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Oxford clinical cases > Chest pain > Flashcards

Chest pain Flashcards

1
Q

What are the most common causes of acute chest pain in a 60+ patient?

A 
Musculoskeletal inflammation 
Acute Coronary syndrome
PE
Pleurisy (Secondary to infection) 
Oesophagitis (secondary to GORD) 
Pneumothorax
Anxiety
Aortic dissection
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2
Q

What are the most common causes of musculoskeletal inflammation leading to chest pain?

A

Sprained muscle e.g. cough
Coxsackie B infection (Bornholm’s disease)
idiopathic costochondritis (Tietze’s syndrome)
Varicella Zoster infection –> neuropathic pain restricted to a dermatome.

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3
Q

Young female on COCP with acute chest pain

A

PE (COCP thrombogenic)
Pneumothorax (Especially if tall and thin)
Cocaine induced coronary spasm (still quite rare)

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4
Q

Which conditions which present with acute chest pain require immediate management?

A 
ACS
Pneumothorax
Aortic dissection 
PE 
Boerhaave's perforation
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5
Q

What is boerhaave’s perforation?

A

Spontaneous transmural rupture of the oesophagus. Usually occurs after forced emesis.

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6
Q

What are some features of Acute coronary syndrome?

A

Central, crushing pain in the chest.
Radiates to one or both arms, neck or jaw
Usually lasts a few mins to half an hour.

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7
Q

What are some cardiovascular risk factors?

A 
Hypercholesterolaemia 
Diabetes mellitus 
Smoking 
Hypertension 
Family history
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8
Q

What are some signs of hypercholesterolaemia

A

Xanthelasma, Corneal arcus (although this is normal in older people), xanthomata (cholesterol deposits around the tendons e.g. back of hands or on bony prominences)

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9
Q

Signs of peripheral (atherosclerotic) vascular disease

A 
Weak peripheral pulses
Peripheral cyanosis
Carotid bruits
Cold peripheries 
Atrophic skin 
Ulcers
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10
Q

Why is an arrhythmia relevant in ACS?

A

The arrhythmia may be the cause of the ischaemia as both brady and tachyarrhythmias cause a drop in CO. Secondly, most arrhythmias around in or around the scarred myocardium, both from old infarcts and acute ones.

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11
Q

What symptom does ventricular tachycardia commonly cause?

A

Shock

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12
Q

What symptom does heart block commonly cause?

A

Chest pain

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13
Q

What is a common history in an aortic dissection case?

A

Sudden onset tearing chest pain radiating to the back
Absent pulse in one arm.
Hypertension (50%)
OR hypotension (25%)
difference in blood pressure in arms 1/3 cases >20mmHg
New onset aortic regurgitation

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14
Q

What are the two types of aortic dissection?

A

Type A and B.
A: ascending aorta (most common)
B: descending aorta

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15
Q

Risk factors for aortic dissection

A 
Hypertension (most common) 
Male between 40-60 
Smoking
Atherosclerosis
Crack cocaine 
Aortic valve replacement
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16
Q

Which branches of the aorta can be obstructed during aortic dissection?

A

Carotid (Hemiparesis, dysphasia, blackout)
Coeliac (abdominal pain as ischaemic bowel)
Subclavian (ataxia, loss of consciousness)
Renal (renal failure, anuria)
Coronary (chest pain, angina or MI)
Anterior spinal (paraplegia)

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17
Q

Features of pneumothorax

A

Sudden onset pleuritic chest pain with breathlessness (could also be painless)
Hyperinflated chest wall with impaired expansion
Absent breath sounds
Hyper-resonance over affected lung
Tracheal deviation
NOTE: tracheal deviation in tension pneumothorax can lead to compression of the heart and cardiopulmonary arrest . Thus a trachea that deviates away from the pneumothorax is a medical emergency.

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18
Q

What are the 3 types of pneumothorax?

A

Spontaneous
Secondary
Traumatic

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19
Q

How do you manage a tension pneumothorax?

A

Maximum O2
Insert a large bore needle into 2nd ICS MCL to relieve pleural pressure
Insert a chest drain soon after

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20
Q

How do you classify a small and moderate pneumothorax?

A

Small: <2cm lung-pleural margin
Moderate: >2cm lung-pleural margin

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21
Q

How do you manage a small and moderate pneumothorax?

