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Chest Pain. LSU Medical Student Clerkship, New Orleans, LA. 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

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chest pain
Chest Pain

LSU Medical Student Clerkship, New Orleans, LA

slide2
Goals
  • Review the pathophysiology, diagnosis and treatment of life threatening causes of chest pain.
slide3
Epidemiology
  • 5% of all ED visits
  • Approximately 5 million visits per year
slide4
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
slide5
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.
slide6
Initial Approach
  • ABC’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
slide7
History
  • O- onset
  • P-provocation /palliation
  • Q- quality/quantity
  • R- region/radiation
  • S- severity/scale
  • T- timing/time of onset
history
History
  • Change in pain pattern
  • Associated symptoms: DOE, SOB, diaphoresis, vomiting, heart burn, food intolerance
  • PHx
  • Social history
  • FHx
slide9
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)
physical exam
Physical Exam
  • Neck: JVD, crepitence, bruits
  • Abdomen
  • Extremities: swelling, pulses, tenderness, Homan’s
slide12
Life Threatening Causes of Chest Pain
  • Acute Coronary Syndromes
  • Pulmonary Embolus
  • Tension Pneumothorax
  • Aortic Dissection
  • Esophageal Rupture
  • Pericarditis with Tamponade
slide13
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
slide14
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)
slide15
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
echocardiogram
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
slide22
Acute Coronary Syndromes - Treatment
  • Aspirin
  • Nitroglycerin
  • Oxygen
  • Analgesia
treatment
Treatment
  • Beta-Blockers
  • Anticoagulation
  • Anti-Platelet Agents
  • Thrombolysis
  • Percutaneous Coronary Interventions (PCI)
stress echocardiograms
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
slide25
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)
slide26
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
slide27
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, PURSUIT, and HEART can be helpful but are no substitute for clinical judgment
slide28
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
slide29
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
slide30
Pulmonary Embolism – Physical Exam
  • Tachycardia, tachypnea, diaphoresis, hypotension, hypoxia, low grade fever, anxiety, cardiovascular collapse, right ventricular heave
slide31
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
slide32
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

slide34
Pulmonary Embolism – Treatment/Disposition
  • Unfractionated heparin vs low molecular weight heparin (some studies suggest superiority of LMWH)
  • Thrombolysis (for cardiovascular collapse)
  • Floor vs ICU
slide41
Aortic Dissection - Pathophysiology
  • Intimal tear of the aorta leads to dissection of the layers of the aorta creating a false lumen
slide42
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
slide44
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.
slide46
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.
slide47
Tension Pneumothorax - Pathophysiology
  • Collection of air in the pleural space causes collapse of the ipsilateral lung and then cardiovascular collapse as intrathoracic pressures increase.
slide48
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
slide50
Tension Pneumothorax - Treatment
  • Needle decompression
  • Tube thoracostomy
slide51
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
slide52
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
slide53
Subtle

Not so subtle

slide55
Esophageal Rupture - Treatment
  • Antibiotics
  • Supportive Care
  • Small tears with minimal extraesophageal involvement can be managed conservatively
  • Surgical consult for all regardless of size
slide56
Take Home Points
  • ABC’s first
  • History is key
  • Have a low threshold for missed MI
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