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Y3 Oxford Cases > Chest Pain > Flashcards

Chest Pain Flashcards

1
Q

What are the most common causes of acute chest pain in an individual >60

A 
Musculoskeletal inflammation
ACS
PE
Stable angina
Pleurisy (secondary to infection)
Oesophagitis (GORD or hiatus hernia)
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2
Q

What kind of musculoskeletal inflammation may cause chest pain

A

Sprained muscle e.g. due to coughing
Coxsackie B infection (Bornholm’s disease)
Idiopathic costochondritis (Tietze’s syndrome)
Varicella Zoster infection -> neuropathic pain restricted to dermatome

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3
Q

What are less common causes of chest pain in an individual >60

A 
Pneumothorax
Anxiety 
Peptic ulcer disease or gastritis 
Myopericarditis (includes Takotsubo)
Cholecystitis 
Acute pancreatitis
Thoracic aortic dissection or aneurysm 
Coronary vasospasm
Oesophageal spasm
Boerhaave's perforation
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4
Q

What would the differential for chest pain be in a young female on COCP

A

PE
Pneumothorax (esp. tall and thin)
Cocaine-induced coronary spasm

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5
Q

Which causes of chest pain are potentially fatal and require immediate management?

A 
ACS
Aortic dissection
Pneumothorax
PE
Boerhaave's perforation
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6
Q

What are the presenting features you might see in ACS

A

Sudden-onset, central, crushing pain radiation to arms/shoulders/neck/jaw, minutes-hour
History of ACS, smoking, HTN, cholesterol, DM, family history

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7
Q

What signs may be seen in a patient with ACS on exam

A

Signs of high cholesterol: xanthochromia/lasma, corneal arcus

Signs of peripheral vascular disease: weak pulse, cyanosis, cold, atrophic skin, ulcers, bruises, carotid bruits

Signs of brady or tachy arrhythmia esp on ECG

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8
Q

What are the presenting features you might see in aortic dissection

A

Sudden onset tearing chest pain that radiates to the back
Very intense from onset
History of HTN, smoking, atherosclerosis, IHD

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9
Q

What signs may be seen in a patient with aortic dissection on exam

A

Absent pulse in one arm (due to occlusion by the dissection flap)
Hypertension or hypotension
Difference in blood pressure between arms >20mmHg
New-onset aortic regurgitation
Pleural effusion (usually on let)

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10
Q

What are the presenting features you might see in pneumothorax

A

Sudden-onset pleuritic chest pain + SOB

Could also be painless breathlessness

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11
Q

What signs may be seen in a patient with pneumothorax on exam

A

Hyperinflated chest wall with reduced expansion
Hyper-resonant percussion over the affected area
Absent breath sounds over affected area
Tracheal deviation in tension pneumothorax - EMERGENCY

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12
Q

What are the presenting features you might see in PE

A

Sudden onset SOB and/or pleuritic chest pain and/or haemoptysis
Inflamed limb
Risk factors for clots e.g. surgery, malignancy, COCP, long haul flight (stasis)

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13
Q

What signs may be seen in a patient with PE on exam

A

Tachycardia

Signs of hypoxia (rare)

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14
Q

What are the presenting features you might see in Boerhaave’s perforation

A

Sudden onset severe chest pain immediately after vomiting

SOB and pleuritic pain develops after due to subsequent pleurisy and effusion

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15
Q

What signs may be seen in a patient with Boerhaave’s perforation on exam

A 
Signs of pleural effusion: dull percussion, absent breath sounds, reduced resonance
Subcutaneous emphysema 
Abdominal rigidity, swelling
Fever
Tahcycardia
Hypotension
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16
Q

What tests should be ordered for suspected ACS

A

ECG
Bloods esp. troponin
CXR
Second line: D-dimer (If wells score >4)

17
Q

What is the purpose of ECG for ACS testing

A

Either 2 30mins apart, or every 10-15mins with continued pain
ACS: signs of ischaemia, ST Elevation, LBBB
PE: tachycardia, right heart strain signs