A

Small: analgesia
Moderate: Aspiration using large bore cannula (2nd ICS MCL) or catheter. X-ray: just after, 2 hours after, 2 weeks after. If aspiration fails: chest drain (4-6th ICS MCL)

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22
Q

History of a patient with PE from DVT (95% of cases)

A

Small: often asymptomatic. Earliest sign is tachycardia and tachypnoea
Moderate: Tachypnoea, tachycardia, SOB, pleural rub, low saturation O2 despite supplementation
Massive PE: Hypoxia, Shock, cyanosis, Signs of right heart strain. (raised JVP, left parasternal heave)
Multiple recurrent PE: Signs of pulmonary hypertension and right heart failure.

GENERALLY: Tachycardia, haemoptysis, sudden onset shortness of breath, pleuritic chest pain

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23
Q

What investigation should you perform of anyone with suspected cardiac disease?

A

ECGs

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24
Q

What is the most common ECG finding in PE?

A

Tachycardia

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25
Q

What other signs may you see on the ECG in a PE patient?

A

Signs of right heart strain (E.g. RBBB and T wave inversion in the right precordial leads)

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26
Q

What ECG signs would be seen in a patient with STEMI?

A

ST elevation and new-onset LBBB

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27
Q

Why are blood tests performed in patients with suspected cardiac disease?

A

Check for troponin. It has a high sensitivity and specificity for damage to cardiac muscle.

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28
Q

What is a drawback of using troponin as a cardiac marker?

A

It has a minimum 3 hour delay in increased troponin levels.

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29
Q

What other marker can be used?

A

CK-MB. (an isotope of the enzyme creatinine kinase).

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30
Q

What are some pros and cons of using CK-MB?

A

Released more rapidly following damage.

Con: Levels fall back to normal within 2-3 days whereas troponin levels remain high for >7 days.

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31
Q

What does high CK-MB levels >4 days after infarction suggest?

A

Re-infarction

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32
Q

What are some problems associated with using troponin to diagnose ACS?

A

Troponin is specific for cardiac damage but not 100% specific for ACS. Other conditions that cause a raised troponin include: Coronary spasm (Cocaine use), aortic dissection causing ischaemia, myopericarditis, cardiac trauma, PE.
ALSO, troponin is renally excreted so you have to be wary with renal failure patients with a raised troponin level.

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33
Q

Why is it important to assess serum cholesterol ASAP after a suspected MI?

A

An MI will result in a decrease in HDL, LDL and total cholesterol within about 24 hours post MI and it will not return to normal level up to 2-3 months later.

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34
Q

In a FBC what are you looking for?

A

To see if the patient is anaemic as this will exacerbate any deficiency in cardiac perfusion, resulting in ischaemic heart disease.

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35
Q

What should you pay attention to in a patient’s U&Es?

A

Their potassium levels as this could be the cause of an arrhythmia.

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36
Q

What inflammatory markers are you looking for and why?

A

WCC and CRP. These are elevated in inflammatory processes such as pericarditis or Bornholm’s disease. They are also elevated in MI, aortic dissection, which cause inflammation of the affected tissues.

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37
Q

What type of infarcts are diabetics more likely to present with?

A

Silent infarcts. These are MI without pain.

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38
Q

Why do we test for amylase in the blood test?

A

Often acute pancreatitis can present with chest pain and no epigastric tenderness.

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39
Q

What imaging is done in a patient presenting with acute chest pain and why?

A

Erect radiograph. This is to exclude pneumothorax and aortic pathology (dissection –> wide mediastinum). If Booerhave’s perforation of the oesophagus is suspected, chest radiograph will typically show air around the heart shadow, pleural effusion or pneumothorax.

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40
Q

What do you test for in the blood overall?

A 
Troponin
CK-MB
Amylase
Inflammatory markers
FBC
Serum cholesterol
U&amp;Es 
Capillary glucose
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41
Q

What are D-dimer levels symptomatic of?

A

Symptomatic of breakdown of a fibrin clot for whatever reason e.g. recent surgery or trauma.

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42
Q

Why would a D-dimer test be performed in someone with chest pain?

A

Low D-dimer levels can be used to rule out DVT or PE as these are unlikely to occur without any fibrin breaking down.

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43
Q

What can you see on an ECG in a patient with anterior NSTEMI?

A

ST depression in leads V1-V3.

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44
Q

What else could ST depression in leads V1-V3 suggest? How is this treated?

