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Flashcards in Session 10 Deck (52):

What can the causes of chest pain be divided into?

Chest wall


Heart and Great Vessels

Oesophagus and stomach

Other causes


What problems arising from the chest wall could cause chest pain?

Chest Wall (muscle/bone – rib - /skin)

Often localised, movements may increase pain, local pressure application may elicit tenderness

History of trauma/use e.g. broken ribs, overuse of muscles – muscle pain, bone metastases



What problems arising from the lungs could cause chest pain?

Lateral chest pain, sharp (accentuated) on inspiration, respiratory symptoms +

E.g. pneuomonia, pulmonary embolism

Pneumothorax (air that is trapped between a lung and the chest wall – the air gets there either from the lungs such as in rupture of alveoli or from outside the body – spontaneous)



What problems arising from the heart and great vessels could cause chest pain?

Central pain

Pain from ischaemic myocardium – tightening

Stable angina – pain on exertion and relieved by exertion

Ischaemic Heart disease is common and serious

Pericarditis (less common) - inflammation

Aortic dissection (tear in the aorta --> separation of the aorta walls --> bleeding into and along the wall of the aorta) – uncommon but an emergency


What problems arising from the gastrointestinal system could cause chest pain?

Oesophagus/stomach (Gastrointestinal system)

Chest and epigastric pain, GI symptoms +

Gastro-oesophageal reflux, GB disease (Gullain-Barre syndrome – autoimmune attack on the peripheral nervous system), peptic ulcer, Gastroesophageal reflux disease (from stomach into oesophagus), gallbladder inflammation (cholesystitis)


Discuss Ischaemic Heart Disease

Normally increases in myocardial O2 demand are met by increases in myocardial O2 supply. Myocardial ischaemia occurs when supply cannot increase to meet the demand.

Myocardial Oxygen supply depends on coronary blood flow and O2 carrying capacity of blood e.g. Hb

- Coronary blood flow depends on perfusion pressure (diastolic blood pressure – driving force) and coronary artery resistance

Myocardial Oxygen demand depends on heart rate, wall tension and contractility.

- Wall tension depends on pre-load and after-load


What is the commonest cause of Ischaemic Heart Disease?

fixed narrowing of coronary artery/arteries due to atheromatous coronary artery disease


Discuss the physiology of IHD

Coronary flow occurs from epicardium --> endocardium therefore subendocardial muscle is most vulnerable to ischaemia.

Increasing flow to meet demand is by vasodilation but any fixed narrowing of vessels interferes with vasodilation

Coronary flow occurs during diastole (shortening of diastole at rapid heart rates) decreases time for this flow

Collaterals: absent between major arteries on epicardial surface but present between smaller coronary arteries and arterioles.

- Expansion and development of new collaterals occur when myocardium is ischaemic but takes time – may not develop fast enough to prevent an infarction


Apart from atheromatous CAD, what else may cause IHD?

Rarely, ischaemia may be caused by disorders other than atheromatous CAD (but more often they exacerbate existing atheromatous CAD)

A decreased myocardial O2 supply could be due to a decrease in coronary blood flow or severe anaemia

-  A decrease in coronary blood flow could be due to severe hypotension and non-atheromatous causes of coronary artery narrowing.

As myocardial O2 demand increases, this could be due to tachycardias, thyrotoxicosis and aortic stenosis (increased afterload)


What are the risk factors for Coronary Artery Disease?

Same as for atheroma

Non-modifiable: increasing age, male gender (females catch up after menopause), family history

Important modifiable: hyperlipidaemia, cigarette smoking, hypertension (high systolic / diastolic blood pressure), diabetes mellitus (doubles IHD risk)

Other risk factors include lack of exercise, obesity, stress etc.


What is the difference between a stable plaque and an unstable plaque?

Stable: Small necrotic core, thick fibrous cap, cap is less likely to fissure/rupture

Vulnerable: Large necrotic core, thin fibrous cap, cap more likely to fissure/rupture


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What may happen to a Vulnerable/Unstable Plaque?

Fibrous cap can undergo erosion or fissuring.