18
Q

What bloods should be ordered for suspected ACS and why

A

Troponin - 3-12 hours from onset of pain (can also do CK-MB levels)
Serum cholesterol - risk factor (ACS leads to decrease within 24h of even and levels do not return for 3 months)
FBC - anaemia that will exacerbate ischaemia, raised WCC
U&Es - Potassium (may cause arrhythmia)
Inflammatory markers - raised CRP
Capillary glucose - DM risk factor (esp. for silent MI)
Amylase - acute pancreatitis

19
Q

What other than ACS may cause a rise in troponin

A 
Coronary spasm
Aortic dissection
Myopericarditis
Hypertrophic cardiomyopathy 
Severe heart failure
Cardiac trauma f
PE
20
Q

What is the purpose of CXR for ACS testing

A

Erect chest radiograph to exclude pneumothorax and aortic pathology or Boerhaave’s (pneymomediastinum)

21
Q

How should a STEMI be managed acutely

A 
MONABASH 
Morphine (+anti emetic)
Oxygen if sats low
Nitrates e.g. GTN, isosorbide mononitrate for vasodilation
Antiplatelets e.g. aspirin 300mg
Beta blocker 
ACEi
Statins
Heparin 
\+ primary angioplasty or thrombolysis within 12 hours of onset
22
Q

How should a NSTEMI be managed acutely

A 
MONABASH 
Morphine (+anti emetic)
Oxygen if sats low
Nitrates e.g. GTN, isosorbide mononitrate for vasodilation
Antiplatelets e.g. aspirin 300mg
Beta blocker 
ACEi
Statins
Heparin 
Primary angioplasty if high risk
23
Q

When are beta blockers contraindicated

A

Asthma
Heart block
Heart failure

24
Q

What advice and medications should ACS patients be discharged with

A

Lifestyle change: smoking cessation, low-salt diet, exercise and weight loss
BP control i.e. ACEi, or CCB
Statin (or fibrates)
Diabetes control
Low-dose aspirin (life) and clopidogrel (year)

25
Q

What are the complications of MI

A 
Death 
Arrhythmia
Rupture
Tamponade
Heart failure
Valve disease
Aneurysm 
Dressler's syndrome
Embolism
Recurrence
26
Q

How does Dressler’s syndrome present

A

Pericarditis
Pleuritic chest pain (worse inspiration, relived lying forward)
Fever

27
Q

What are the investigations for suspected Dressler’s syndrome

A 
FBC - leucocytosis
ECG - diffuse saddle-shaped ST elevation across leads without ST depression, PR depression
Echo - pericardial effusion
CXR - pericardial effusion
Troponin - rule out MI
28
Q

What is the management for Dressler’s syndrome

A

Analgesia
Large dose aspirin or NSAIDs/colchicine
PPIs is NSAIDs given
Aspiration (pericardiocentesis) if pericardial effusion

29
Q

How are biliary colic and oesophageal spasm diagnosed

A

Oesophageal spasm - barium swallow and manometry

Biliary colic - Ultrasound

30
Q

What are patients who develop Boerhaave’s likely to dev elop

A

Pleural effusion
Pneumomediastinum
Pneumothorax
Infection by GI flora -> mediastinitis and sepsis

31
Q

How is Boerhaave’s treated

A

Antibiotic therapy and surgical repair

32
Q

Why do some patients get vomiting with acute MIs

A

Bezol-Jarisch reflex

Infarction of the inferior myocardium irritates the diaphragm -> vomiting

33
Q

What investigations should be ordered for suspected angina

A 
Exercise tolerant test (ECG and BP monitored during increasing amounts of exercise) 
Stress echo (given dobutamine)
Myoview scan (thallium injection)
CT coronary angiography 
Angiography/angioplasty
34
Q

What ECG changes would be expected in a patient who suffered a full-thickness inferior MI 2 years previously

A

The infarcted tissue no longer conducts electrical impulses

Deep, pathological Q waves

35
Q

What are the ECG changes you would see over 7 days in a patient with acute STEMI

A
  1. Tented T waves within minutes (localised hyperkalaemia)
  2. ST elevation in affected leads with depression in reciprocal leads (24-48hrs)
  3. T wave inversion in 1-2 days and persists for weeks/months unless treated
  4. Q waves within days (permanent)

Y3 Oxford Cases (29 decks)

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