufficient blood flow
32
Q

Why does stable angina only present with pain during exercise?

A
  • Due to increased metabolic demands and insufficient blood flow
33
Q

What determines whether you get Unstable Angina, NSTEMI or STEMI?

A

Severity of occlusion

34
Q

Describe the pathophysiology of unstable angina (5)

A
  • Partial, chronic (stable) occlusion of a coronary artery with atherosclerotic plaque
  • Plaque ruptures (acute/sudden)
  • Leads to thrombus formation
  • Sudden increased occlusion of coronary vessel by plaque disruption and platelet aggregation
  • Chest pain at rest as well as during exercise
35
Q

Describe the pathophysiology of an NSTEMI (5)

A
  • Partial, chronic (stable) occlusion of a coronary artery with atherosclerotic plaque
  • Plaque ruptures (acute)
  • Leads to thrombus formation
  • Greater sudden increased occlusion of coronary vessel by thrombus formed on plaque - not fully occluding
  • Chest pain at rest as well as during exercise
36
Q

Describe the pathophysiology of a STEMI (5)

A
  • Partial, chronic (stable) occlusion of a coronary artery with atherosclerotic plaque
  • Plaque ruptures (acute)
  • Leads to thrombus formation
  • Complete sudden occlusion of coronary vessel - thrombus fully occludes vessel
  • Chest pain at rest as well as during exercise
37
Q

What differentiates stable angina from an acute coronary syndrome?

A

ACS has atheromatous plaque actually rupturing and thrombus formation, leading to sudden occlusion of the coronary vessel SA doesn’t

38
Q

Describe the difference in management of someone with stable angina, vs someone with ACS

A
  • SA patients do not need hospitalisation and can be treated with drug and lifestyle advice
  • ACS patients need to be in hospital
39
Q

What will all ACS present with?

A

Cardiac ischaemic sounding chest pain

40
Q

Describe the signs and symptoms of angina (5)

A
  • Chest pain
  • Heaviness or tightness in your chest, can radiate to shoulders, arms, neck, jaw, back
  • Shortness of breath
  • No associated anatomical features ie sweating, nausea
  • Ischeamic heart disease risk factors
41
Q

Distinguish the characteristics of unstable angina from stable angina (6)

A

Characteristics between stable and unstable angina: (6)

  • Stable relieves upon rest, unstable doesn’t and chest pain is present at rest
  • No changes on ECG for stable generally
  • Changes on ECG for unstable due to ischaemia, ST depression or T wave inversion
  • Pain may be more intense in Unstable
  • Pain may last longer in unstable
  • Risk of deteriorating further (NSTEMI/STEMI) in unstable
42
Q

Describe the signs and symptoms of myocardial infarction (7)

A

2 types of myocardial infarction = NSTEMI or STEMI

Signs/symptoms:

  • Central Crushing chest pain at rest
  • Pain can radiate from the chest to the jaw, neck, arms and back
  • Cold sweat
  • Nausea
  • Looks unwell (sweaty/pallor)
  • Shortness of breath
  • Feeling weak or lightheaded
43
Q

Explain the difference between unstable angina, NSTEMI and STEMI

A

Unstable angina - partial sudden occlusion of a coronary artery, due to plaque disruption and platelet aggregation, without necrosis of cardiac muscle tissue
NSTEMI - greater sudden occlusion of coronary vessel by thrombus , leading to necrosis of cardiac muscle tissue
STEMI - complete sudden occlusion of coronary vessel by thrombus, leading to necrosis of cardiac muscle tissue

44
Q

Describe the use of the ECG in the diagnosis of MI, distinguishing STEMI from a NSTEMI and unstable angina

A
  • NSTEMI and unstable angina would show ST depression and maybe T wave inversion (or ECG could be normal)
  • STEMI would show ST elevation
45
Q

Describe the use of cardiac biomarkers as a marker for MI and to distinguish between NSTEMI & unstable angina in a patients with Acute Coronary Syndrome

A
  • NSTEMI and STEMI would have elevated troponin due to cardiac myocyte death
  • Unstable angina would have no elevated troponin
46
Q

Describe the investigations for ACS

A

2 main investigations

  1. ECG
    - NSTEMI and unstable angina would show ST depression and maybe T wave changes (t wave inversion - or the ECG could be normal)
    - STEMI would show ST elevation

2 . Troponin blood test
- Unstable angina would not have elevated troponin
- NSTEMI and STEMI would have elevated troponin

  1. Chest x-ray
    Allows DR to check size of heart and blood vessels and look for fluid in lungs - pulmonary oedema
    If widened mediastinum = aortic dissection maybe
47
Q

Blood tests NSTEMI (5)

A
  • Haemoglobin (rule out anaemia as considering antiplatelets)
  • Renal function (angiogram iodine-based contrasts can induce nephropathy in patients with renal impairments)
  • Cholesterol
  • HBA1C (diabetes)
  • Troponin
48
Q

1) When is troponin raised?
2) When does it peak?
3) How long does it remain elevated for?

A

Raised within 3 hours of damage
Peaks at 24-48 hours
Remains elevated 2+ weeks

49
Q

If there is ST elevation but no troponin present in the blood, what is the diagnosis?

