Student Lecture Series

CHEST PAIN
Differential Diagnosis
and Diagnostic Challenge

Raymond P. Kelly DO
FACOEP
 WHAT DO YOU
NEED TO THINK ABOUT
WHEN SOMEONE FLIES IN WITH…

CHEST PAIN?
 Impact of Chest Pain In the
Emergency Department

• 5 Million patients present annually

to the Emergency Department (ED)
complaining of chest pain
• This is = approximately 5% of all
annual ED visits
• 1.5 Million patients are admitted
each year for acute coronary
syndrome (ACS)
 Impact of Chest Pain In the
Emergency Department
• Acute Myocardial Infarction (AMI) and
ACS are missed at a rate of 2% and 5%
• Mortality in mistakenly discharged
patients is twice that of admitted
patients with similar risk
• 20% of malpractice dollars in
emergency medicine are related to
missed acute MI
 Pathophysiolgy of Chest Pain

• Afferent Pain fibers

–SOMATIC pain fibers from the
dermis and parietal pleura
• Enter the spinal cord at specific
levels, arranged in dermatomal
patterns
• Map to specific levels of the parietal
cortex
 Pathophysiolgy of Chest Pain

• Afferent Pain fibers

– VISCERAL pain fibers from internal
organs such as the esophagus, visceral
pleura, and blood vessels
• Enter the spinal cord at multiple levels, along
with the somatic pain fibers
• Map to areas of the parietal cortex
corresponding to levels shared with the somatic
fibers
 Pathophysiolgy of Chest Pain

• Pain from somatic fibers is usually

easily described, precisely located,
and sharp in nature
• Visceral pain is imprecisely
localized and often described as
discomfort, heaviness, or aching
 Pathophysiolgy of Chest Pain

• Cardiac ischemic pain

(angina)
– Is initiated by stimulation of visceral
afferent fibers arranged in the superficial
and deep cardiac plexus and sympathetic
ganglia
– Enter the spinal cord through the lower
cervical and upper 5 five thoracic spinal
nerve roots
 Pathophysiolgy of Chest Pain

KBecause of this wide spinal cord

distribution of the cardiac pain fibers,
the cerebral cortex often misinterprets
the location and origin of the pain
KTherefore, myocardial ischemia is
easily confused with pain from other
structures in the chest
 Anatomical Considerations
In Differential Diagnosis
K HEART: ACS (MI, Angina), pericarditis, myocarditis, valvular
diseases (aortic stenosis, mitral valve prolapse)
K LUNGS: pneumonia, pneumothorax, pulmonary embolism,
COPD exacerbation, pleuridynia
K AORTA: dissection, aneurysm
K UPPER ABDOMEN: pancreatitis, cholecystitis, ulcer, hepatic
K ESOPHAGUS: GERD, spasm, esophagitis, foreign body,
rupture (Boerhaave’s syndrome) biliary disease
K CHEST WALL: costochondritits, fracture, muscle tear
 Coronary Artery Disease
RISK FACTORS
– Male > 35 – Family History
– Female > 45, – Diabetes
postmenopausal – Smoking
– Hypercholesterol – Truncal Obesity
emia – Sedentary
– Hypertension Lifestyle
 Coronary Artery Disease
RISK FACTORS
• Lack of cardiac risk factors does not
by itself place an emergency
department patient at low risk for
acute cardiac events
 Coronary Artery Disease
SIGNS AND SYMPTOMS

– Pressure or – Nausea/Vomiting*
Squeezing pain – Fatigue*
– Radiation to – Diaphoresis*
Arm/Jaw – Signs of CHF*
– Anxiety – Shortness of Breath/
Wheezing*
– Tachycardia/
Bradycardia
∗ Anginal Equivalents
 Coronary Artery Disease
SIGNS AND SYMPTOMS

• “Classic” description of angina pectoris is

retrosternal, left anterior chest or epigastric
discomfort described as crushing, tightening,
squeezing, or pressure
• Atypical pain is the rule rather than the
exception. Up to 22% of patients with AMI
describe their symptoms as sharp, stabbing
in nature. Six percent describe a pleuritic
component
 Coronary Artery Disease
SIGNS AND SYMPTOMS