This exposes blood to the thrombogenic material in the necrotic core, initiating platelet adhesion and aggregation --> activating platelet clotting cascade --> platelet ‘clot’ followed by fibrin thrombus

- Sudden reduction in artery lumen à acute severe reduction in blood flow à critical ischaemia

- May be sufficient to cause myocyte injury / necrosis

Clinically present with Acute Coronary Syndrome – medical emergency

NOTE; thrombus doesn’t always form – maybe endothelialised – plaque grows bigger

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What symptoms does a Stable Plaque present?

No symptoms or stable angina


Discuss Stable Angina Pectoris

Moderate reduction in blood flow

Flow sufficient at rest

Transient ischaemia during periods of increased O2 demand relieved when demand stop – chest pain during exercise, exertion

No myocyte injury or necrosis

May progress gradually over time to severe fixed narrowing --> over the years , could lead to  ischaemia with less demand

Site: central, diffuse (‘spread out’) chest pain

Quality of pain: tightening (heavy, pressing)

Picture shows typical radiation of power

Brief episodes; mild to moderate central crushing pain with typicalradiation to left/right/both arms or shoulders, neck, jaw, back and epigastrium

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How does Stable Angina present?

Brought on by exertion, emotional stress

Particularly exertion after meals, in cold weather.

Pain, is often predictable: i.e. a reproducible with same amount of exertion.

Relieved by rest or nitrates within about 5 minutes

Presence of risk factors


How is a Clinical Diagnosis of Stable Angina made?

based on history:

Examination: no specific signs but may have signs related to risk factors e.g. increased blood pressure, corneal arcus in hyperlipidaemia

Signs of atheroma elsewhere e.g. absent pulses (PVD) in the feet

LV dysfunction

Resting ECG – usually normal. May show changes (pathological Q waves) of previous MI


What happens if the diagnosis of stable angina is uncertain?

Exercise (ECG) stress test may be done to confirm the diagnosis.

Graded exercise on a treadmill until target heart rate reached or chest pain occurs or ECG changes + or other problems – arrhythmias, decreased blood pressure

Transient sub-endocardial ischaemia with exercise in stable angina – manifests as ST segment depression.

With rest, the ischaemia disappears – ST segment back to baseline

Test is positive if ECG shows ST depressions of greater than or equal to 1mm (horizontal/down slopping)

Test is negative if target heart rate is reached without any ECG changes


A strongly positive test indicates critical stenosis

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What are the ways to treat stable angina?

  • Reduce myocardial O2 demand
  • Increase blood flow by revascularisation
  • Prevent progression of atheroma, stabilise plaques, prevent thrombosis


How does treatment to reduce myocardial oxygen demand for stable angina work?


  • Reduce preload and afterload (nitrates are venodilators and decrease preload, calcium channel blockers decrease afterload by peripheral vasodilation)
  • Reduce heart rate (beta blockers decrease heart rate and contractility)

  • Reduce myocardial contractility


When treating stable angina, what is meant by revascularisation (to increase blood flow)?

An angiography is undertaken to study coronary artery anatomy when revascularisation is planned

Revascularisation: stenting (carried out by using a percutaneous coronary intervention – PCI – method) and/or coronary artery bypass grafting (CABG)

Choice of procedure is influenced by angiography findings


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What arteries and veins are used in a CABG?

internal mammary artery (aka internal thoracic artery), radial artery and saphenous vein (using reversed segment of vein so valves ensure correct blood flow) – grafts are used.

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Explain about treatment used to prevent progression of atheroma

To prevent progression of atheroma, stabilise plaques, prevent thrombosis

  • Aspirin: decreases platelet aggregation hence thrombus formation if plaques disrupted
  • Statins decrease LDL cholesterol and decrease progression of atherosclerosis and increase plaque stability, secondary prevention


What is Acute Coronary Syndrome?

Plaque fissure and thrombus formation can cause: STEMI, NSTEMI, Unstable Angina

  • STEMI: ST segment Elevation Myocardial Infarction (persistent complete cocclusion of an artery resulting in necrosis), biomarkers of necrosis (+ve) – leaked cellular contents; ECG: ST segment elevated
  • NSTEMI: Non ST segment Elevation Myocardial Infarction (no ST elevation on ECG, necrosis, biomarkers (+VE))
  • Unstable Angina: ischaemia but no myocyte necrosis (ECG – no ST elevation, no necrosis, biomarkers (-ve) – as no leakage of cell contents)


What is a STEMI?

