Lecture 6.1: Chest Pain & Ischaemic Heart Disease Flashcards

1
Q

What are the broad systems that can account for chest pain? (6)

A

• MSK
• Cardiac
• Pulmonary
• Gastrointestinal
• Vascular
• Other

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2
Q

What are some Cardiac causes of Chest Pain? (8)

A

• Chronic Stable Angina
• Unstable Angina
• Non-ST Elevation MI
• ST-Elevation MI
• Pericarditis
• Infective Endocarditis
• Valve Stenosis
• Heart Failure

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3
Q

What are some Pulmonary causes of Chest Pain? (4)

A

• Pneumonia
• Pleurisy
• Pleural Effusion
• Pneumothorax

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4
Q

What are some Gastrointestinal causes of Chest Pain? (5)

A

• GERD
• Gastric/Duodenal ulcer
• Pancreatitis
• Cholecystitis
• Oesophageal Spasm

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5
Q

What are some MSK causes of Chest Pain? (5)

A

• Costochondritis
• Spinal OA
• Fibromyalgia
• Intercostal Neuralgia
• Trauma

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6
Q

What are some Vascular causes of Chest Pain? (2)

A

• Aortic Dissection
• Pulmonary Embolism

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7
Q

What are some Other causes of Chest Pain? (2)

A

• Intercostal Neuralgia
• Herpes Zoster

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8
Q

What is Ischaemic Chest Pain?

A

Chest pain that happens because there isn’t enough blood going to part of your heart

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9
Q

Where is Ischaemic Chest Pain felt? What is the quality of the pain?

A

• Site: Central (Retrosternal), or Left Sided, diffuse pain
• Radiation: Left /Right/Both Arms & Shoulders, Neck, Jaw , Epigastrium, Back
• May present with isolated pain at these sites without chest pain
• ‘Tightening’ ‘heavy’ ‘crushing’ ‘constricting’ ‘pressure’

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10
Q

Gender Differences in Chest Pain

A

• Present with different symptoms
• Both can present with chest pain
• Women might also more non-chest pain symptoms
• Women get less obvious warning signs
• Gender impacts treatment

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11
Q

Causes of Ischaemic Heart Disease (5)

A

• Chronic Stable Angina
• Acute Coronary Syndrome
• Unstable angina (UA)
• Non-ST elevation Myocardial Infarction (NSTEMI)
• ST elevation Myocardial Infarction (STEMI/STE-ACS)

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12
Q

What is Coronary Artery Disease? When is it a problem?

A

• Atheromatous Plaque
• Partially occludes coronary artery
• >70% occlusion = compromised blood flow
when O2 demand increases
• 90% occlusion = ischaemia at rest

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13
Q

Coronary Blood Flow: In Systole

A

• Small intramuscular vessels are compressed
by forces generated in the cardiac muscle
• → coronary flow through LV muscle ↓ to a
minimum
• Coronary flow occurs during diastole when
heart muscle is relaxed
• But: shortening of diastole (at rapid heart
rates) reduces time for this flow

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14
Q

Why is the Subendocardial Area most vulnerable to Ischaemia?

A

• Heart muscle is perfused from the epicardial
surface to endocardial surface
• Myocardial wall pressure is greatest in in the
subendocardial area which is closest to LV
cavity

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15
Q

Risk Factors for IHD: Non-Modifiable (3)

A

• Increasing Age
• Male Gender (females catch up after
menopause)
• Family History

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16
Q

Risk Factors for IHD: Most Important 4 Modifiable Factors

A

• Hyperlipidaemia (metabolism unit)
• Cigarette Smoking
• Hypertension (high systolic/diastolic BP)
• Diabetes Mellitus- doubles IHD risk
(metabolism unit)

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17
Q

Risk Factors for IHD: Modifiable

A

• Lack of exercise
• Obesity
• Stress
• Depression
• Harmful Alcohol Use
• Unhealthy Diet (rich in salt, sugar, fat and
calories)

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18
Q

Chronic Stable Angina / Angina Pectoris: Cause? When is it felt? What makes it better?

A

• Stable plaque (no thrombus) → coronary
artery narrowing
• Moderate reduction in flow, blood flow
sufficient at meet needs at rest
• Ischaemia only when oxygen demand
increases (exertion/emotional stress)
• Relieved when demand ceases
• Angina reproducible with same amount of
exertion

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19
Q

Chest Pain Character in Stable Angina (3)

A

1) Brief episodes of Ischaemic Pain (mild to
moderate pain)
2) Brought on by exertion/emotion (particularly
exertion after meals/in cold weather)
3) Relieved by rest or nitrates, within about 5
minutes

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20
Q

What is the Exercise (ECG) Stress Test? How is it done?

