Chest Pain
LSU Medical Student Clerkship,
New Orleans, LA
Chest Pain
Goals
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Review the pathophysiology, diagnosis and
treatment of life threatening causes of chest pain.
Chest Pain
Epidemiology
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5% of all ED visits
Approximately 5 million visits per year
Chest Pain
Visceral Pain
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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
Chest Pain
Parietal Pain
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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.
Chest Pain
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
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Chest Pain
History
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O- onset
P-provocation /palliation
Q- quality/quantity
R- region/radiation
S- severity/scale
T- timing/time of onset
Chest Pain
History
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Change in pain pattern
Associated symptoms: DOE, SOB,
diaphoresis, vomiting, heart burn, food
intolerance
PHx
Social history
FHx
Chest Pain
Physical Exam
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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)
Chest Pain
Physical Exam
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Neck: JVD, crepitence, bruits
Abdomen
Extremities: swelling, pulses, tenderness,
Homan’s
Chest Pain
Differential Diagnoses
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 (MalloryWeiss), 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
Chest Pain
Life Threatening Causes of Chest Pain
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Acute Coronary Syndromes
Pulmonary Embolus
Tension Pneumothorax
Aortic Dissection
Esophageal Rupture
Pericarditis with Tamponade
Chest Pain
Acute Coronary Syndromes - Epidemiology
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In a typical ED population of adults over the age
of 30 presenting with visceral-type chest pain,
about 15 percent will have AMI and 25 to 30
percent will have UA
Chest Pain
Acute Coronary Syndromes - History
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“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)
Chest Pain
Acute Coronary Syndromes – EKG Findings
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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
Chest Pain
Chest Pain
Chest Pain
Acute Coronary Syndromes – Cardiac Markers
Marker
Initial
Rise
Peak
Return to
normal
Troponin
2-4 hr
10 -24 hr 5 -10 days
CK-MB
3-4 hr
10-24 hr
LDH
10 hr
24 -72 hr 14 days
Myoglobin
1-2 hr
4 -8 hr
2 – 4 days
24 hours
Benefits
Sensitive and specific
Unaffected by renal failure
Very sensitive, powerful
negative predictive value
Chest Pain
Acute Coronary Syndromes – Cardiac Markers
Chest Pain
Echocardiogram
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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
Chest Pain
Echo
Chest Pain
Acute Coronary Syndromes - Treatment
Aspirin
 Nitroglycerin
 Oxygen
 Analgesia
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Chest Pain
Treatment
Beta-Blockers
 Anticoagulation
 Anti-Platelet Agents
 Thrombolysis
 Percutaneous Coronary Interventions
(PCI)
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Chest Pain
Stress echocardiograms
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Sensitivity 60-90%
Specificity 75% ?
Should be employed with moderate to high
risk stratification
Limitations of reader, image quality, and
previous functional impairment
Negative test has time limited value
Chest Pain
Acute Coronary Syndromes - Treatment
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STEMI (ASA, B-blocker, NTG, anti-platelet,
anticoagulation, thrombolysis, PCI)
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NSTEMI (ASA, B-blocker, NTG, anti-platelet,
anticoagulation, PCI)
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Unstable Angina (ASA, B-blocker, NTG,
anticoagulation, risk stratification)
Chest Pain
Acute Coronary Syndromes - Disposition
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Mortality is twice as high for missed MI
Missed MI is the most successfully litigated
claim against EP's. EP’s miss 3-5% OF AMI,
this accounts for 25% of malpractice costs
against EP’s
Chest Pain
Acute Coronary Syndromes - Disposition
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A single set of cardiac enzymes is rarely of use
Risk Stratification: goal is to predict the
likelihood of an adverse cardiovascular event
Combination of H+P, EKG, Biomarkers
No single globally accepted algorithm
Mathematical models such as TIMI, GRACE,
PURSUIT, and HEART can be helpful but are
no substitute for clinical judgment
Chest Pain
Pulmonary Embolism - Pathophysiology
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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
Chest Pain
Pulmonary Embolism – History
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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
Chest Pain
Pulmonary Embolism – Physical Exam
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Tachycardia, tachypnea, diaphoresis,
hypotension, hypoxia, low grade fever, anxiety,
cardiovascular collapse, right ventricular heave
Chest Pain
Pulmonary Embolism – Diagnostic Testing
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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
Chest Pain
Pulmonary Embolism – Wells Criteria
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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
<2 = Low risk, 2.5-6 = moderate risk, >6 = high risk
Chest Pain
Pulmonary Embolism – Diagnostic Imaging Algorithm
Chest Pain
Pulmonary Embolism – Treatment/Disposition
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Unfractionated heparin vs low molecular weight
heparin (some studies suggest superiority of
LMWH)
Thrombolysis (for cardiovascular collapse)
Floor vs ICU
Chest Pain
PE CXR
Chest Pain
Chest Pain
Chest Pain
Chest Pain
Chest Pain
Chest Pain
Aortic Dissection - Pathophysiology
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Intimal tear of the aorta leads to dissection of the
layers of the aorta creating a false lumen
Chest Pain
Aortic Dissection - Diagnosis
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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
Chest Pain
Chest Pain
Aortic Dissection - Classification
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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.
Chest Pain
Chest Pain
Aortic Dissection - Treatment
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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 a life-threatening complication such as
aortic regurgitation, cardiac tamponade, or myocardial infarction.
Chest Pain
Tension Pneumothorax - Pathophysiology
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Collection of air in the pleural space causes
collapse of the ipsilateral lung and then
cardiovascular collapse as intrathoracic
pressures increase.
Chest Pain
Tension Pneumothorax - Diagnosis
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Risk factors: COPD; connective tissue disease,
trauma, recent instrumentation, positive
pressure ventilation
Absent breath sounds unilaterally, hypotension,
distended neck veins, tracheal deviation
Chest Pain
Chest Pain
Tension Pneumothorax - Treatment
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Needle decompression
Tube thoracostomy
Chest Pain
Esophageal Rupture - Pathophysiology
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Tear in the esophagus leads to leaking of
gastrointestinal contents into the mediastinum
Inflammation followed by infection cause rapid
deterioration, sepsis and death
Chest Pain
Esophageal Rupture - Diagnosis
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Rare but devastating
Risk Factors: Iatrogenic, heavy retching,
trauma, foreign bodies, toxic ingestion
Radiology: Mediastinal air on plain films or CT
scan
Chest Pain
Subtle
Not so subtle
Chest Pain
Imaging
Chest Pain
Esophageal Rupture - Treatment
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Antibiotics
Supportive Care
Small tears with minimal extraesophageal
involvement can be managed conservatively
Surgical consult for all regardless of size
Chest Pain
Take Home Points
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ABC’s first
History is key
Have a low threshold for missed MI