Chest Pain
Dr. Mohannad F Allehyani
Emergency Medicine Demonstrator
KAUH – Faculty of Medicine
Goals
Review the pathophysiology,
diagnosis and treatment of life
threatening causes of chest pain.
Epidemiology
5% of all ED visits
Approximately 5 million visits per year
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
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.
Initial Approach
ABC’s first, always (look for
conditions requiring immediate
intervention)
Aspirin for potential ACS
EKG
Cardiac and vital sign monitoring
History
O- onset
P-provocation /palliation
Q- quality/quantity
R- region/radiation
S- severity/scale
History
Change in pain pattern
Associated symptoms: DOE,
SOB, diaphoresis, vomiting, heart
burn, food intolerance
PHx
Social history
FHx
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)
Physical Exam
Neck: JVD, crepitence, bruits
Abdomen
Extremities: swelling, pulses,
tenderness, Homan’s
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
Life Threatening Causes of
Chest Pain
Acute Coronary Syndromes
Pulmonary Embolus
Tension Pneumothorax
Aortic Dissection
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
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
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
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
Acute Coronary Syndromes –
Cardiac Markers
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
Echo
Acute Coronary Syndromes Treatment
Aspirin
Nitroglycerin
Oxygen
Analgesia
Treatment
Beta-Blockers
Anticoagulation
Anti-Platelet Agents
Thrombolysis
Percutaneous Coronary
Interventions (PCI)
Stress echocardiograms
Sensitivity 60-90%
Specificity 75% ?
Should be employed with
moderate to high risk
stratification
Limitations of reader, image
quality, and previous functional
Acute Coronary Syndromes Treatment
STEMI (ASA, B-blocker, NTG,
anti-platelet, anticoagulation,
thrombolysis, PCI)
NSTEMI (ASA, B-blocker, NTG,
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%
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,
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
Pulmonary Embolism – History
Dyspnea is the most common
symptom, present in 90% of
patients diagnosed with PE
Sharp pleuritic chest pain,
syncope,
Prolonged immobilization,
Pulmonary Embolism –
Physical Exam
Tachycardia, tachypnea,
diaphoresis, hypotension,
hypoxia, low grade fever, anxiety,
cardiovascular collapse, right
ventricular heave
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
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
Pulmonary Embolism – Diagnostic
Imaging Algorithm
Pulmonary Embolism –
Treatment/Disposition
Unfractionated heparin vs low
molecular weight heparin (some
studies suggest superiority of LMWH)
Thrombolysis (for cardiovascular
collapse)
PE CXR
Aortic Dissection Pathophysiology
Intimal tear of the aorta leads to
dissection of the layers of the aorta
creating a false lumen
Aortic Dissection - Diagnosis
Tearing chest pain radiating to the
back
Risk Factors: HTN, connective tissue
disease
Exam: HTN, pulse differentials, neuro
deficits
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
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
Tension Pneumothorax Pathophysiology
Collection of air in the pleural
space causes collapse of the
ipsilateral lung and then
cardiovascular collapse as
Tension Pneumothorax Diagnosis
Risk factors: COPD; connective
tissue disease, trauma, recent
instrumentation, positive
pressure ventilation
Tension Pneumothorax Treatment
Needle decompression
Tube thoracostomy
Esophageal Rupture Pathophysiology
Tear in the esophagus leads to
leaking of gastrointestinal
contents into the mediastinum
Inflammation followed by
Esophageal Rupture Diagnosis
Rare but devastating
Risk Factors: Iatrogenic, heavy
retching, trauma, foreign bodies,
toxic ingestion
Not so subtle
Subtle
Imaging
Esophageal Rupture Treatment
Antibiotics
Supportive Care
Small tears with minimal
extraesophageal involvement can
Take Home Points
ABC’s first
History is key
Have a low threshold for missed
MI