90% of STEMIs have total occlusion of an artery; persistent complete occlusion of an artery supplying a significant area of myocardium without adequate collateral circulation

Injury extends to sub-epicardal area --> manifested as ST elevation in leads facing injured area

Proved benefit from emergency re-opening artery by PCI (stenting) or Thrombolysis (i.e. dissolving thrombus)

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What is NSTEMI and Unstable Angina?

Results from non-occlusive thrombus, small risk area, brief or partial occlusion or an occlusion with adequate collaterals

Manifested as ST depression in leads facing injured area

  • NSTEMI: cell necrosis + cardiac biomarkers are (+ve)
  • Unstable angina: no cell necrosis = biomarkers are (-ve)


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What is the History of Unstable Angina?

(Crescendo angina)

More frequent

More severe pain

Longer, more persistent duration

Angina at rest (previously angina upon exertion)

Recent onset of new, effort-limiting angina

Presence of risk factors

Important to realise at the moment thrombus is partially occluding artery à could lead to complete occlusion


What is the History of Myocardial Infarction?

Central, crushing chest pain with typical radiation (shoulders, arms, jaw, back, epigstrium)

Severe pain, patient distressed, ‘feeling of impending death’

Persistent pain

Pain at rest, often no precipitant (50% of time)

Not relieved by rest / nitrate spray

Autonomic features present: sweating, pallow

Other features: nausea, vomiting, breathlessness, (due to LV dysfunction), Faint

Risk factors +


What is the Examination for Acute Coronary Syndrome?

Patient anxious, distressed

Sweating, pallor

Cold, clammy skin

Tachycardia / Arrhythmias +/-

Low BP +/-

Signs of Heart failure: S3, S4, crackles in lung bases (Left ventricular failure --> pulmonary oedema)


What initial investigations would you do for Acute Coronary Syndrome?


Cardiac Biomarkers


Discuss the management of Acute Coronary Syndrome

Priority is to differentiate STEMI from NSTEMI/UA because the treatment is different

Clinical history alone may not differentiate

ECG for a STEMI: ST elevation in 2 or more leads facing same area (1mm in limb leads, 2mm in chest leads); New Left bundle branch block (LBBB)

ECG for a UA/NSTEMI: ST segment depression, T wave inversion OR no ECG changes


What Biomarkers are there for myocyte damage?

Cardiac Troponin I (cTnI) and Troponin T (cTnT)

  • Protein important in actin/myosin interaction
  • Released in myocyte death
  • Very specific and sensitive marker
  • Starts to rise 3-4 hours after onset of pain
  • Peak at 18-36 hours
  • Decline slowly – (+) up to 10-14 day

Creatine kinase (CK)

  • Enzyme present in skeletal muscle, heart, brain
  • 3 iso enzymes; CK-MB is the cardiac isoenzyme
  • Rise 3-8 hours after onset; peak at 24 hours
  • Back to normal 48-72 hours

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What are the ECG changes of a fully involved STEMI? (in the leads facing the infarcted area)

Pathological Q waves

ST segment elevation

T wave inversion



Describe the genesis of a pathological Q wave

The dead tissue creates an electrical hole or ‘window’ as it is no longer able to conduct an electrical current.

As a result, all of the electrical forces of the heart will be directed away from the area of the infarction.

An electrode overlying the infarct will therefore record a deep negative deflection, a Q wave.

Q waves are normally isoelectric


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What causes ST elevation?


When cardiac myocardium gets damaged, it becomes leaky so there is an efflux of K+ ions making it more prone to depolarisation causing ST elevation




Describe the evolution of the ECG during a STEMI


Hyperacute T-wave minutes-hours

ST-elevation 0-12 hours

Q wave develops over 1-12 hours

ST elevation with T-wave inversion 2-5 days

T-wave recovery weeks-months

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If there was an a Inferior area of infarction, what leads would show the ECG changes and what artery is occluded?

Leads II, III, aVF

Artery: Right Coronary Artery

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If there was a antero-septal infarction, what would the ECG leads and artery be?


Leads: V1 - V2

Artery: Left anterior descending artery

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If there was a Anterior Apical Infarction, what leads and artery would it be?

Leads: V3-V4

Artery: LAD (distal)


If there was a Antero-lateral infarction, what leads and artery would it be?

Leads: I, aVL, V5-V6

Artery: Circumflex


If there was a Extensive Anterior infarction, what leads and artery would it be?

