1. Chest Pain Dr. Mohannad F Allehyani Emergency Medicine Demonstrator KAUH – Faculty of Medicine

2. Goals Review the pathophysiology, diagnosis and treatment of life threatening causes of chest pain.

3. Epidemiology 5% of all ED visits Approximately 5 million visits per year

4. 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

5. 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.

6. 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

7. History O- onset P-provocation /palliation Q- quality/quantity R- region/radiation S- severity/scale T- timing/time of onset

8. History Change in pain pattern Associated symptoms: DOE, SOB, diaphoresis, vomiting, heart burn, food intolerance PHx Social history FHx

9. 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)

10. Physical Exam Neck: JVD, crepitence, bruits Abdomen Extremities: swelling, pulses, tenderness, Homan’s

11. 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

12. Life Threatening Causes of Chest Pain Acute Coronary Syndromes Pulmonary Embolus Tension Pneumothorax Aortic Dissection Esophageal Rupture Pericarditis with Tamponade

13. 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

14. 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)

15. 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

18. MarkerInitial Rise PeakReturn to normal Benefits Troponin2-4 hr10 -24 hr5 -10 daysSensitive and specific CK-MB3-4 hr10-24 hr2 – 4 daysUnaffected by renal failure LDH10 hr24 -72 hr14 days Myoglobin1-2 hr4 -8 hr24 hoursVery sensitive, powerful negative predictive value Acute Coronary Syndromes – Cardiac Markers

20. 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

21. Echo

22. Acute Coronary Syndromes - Treatment Aspirin Nitroglycerin Oxygen Analgesia

23. Treatment Beta-Blockers Anticoagulation Anti-Platelet Agents Thrombolysis Percutaneous Coronary Interventions (PCI)

24. 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

25. 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)

26. 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

27. 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

28. 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

29. 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

30. Pulmonary Embolism – Physical Exam Tachycardia, tachypnea, diaphoresis, hypotension, hypoxia, low grade fever, anxiety, cardiovascular collapse, right ventricular heave

31. 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

32. 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 6 = high risk

33. Pulmonary Embolism – Diagnostic Imaging Algorithm

34. Pulmonary Embolism – Treatment/Disposition Unfractionated heparin vs low molecular weight heparin (some studies suggest superiority of LMWH) Thrombolysis (for cardiovascular collapse) Floor vs ICU

35. PE CXR

41. Aortic Dissection - Pathophysiology Intimal tear of the aorta leads to dissection of the layers of the aorta creating a false lumen

42. 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

44. 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.

46. 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.

47. Tension Pneumothorax - Pathophysiology Collection of air in the pleural space causes collapse of the ipsilateral lung and then cardiovascular collapse as intrathoracic pressures increase.

48. 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

50. Tension Pneumothorax - Treatment Needle decompression Tube thoracostomy

51. 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

52. 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

53. Subtle Not so subtle

54. Imaging

55. Esophageal Rupture - Treatment Antibiotics Supportive Care Small tears with minimal extraesophageal involvement can be managed conservatively Surgical consult for all regardless of size

56. Take Home Points ABC’s first History is key Have a low threshold for missed MI