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

Parietalpain, 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
ABCs 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,

Homans
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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)

UnstableAngina (ASA, B-blocker, NTG,

anticoagulation, risk stratification)
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Acute Coronary Syndromes - Disposition

Mortalityis twice as high for missed MI
Missed MI is the most successfully litigated
claim against EP's. EPs miss 3-5% OF AMI,
this accounts for 25% of malpractice costs
against EPs
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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

ABCs first
History is key

Have a low threshold for missed MI