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
What drugs can prevent cardiac events in stable angina? (3)
• Aspirin • Statins • ACEI
26
What are the 2 Types of Revascularisation Surgeries often done in Stable Angina?
• Percutaneous Coronary Intervention (PCI) • Coronary Artery Bypass Grafting (CABG)
27
What is done in Percutaneous Coronary Intervention (PCI)?
• Coronary Angioplasty (widen and open up narrowed or blocked arteries) • Stenting
28
What is done in Coronary Artery Bypass Grafting?
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
What Arteries can be harvested for CABG Grafting?
• LIMA (L internal mammary) • RIMA(R internal mammary) • RA (radial artery)
30
What Veins can be harvested for CABG Grafting?
• Saphenous Vein
31
What diagnosis come under "Acute Coronary Syndrome"? (3)
• Unstable angina (UA) • Non-ST elevation myocardial infarction NSTEMI orNSTE-ACS • ST elevation myocardial infarction STEMI or STE-ACS
32
General Clinical Presentation of ACS (3)
• Recurrent chest pain • Occurring frequently and with little or no exertion • Episodes lasting > 15 minutes is suggestive of an acute coronary syndrome
33
What is the priority when a patient is presenting with ACS?
Priority is to differentiate into: • STEMI • NSTEMI • Unstable Angina (UA)
34
What is seen in a History of Unstable Angina? (6)
• 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
What is seen in a History of MI?
• 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
What are some Autonomic Features present in an MI? (3)
• Sweating • Pallor • Cold Clammy
37
What are some Secondary Symptoms of an MI? (4)
• 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
Initial investigations for Acute Coronary Syndrome (ACS) (2)
• ECG • Cardiac Biomarkers (Troponins)
39
What is seen on ECG of a STEMI?
• 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
What is seen on ECG of a NSTEMI?
• ST segment depression • T wave inversion • Or No ECG changes
41
What is seen on ECG of Unstable Angina (UA)?
• Normal ECG
42
Why can there be ST-segment depression (in ECG leads facing injured area) in UA and NSTEMI?
• 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
Why is there ST-elevation in a STEMI?
• 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
Are Cardiac Biomarkers present in UA?
• Cardiac Biomarkers = Negative • No evidence cell necrosis → Unstable Angina
45
Are Cardiac Biomarkers present in NSTEMI?
• Cardiac Biomarkers = Positive • Cell Necrosis Present → NSTEMI
46
Are Cardiac Biomarkers present in a STEMI?
• Cardiac Biomarkers Positive
47
ECG Evolution of a STEMI (Mins/Hours all the way to Weeks later)
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
How much of the coronary arteries is occluded in a NSTEMI?
Partial Occlusion
49
How to treat an NSTEMI?
• 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
How much of the coronary arteries is occluded in a STEMI?
• Total Occlusion • Large amount of myocardium at risk & no time to lose
51
How to treat an STEMI?
• 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
Complications of MI (8)
• 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
What is Cardiogenic Shock?
It is when your heart cannot pump enough blood and oxygen to the brain and other vital organs
54
Creatine Kinase (CK) as a Biomarker in MI's
• 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
What is Peptic Ulcer Disease? Symptoms? Treatment?
• 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
What is Biliary Colic? Symptoms? Treatment?
• 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
What is an Aortic Dissection?
• 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
Symptoms of Aortic Dissection
• Severe, ‘tearing’ type of chest pain • Which radiates to the back to between the shoulder blades • Very abrupt onset
59
Signs of Aortic Dissection
• Unequal pulses in the two arms • Signs of Aortic Regurgitation may be present • Occlusion of aortic branches may cause a variety of complications
60
96% of acute aortic dissections can be identified based upon some combination of the following three clinical features....?
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
What is Pericarditis? Symptoms?
• Pericarditis is inflammation of the lining around your heart • Central / left sided chest pain • Sharp, worse with inspiration • Improved by leaning forward
62
Examinations to Diagnose Pericarditis
• Pericardial Rub • Signs of pericardial effusion (if present)
63
Treatment of Pericarditis
• Treat Cause • If effusion causing tamponade then pericardiocentesis