Chest Pain

LSU Medical Student Clerkship,

New Orleans, LA
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Goals
 Review the pathophysiology, diagnosis and
treatment of life threatening causes of chest pain.
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Epidemiology

 5% of all ED visits
 Approximately 5 million visits per year
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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
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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.
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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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History
 O- onset
 P-provocation /palliation
 Q- quality/quantity
 R- region/radiation
 S- severity/scale
 T- timing/time of onset
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History

 Change in pain pattern

 Associated symptoms: DOE, SOB,
diaphoresis, vomiting, heart burn, food
intolerance
 PHx
 Social history
 FHx
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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)
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Physical Exam

 Neck: JVD, crepitence, bruits

 Abdomen
 Extremities: swelling, pulses, tenderness,
Homan’s
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Differential Diagnoses
Acute myocardial infarction, Acute coronary ischemia, Aortic dissection, Cardiac
Cardiovascular tamponade, Unstable angina, Coronary spasm, Prinzmetal's angina, Cocaine
induced, Pericarditis, Myocarditis, Valvular heart disease, Aortic stenosis, Mitral
valve prolapse, Hypertrophic cardiomyopathy
Pulmonary embolus, Tension pneumothorax, Pneumothorax, Mediastinitis,
Pulmonary Pneumonia, Pleuritis, Tumor, Pneumomediastinum

Esophageal rupture (Boerhaave), Esophageal tear (Mallory-

Gastrointestinal Weiss), Cholecystitis, Pancreatitis, Esophageal spasm, Esophageal
reflux, Peptic ulcer, Biliary colic
Muscle strain, Rib fracture, Arthritis, Tumor, Costochondritis, Nonspecific chest
Musculoskeletal wall pain

Spinal root compression, Thoracic outlet, Herpes zoster, Postherpetic neuralgia

Neurologic
Psychologic, Hyperventilation
Other
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Life Threatening Causes of Chest Pain

 Acute Coronary Syndromes

 Pulmonary Embolus
 Tension Pneumothorax
 Aortic Dissection
 Esophageal Rupture
 Pericarditis with Tamponade
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Acute Coronary Syndromes - Epidemiology

 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
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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!
 Cardiac Risk Factors (Age, DM, HTN, FH,
smoking, hypercholesterolemia, cocaine abuse)
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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 completely normal
EKGs
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Acute Coronary Syndromes – Cardiac Markers

Marker Initial Peak Return to Benefits

Rise normal
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
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Acute Coronary Syndromes – Cardiac Markers

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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:
aneurysms, valve abnormalities, other
structural destruction
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Echo
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Acute Coronary Syndromes - Treatment

 Aspirin
 Nitroglycerin
 Oxygen
 Analgesia
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Treatment

 Beta-Blockers
 Anticoagulation
 Anti-Platelet Agents
 Thrombolysis
 Percutaneous Coronary Interventions
(PCI)
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Stress echocardiograms

 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
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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)
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Acute Coronary Syndromes - Disposition

 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
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Acute Coronary Syndromes - Disposition

 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
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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
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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
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Pulmonary Embolism – Physical Exam

 Tachycardia, tachypnea, diaphoresis,
hypotension, hypoxia, low grade fever, anxiety,
cardiovascular collapse, right ventricular heave
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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
 D-Dimer in a low risk patient can be used to rule
out PE
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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

<2 = Low risk, 2.5-6 = moderate risk, >6 = high risk

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Pulmonary Embolism – Diagnostic Imaging Algorithm

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Pulmonary Embolism – Treatment/Disposition

 Unfractionated heparin vs low molecular weight

heparin (some studies suggest superiority of
LMWH)
 Thrombolysis (for cardiovascular collapse)
 Floor vs ICU
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PE CXR
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Aortic Dissection - Pathophysiology

 Intimal tear of the aorta leads to dissection of the

layers of the aorta creating a false lumen
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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 angio
chest, echo
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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, regardless of the site of the
primary intimal tear, and all other dissections as type B.
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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 for a life-threatening complication such as
aortic regurgitation, cardiac tamponade, or myocardial infarction.
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Tension Pneumothorax - Pathophysiology

 Collection of air in the pleural space causes

collapse of the ipsilateral lung and then
cardiovascular collapse as intrathoracic
pressures increase.
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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
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Tension Pneumothorax - Treatment

 Needle decompression
 Tube thoracostomy
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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
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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
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Subtle Not so subtle

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Imaging
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Esophageal Rupture - Treatment

 Antibiotics
 Supportive Care
 Small tears with minimal extraesophageal
involvement can be managed conservatively
 Surgical consult for all regardless of size
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Take Home Points

 ABC’s first
 History is key
 Have a low threshold for missed MI