A

Posterior infarct. This is treated like a STEMI despite the lack of ST elevation.

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45
Q

Why is chest pain not always a feature in diabetics?

A

Long standing diabetics often have neuropathy and dulled pain sensation.

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46
Q

What is a main difference between a STEMI and an NSTEMI

A

A STEMI is a full thickness infarct (full occlusion) whereas an NSTEMI is a partial-thickness infarct.

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47
Q

All patients with any ACS are started on a cocktail of drugs which are remembered by which mnemonic?

A

MONABASH

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48
Q

MONABASH

A

Morphine and an anti-emetic e.g. Metoclopramide
Oxygen: ONLY to maintain oxygen saturation at 94%
Nitrates e.g. GTN
Antiplatelets: aspirin and clopidogrel
Beta blockers
ACE inhibitors (improve endothelial function)
Statins (improve endothelial function and modulate inflammatory responses)
Heparin (LMWH), prevent coronary thrombosis

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49
Q

When are beta blockers contraindicated?

A

Heart block
Asthma
Signs of acute heart failure

50
Q

Some advantages of ACEi post MI

A

Attenuation of post-infarct ventricular remodelling that can cause arrhythmias.
Reduction of AngII induced vasoconstriction
Beneficial effects on endothelial function

51
Q

Some benefits of statins post MI

A 
Reduce cholesterol levels
Improve endothelial function 
modulate inflammatory responses 
Maintain atherosclerotic plaque stability 
Prevent thrombus formation
52
Q

What should STEMI patients also receive?

A

Either primary angioplasty or thrombolysis within 12 hours of onset of pain.

53
Q

which is preferred over thrombolysis and angioplasty?

A

Angioplasty

54
Q

Under what circumstances would an NSTEMI patient have angioplasty?

A

Haemodynamically unstable, ongoing chest pain, severe left ventricular dysfunction, mitral regurgitation, VSD, sustained ventricular tachyarrhythmias.

55
Q

What are prominent R waves suggestive of?

A

Posterior MI

56
Q

What other drug do you give if statins are not tolerateD?

A

Fibrins

57
Q

What is the GRACE score?

A

It provides a schema for risk stratifying NSTEMI patients.

58
Q

How does a post MI patient reduce their thromboembolic risk?

A

Aspirin life long and ADP receptor blocker e.g. clopidogrel for 1 year.

59
Q

What are the common complications of MI? (DARTH VADER)

A 
Death
Arrhythmia
Rupture (either of the septum or the outer walls)
Tamponade
Heart failure
Valve disease
Aneurysm
Dressler's syndrome
Embolism
Reinfarction
60
Q

what is Dressler’s syndrome?

A

autoimmune pericarditis 2-10 weeks post-MI; note that simple post-MI pericarditis is more common and presents within 2-4 days.

61
Q

What would a full blood count show in dressler’s syndrome?

A

Leucocytosis

62
Q

Why would you also perform an ECG and Troponin test?

A

To exclude reinfarction or pulmonary pathology.

63
Q

How should we treat the patient with suspected pericarditis?

A

Immediately start the patient on analgesia. large doses of anti-inflammatory drugs such as aspirin, other NSAIDs and/ or colchicine may be given and are usually sufficient. Patients may require PPIs e.g. omeprazole to prevent gastric irritation from the high dose aspirin or NSAIDs. If there is a significant pericardial effusion, it can be aspirated (pericardiocentesis).

64
Q

What should you check in a patient that is started on high dose ACEinhibitors and aspirin?

A

Their renal function should be assessed frequently

65
Q

What is colchicine most commonly used to treat?

A

Gout

66
Q

Other than angina, what else can GTN spray relieve?

A

Oesophageal spasm

67
Q

How can you diagnose gall stones (Causing biliary colic?

A

Ultrasound

68
Q

How can oesophageal spasm be detected?

A

Barium swallow and manometry (although a normal result does not exclude it)

69
Q

What is oesophageal manometry?

A

A test used to identify problems with movement and pressure within the oesophagus which may lead to problems like heart burn. Manometry measures the strength and muscle coordination of your oesophagus when you swallow.

70
Q

What do you prescribe to someone with oesophageal spasm secondary to reflux?

A

PPIs

71
Q

What is variant or prinzmetal angina?

A

It is a syndrome with angina caused by coronary artery vasospasm, and most commonly occurs in individuals at rest, asleep or lying down.

