1. APPROACH TO CHEST PAIN
DR SAZWAN REEZAL BIN SHAMSUDDIN
EMERGENCY MEDICINE SPECIALIST
MEDTWEETMY
2. Objectives:
• Anatomy.
• Relationship of coronary arteries with ECG.
• Pathophysiology of chest pain.
• Risk stratification/Scoring system.
• Acute coronary syndrome.
• Interpretation of cardiac enzymes/biomarkers.
• Management
• Other life threatening chest pain
• Stepwise approach
3. Scenario.
• 40/Male
• DM/HPT x 5years
• c/o central chest x 2 hours.
• Heaviness, non radiating
• Assoc nausea+ sweating+
• First episode
• 52/female
• Post op D3, TKR
• c/o central chest pain
• Associated with breathlessness.
• Sweating+
• Coughing out streak of blood
6. Pathophysiology of chest pain (1)
• Somatic Pain fibers
– Dermis and parietal
pleura innervations
– These enter the spinal
cord at specific levels
and arranged in a
dermatomal pattern.
• Visceral Pain fibers
– Found in internal organs
such as heart and
esophagus and blood
vessels
– Enter the cord at
multiple levels and
“share” parietal cortex
space with the somatic
fibers.
7. Pathophysiology of chest pain(2)
• Somatic Pain fibers
– Pain is usually easily
described.
– Precisely located.
– Described as a sharp
sensation.
• Visceral Pain fibers
– Imprecisely localized.
– Difficult to describe.
– Often described as
aching, discomfort,
heaviness.
– Often misinterpreted
because the pain is
referred to a different
area by the adjacent
somatic nerve.
8. Pathophysiology of chest pain(3)
• Several modifying factors to the pain
sensation.
• Comorbidities, age, gender,
medications, drugs, alcohol.
• Cultural and language difference :
sekok, kenaleng
• Group with atypical chest
pain:
Elderly
Female
Diabetic
Mentally challenge.
9. 1) Acute Coronary Syndrome (ACS)
• Spectrum of ischaemic heart
disease.
• Range from Unstable Angina
NSTEMI STEMI.
• Increasing in trend because of
non communicable disease, life
style and stress.
• Time is myocardium!
Risk factors:
• Age > 40
• Male
• Hypertensive
• Diabetes mellitus
• Hypercholestrolemia
• Smoker
• Family history of IHD
10. Pathophysiology of ACS
• Plaques (a thin fibrous cap & a
large lipid pool) are vulnerable
to disruption.
• Disruption of the plaque leads to
exposure to circulating platelets,
platelet adhesion, activation,
and aggregation.
• Plaque rupture and a platelet-
rich thrombus develop, leading
to decreased blood flow and
ischemia.
11. Effect on ECG
• Within minutes of the onset of
infarction, there will be
alterations in the electrical
potential of the cardiac
myocytes, which can be seen on
ECG as ST-segment elevation.
15. STEMI
• STEMI is diagnosed when there
is:
➢ST elevation of >1 mm in 2
contiguous leads or
➢a new onset LBBB in the resting
ECG in a patient with
➢ischaemic type chest pains of >
30 minutes
➢and accompanied by a rise and
fall in cardiac biomarkers.
16.
17.
18. Unstable Angina & NSTEMI
• Patients having prolonged ischaemic type chest pain of > 30 minutes
and having:
➢ a normal ECG or ST segment depression may be having either
Unstable angina (UA) or Non- ST Elevation MI (NSTEMI).
20. Cardiac biomarkers. Test Sensitivity &
specificity
Peak
Troponin T/I The most
sensitive and
specific test for
myocardial
damage.
12 hours
CKMB It is relatively
specific when
skeletal muscle
damage is not
present.
10–24 hours
Myoglobin low specificity
for myocardial
infarction
2 hours
*High sensitivity Trop T/I
22. Tik… tok… tik… tok…
• Given the potentially serious concerns the
patient should be addressed quickly and
systematically.
• IV, O2, Monitor
• Immediate life threats should be addressed
systematically:
Airway
Breathing
Circulation
25. Pulmonary embolism.
• is a blockage in
the pulmonary arteries in the
lungs.