• Patients predisposed to sensory impairment

due to diabetes, advanced age, or altered
mental status are especially likely to present
in atypical ways
• Atypical chest pain is more common in
women than men
• Chest pain at rest but not during exercise
does not decrease the likelihood of disease in
women as it does men
 Coronary Artery Disease
SIGNS AND SYMPTOMS
• Up to 1/3 of AMIs may
be silent
 Aortic Dissection

• Dissection of the layers of the aorta

initiated by an intimal tear
• Blood dissects into the layers of the
media and a false lumen develops
• Blood flow may be limited in any of the
branches of the aorta
• Proximal dissections occur 2x distal
• Men affected 2:1, most commonly
between the ages of 40 and 70
 Aortic Dissection

• The overall mortality rate is 20-25%

• Most common causes of death are
hemorrhage and acute heart failure
(when proximal dissection involves the
aortic valve rendering it incompetent)
• Post dissection aneurysm is a late
complication in survivors
 Aortic Dissection
RISK FACTORS
– Hypertension – Family History
– Connective – Coarctation of
Tissue Disorder Aorta
(Marfan’s) – Valvular Disease
– Pregnancy – Increasing Age
 Aortic Dissection
SIGNS AND SYMPTOMS
– Sudden onset of
tearing pain
– Differential
– Maximal pulses and blood
intensity early pressures
– Radiation to – Hypertension
back
– Associated
neurological
changes
 Pulmonary Embolism
• Approximately 650,000 cases/yr in the US
• >200,000 die each year with about 1/3 dying
in the first hour and over 16,000 dying despite
treatment
• Untreated PE mortality approximately 30%
• Majority are caused by thromboembolism
• Lower extremity DVT 80-90% of cases
• Upper extremity DVT 10-20% of cases
 Pulmonary Embolism
RISKS FACTORS
• VIRCHOW’S TRIAD
–Stasis
–Hypercoagulable
–Endothelial Injury
 Pulmonary Embolism
RISKS FACTORS

– Immobilization/ – Prior
Immobility Thromboembolism
– Postoperative – Pregnancy/Postpart
(Pelvic and Lower – Estrogen Use
Abdominal – Cancer
Surgery in past 6
months) – Oral Contraceptives
– Family History – Prolonged travel
 Pulmonary Embolism
SIGNS AND SYMPTOMS

– Pleuritic Chest Pain – Tachypnea,Tachycar

– Shortness of dia
Breath – Low Grade Fever
– Anxiety – Wheezes*
– Diaphoresis – Localize Rales
– SYNCOPE
 Acute Pericarditis
RISK FACTORS

KTrauma KCollagen
KCancer Vascular
KRecent MI or Diseases
Surgery – Dressler’s KDrugs
syndrome KAnticoagulants
KRecent Viral
Infection
 Acute Pericarditis
SIGNS AND SYMPTOMS
KSubsternal Pain KAnxiety
KVaries with KAnorexia
Respiration
KFever
KIncreased with
Recumbency KPericardial
KRelived by Friction Rub
Leaning Forward
 Acute Pericarditis
• EKG evolves over 4 stages:
– I – (most common presentation) ST
elevation and PR depression =
“classic diagnostic finding”
– II – normal EKG
– III – Deep symmetric T-wave
inversions throughout
– IV – Normal EKG
 Acute Pericarditis
CARDIAC TAMPONADE
• Is the most serious complication of
pericarditis
• Presentation – tachycardia, hypotension,
elevated jugular venous pressure, and
pulsus paradoxus (> 10mm decrease in
systolic BP during inspiration)
• BECK’S TRIAD – Muffled heart sounds,
elevated jugular venous distention (JVD),
and hypotension
 Acute Pericarditis
Findings With Tamponade
• CXR – Enlarged cardiac silhouette in absence of
findings of heart failure
• EKG – Low voltage and electrical alternans
• Echocardiography – is the study of choice and
will confirm the presence of pericardial fluid as
well as impaired filling of the atrium and right
ventricle
 Acute Pericarditis
• Emergent pericardiocentesis is the treatment of
choice for hemodynamically unstable patients
• Removal of even small amounts of fluid can lead
to dramatic improvement
• Can be done with ultrasound guidance if patient
is stable
• Intubation of these patients with PPV can lead to
precipitous drops in blood pressure due to
increased preload reduction
 Cocaine Chest Pain
RISK FACTORS
• Younger patients with classic angina
– Known drug abuse history – always ask
about recent use (< 24 hrs)
– Cocaine use also associated with:
• Aortic Dissection
• Pulmonary Infiltrates (Crack Lung)
 Pneumothorax
• Traumatic
– Penetrating Trauma
– Blunt trauma with associated rib
fractures or ruptured bleb
– S/P Chest Instrumentation – CVP Lines,
Nerve Blocks
• Spontaneous
– Primary - Rupture of a small
unrecognized bleb
– Secondary – Changes in barometric
pressure, PPV, COPD, Lung infections
 Mitral Valve Prolapse
• MVP is the most frequently diagnosed
valvular abnormality
• More common in women than men
• Discomfort associated is often atypical
and associated with dizziness,
hyperventilation, anxiety, depression,
palpations, and fatigue
• Mid-systolic click and late systolic
murmur
• Beta blockers are often helpful
 Pneumonia