A

• Done to assess the heart’s response to stress or exercise

Graded exercise on a Treadmill until one of the following:
• Target Heart Rate Reached
• Chest Pain
• ECG Changes
• Other Problems (Arrhythmias,↓BP)

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21
Q

Treating Angina: Drugs that Reduce the Work Load of the Heart (5)

A

• ACE Inhibitor / ARB
• β-adrenoceptor blockers
• Ca2+ Channel Antagonists
• Organic Nitrates (venodilator, preload↓)
• I(f) Channel Blockers (slow pacemaker)

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22
Q

Treating Angina: Improve the Blood Supply to the Heart itself (4)

A

• Ca2+ Channel Antagonists
• Antiplatelets which prevent thrombusformation (e.g. Aspirin)
• Cholesterol Reduction (Statins)
• Angiography +/- stents -revascularise

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23
Q

How to Treat Acute episodes of Angina?

A

• Sub-lingual nitrate spray/ tablet eg sublingual glyceryl trinitrate (GTN)

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24
Q

What drugs can prevent episodes of Angina? (3)

A

• Beta Blockers
• Calcium Channel Blockers
• Oral Nitrates

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25
Q

What drugs can prevent cardiac events in stable angina? (3)

A

• Aspirin
• Statins
• ACEI

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26
Q

What are the 2 Types of Revascularisation Surgeries often done in Stable Angina?

A

• Percutaneous Coronary Intervention (PCI)
• Coronary Artery Bypass Grafting (CABG)

27
Q

What is done in Percutaneous Coronary Intervention (PCI)?

A

• Coronary Angioplasty (widen and open up
narrowed or blocked arteries)
• Stenting

28
Q

What is done in Coronary Artery Bypass Grafting?

A

Taking a blood vessel from another part of the body and attaching it to the coronary artery above and below the narrowed area or blockage

29
Q

What Arteries can be harvested for CABG Grafting?

A

• LIMA (L internal mammary)
• RIMA(R internal mammary)
• RA (radial artery)

30
Q

What Veins can be harvested for CABG Grafting?

A

• Saphenous Vein

31
Q

What diagnosis come under “Acute Coronary Syndrome”? (3)

A

• Unstable angina (UA)
• Non-ST elevation myocardial infarction NSTEMI orNSTE-ACS
• ST elevation myocardial infarction STEMI or STE-ACS

32
Q

General Clinical Presentation of ACS (3)

A

• Recurrent chest pain
• Occurring frequently and with little or no exertion
• Episodes lasting > 15 minutes is suggestive of an acute coronary syndrome

33
Q

What is the priority when a patient is presenting with ACS?

A

Priority is to differentiate into:
• STEMI
• NSTEMI
• Unstable Angina (UA)

34
Q

What is seen in a History of Unstable Angina? (6)

A

• Acute worsening of stable angina (crescendo angina)
• Pain more frequent and severe
• Longer duration
• Angina at rest
• Recent onset of new, effort limiting angina
• Presence of risk factors

35
Q

What is seen in a History of MI?

A

• Typical Ischaemic Chest Pain
• Severe Persistent Pain
• Pain at rest , often no precipitant (50% of time)
• Not relieved by rest /nitrate spray
• Patient distressed (often a `feeling of impending death’)

36
Q

What are some Autonomic Features present in an MI? (3)

A

• Sweating
• Pallor
• Cold Clammy

37
Q

What are some Secondary Symptoms of an MI? (4)

A

• Nausea/Vomiting
• Bladder/Bowel urgency
• Breathlessness (due to pulmonary oedema from LV systolic dysfunction)
• Presyncope/Syncope (due to ventricular tachyarrhythmias, bradyarrhythmias
or cardiogenic shock)

38
Q

Initial investigations for Acute Coronary Syndrome (ACS) (2)

A

• ECG
• Cardiac Biomarkers (Troponins)

39
Q

What is seen on ECG of a STEMI?

A

• ST elevation in ≥ 2 leads facing same area
• 1 mm in limb leads
• 2 mm in chest leads
• New Left bundle branch block (LBBB)

40
Q

What is seen on ECG of a NSTEMI?

A

• ST segment depression
• T wave inversion
• Or No ECG changes

41
Q

What is seen on ECG of Unstable Angina (UA)?

A

• Normal ECG

42
Q

Why can there be ST-segment depression (in ECG leads facing injured area) in UA and NSTEMI?

A

• Thrombus partially occluding lumen of a coronary artery
• Affects vulnerable subendocardial areas of myocardium
• K+ leak from injured subendocardial cells, causes depolarisation
• This manifests as ST segment depression in ECG leads facing injured area

43
Q

Why is there ST-elevation in a STEMI?

A

• 90% of STEMI s = total occlusion CA
• Extensive ischaemic injury
• K+ leak from injured sub epicardial myocytes = causes depolarisation
• Manifests as ST segment elevation in ECG leads facing injured area

44
Q

Are Cardiac Biomarkers present in UA?