Leads: I, aVL, V2-V6

Artery: Proximal Left Coronary Artery


If there was a true posterior infarction, what leads and artery would it be?

Tall R Wave in V1

Right Coronary artery


What would an Anterior MI look like?

Occlusion of proximal left anterior descending coronary artery

Leads: I, V2-V4

Pathological Q waves, T Waves inversion, ST elevation

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What would a Lateral MI look like?

Occlusion of

Left Circumflex Coronary Artery

Marginal branch of left circumflex artery

Margian branch of left anterior descending artery

Leads: I, aVL, V5, V6

ST elevation, pathological Q waves, T wave inversions

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What would a Posterior MI look like?

Tall R wave in V1


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What does an Inferior MI look like?

Leads: II, III, aVF, V6

Artery: Right Coronary Artery

T wave inversions, Pathological Q waves

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What is the aim of treatment for Acute Coronary Syndrome?


Restore perfusion, prevent muscle loss




What is the Treatment for STEMI?

Total occlusion: large amount of myocardium at risk and no time to lose

If emergency PCI (angioplasty and stenting) is available In 90-120 minutes, perform Primary PCI – gives better results

If emergency PCI is not available in the time frame, perform firbinolytic therapy if there are no contraindications (e.g. recent surgery or stroke --> risk of severe bleed), with subsequent revascularisation

General: monitoring in CCU, pain control, O2 if needed

Anti-platelet agents: aspirin + Clopidogrel

Anti ischaemic therapy: IV nitrates, beta blockers

ACEI – especially if left ventricle dysfunction – prevents harmful remodelling of heart

Statins (reduce cholesterol synthesis in tissues)


What are drugs used in ACS and how do they work?

Prevent Thrombosis by acting on platelet pathways (anti-platelet drugs e.g. aspirin) and coagulation pathways (anti coagulants e.g. heparin)

Dissolve thrombus (fibrinolytic agents)



What is the treatment of Non-STEMI?


Partial occlusion


Prevent extension of thrombus with anti thrombotic therapy

Early restoration of perfusion in partially occluded vessels – angiography  -> PCI / CABG

Prevent progression of thrombosis with anti platelet agents : aspirin + clopidogrel, anticoagulants: LMW heparin

Note: Thrombolytics not used

Risk assessment: High risk – early PCI / CABG, Low risk – initially medial treatment à elective angio

General measures:anti-platelet agents, anti-ischaemic therapy, statins, ACEI


Discuss Long Term Treatment after MI

Aspirin: decrease mortality and re-infarction

Beta blocker – decrease mortality and re infarction

ACEI – improved survival

Statin – decrease mortality and re infarction

Manage risk factors – life style modifications – weight loss, exercise, diet, stop smoking, decrease alcohol



List some complications of MI

Sudden Cardiac Death – ventricular fibrillation / asytole


~Sinus tachycardia (pain, anxiety, heart failure)

~Sinus bradycardia (SA node ischaemia)

~Heart block 1/2/3 degrees – (AV node ischaemia), 2nd/3rd degree heart block may require temporary pacemaker

~Ventricular tachycardia/ Ventricular fibrillation (ventricular ischaemia causing re-entry circuits or increased automaticity)

~Atrial fibrillation

Heart failure – loss of myocardium leading to decreased myocardial contractility

Cardiogenic shock – when >40% of myocardium infracted, severely decreased cardiac output, systolic blood pressure <90mmHg, with inadequate perfusion of tissues


Explain about Pericarditis

In most cases the pericardium becomes acutely inflamed, with pericardial vascularisation and infiltration with polymorphonuclear leukocytes. A fibrinous reaction frequently results in exudate and adhesions within the pericardial sac, and a serous or haemorrhagic effusion may develop. In some conditions (eg, tuberculosis, sarcoidosis, fungal infections and rheumatoid arthritis), a granulomatous pericarditis develops.

- Chest Pain (Aggravated by inspiration, swallowing, coughing and lying flat. Relieved by sitting up and leaning forward.) Other symptoms can include a nonproductive cough, chills and weakness.

- Signs: pericardial friction rub present upon auscultation, tachypnoea (rapid breathing), tachycardia, fever.

- Cardiac tamponade could arise due to restriction of heart pumping due to fluid buildup between myocardium and pericardium