• Discomfort is usually sharp and pleuritic

• Associated with fever, cough, and
hypoxia
• Exam – rales over affected lobe(s),
decreased breath sounds, signs of
consolidation
• Chest xray confirms the diagnosis
 Gastrointestinal Causes

KBiliary Colic
KPancreatitis
KEsophageal Spasm
KEsophageal Reflux
KGastritis/ Peptic Ulcer Disease
KEsophageal Rupture (Boerhaave’s
Syndrome)
 Gastrointestinal Causes
• Avoid the “GI cocktail” as a diagnostic
challenge
• No data to support chest discomfort relieved
by antacids is more likely to be noncardiac
than pain that is not so relieved
• Conversely, nitroglycerine is a smooth
muscle dilator that may relive esophageal
spasm or biliary colic
• Diagnostic decisions should not be influenced
by response to a therapeutic trial
 Musculoskeletal Chest Pain
and Other Considerations
• Palpation of the chest should REPRODUCE,
not produce the pain
• If you don’t completely expose and inspect
the chest you may never find the lesions of
Herpes Zoster that have appeared on the
chest wall
• Costochondritis is inflammation of the costal
cartilages and is often sharp and varies with
respirations
 Musculoskeletal Chest Pain
and Other Considerations
• Other funny words
– Tietze Syndrome = erythema, tenderness,
and swelling of the costochondral cartilage
– Xiphodynia
– Texidor Twinge – short, lancinating
discomfort at cardiac apex associated with
breathing and poor posture/ inactivity
– Epidemic Pleuridynia – the “Devil’s Grip”
 Chest Pain Diagnosis
• The HISTORY is the single most important tool
to distinguish between the various causes
• The key is to ask questions in such a way that
allows the patient to describe their symptoms in
their own words
 Chest Pain Diagnosis

• Duration • Frequency
• Constant
• Location • Intermittent
• Retrosternal • Sudden vs.
• Subxyphoid Delayed Onset
• Diffuse
 Chest Pain Diagnosis

• Precipitatin • Quality
g Factors • Burning
• Exertion • Squeezing
• Stress • Dull
• Food • Sharp
• Respiration
• Tearing
• Movement
• Heavy
 Chest Pain Diagnosis
ASSOCIATED SYMPTOMS
• Shortness of • Back Pain
Breath • Radiation to
• Diaphoresis neck or arms
• Palpitations
• Nausea
• Weakness
• Vomiting
• Fatigue
• Jaw Pain
 Electrocardiogram
Cardiac Ischemia
• Inexpensive and readily available
• Sensitivity of initial tracing is less than
40%
– Serial EKGs may be helpful if ACS is
suspected
• Increased suspicion if have:
– T-wave inversions
– ST abnormalities
• Comparison to old tracings often helpful
 Electrocardiogram
Pulmonary Embolism

– “Classic” S1, Q3, T3 pattern

– Low sensitivity – seen in less that
20%
– Sinus tachycardia is most common
finding
 Electrocardiogram
Aortic Dissection
• Aortic Dissection
– May present with a EKG consistent with
AMI due to dissection into the coronary
artery. Thus, a positive EKG does not rule
out dissection
– A negative EKG supports the diagnosis of
dissection in patients with severe chest
pain
– Signs of preexisting hypertension (LVH,
Strain pattern) often seen
 Chest Radiograph

