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Chest Pain
Dr. Mohannad F AllehyaniEmergency 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
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
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.
Initial ApproachABC’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
History
O- onset
P-provocation /palliation
Q- quality/quantity
R- region/radiation
S- severity/scale
T- timing/time of onset
History
Change in pain pattern
Associated symptoms: DOE, SOB, diaphoresis, vomiting, heart
burn, food intolerance
PHx
Social history
FHx
Physical ExamGeneral 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)
Physical Exam
Neck: JVD, crepitence, bruits
Abdomen
Extremities: swelling, pulses, tenderness, Homan’s
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 (Mallory-Weiss), 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
Differential Diagnoses
Life Threatening Causes of Chest Pain
Acute Coronary Syndromes
Pulmonary Embolus
Tension Pneumothorax
Aortic Dissection
Esophageal Rupture
Pericarditis with Tamponade
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 NOT present with these
symptoms!
Cardiac Risk Factors (Age, DM, HTN, FH, smoking,
hypercholesterolemia, cocaine abuse)
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
Marker Initial Rise
Peak Return to normal
Benefits
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
Acute Coronary Syndromes – Cardiac Markers
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 complications: aneurysms, valve
abnormalities, other structural destruction
Echo
Acute Coronary Syndromes - Treatment
AspirinNitroglycerin
OxygenAnalgesia
Treatment
Beta-BlockersAnticoagulation
Anti-Platelet AgentsThrombolysis
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
impairment
Negative test has time limited value
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)
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
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 eventCombination of H+P, EKG,
BiomarkersNo single globally accepted
algorithmMathematical models such as TIMI, GRACE, PURSUIT, and
HEART can be helpful but are no substitute for clinical judgment
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
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
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 PE
D-Dimer in a low risk patient can be used to rule out PE
Pulmonary Embolism – Wells Criteria
Clinical Signs and Symptoms of DVT? Yes +3PE is #1 Diagnosis, or Equally Likely? Yes +3
Heart Rate > 100? Yes +1.5Immobilization at least 3 days, or Surgery in the
Previous 4 weeks? Yes +1.5Previous, objectively diagnosed PE or
DVT? Yes +1.5Hemoptysis? Yes +1
Malignancy w/ Treatment within 6 mo, or palliative? Yes +1
<2 = Low risk, 2.5-6 = moderate risk, >6 = high risk
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)
Floor vs ICU
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
Radiology: Wide mediastinum on CXR, CT angio chest, echo
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.
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.
Tension Pneumothorax - Pathophysiology
Collection of air in the pleural space causes collapse of the
ipsilateral lung and then cardiovascular collapse as
intrathoracic pressures increase.
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
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 infection cause rapid
deterioration, sepsis and death
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
Subtle
Not so subtle
Imaging
Esophageal Rupture - Treatment
Antibiotics
Supportive Care
Small tears with minimal extraesophageal involvement can
be managed conservatively
Surgical consult for all regardless of size
Take Home Points
ABC’s first
History is key
Have a low threshold for missed MI