A

Aborted STEMI

50
Q

Main cause of acute coronary syndrome

A

Atheromatous plaque rupture, leading to thrombus formation, leading to decreased blood flow through coronary arteries

51
Q

Other pathologies myocardial infarction apart from atheromatous plaque rupture

A
  • Coronary dissection (tear in tunica media)
  • Coronary spasm
52
Q

Give 5 things that can confirm the diagnosis of an MI

A
  • Symptoms of ischaemia ie retrosternal chest pain that can radiate to jaw/arm
  • With rise and/or fall in cardiac biomarker preferably cardiac troponin
  • Pathological Q waves (patient had their infarct a few days ago and myocardium is dead)
  • Imaging evidence of wall abnormality (echocardiogram)
  • Coronary angiography detects thrombus
53
Q

What is type 1 MI?

A

Atheromatous plaque rupture, leading to thrombus formation, leading to decreased blood flow through coronary arteries and subsequent myocardial necrosis

54
Q

Coronary artery anatomy

A
55
Q

What are the anterior leads of the heart and what do they look at?

A

V1-V6

Look at the front of the heart

56
Q

What are the:
- Lateral leads of the heart
- What do they look at?
- Which artery supplies them?

A
  • I, aVL, (high lateral)
    V5, V6
  • They are supplied by the left circumflex artery

L for Lateral for LEFT

57
Q

What are the:
- Inferior leads of the heart
- What do they look at?
- Which artery supplies them?

A
  • II, III and aVF
  • They look at the bottom part of the heart
  • They are supplied by the right coronary artery
58
Q

Anteroseptal ECG leads
What artery supplies them?

A

V1
V2
=. Septal

V3
V4
= Anterior

(left anterior descending)

59
Q

Describe the management of STEMI (7)

A

1) Aspirin (300mg)
2) P2Y12 inhibitor (thin blood even more) such as Ticagrelor 180mg
3) Morphine 5-10mg (ease pain) + antisickness drug (metoclopramide 10mg IV) as morphine can cause nausea
4) Nitrate 2 puffs under tongue if SBP>110mmHg (vasodilator)
5) Oxygen if low sats
6) Direct transfer catheter lab for PCI

  • Time is muscle!
60
Q

Describe the principles of management of NSTEMI (4)

A

1) Antiplatlets and antithrombotics (Aspirin and Ticagrelor/Clopidogrel - P2Y12 inhibitors)
2) Anti-ishcaemics (Bisoprolol and GTN infusion - slow the heart rate down)
3) Secondary prevention (e.g. statins, ACE inhibitors - help with positive remodelling)
4) Consider referral to the catheter lab

61
Q

When should a patient with NSTEMI when to go to catheter lab for urgent percutaneous coronary intervention? (2)

A
  • If chest pain persists with dynamic ECG changes (ECG is evolving)
  • If patient develops arrhythmias
62
Q

Describe the principles of the management of stable angina (5)

A
  • GTN spray (Sublingual glyceryl trinitrate) -
    to reduce symptoms of angina and for use before performing activities known to cause symptoms of angina.
  • Beta blockers long term (e.g. Bisoprolol) or a calcium-channel blocker to reduce the symptoms of stable angina.
  • Stop smoking
  • Low fat and low salt diet
  • Exercise
63
Q

Describe the principles of management of unstable angina (3)

A
  • Antiplatlets and antithrombotics (e.g. Aspirin and Ticagrelor/Clopidogrel) to thin blood
  • Consider referral to catheter lab for percutanous coronary intervention (stent)
  • Lifestyle changes ie stop smoking, exercise, low fat and salt diet
64
Q

What does GTN do?
What condition can it be given in?
What condition can’t it be given in?

A
  • GTN causes vasodilation of veins to decrease the workload of the heart by reducing cardiac return.
  • Relives stable angina
  • Does not work in unstable angina
65
Q

What does invasive coronary angiogram do?

A
  • Establishes the type of leison and its location so we can treat it with stents
66
Q

Describe invasive coronary angiogram (9)

A
  • 30 min procedure
  • Local anaesthetic (to access radial or femoral artery)
  • Catheter guided through artery in arm or leg into coronary arteries
  • Then a liquid dye is injected through catheter
  • Allows doctors to identify blockages by tracing flow of dye
  • Wire occluded vessel with catheter with small inflatable balloon and stent at tip
  • Inflate balloon so anything causing the blockage is pushed towards the edges and to put stent in place
  • Stent acts as metal scaffold to keep vessel open
  • Catheter withdrawn
67
Q

Describe some non-surgical managements of ACS and SA (8)

A

1) Life style changes (low fat/salt, regular exercise, stop smoking)

2) Dual antiplatelets for 12 months min - Ticagrelor/Clopidogrel, Prasugrel

3) Aspirin for life

4) Statins to reduce cholesterol to less than 4mmol/L, LDL cholesterol below 2mmol/L

5) Bisoprolol (beta-blocker) aiming for HR around 70bpm

6) ACE inhibitor aiming for BP <140/80

7) If echocardiogram shows the ejection fraction is below 40%, then eplerenone

8) If ejection fraction is consistently low for 3 months, implantable cardiac defibrillator

68
Q

Describe an alternative surgical treatment to stent placement (LEARN IF TIME)

A

Coronary artery bypass graft surgery

  • Diverts blood around narrowed or clogged parts of major arteries, and provides an alternative route for blood to flow to improve blood flow and oxygen supply

CVS 2023 (26 decks)

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