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CVS ILO's > Session 9 ILOS - Chest Pain and Acute Coronary Syndromes COPY > Flashcards

Session 9 ILOS - Chest Pain and Acute Coronary Syndromes COPY 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 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
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29
Q

What can acute coronary syndromes lead to?

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

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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
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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
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 left ventricle
  • They are supplied by the right coronary artery
58
Q

Anteroseptal ECG leads

A

V1
V2
V3
V4

(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 (Bisopolol 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 (VT, VF with compromise
62
Q

Describe the principles of the management of stable angina

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

Describe the principles of management of unstable angina

A
  • Antiplatlets and antithrombotics (e.g. Aspirin and Ticagrelor/Clopidogrel)
  • Anti-ishcaemics (e.g. Bisopolol, GTN)
  • Consider referral to catheter lab for percutanous coronary intervention (stent)
64
Q
A

GTN can be given to relieve stable angina, though it does not work in unstable angina. GTN causes vasodilation of veins to decrease the workload of the heart by reducing cardiac return.

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
  • Predilate the narrowed section with balloons
  • Stent acts as metal scaffold to keep vessel open
  • Catheter withdrawn
67
Q

Describe an alternative surgical treatment to stent placement

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 to heart
68
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

69
Q

Examination of suspected ACS (LEARN IF TIME)

A
  • BP if systolic <90 - hypotensive could result in cardiogenic shock)
  • Tachycardia - seen in fight or flight response. You will have that fight or flight response in a MI
  • Bradycardia due to occlusion of right coronary artery, which supplies the SA node (2:1 heart block/complete heart block)
  • JVP - if elevated, may indicate right heart failure or pulmonary oedema
  • Heart murmur
  • Lungs - clear or wet - wet with lots of crackles = large MI
  • Cool peripheries? - shut down due to shock
70
Q

Assessment of suspected acute coronary syndrome (7) (LEARN IF TIME)

A

History:
- Cardiac sounding?
Squeezing, pressure pain?
- Radiation to neck/left arm/jaw?
- Relieved with GTN?
- How long have you had it?
- Is pain getting worse?
- Pleuritic? ie worse if you breath in - maybe you have a pulmonary embolism

Risk factors present? (eg diabetes, smoker, high cholesterol, family history, thrombophillia)

71
Q

What do we use echocardiogram for?

A

LV function (normal or impaired)
Wall motion (regional or global motion)
Valvular disease (mitral regurg)
Complications from MI eg VSD - ventricular septal defect

72
Q

Echocardiogram views

A

Apical 2 chamber view : LAD and RCA

Apical 4 chamber view: LAD, RCA and LCA

73
Q

What does ST elevation imply?

A
  • Sudden occlusion
  • or can persist long term as a marker of LV aneurysm (Q waves usually present)
74
Q

What does ST depression imply?

A
  • Under supply of blood to myocardium but not sudden full occlusion
  • If in anterior leads (V1-V6) can be due to posterior STEMI
75
Q

T wave inversion means

A

Under supply of blood but not sudden occlusion

76
Q

Describe the Evolution of waves in STEMI

A

Hyperacute T waves + ST elevation (acute)
Q wave begins + ST elevation (hours)
T wave inversion + deeper Q wave (day 1-2)
ST normalise + inverted T waves (days)
ST and T normal, Q wave persists (pathological Q waves, weeks)

77
Q

What is type 2 MI?

A

When something other than coronary plaque contributes to an imbalance between supply and demand of myocardial oxygen, leading to a rise and fall in cardiac enzymes

78
Q

Give 7 causes of type 2 MI

A
  • Coronary artery spasm
  • Coronary endothelial dysfunction
  • Tachyarrhthmias/Bradyarryhthmias
  • Anaemia
  • Respiratory failure
  • Hypotension
  • Severe Hypertension

CVS ILO's (15 decks)

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