72
Q

What is coronary syndrome X?

A

Cardiac syndrome X (CSX) is typical anginalike chest pain with evidence of myocardial ischemia in the absence of flow-limiting stenosis on coronary angiography

73
Q

What is a common ECG finding in a patient with pericarditis?

A

Saddle shaped ST elevation in a number of leads not conforming to the territory of a single coronary artery

74
Q

What can Marfan’s syndrome predispose to?

A

Dissected thoracic aorta/ dissected aortic aneurysm or a spontaneous pneumothorax.

75
Q

What would a chest X-ray show in an individual with aortic dissection?

A

Widened mediastinum

76
Q

Why should you pay attention to a patient’s blood pressure with suspected aortic aneurysm/dissection?

A

Patients with aortic aneurysm are often hypertension but can become hypotensive if they dissect back into the pericardial space and develop cardiac tamponade (along with muffled heart sounds and distended neck veins)

77
Q

How is an aortic dissection classified?

A

Stanford classification divides dissection into:
Type A with ascending aorta tear (most common)
Type B with descending aorta tear distal to the left subclavian artery

78
Q

How do you treat a type A and type B dissection?

A

Type A dissection is a surgical emergency because of the risk of cardiac tamponade.
Type B dissection can be treated medically, surgically or by endovascular stunting.

79
Q

What coronary problems can cocaine usage cause?

A

Coronary artery spasm

80
Q

What are nausea and vomiting commonly associated with in patients with chest pain?

A

Inferior MI

81
Q

What is Booerhave’s syndrome?

A

Spontaneous tear in the oesophageal wall due to increased intraoesophageal pressure from vomiting.

82
Q

What are some symptoms of Boeerhave’s syndrome?

A

Chest pain following severe vomiting, dyspnea, fever, shock, cyanosis

83
Q

How can you differentiate between Boeerhave’s and MI?

A

In Boeerhave’s the vomiting precedes the pain. In MI, the pain precedes the vomiting.

84
Q

Why can you get vomiting post-MI?

A

The post-infarct inflammation irritates the diaphragm

85
Q

What can patients with Booerhave’s go on to develop?

A

Pleural effusion, pneumomediastinum, and/or pneumothorax perhaps followed by infection with GI flora.

86
Q

What dose treatment of Boerhaave’s syndrome consist of?

A

Prompt antibiotic therapy and surgical repair of the oesophagus with mediastinal washout.

87
Q

What is the prognosis for patients with Boerhaave’s?

A

Prognosis is grim with a 30% mortality if surgical intervention is initiated within 24 hours.
50-60% mortality if surgery is delayed beyond 24 hours.

88
Q

What would you expect to hear on auscultation in a patient with pulmonary oedema?

A

Bibasal crackles

89
Q

Why do some patients with acute MI get n&v but not all?

A

This is called the Bezold-Jarisch reflex. Infarction of the interior myocardium irritates the diaphragm, resulting in vomiting.

90
Q

Why else may a patient with chest pain present with n&v?

A

If a patient is undergoing angiography

91
Q

what are the ECG findings of an anterior infarct?

A

ST elevation in leads V2,3,4. This indicates infarction of the anterior surface of the left ventricle, supplied by LAD.

92
Q

What are the ECG findings of a right/inferior infarct?

A

ST elevation in leads II,III and avF indicates infarction of the inferior surface supplied by the Right coronary artery.

93
Q

What are the ECG findings of a lateral infarct?

A

ST elevation in leads V5,V6. This indicates infarction of the lateral surface of the left ventricle and may be involved in a circumflex or LAD lesion.

94
Q

What are the ECG findings of a posterior infarct?

A

ST DEPRESSION in V1-V3 with tall R waves. This is indicative of circumflex occlusion i.e. true posterior infarct. Look particularly for a dominant R wave in V1.

95
Q

What are the earliest biochemical changes in MI?

A

Troponin

CK-MB (levels detected sooner but less specific for cardiac damage)

96
Q

Why are troponin levels used?

A

Because they have a very high sensitivity and specificity for cardiac damage

97
Q

Describe the MOA of aspirin

A

Aspirin is an anti-platelet and irreversible COX inhibitor which synthesises inflammatory mediators including the platelet aggregator TxA2. Aspirin’s action is reversed on synthesis of new platelets.

