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Core clinical problems > 46. Chest pain > Flashcards

46. Chest pain Flashcards

1
Q

Systems to consider for chest pain?

A

Cardiovascular
Respiratory
Gastrointestinal
MSK
Psych

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2
Q

History taking chest pain

A

SOCRATES
Character: tightening
Radiation: jaw, arm, back
Exacerbating and relieving: exercise?breathing? Movement? Coughing? GTN spray? sitting forwards?

Cardiac system: palpitations? Sweating? Syncope?
Respiratory system: shortness of breath, cough, haemoptysis
GI system: indigestion? Dysphagia?
MSK system: twisting movements?
Psychiatry: ‘In the past six months, did you ever have a spell or an attack when you suddenly felt anxious or frightened or very uneasy?’

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3
Q

Examination chest pain

A

Cardiac
Respiratory
GI
MSK - localise pain and palpate for tenderness

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4
Q

Invetsigations chest pain

A

Full set of observations including a blood pressure in both arms

Bedside
ECG

Bloods
Troponin
D-dimer
CRP/ESR
Full blood count (FBC)
Urea & electrolytes/liver function tests
Bone profile
Thyroid function tests
Blood glucose and lipid profile

Imaging
CXR
CT for rib fracture

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5
Q

chest pain

heavy, central chest pain they may radiate to the neck and left arm
nausea, sweating
elderly patients and diabetics may experience no pain
Risk factors for cardiovascular disease

A

MI

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6
Q

chest pain

History of asthma, Marfan’s etc
Sudden dyspnoea and pleuritic chest pain

A

pneumothorax

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7
Q

chest pain

Sudden dyspnoea and pleuritic chest pain
Calf pain/swelling
Current combined pill user, malignancy

A

PE

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8
Q

chest pain

Sharp pain relieved by sitting forwards
May be pleuritic in nature

A

Pericarditis

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9
Q

chest pain

Tearing’ chest pain radiating through to the back
Unequal upper limb blood pressure

A

Dissecting aortic aneurysm

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10
Q

chest pain

Burning retrosternal pain
Other possible symptoms include regurgitation and dysphagia

A

GORD

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11
Q

chest pain

The pain is often worse on movement or palpation.
May be precipitated by trauma or coughing

A

Musculoskeletal chest pain

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12
Q

chest pain followed by a rash

A

Shingles

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13
Q

pathophysiology ischaemic heart disease

A

Triggers such as smoking, high blood pressure and high blood sugar damage the lining of the heart –> inflamamtion –> fatty deposits worsened by high cholesterol –> plaques
- narrow = reduced blood flow
- rupture = completely block

  1. endothelial dysfucntion (triggered by smoking, HTN, hyperglycaemia)
  2. pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
  3. fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
  4. monocytes tun into foam cells and further propagate the inflammatory process
  5. Smooth muscle proliferation

= plaque
1. narrow lumen
2. rupture

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14
Q

NICE defintion of angina

A
  1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. precipitated by physical exertion
  3. relieved by rest or GTN in about 5 minutes
  • patients with all 3 features have typical angina
  • patients with 2 of the above features have atypical angina
  • patients with 1 or none of the above features have non-anginal chest pain
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15
Q

Investigation ?angina

A

1st line: CT coronary angiography

2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia) eg stress echocardiography

3rd line: invasive coronary angiography

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16
Q

Management of angina

A

+ aspirin, statin and GTN
1. Beta blocker OR CCB (non-dihydropyridine eg verapamil or dilatizem (DeaV is a risk)

  1. Increase above to max
  2. Beta blocker AND CCB (dihydropyridine eg amlodipine or MR-nifedipine
  3. If above not tolerated, consider
    - long acting nitrate eg Isosorbide mononitrate
    - ivabradine
    - nicorandil
    - ranolazine
  4. Three drugs only if awaiting assessment for PCI or CABG
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17
Q

first step management of angina

A

+ aspirin, statin and GTN
1. Beta blocker OR CCB (non-dihydropyridine eg verapamil or dilatizem (DeaV is a risk)

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18
Q

symptomatic/uncontrolled angina pt on aspirin, statin, GTN, BB

A

increase BB to max dose

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19
Q

symptomatic/uncontrolled angina pt on aspirin, statin, GTN, CCB verapamil

A

increase verapamil to max dose

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20
Q

symptomatic/uncontrolled angina pt on aspirin, statin, GTN, CCB verapamil or BB on max dose