A

• Cardiac Biomarkers = Negative
• No evidence cell necrosis → Unstable Angina

45
Q

Are Cardiac Biomarkers present in NSTEMI?

A

• Cardiac Biomarkers = Positive
• Cell Necrosis Present → NSTEMI

46
Q

Are Cardiac Biomarkers present in a STEMI?

A

• Cardiac Biomarkers Positive

47
Q

ECG Evolution of a STEMI (Mins/Hours all the way to Weeks later)

A

Mins/Hours: ST-elevation, T-wave upright
Day 1: ST-elevation, T-wave downwards, reduced R-wave, Q-wave begins
Day 1/2: Q-wave deeper, T-wave inverted
Days Later: ST-normalises, T-wave inverted, Q-wave persists
Weeks Later: ST & T normal, Q-wave persists

48
Q

How much of the coronary arteries is occluded in a NSTEMI?

A

Partial Occlusion

49
Q

How to treat an NSTEMI?

A

• Prevent extension of thrombus with anti thrombotic therapy
• Early restoration of perfusion in partially occluded vessels
• Angiography
• PCI
• CABG
• Anti ischaemic therapy: IV nitrates, Beta blockers Statins, ACEI

50
Q

How much of the coronary arteries is occluded in a STEMI?

A

• Total Occlusion
• Large amount of myocardium at risk & no time to lose

51
Q

How to treat an STEMI?

A

• Monitor: ECG, HR, BP, SpO2
• O2 if SpO2 of less than 94%
• IV access
• Pain relief → Diamorphine 2.5-5 mg IV (+metoclopramide 10 mg)
• Anti-platelet (loading dose) → Aspirin 300 mg / Ticagrelor 180mg OR clopidogrel
300 mg (local policy dependent)
• Emergency PCI if available within 120 mins
• Otherwise Fibrinolytic therapy if no contraindications

52
Q

Complications of MI (8)

A

• Sudden Cardiac Death - Arrhythmia (VF / asystole)
• Arrhythmias: Sinus tachycardia (pain, anxiety, heart failure), Sinus bradycardia
(SA node ischaemia )
• Primary/2ndary / 3rtiary heart block (AV node ischaemia)
• 2ndary / 3rtiary block may require temporary pacemaker
• Ventricular tachycardia / Ventricular fibrillation
• Atrial fibrillation
• Heart failure
• Cardiogenic shock

53
Q

What is Cardiogenic Shock?

A

It is when your heart cannot pump enough blood and oxygen to the brain and other vital organs

54
Q

Creatine Kinase (CK) as a Biomarker in MI’s

A

• Enzyme present in skeletal muscle, heart, brain
• 3 iso enzymes: CK –MB is the cardiac iso enzyme
• Rise 3-8 hrs after onset
• Peak at 24 hrs
• Back to normal 48-72 hrs

55
Q

What is Peptic Ulcer Disease? Symptoms? Treatment?

A

• Peptic ulcers occur when acid in the digestive tract eats away at the inner
surface of the stomach or small intestine
• Epigastric ache or burning
• Occurs after meals
• Unrelated to exertion
• Relieved with antacids

56
Q

What is Biliary Colic? Symptoms? Treatment?

A

• If a gallstone blocks one of the bile ducts, it can cause sudden, severe
abdominal pain, known as biliary colic
• Constant deep pain in the right upper quadrant
• Surgical removal of the gallbladder

57
Q

What is an Aortic Dissection?

A

• A tear occurs in the inner layer of the aorta
• Blood rushes through the tear, causing the inner and middle layers of the aorta
to split (dissect)

58
Q

Symptoms of Aortic Dissection

A

• Severe, ‘tearing’ type of chest pain
• Which radiates to the back to between the shoulder blades
• Very abrupt onset

59
Q

Signs of Aortic Dissection

A

• Unequal pulses in the two arms
• Signs of Aortic Regurgitation may be present
• Occlusion of aortic branches may cause a variety of complications

60
Q

96% of acute aortic dissections can be identified based upon some combination of the following three clinical features….?

A

1) Immediate onset of aortic pain with a tearing and/or ripping character
2) Variation in pulse and/or blood pressure between the right and left arm
3) Mediastinal and/or aortic widening on chest radiograph

61
Q

What is Pericarditis? Symptoms?

A

• Pericarditis is inflammation of the lining around your heart
• Central / left sided chest pain
• Sharp, worse with inspiration
• Improved by leaning forward

62
Q

Examinations to Diagnose Pericarditis

A

• Pericardial Rub
• Signs of pericardial effusion (if present)

63
Q

Treatment of Pericarditis

A

• Treat Cause
• If effusion causing tamponade then pericardiocentesis