98
Q

Describe the MOA of clopidogrel

A

Anti-platelet that irreversible blocks the ADP receptor on platelet cell membranes that prevents them binding to fibrinogen and hence inhibits platelet aggregation.

99
Q

Describe the MOA of abciximab and tirofiban

A

Anti-platelets which reversibly block fibrinogen binding to glpIIb/IIIa receptors on platelet cell membranes that mediate platelet aggregation

100
Q

What is bivalirudin?

A

A direct thrombin inhibitor and anti-platelet. It is sometimes used instead of heparin (An indirect thrombin inhibitor)

101
Q

What investigations should you request for a patient presenting with new-onset angina?

A 
Exercise tolerance test (a patient's ECG and blood pressure are monitored during increasing amounts of exercise)
Stress Echocardiogram
Myoview Scan
CT coronary angiography
Angiography/angioplasty
102
Q

What features in an exercise tolerance test indicate stenosis of the coronary arteries?

A

ST depression of >2mm
Symptoms of exertion angina
ST elevation >1mm

103
Q

What does a drop in BP during an exercise tolerance test indicate?

A

A poor prognostic sign

104
Q

What does 70% specificity mean?

A

That 30% of positive results will be false positives.

105
Q

Why would we perform a stress echocardiogram instead of an exercise tolerance test?

A

For those patients who cannot perform an exercise tolerance test e.g. cannot walk or have severe arthritis. Patient given dobutamine to stimulate stress while an echo is performed.

106
Q

What does the echocardiogram of an ischaemic myocardium show?

A

An ischaemic myocardium is hypo kinetic

107
Q

What score can be calculated from a CT coronary angiography?

A

The calcium score which reflects the degree of atherosclerosis

108
Q

Under what circumstances would an angioplasty/angriography be performed?

A

If any of the other tests are positive then the patient is eligible for diagnostic testing.

109
Q

Would you expect to see findings on an eCG of a patient who had an MI two years previously?

A

Yes,old infarcts are visible on ECG as the infarcted tissue no longer conducts electrical impulses

110
Q

What ECG signs would you see in a patient that suffered a full thickness inferior MI 2 years ago?

A

Deep, pathological Q waves >2mm

111
Q

What ECG changes would you see over a week in a patient presenting with acute STEMI?

A
  1. Tented T waves in the affected leads within minutes of occlusion due to hyperkalaemia following myocyte ischaemia
  2. ST elevation in the affected leads with ST depression in the reciprocals, lasting 24-48 hours
  3. T wave inversion developing in 1-2 days and persisting for weeks or months unless the MI is treated.
  4. Q waves developing within days and remaining indefinitely
112
Q

What ECG sign do you see in a patient with hyperkalemia?

A

Tented T-waves

113
Q

What D-Dimer finding rejects diagnosis of PE?

A

A Wells score <4 and a D dimer <500ng/mL predicts with 98% certainty that the patient does not have PE. If D-dimer <500 and PE still suspected then start them on LMWH and perform a CTPA.

114
Q

What is the treatment for a CTPA verified PE?

A

Start the patient on anticoagulation therapy (Warfarin or rivaroxaban). This is usually continued for a minimum of 3 months. (The patient will have been on LMWH whilst CTPA performed etc)

115
Q

If a hyperlipidaemic patient is intolerant of statins, what is the second line drug you’d give them?

A

Ezetimibe

116
Q

How does ezetimibe work?

A

It works by inhibiting the absorption of cholesterol from the small intestine and decreases the amount of cholesterol available to the liver cells so they absorb the cholesterol from the circulation

117
Q

What is the definition of Hernia?

A

The abnormal protrusion of a body viscous through its normal anatomical constraints.

118
Q

3 Causes of AF

A

Hypertension
Thyrotoxicosis
Valvular heart disease

119
Q

3 Causes of AF

A

Hypertension
Thyrotoxicosis
Valvular heart disease

120
Q

Stages of hypertension

A

130-140 Stage 1
140-160 stage 2
160-180 stage 3
>180 stage 4

121
Q

Causes of secondary hypertension

A

Renal: renal artery stenosis, chronic pyelonephritis, glomerulonephritis, interstitial kidney disease

Endocrine: Cushing’s disease, thyrotoxicosis, phaeochromocytoma, Conn’s

Drug induced hypertension: cocaine, NSAIDs, salicylic acid

NOTE: typically under age of 35/40

Oxford clinical cases (4 decks)

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