A

Beta blocker AND CCB (dihydropyridine eg amlodipine or MR-nifedipine

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21
Q

if BB and amlodipine/nifedepine not tolerated, next step amangement of angina

A

If above not tolerated, consider
- long acting nitrate eg Isosorbide mononitrate
- ivabradine
- nicorandil
- ranolazine

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22
Q

history ACS

A

heavy, central chest pain
elderly patients and diabetics may experience no pain
Retrosternal pressure, tightness, constricting
Radiation to shoulders/arms/neck/jaw
Crescendo in nature, related to exertion
Associated with diaphoresis, sweating, nausea, pallor

SH: Risk factors for cardiovascular disease

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23
Q

examination ACS

A

Patients presenting with ACS often have very few physical signs to elicit:
pulse, blood pressure, temperature and oxygen saturations are often normal or only mildly altered e.g. tachycardia

if complications of the ACS have developed e.g. cardiac failure then clearly there may a number of findings

the patient may appear pale and clammy

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24
Q

Immediate management of ACS

A

MONA

Morphine IV (IF SEVERE PAIN- used to be routine)

Oxygen (IF <94)

Nitrates IV or sublingual (caution if hypotensive)

Aspirin 300mg

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25
Q

immediate invetsigation ACS

A

ECG

Troponin

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26
Q

how is a STEMI diagnosed

A

Symptoms + ECG changes

ST-segment elevation
New left bundle branch block

troponin confirms

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27
Q

How is an NSTEMI diagnosed

A

Troponin

NSTEMI has to be diagnosed based on troponin
NOT ECG, this just supports
IF trop negative = unstable angina

supported by:
ST segment depression
T wave inversion

Pathological Q waves suggest a deep infarction involving the full thickness of the heart muscle (transmural) and typically appear 6 or more hours after the onset of symptoms.

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28
Q

How much does ST have to be elevated to count as ST elevation

A

2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads

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29
Q

what ECG changes support a diagnosis of NSTEMI

A

ST segment depression
T wave inversion

Pathological Q waves suggest a deep infarction involving the full thickness of the heart muscle (transmural) and typically appear 6 or more hours after the onset of symptoms.

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30
Q

what leads are involved in are inferior? what artery?

A

II, III, aVF

Right coronary artery

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31
Q

what leads are anterior? what artery?

A

V1-V2 - septal leads - proximal LAD
V3-V4 - anterior leads - LAD

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32
Q

what leads are lateral? which artery?

A

I, aVL, v5, v6

circumflex

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33
Q

which leads are septal leads

A

v1-v2

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34
Q

which leads are ‘high lateral’

A

I and avL

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35
Q

Posterior stemi on ecg?

A

shows the reciprocal changes in A and S
PAILS

V1-V3
horizontal ST depression
Upright T waves
tall broad R waves >30ms
dominant R wave (R/S ratio >1) in V2

Posterior infarction is confirmed by the presence of ST elevation and Q waves in the posterior leads (V7-9)

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36
Q

mneumonic for reciprocal changes

A

PAILS

write in a ring , reciprocal changes will be seen in adjacent zones, especially going in P–>S direction

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37
Q

first cardiac enzyme to rise

A

myoglobin

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38
Q

what cardiac enzyme is useful to look at for reifarction

A

CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days (troponin T remains elevated for up to 10 days)

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39
Q

troponin T begins to rise, peak and return to normal

A

begin to rise 4-6 hours
peak value 12-24 hours
returns to normal 7-10 days

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40
Q

what troponin level can rule out MI

A

troponin <14ng/l
AND
pain > 6 hours

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41
Q

what to do if troponin 14-30ng/l

A

if low risk test troponin again >3 hours later

if moderate/high tisk or symptomatic –> probable MI

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42
Q

troponin 20 low risk, tested again >3 hours later… what makes it MI or not

A

change >7 or reached threshold of 30 = probable MI

change <7 and not reached 30 –> rev alt causes

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43
Q

what troponin result rules in MI

A

troponin > 30ng/l

WITH history of cardiac symptoms

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44
Q

broad categories of management options STEMI

A

medical

priamry PCI

fibrinolysis

45
Q

how do you decide which management option is right for a pt STEMI

A

eligible for PCI?

have they presented within 12 hours?

is PCI available in 120 mins?

