Emergency Department Evaluation of Chest Pain

1. Emergency Department Evaluation of Chest Pain Indiana University SOM Department of Emergency Medicine MS-IV Lecture Series

2. Why this is important • Many of the causes of chest pain are imminently or potentially life threatening • Therapy for many of these conditions can be lifesaving and must be started in the ED • Failure to recognize and treat serious causes of chest pain will be costly to your patients and to you.

3. Caring for Chest Pain:Two Major Goals • Distinguish serious from non-serious causes • Institute appropriate interventions

4. Causes of Chest Pain • Imminently life threatening: • MI/ACS, aortic dissection, pulmonary embolus • Potentially life threatening: • Pneumothorax, Boehaave’s, pericarditis, pneumonia, others • Non-emergent: • Chest wall pain, GERD, many others

5. Case #1 • 54 yo F presents with SSCP. She is being placed into the bed as you walk in. She looks sweaty and uncomfortable. • What do you want the nurses to begin doing as you start your H&P?

6. Chest Pain: Initial Interventions • Vitals, including pulse oximetry • EKG • Within 10 minutes after arrival to the ED • “Safety net” • IV • *02 • Monitor *ACLS 2010: “there is insufficient evidence to support its (supplemental oxygen’s) routine use in uncomplicated ACS. If the patient is dyspneic, hypoxemic, or has obvious signs of heart failure, providers should titrate therapy, based on monitoring of oxyhemoglobin saturation, to <94%”

7. Chest Pain: Initial Interventions • ASA • Cheap, little downside, 23% reduction in mortality in AMI. • Give it to (almost) everyone with CP and give it early

8. Case #1 (continued) • You begin to ask your patient about her pain. • What type of pain typifies the following: • Myocardial ischemia? • Aortic Dissection? • Pulmonary Embolism?

9. Case #1 (continued) • Your patient has been having intermittent episodes of sub-sternal squeezing pressure for one day, with radiation to both arms. Episodes last 10-15 minutes. Currently, the pain is more severe and has been ongoing for one hour. • The nurse hands you the EKG…

10. What does the EKG show?What therapies need to be instituted?

11. Acute MI: Treatment • Reperfusion Therapy • Primary angioplasty (Percutaneous Coronary Intervention - PCI) or thrombolytics • PCI generally preferred (better outcomes), but not available 24/7 in most hospitals • Time is critical • Door-to-lytic time should be < 30 minutes • Door-to-balloon time should be < 90 min • “Time is tissue”

12. Acute MI: TreatmentReperfusion Therapy • Thrombolytics • Convert plasminogen to plasmin, which is fibrinolytic • Coronary artery thrombus is lysed, allowing myocardial reperfusion • Marked reduction in mortality (~20%) • Many agents now available: streptokinase, alteplase (t-PA), retevase, tenecteplase (TNK)

13. Acute MI: TreatmentReperfusion Therapy Thrombolytics – eligibility criteria: H&P consistent with AMI + Symptom duration < 12 hours + • ST elevation > 1mm in two or more contiguous limb or precordial leads, or • New or presumed new LBBB Decision to reperfuse based on H&P and EKG, not labs

14. Acute MI: TreatmentOther therapies • Aspirin • Nitrates • Decrease preload (and thus myocardial O2 demand) and cause some direct vasodilatation of the coronary arteries • Sublingual or IV in setting of STEMI • Avoid if PDE inhibitor (e.g. sildenafil) taken in past 24-48 hrs (intractable hypotension)

15. Acute MI: TreatmentOther therapies • Beta blockers – Controversial • Decrease myocardial 02 demand • Increase risk of cardiogenic shock • Routine use currently not recommended • Contraindications: • Hypotension • Bradycardia • AV block • Heart failure • Cocaine intoxication

16. Acute MI: TreatmentOther therapies • Heparin • Unfractionated or Low Molecular Weight (enoxaparin) • Used in addition to thrombolytics or PCI • Direct thrombin inhibitors • Bivalirudin (Angiomax) • An alternative to heparin/LMWH • Does not cause thrombocytopenia • Exact role still emerging

17. Acute MI: TreatmentOther therapies • Platelet inhibitors • Clopidogrel (Plavix) • Prasugrel (Effient) • Inhibit platelet aggregation by a different mechanism than ASA (irreversibly inhibit platelet ADP receptor)

