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1. ApproachtoChestPain

2. Introduction:
• Chest pain is one of most common symptoms presenting
in emergency department and it is worried us because it
is widely range differential diagnosis between life
threatening conditions such as Acute coronary symptoms
(ACS), Pulmonary Embolism (PE), Aortic dissection,
pericarditis with tamponade, pneumothorax and
esophageal rupture or maybe the Chest pain can be
caused by non–emergent conditions such as esophageal
reflux, peptic ulcer, biliary colic, muscle strain,
costocondritis, pleurisy, Pneumonia and non specific chest
wall pain.

3. Introduction:
• It is important as emergency physicians to have
approach to chest pain to able recognized life-
threatening conditions from non - emergent
conditions .

4. LifeThreateningCausesofChestPain:
• Acute Coronary Syndromes
• Pulmonary Embolus
• Tension Pneumothorax
• Aortic Dissection
• Esophageal Rupture
• Pericarditis with Tamponade

5. HISTORY?
• General approach — Obtain a detailed history of the patient's chest pain,
including:
• Onset of pain (eg, abrupt or gradual)
• Provocation/Palliation (which activities provoke pain; which alleviate pain)
pain)
• Quality of pain (eg, sharp, squeezing, pleuritic)
• Radiation (eg, shoulder, jaw, back)
• Site of pain (eg, substernal, chest wall, back, diffuse, localized)
• Timing (eg, constant or episodic, duration of episodes, when pain began)
• Prior diagnostic studies or prior procedures (eg, stress test or coronary
CT angiography , cardiac catheterization)
• Comorbidities: hypertension, diabetes mellitus, peripheral artery disease,
malignancy, connective tissue disorders, bicuspid aortic valve, recent
pregnancy

6. AcuteCoronarySyndromes-History
• “Typical” Chest Pain Story (Pressure-like, squeezing,
crushing pain, worse with exertion, SOB,
diaphoresis, radiates to arm or jaw) The majority of
patients with ACS DO NOT present with these
symptoms!
• Cardiac Risk Factors (Age, DM, HTN, FH, smoking,
hypercholesterolemia, cocaine abuse)

7. • STEMI - ST segment elevation (>1 mm) in
contiguous leads; new LBBB
• T wave inversion or ST segment depression in
contiguous leads suggests subendocardial ischemia
• 5% of patients with AMI have completely normal
EKGs
ACUTECORONARYSYNDROMES- ECG

8. Marker Initial
Rise
Peak Return to
normal
Benefits
Troponin 2-4 hr 10 -24 hr 5 -10 days Sensitive and specific
CK-MB 3-4 hr 10-24 hr 2 – 4 days Unaffected by renal failure
LDH 10 hr 24 -72 hr 14 days
Myoglobin 1-2 hr 4 -8 hr 24 hours Very sensitive, powerful
negative predictive value
ACUTECORONARY SYNDROMES-MARKERS

9. • Wall abnormalities occur within minutes
• Will detect abnormalities in 80% of AMI
• Normal resting echo in setting of chest pain gives low
probability
• Early screen for AMI complications: aneurysms, valve
abnormalities, other structural destruction
ACUTECORONARYSYNDROMES- ECHO

10. AcuteCoronarySyndromes-Treatment
• Aspirin
• Nitroglycerin
• Oxygen
• Analgesia
• Beta-Blockers
• Anticoagulation
• Anti-Platelet Agents
• Thrombolysis
• Percutaneous Coronary Interventions (PCI)

11. AcuteCoronarySyndromes-Treatment
• STEMI (ASA, B-blocker, NTG, anti-platelet,
anticoagulation, thrombolysis, PCI)
• NSTEMI (ASA, B-blocker, NTG, anti-platelet,
anticoagulation, PCI)
• Unstable Angina (ASA, B-blocker, NTG,
anticoagulation, risk stratification)

13. PulmonaryEmbolism-Pathophysiology
• Thrombosis of a pulmonary artery >90% arise
from DVT .
• Clot from a DVT travels through the venous
system and lodges in the pulmonary
vasculature creating a ventilation/perfusion
mismatch.

14. PulmonaryEmbolism–History
• Dyspnea is the most common symptom, present in
90% of patients diagnosed with PE.
• Sharp pleuritic chest pain, syncope, prolonged
immobilization, neoplasm, known hypercoagulable
disorder.

15. PulmonaryEmbolism–PhysicalExam
Tachycardia, tachypnea, diaphoresis, hypotension,
hypoxia, low grade fever, anxiety, cardiovascular
collapse, right ventricular heave.

16. PulmonaryEmbolism–DiagnosticTesting
• Sinus Tachycardia is the most frequent EKG finding
• Classic S1,Q3,T3 finding is seen in less than 20%
• ABG plays no role in ruling out PE
• D-Dimer in a low risk patient can be used to rule
out PE

17. PulmonaryEmbolism–WellsCriteria

19. PulmonaryEmbolism –Treatment/Disposition
• Unfractionated heparin vs low molecular
weight heparin (some studies suggest
superiority of LMWH)
• Thrombolysis (for cardiovascular collapse)
• Floor vs ICU

22. AorticDissection-Diagnosis
• Tearing chest pain radiating to the back
• Risk Factors: HTN, connective tissue disease
• Exam: HTN, pulse differentials, neuro deficits
• Radiology: Wide mediastinum on CXR, CT angio
chest, echo .

24. AorticDissection-Classification
• De Bakey system:
• Type I dissection involves both the ascending and
descending thoracic aorta.
• Type II dissection is confined to the ascending
aorta.
• Type III dissection is confined to the descending
aorta.
• The Daily system classifies dissections that involve
the ascending aorta as type A, regardless of the site
of the primary intimal tear, and all other dissections
as type B.

26. AorticDissection-Treatment
• Patients with uncomplicated aortic dissections
confined to the descending thoracic aorta (Daily type B
or De Bakey type III) are best treated with medical
therapy.
• Medical Therapy: Goal to decrease the blood pressure and
the velocity of left ventricular contraction, both of
which will decrease aortic shear stress and minimize
the tendency to further dissection.
• Acute ascending aortic dissections (Daily type A or De
Bakey type I or type II) should be treated surgically
whenever possible since these patients are a high risk
for

27. TensionPneumothorax-Pathophysiology
• Collection of air in the pleural space causes
collapse of the ipsilateral lung and then
cardiovascular collapse as intrathoracic pressures
increase.

28. TensionPneumothorax-Diagnosis
• Risk factors: COPD; connective tissue disease,
trauma, recent instrumentation, positive
pressure ventilation
• Absent breath sounds unilaterally,
hypotension, distended neck veins, tracheal
deviation

30. TensionPneumothorax-Treatment
• Needle decompression
• Tube thoracostomy

31. EsophagealRupture-Pathophysiology
• Tear in the esophagus leads to leaking of
gastrointestinal contents into the mediastinum
• Inflammation followed by infection cause rapid
deterioration, sepsis and death .

32. EsophagealRupture-Diagnosis
• Rare but devastating
• Risk Factors: Iatrogenic, heavy retching, trauma,
foreign bodies, toxic ingestion
• Radiology: Mediastinal air on plain films or CT scan .

33. Subtle Not so subtle

35. EsophagealRupture-Treatment
• Antibiotics
• Supportive Care
• Small tears with minimal extraesophageal
involvement can be managed conservatively
• Surgical consult for all regardless of size