46
Q

STEMI management not eligible for reperfusion therapy

A

Medical
1. ticagrelor + aspirin

If high bleeding risk, offer clopidogrel + aspirin, or aspirin alone

PLUS cardiac rehabilitation and secondary prevention

47
Q

STEMI management Presenting within 12 hours and PCI available within 120 mins

A
  1. CT coronary angiography with follow on primary PCI

+ Drug therapy for primary PCI:
- Prasugrel with aspirin if not taking another anticoagulant
- Clopidogrel with aspirin if taking another anticoagulant

PLUS cardiac rehabilitation and secondary prevention

48
Q

STEMI management Presenting within 12 hours and PCI not available within 120 mins

A

Fibrinolysis
Ticagrelor + aspirin

PLUS cardiac rehabilitation and secondary prevention

49
Q

Management NSTEMI

A

B – Base the decision about angiography and PCI on the GRACE score
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)
M – Morphine titrated to control pain
A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)
N – Nitrate (GTN)

50
Q

alternative causes for raised troponin

A

Chronic kidney disease
Sepsis
Myocarditis
Aortic dissection
Pulmonary embolism

51
Q

apart from ECG and troponin, what other tests would you do ?ACS

A

Baseline bloods, including FBC, U&E, LFT, lipids and glucose

Chest x-ray to investigate for pulmonary oedema and other causes of chest pain

Echocardiogram once stable to assess the functional damage to the heart, specifically the left ventricular function

52
Q

general rule for ACS management of the second antiplatelt to choose? dosing?

A

Ticagrelor 180mg stat dose (loading)
then 90 mg twice daily usually for up to 12 months

  • clopidogrel if high bleeding risk
  • prasugrel if having angiography
53
Q

what is the GRACE tool

A

The GRACE score gives a 6-month probability of death after having an NSTEMI.

3% or less is considered low risk
Above 3% is considered medium to high risk

54
Q

Secondary prevention of MI

A

Aspirin 75mg once daily indefinitely
Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril) titrated as high as tolerated (ARB if intolerant)
Atenolol (or another beta blocker – usually bisoprolol) titrated as high as tolerated (if CI, use diltiazem or verapamil if no pulmonary congestion or LV dysfunction)

Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily) - MONITOR renal function closely if taking this and ACEi/ARB - risk of fatal hyperkalameia

55
Q

monitoring if taking spironolactone and ACEi

A

MONITOR renal function closely - risk of fatal hyperkalameia

56
Q

complications of MI

A

D – Death
R – Rupture of the heart septum or papillary muscles
E – “oEdema” (heart failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome

57
Q

pleuritic chest pain, low grade fever and pericardial rub post MI

A

Dressler’s Syndrome

58
Q

pathophysiology dresslers syndrome

A

localised immune response that results in inflammation of the pericardium, the membrane that surrounds the heart (pericarditis).

59
Q

investigation dresslers syndrome

A

ECG (global ST elevation and T wave inversion),
Echocardiogram (pericardial effusion)
ESR raised inflammatory markers (CRP and ESR).

60
Q

management dresslers

A

Management is with NSAIDs (e.g., aspirin or ibuprofen) and, in more severe cases, steroids (e.g., prednisolone). Pericardiocentesis may be required to remove fluid from around the heart, if there is a significant pericardial effusion.

61
Q

types of myocardial infarction

A

ACDC mneumonic

Type 1: A – ACS-type MI

Type 2: C – Can’t cope MI
Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)

Type 3: D – Dead by MI
Sudden cardiac death or cardiac arrest suggestive of an ischaemic event

Type 4: C – Caused by us MI
MI associated with procedures such as PCI, coronary stenting and CABG

62
Q

referral of cardiac chest pain from primary care??

