Visceral pain from chest organs is poorly localized and described as dull, while parietal pain from the chest wall is sharp and localized. Chest pain evaluations start with ABCs and aspirin, then involve EKG, monitoring, and pain relief. A thorough history and physical exam aim to differentiate causes like acute coronary syndrome, aortic dissection, pulmonary embolism, pneumonia, or musculoskeletal issues. Diagnostic testing may include markers, echocardiogram, Wells criteria, CT scans, and management depends on the specific diagnosis and stability of the patient.

1. Chest Pain

2. Visceral Pain
Visceral fibers enter the spinal cord at several
levels leading to poorly localized, poorly
characterized pain. (discomfort, heaviness, dull,
aching)
Heart, blood vessels, esophagus and visceral
pleura are innervated by visceral fibers
Because of dorsal fibers can overlap three levels
above or below, disease of thoracic origin can
produce pain anywhere from the jaw to the
epigastrum

3. Parietal Pain
Parietal pain, in contrast to visceral
pain, is described as sharp and can
be localized to the dermatome
superficial to the site of the painful
stimulus.
The dermis and parietal pleura are
innervated by parietal fibers.

4. Initial Approach
ABC’s first, always (look for conditions
requiring immediate intervention)
Aspirin for potential ACS
EKG
Cardiac and vital sign monitoring
Pain relief
Because of the wide differential, H+P will
guide the diagnostic workup

5. History
O- onset
P-provocation /palliation
Q- quality/quantity
R- region/radiation
S- severity/scale
T- timing/time of onset

6. History
Change in pain pattern
Associated symptoms: DOE, SOB,
diaphoresis, vomiting, heart burn,
food intolerance
PHx
Social history
FHx

7. Physical Exam
General Appearance and Vitals (sick vs not
sick)
Chest exam
-Inspection (scars, heaves, tachypnea, work
of breathing)
-Auscultation (murmurs, rubs, gallops,
breath sounds)
-Percussion (dullness)
-Palpation (tenderness, PMI)

8. Physical Exam
Neck: JVD, crepitence, bruits
Abdomen
Extremities: swelling, pulses,
tenderness, Homan’s

9. Cardiovascular Acute myocardial infarction, Acute coronary ischemia, Aortic
dissection, Cardiac tamponade, Unstable angina, Coronary spasm, Prinzmetal's
angina, Cocaine induced, Pericarditis, Myocarditis, Valvular heart
disease, Aortic stenosis, Mitral valve prolapse, Hypertrophic cardiomyopathy
Pulmonary Pulmonary embolus, Tension pneumothorax, Pneumothorax, Mediastinitis,
Pneumonia, Pleuritis, Tumor, Pneumomediastinum
Gastrointestinal Esophageal rupture (Boerhaave), Esophageal tear (Mallory-
Weiss), Cholecystitis, Pancreatitis, Esophageal spasm, Esophageal
reflux, Peptic ulcer, Biliary colic
Musculoskeletal Muscle strain, Rib fracture, Arthritis, Tumor, Costochondritis, Nonspecific
chest wall pain
Neurologic Spinal root compression, Thoracic outlet, Herpes zoster, Postherpetic
neuralgia
Other Psychologic, Hyperventilation
Differential Diagnosis

11. Acute Coronary Syndromes - 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!

12. Acute Coronary Syndromes – EKG Findings
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

13. 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
Myoglobi
n
1-2 hr 4 -8 hr 24 hours Very sensitive, powerful
negative predictive value
Acute Coronary Syndromes – Cardiac Markers

14. Echocardiogram
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:

15. Acute Coronary Syndromes -
Treatment
Aspirin
Nitroglycerin
Oxygen
Analgesia

16. Treatment
Beta-Blockers
Anticoagulation
Anti-Platelet Agents
Thrombolysis
Percutaneous Coronary
Interventions (PCI)

17. Acute Coronary Syndromes -
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)

20. Pulmonary Embolism -
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

21. Pulmonary Embolism – 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

22. Pulmonary Embolism – Physical
Exam
Tachycardia, tachypnea,
diaphoresis, hypotension, hypoxia,
low grade fever, anxiety,
cardiovascular collapse, right
ventricular heave

23. Pulmonary Embolism – Diagnostic
Testing
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

24. Pulmonary Embolism – Wells Criteria
Clinical Signs and Symptoms of DVT? Yes +3
PE is #1 Diagnosis, or Equally Likely? Yes +3
Heart Rate > 100? Yes +1.5
Immobilization at least 3 days, or Surgery in the
Previous 4 weeks? Yes +1.5
Previous, objectively diagnosed PE or DVT? Yes +1.5
Hemoptysis? Yes +1
Malignancy w/ Treatment within 6 mo, or
palliative? Yes +1

25. Pulmonary Embolism – Diagnostic Imaging
Algorithm

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

28. Aortic Dissection - Pathophysiology
Intimal tear of the aorta leads to
dissection of the layers of the aorta
creating a false lumen

29. Aortic Dissection - 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

30. Aortic Dissection - 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,

31. Aortic Dissection - 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

32. Tension Pneumothorax -
Pathophysiology
Collection of air in the pleural space
causes collapse of the ipsilateral
lung and then cardiovascular
collapse as intrathoracic pressures
increase.

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

34. Tension Pneumothorax -
Treatment
Needle decompression
Tube thoracostomy

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

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

37. Esophageal Rupture - Treatment
Antibiotics
Supportive Care
Small tears with minimal
extraesophageal involvement can
be managed conservatively
Surgical consult for all regardless of
size