• thrombus originates in the deep
venous system of the lower
extremities e.g. DVT
• Virchow’s triad-
Decreased blood flow- stasis
Damage to vessel wall
Hypercoagulability
Risk factors
Recent surgery
Hospitalization
Advanced age
Obesity
Immobilization
Thrombophilia-
ATIII/protein C or
S deficiency
Pregnancy
Estrogen
containing OCP
Smoker
Prolonged air
travel
Cancer
Infection
27. ECG in PE
• RBBB – associated with increased mortality; seen
in 18% of patients.
• Right ventricular strain pattern – T wave inversions
in the right precordial leads (V1-4) ± the inferior
leads (II, III, aVF). This pattern is seen in up to 34%
of patients and is associated with high pulmonary
artery pressures.
• Right axis deviation – seen in 16% of patients.
• Dominant R wave in V1 – a manifestation of acute
right ventricular dilatation.
• S1 Q3 T3 pattern – deep S wave in lead I, Q wave
in III, inverted T wave in III. This “classic” finding is
neither sensitive nor specific for pulmonary
embolism; found in only 20% of patients with PE.
• Non-specific ST segment and T wave changes,
including ST elevation and depression. Reported in
up to 50% of patients with PE.
29. Thoracic Aortic Dissection.
• separation of the layers within the
aortic wall.
• tears in the intimal layer result in
the propagation of dissection
(proximally or distally) secondary
to blood entering the intima-media
space.
Signs
• Sudden onset of severe chest pain
(tearing).
• Anterior chest pain: Usually
associated with anterior arch or
aortic root dissection.
• Neck or jaw pain: With aortic
arch involvement and extension
into the great vessels
• Tearing intrascapular pain: May
indicate dissection involving the
descending aorta
30. • Syncope
• Cerebrovascular accident (CVA)
symptoms (eg, hemianesthesia,
and hemiparesis, hemiplegia)
• Dyspnea
• Hemoptysis
• Clinical sign:
• BP would be high initially.
• Low BP is not a good sign.
• Interarm blood pressure
differential greater than 20
mmHg
• Wide pulse pressure.
• Tachycardia.
• Radio-radial/radio-femoral delay.
31. Ix:
widening mediastinum - ≥8 cm or >1/3rd the transthoracic
distance at the level of the aortic knob on a supine AP film.
haemothorax
CT with contrast
33. Pericarditis.
• an inflammation of the pericardium.
Symptoms:
• Chest pain (pleuritic)
• +/- fever
• preceded by cough/sorethroat
• weight loss
• related to the cause
• Causes:
Idiopathic causes
Infectious conditions, such as viral,
bacterial, and tuberculous infections
Inflammatory disorders, such as RA, SLE,
scleroderma, and rheumatic fever
Metabolic disorders, such as renal failure
and hypothyroidism
Cardiovascular disorders, such as acute
MI, Dressler syndrome, and aortic
dissection
Miscellaneous causes, such as iatrogenic,
neoplasms, drugs, irradiation, sarcoidosis,
cardiovascular procedures, and trauma
34. ECG in pericarditis
• Widespread concave ST
elevation and PR depression
throughout most of the limb
leads (I, II, III, aVL, aVF) and
precordial leads (V2-6)
• Reciprocal ST depression and PR
elevation in lead aVR (± V1)
37. Perforated peptic ulcer
History of :
• peptic ulcer
• ingestion of NSAIDs
• Intermittent epigastric pain
• Symptoms:
lower sharp chest pain
extending to the back or
shoulder.
may start from epigastric region.
pain worsen by movement
39. Pneumothorax.
• presence of air or gas in the
pleural cavity (space between
the visceral and parietal pleura
of the lung).
• in most patients occurs from
the rupture of blebs and
bullae.
• Risk factor for spontaneous
pneumothorax:
Smoking
Tall, thin stature in a healthy
person
Marfan syndrome
Pregnancy
Familial pneumothorax
40. • Symptoms:
sudden onset of chest pain with
respiration.
difficulty to breath
• Clinical
tachypnea
restless
saturation < 95%
hyper-resonance on percussion
reduced air entry
?trachea