A

current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency admission

chest pain 12-72 hours ago: refer to hospital the same-day for assessment

chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action

63
Q

What is cardiac rehabilitation

A

start before discharge - assessment appt to take place within 10 days of discharge

includes:
- physical activity
- lifestyle advice including on driving, flying and sex
- stress management
- health education

64
Q

diet advice cardiac rehabilitation

A

Mediterranean diet (fish, fruit, veg, olive oil)

65
Q

exercise advice cardiac rehabilitation

A

regular physical activity - 20-30 mins to point of slight breathlessness

66
Q

define acute pericarditis

A

Acute pericarditis is a condition referring to inflammation of the pericardial sac, lasting for less than 4-6 weeks

67
Q

causes pericarditis

A

infections:
viral infections (Coxsackie)
tuberculosis

systemic:
uraemia
post-myocardial infarction
connective tissue disease
systemic lupus erythematosus
rheumatoid arthritis
hypothyroidism
malignancy
lung cancer
breast cancer

trauma
radiotherapy

68
Q

features percarditis

A

chest pain: may be pleuritic. Is often relieved by sitting forwards

other symptoms include a non-productive cough, dyspnoea and flu-like symptoms

pericardial rub

69
Q

types of post-MI pericarditis

A

early (1-3 days): fibrinous pericarditis
late (weeks to months): autoimmune

pericarditis (Dressler’s syndrome)

70
Q

ecg changes pericarditis

A

global/widespread
‘saddle-shaped’ ST elevation
PR depression

71
Q

most specific ecg change pericarditis

A

PR depression

72
Q

invetsigations pericarditis

A

transthoracic echocardiography

bloods
- inflammatory markers
- troponin: around 30% of patients may have an elevated troponin - this indicates possible myopericarditis

73
Q

management pericarditis

A

NSAIDS AND COLCHICINE if idio[athic or viral until symptom resolution and normalisation of inflammatory markers (usually 1-2 weeks) followed by tapering of dose recommended over

+ decide if need admission
- majority - no
- fever >38 or elevated troponin

+ treat underlying cause
- majority is viral so no treatment

+ avoid strenuous activity until symptoms and inflammatory markers normalised

74
Q

who with pericarditis should be managed as an inpatient

A

high-risk features such as fever > 38°C or elevated troponin should be managed as an inpatient

75
Q

how long should colchicine and nsaids be used for pericarditis

A

until symptom resolution and normalisation of inflammatory markers (usually 1-2 weeks) followed by tapering of dose recommended over

76
Q

causes of constrictive pericarditis

A

any cause of pericarditis
particularly TB

77
Q

features of constrictive pericarditis

A

dyspnoea
right heart failure: elevated JVP, ascites, oedema, hepatomegaly
JVP shows prominent x and y descent
pericardial knock - loud S3
Kussmaul’s sign is positive

78
Q

CXR constrictive pericarditis

A

pericardial calcification

79
Q

what is kussmauls sign

A

a paradoxical rise in JVP during inspiration

present in constrictive pericarditis

80
Q

JVP features cardiac tamponade vs constrictive pericarditis

A

TAMpaX = just X (absent y descent)

constrictive pericarditis = X and Y present

81
Q

what is pulsus paradoxocus

A

During normal inspiration, there is a slight fall in systolic blood pressure (<10 mm Hg) as venous return to the left ventricle decreases (because of increase in lung capacitance as lung volume increases) and as inspiratory negative intrapleural (intrathoracic) pressures are superimposed onto the aorta.

pulsus paradoxocus >10mmHg
- present in cardiac tamponade

82
Q

what is myocarditis

A

inflammation of the myocardium

83
Q

causes myocarditis

A

viral: coxsackie B, HIV
bacteria: diphtheria, clostridia
spirochaetes: Lyme disease
protozoa: Chagas’ disease, toxoplasmosis
autoimmune
drugs: doxorubicin

84
Q

presentation myocarditis

A

usually young patient with an acute history
chest pain
dyspnoea
arrhythmias

85
Q

invetsigations myocarditis

A

ecg
tachycardia
arrhythmias
ST/T wave changes including ST-segment elevation and T wave inversion

bloods
↑ inflammatory markers in 99%
↑ cardiac enzymes
↑ BNP

86
Q

management myocarditis

A

treatment of underlying cause e.g. antibiotics if bacterial cause

supportive treatment e.g. of heart failure or arrhythmias

87
Q

complications myocarditis

A

heart failure
arrhythmia, possibly leading to sudden death
dilated cardiomyopathy: usually a late complication

88
Q

what is pleurisy

A

also known as pleuritis, is inflammation of the membranes that surround the lungs and line the chest cavity (pleurae).[1] This can result in a sharp chest pain while breathing.

