Slide 1*
*
Approximately 5 million visits per year
*
Chest Pain
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
*
Chest Pain
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.
*
ABC’s first, always (look for conditions requiring immediate intervention)
Aspirin for potential ACS
Pain relief
*
PHx
Chest exam
-Auscultation (murmurs, rubs, gallops, breath sounds)
-Percussion (dullness)
Chest Pain
Differential Diagnoses
Pulmonary
Gastrointestinal
Musculoskeletal
Neurologic
Other
Acute Coronary Syndromes
Acute Coronary Syndromes - Epidemiology
*
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!
*
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
*
*
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
Chest Pain
Negative test has time limited value
Chest Pain
NSTEMI (ASA, B-blocker, NTG, anti-platelet, anticoagulation, PCI)
Unstable Angina (ASA, B-blocker, NTG, anticoagulation, risk stratification)
*
Mortality is twice as high for missed MI
*
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
*
>90% arise from DVT
*
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
*
*
Classic S1,Q3,T3 finding is seen in less than 20%
ABG plays no role in ruling out PE
*
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
*
*
Unfractionated heparin vs low molecular weight heparin (some studies suggest superiority of LMWH)
Thrombolysis (for cardiovascular collapse)
Aortic Dissection - Pathophysiology
*
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.
*
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.
*
Tension Pneumothorax - Pathophysiology
*
*
Esophageal Rupture - Pathophysiology
Tear in the esophagus leads to leaking of gastrointestinal contents into the mediastinum
*
*
Surgical consult for all regardless of size
*
*