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

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.

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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 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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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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Differential Diagnoses
Cardiovascular Pulmonary Gastrointestinal Musculoskeletal Neurologic Other
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 embolus, Tension pneumothorax, Pneumothorax, Mediastinitis, Pneumonia, Pleuritis, Tumor, Pneumomediastinum Esophageal rupture (Boerhaave), Esophageal tear (MalloryWeiss), Cholecystitis, Pancreatitis, Esophageal spasm, Esophageal reflux, Peptic ulcer, Biliary colic Muscle strain, Rib fracture, Arthritis, Tumor, Costochondritis, Nonspecific chest wall pain Spinal root compression, Thoracic outlet, Herpes zoster, Postherpetic neuralgia

Psychologic, Hyperventilation

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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 Troponin CK-MB LDH Initial Rise 2-4 hr 3-4 hr 10 hr Peak Return to normal Benefits Sensitive and specific Unaffected by renal failure

10 -24 hr 5 -10 days 10-24 hr 2 4 days

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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Acute Coronary Syndromes - Treatment

Aspirin Nitroglycerin Oxygen Beta-Blockers Anticoagulation Anti-Platelet Agents Thrombolysis Percutaneous Coronary Interventions (PCI)

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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) Unstable Angina (ASA, B-blocker, NTG, anticoagulation, risk stratification)

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Acute Coronary Syndromes - Disposition

Mortality is 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, and PURSUIT 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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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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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