89
Q

causes pleurisy

A

Most common cause: viral infection
Other causes include bacterial infection, pneumonia, pulmonary embolism, autoimmune disorders, lung cancer, following heart surgery, pancreatitis and asbestosis.

90
Q

most common cause pleurisy

A

viral infection

91
Q

complications pleurisy

A

Pleural effusion
Pneumothorax
Hemothorax

92
Q

Causes MSK chest pain

A

Costochondritis
Lower rib pain syndromes
Rib fractures/chest trauma
Fibromyalgia
Primary or secondary bone metastases in the rib
Inflammatory arthritides - generally there will be other joint involvement
Tietze syndrome
Spinal disorders (disc prolapse, cervical spondylosis, facet joint dysfunction)

93
Q

features of MSK chest pain

A

sharp and often nagging. Often, the pain is localized but can radiate.

Pain is generally worsened by movement, changes in position, and deep inspiration.

94
Q

features rib fracture - history, symptoms, signs

A

History — previous history of trauma or coughing.
Symptoms — unilateral, sharp chest pain, worse with inspiration.
Signs — bruising and tenderness on palpation over the affected rib.

95
Q

best investigation rib fracture

A

CT scan of the chest

96
Q

management rib fracture

A
  1. conservative with good analgesia
  2. surgical fixation if pain and fractures have failed to heal following 12 weeks of conservative management
97
Q

why is it important that pain for rib fractures are managed well?

A

inadequate ventilation may predispose to chest infections

98
Q

features costochondritis

A

recent history of cough, vomiting, over-exercising, or similar.

Symptoms — unilateral, sharp, anterior chest-wall pain, exaggerated by breathing, activity, or a particular posture. Usually preceded by exercise or an upper respiratory tract infection, and can last for months.

Signs — tenderness over the costochondral junction and pain in the affected area when palpating the chest wall.

99
Q

what is tietzes syndrome?

A

a more severe form of costochondritis

tender, fusiform swelling of the costal cartilage at the costochondral junction.

100
Q

features lower rib pain syndrome

A

Lower rib pain syndrome generally causes lower chest pain/upper abdominal pain with an identifiably tender spot on the costal margin.

Pain may be reproduced during examination by pressing on this spot.
Pain is also reproduced using the ‘hooking manoeuvre’
Hooking manoeuvre = the examine hooks fingers under the patient’s ribs and pulls gently forward.
It may be difficult to perform the manoeuvre in patient with this syndrome due to exquisite sensitivity in the subcostal margins

101
Q

features of fibromyalgia chest pain

A

Chest pain in fibromyalgia is typically sharp and worse on inspiration and movement.
There is often tenderness to palpation.
Most commonly of the second anterior costochondral junctions.
Typically affecting more than one rib.
Other symptoms of fibromyalgia typically present (e.g. pain in other areas, symptoms of depression and anxiety, cognitive impairment, etc.).

102
Q

what is boerhaave syndrome

A

Spontaneous rupture of the oesophagus DUE TO episodes of repeated vomiting often in association with alcohol excess
Typically there is an episode of repetitive vomiting followed by severe chest and epigastric pain

103
Q

plan ?boerhaave syndrome

A

Invetsigation:
Diagnosis is by CT and contrast studies

Management:
Treatment is surgical; during first 12 hours primary repair, beyond this usually creation of controlled fistula with a T Tube, delay beyond 24 hours is associated with fulminent mediastinitis and is usually fata

104
Q

features oeseophageal rupture

A

History — a recent history of a medical procedure, foreign body ingestion, or oesophageal cancer.
Symptoms — thoracic oesophageal perforation leads to chest pain, dyspnoea, and odynophagia.
Signs — classical findings include fever and subcutaneous emphysema (around the neck and upper chest wall).

105
Q

odynophagia defintion

A

pain on swallowing

106
Q

what is diffuse oeseophageal spasm

A

esophageal motility disorder that often manifests as dysphagia. If the diagnosis is delayed, diffuse esophageal spasm is associated with high morbidity.

107
Q

what may barium swallow show for esopheageal spasm

A

‘nutcracker oesophagus’

108
Q

features oeseophgeal spasm

A

dysphagia

chest pain

Core clinical problems (94 decks)

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