• PNEUMOTHORAX
– A missed tension pneumothorax is
immediately life threatening
• PNEUMONIA
– Sometimes occurs as a consequence
of ischemic heart disease and
congestive heart failure
 Chest Radiograph
• AORTIC DISSECTION
– Widened mediastinum seen in
approximately 80% of patients
– A normal chest x-ray does not rule it out
• ACUTE PERICARDITIS
– Usually normal unless massive pericardial
effusion
• ESOPHAGEAL RUPTURE
– Usually will show mediastinal air or a left
pleural effusion
 Laboratory
• Cardiac Enzymes (CK-MB and
Troponin)
– High positive predictive value
– If initially negative, cannot be used to R/O
MI**
– Negative cardiac markers do not exclude
unstable angina**
• D-Dimer
– Sensitive, but poor specificity for
pulmonary embolism (PE)
 Laboratory
• CBC/ SMA-7
– Basic metabolic screening in chest pain patients
• Coagulation Studies (PT/PTT)
– Essential if considering use of thrombolytic agents
or heparin
• Liver Function Studies/ Amylase
– To rule out GI causes
• Toxicological Screen – if suspecting cocaine
use
 Laboratory

• Arterial Blood Gas (ABG)

– To assess pO2 and pCO2
– PE is possible with normal A-a
gradient
– NOT USEFUL in the diagnosis of PE
 Special Imaging Tests

• MYOCARDIAL IMAGING
– Echocardiography
• Wall motion abnormalities due to
ischemia or infarction
• Helpful in diagnosing pericardial and
valvular heart disease
• Useful in detecting aortic dissections,
particularly the transesophageal method
 Special Imaging Tests

• MYOCARDIAL IMAGING
– Echocardiography - A Stress
echocardiogram is only for
patients who have ruled out for
infarction
 Special Imaging Tests

• MYOCARDIAL IMAGING
– Perfusion Imaging uses an intravenously
injected radioactive tracer that is rapidly
redistributed in the tissues. Areas without
uptake represent either infarcted or
ischemic myocardium
• Thallium studies
• Technetium/ Sestamibi – more useful
 Special Imaging Tests

• CT Scanning
– Sensitive for aortic dissection
– Useful in some centers for detecting
pulmonary embolism using spiral CT and
IV contrast
• Accurate for PE in proximal pulmonary vascular
tree
• May be normal with small distal PE
– Always done on STABLE patients
 Special Imaging Tests
• V/Q Scan
• For diagnosing Pulmonary Embolism
(PE)
• Reported as high, intermediate, or low
probability of PE
• If result is intermediate, or low, and
clinical suspicion is high, must proceed
to pulmonary angiography
 Special Imaging Tests
• Pulmonary Angiography
– “Gold Standard for Diagnosis of PE
– Used when PE is not excluded or
confirmed
• “normal” spiral CT (possible distal PE)
• Intermediate probability V/Q scan
– Associated with higher morbidity and
mortality than other studies described
 Initial Stabilization and
Treatment
• ABC’s
• Oxygen
• IV access
• Pulse Oximiter
• Cardiac Monitoring
• Continuous BP Monitoring
• Prompt evaluation of the EKG
 Initial Stabilization and Treatment
ACLS Guidelines
• Reduce pain and anxiety
• Reduce work load of the heart
• Control extremes of blood pressure
• Assess and treat cardiogenic shock
• Assess and treat congestive heart failure
• Evaluate conduction disturbances -
anticipate appropriate interventions
 Initial Stabilization and
Treatment – More ACLS
• If ACS is suspected, remember that
“MONA” greets the patient at the door
– Morphine – for immediate pain
management
– Oxygen – Is good
– Nitroglycerine dilate coronary arteries
– Aspirin – reduce platelet adherence
 Initial Stabilization and
Additional Treatments
– Metoprolol – Adenosine
– Labetalol – Diltiazem
– Nitroprusside – Lidocaine
– Atropine – Procainamide
– Magnesium – Amiodarone
– Epinephrine – Vasopressin
 Initial Stabilization and
Additional Treatments
– Heparin
– Low Molecular Weight Heparin
– Glycoprotein IIb/IIIa Inhibitors
– Thrombolytic agent du jour
– Angiontensin Converting Enzyme Inhibitors
– Percutaneous Transluminal Coronary
Angioplasty
– Intraaortic Balloon Pump
 Summary Points
• Consider the deep differential in
patients with chest pain
• Do not exclude ACS on the absence of
risk factors
• A single negative cardiac marker does
not exclude AMI
• Negative cardiac markers do not
exclude unstable angina
• A normal ABG does not rule out PE
• All that wheezes is not asthma
?