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APPROACH TO CHEST PAIN
DR SAZWAN REEZAL BIN SHAMSUDDIN
EMERGENCY MEDICINE SPECIALIST
MEDTWEETMY
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
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
Working diagnosis.
1) Acute Coronary Syndrome
(ACS).
2) Pulmonary embolism.
3) Thoracic aortic dissection.
4) Pericarditis.
5) Pneumonia.
6) Perforated peptic ulcer
7) Pneumothorax.
8) Esophageal rupture.
Anatomy
Parietal pericardium is the outermost.
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.
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.
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.
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
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.
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.
Likelihood that signs and symptoms represent
an Acute Coronary Syndrome.
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.
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).
Short-Term Risk of Death or Nonfatal MI in
Patients With UA/NSTEMI
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
TIMI UA/NSTEMI risk score.
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
Treatment
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
Symptoms
• Pleuritic chest pain
• Dyspnea
• Hemoptysis
Clinically
• Tachypnea
• Tachycardia
• O2 desaturation
• hypotension Wells Score for PE
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.
Ix:
• CXR -?Westermark sign ?Hamptom sign
• CT Pulmonary Angiograph (CTPA)
• VQ Scan
Rx:
-Anticoagulation
 LMWH/Fondaparinux/Heparin
-Thrombolysis
 PE with hemodynamic instability
-Surgical thrombectomy
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
• 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.
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
Rx:
• Analgesia
• IVI B-Blocker e.g Labetolol
Surgery.
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
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)
POCUS
• Pericardial effusion
Pneumonia.
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
Clinical signs:
• pale
• hypotensive
• tachycardia
• tender & guarded abdomen
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
• Symptoms:
sudden onset of chest pain with
respiration.
difficulty to breath
• Clinical
tachypnea
restless
saturation < 95%
hyper-resonance on percussion
reduced air entry
?trachea
• Mx
• air aspiration
• chest tube insertion
Esophageal rupture (Boerhaave Synd)
• sudden onset of chest pain after
an episode of forceful vomiting.
• Clinically :
- ill looking
- sweating++
- Tachypnea
• pneumomediastinum
• pneumothorax
• pleural effusion
• subcutaneous emphysema
Stepwise approach
1) History (+ECG)
- chest pain
- risk stratification
2) Vital signs
-blood pressure (dual)
-heart rate
-respiratory rate
-T
-pain score
3) Physical examination
- pallor
- pulse
- CVS- murmur, pedal edema,
crepitations, JVP
- Lungs- trachea, percussion,
auscultation.
- Abd – tender, guarding, PR
4) ECG interpretation
5) Stabilization & initiation of
treatment.
5) CXR interpretation
6) POCUS
7) Diagnostic investigation (if)
8) Other lab investigation.
References :
• Tintinalli’s Emergency Medicine- A Comprehensive Study Guide 7th Edition.
• Evaluation & Management of ST-Segment Elevation Myocardial Infarction
in Emergency Department, Emergency Medicine Practice,January 2021,
Volume 23,Issue 1.
• Management of Acute ST Segment Elevation Myocardial Infarction (STEMI)
2019- Malaysia CPG
• Stable Coronary Artery Disease 2018 (2nd Edition)- Malaysia CPG
• Primary & Secondary Prevention of Cardiovascular Disease 2017- Malaysia
CPG
• Medscape
Slideshare https://www.criticalultrasoundmalaysia.org/
Thank you.

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Approach to chest pain

  • 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
  • 4. Working diagnosis. 1) Acute Coronary Syndrome (ACS). 2) Pulmonary embolism. 3) Thoracic aortic dissection. 4) Pericarditis. 5) Pneumonia. 6) Perforated peptic ulcer 7) Pneumothorax. 8) Esophageal rupture.
  • 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.
  • 12.
  • 13.
  • 14. Likelihood that signs and symptoms represent an Acute Coronary Syndrome.
  • 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).
  • 19. Short-Term Risk of Death or Nonfatal MI in Patients With UA/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
  • 24.
  • 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
  • 26. Symptoms • Pleuritic chest pain • Dyspnea • Hemoptysis Clinically • Tachypnea • Tachycardia • O2 desaturation • hypotension Wells Score for PE
  • 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.
  • 28. Ix: • CXR -?Westermark sign ?Hamptom sign • CT Pulmonary Angiograph (CTPA) • VQ Scan Rx: -Anticoagulation  LMWH/Fondaparinux/Heparin -Thrombolysis  PE with hemodynamic instability -Surgical thrombectomy
  • 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
  • 32. Rx: • Analgesia • IVI B-Blocker e.g Labetolol Surgery.
  • 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
  • 38. Clinical signs: • pale • hypotensive • tachycardia • tender & guarded abdomen
  • 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
  • 41. • Mx • air aspiration • chest tube insertion
  • 42. Esophageal rupture (Boerhaave Synd) • sudden onset of chest pain after an episode of forceful vomiting. • Clinically : - ill looking - sweating++ - Tachypnea
  • 43. • pneumomediastinum • pneumothorax • pleural effusion • subcutaneous emphysema
  • 44. Stepwise approach 1) History (+ECG) - chest pain - risk stratification 2) Vital signs -blood pressure (dual) -heart rate -respiratory rate -T -pain score 3) Physical examination - pallor - pulse - CVS- murmur, pedal edema, crepitations, JVP - Lungs- trachea, percussion, auscultation. - Abd – tender, guarding, PR
  • 45. 4) ECG interpretation 5) Stabilization & initiation of treatment. 5) CXR interpretation 6) POCUS 7) Diagnostic investigation (if) 8) Other lab investigation.
  • 46. References : • Tintinalli’s Emergency Medicine- A Comprehensive Study Guide 7th Edition. • Evaluation & Management of ST-Segment Elevation Myocardial Infarction in Emergency Department, Emergency Medicine Practice,January 2021, Volume 23,Issue 1. • Management of Acute ST Segment Elevation Myocardial Infarction (STEMI) 2019- Malaysia CPG • Stable Coronary Artery Disease 2018 (2nd Edition)- Malaysia CPG • Primary & Secondary Prevention of Cardiovascular Disease 2017- Malaysia CPG • Medscape