18. Acute MI: TreatmentOther therapies • Morphine • Efficacy not adequately studied • No known mortality benefit • Analgesic and anxiolytic effects may be beneficial • Consider if patient’s pain not relieved with nitrates

19. What if your patient’s EKG had looked like this?

20. Acute Coronary Syndrome • ACS = a spectrum of clinical disease that includes AMI and unstable angina • It is not always possible to distinguish between these entities in the ED • The Acute Coronary Syndromes share a common pathophysiology: a ruptured or eroded atheromatous plaque

21. The spectrum of ACS Unstable angina without EKG changes Non-ST elevation MI Unstable Angina with EKG changes STEMI

22. Treatment of ACS • ASA • Nitrates • Heparin/enoxaparin • Clopidogrel • Beta-blockers* • GP IIb-IIIa receptor inhibitors* *Controversial/evolving role

23. Treatment of ACS • +/- Cath lab • Depending on clinical picture (ongoing pain, etc.) • Thrombolyticsonly for STEMI • Worsen outcome if no acute STE

24. Acute Coronary Syndromes Algorithm The management of ACS is complex, rapidly changing, and constantly evolving

25. What if your patient’s EKG had looked like this? (normal)

26. Risk stratification of CP patients • Most CP patients do not have acute EKG changes, but still may have underlying myocardial ischemia causing their CP. • Risk stratification of these patients determines whether or not they require admission and what therapies are appropriate. • Higher risk patients require more aggressive therapy

27. Risk stratification of CP patients for CAD • The history and EKG are, by far, the most important factors • Other less important factors: • Classic cardiac risk factors • Cardiac markers (CK and troponin) • Normal markers do not rule out ACS • Response to therapy (NTG) • Physical exam findings

28. A difficult patient • The patient with CP somewhat suggestive of myocardial ischemia, but with a normal EKG, normal cardiac markers and no apparent alternative dx. • What are your disposition options?

29. A difficult patient • Discharge/outpatient stress • Low risk, pain free patients only • Rapid (12-24 hr) rule out and stress • Often done in ED CP unit • Admit • High risk patients, known CAD, concern for ACS

30. Case #2 • 57 yo M presents with abrupt onset sharp CP that radiates to his upper back. The pain is constant and not exacerbated by exertion or cough. • PMHx: HTN • Meds: Non-compliant with BP meds x 3 yrs • Vitals: 985F 22 102 224/108 What diagnosis are you concerned about?

31. Separation of the intima and media, creating a false lumen Type A: Any involvement of the ascending aorta Type B: Involves descending aorta only Aortic Dissection

32. Aortic DissectionWhat complications can occur? • Aortic regurgitation • Tamponade • Hemothorax • MI • CVA • Limb/renal/intestinal ischemia • Overall mortality 27%

33. Aortic Dissection • What exam findings are suggestive? • Pulse deficit (present in 15%) • Murmur of AI (32%) • Neuro findings (5%) • Hypertension (49%)

34. Aortic Dissection • What CXR findings are suggestive? • Widened mediastinum (62%) • Abnormal aortic contour (50%) • Pleural effusion (19%) If dissection is suspected, it cannot be ruled out by exam findings or CXR

35. CT MRI TEE Aortography Aortic DissectionDiagnostic Tests

36. Aortic DissectionED Management • BP control is the cornerstone of ED management • Nitroprusside + beta-blocker • May alternatively use labetalol as single agent • Definitive management • Type A: surgical • Type B: medical or surgical

37. Case #3 • 46 yo F presents with 8 hours of left-sided chest pain that is worse “every time I breathe.” The pain began suddenly at rest. It is associated with SOB. • PMHx is unremarkable • No meds or allergies • Vitals: 989F 24 106 138/88 97% RA • You order IV/O2/Monitor/EKG/ASA as you continue your H&P • The nurse hands you the EKG:

38. Case #3

39. Case #3 S1 Q3 T3

40. Pulmonary Embolus • Can be difficult to diagnose • Important clues: • Hx • DVT/PE risk factors • Work-up: controversial • Non-specific tests are rarely helpful • EKG • CXR • ABG

41. Pulmonary Embolus PERC rule • “Pulmonary Embolism Rule-out Criteria” • When applied to low-risk patients, the absence of any of the criteria predicts a very low (<2%) risk of PE, obviating the need for further testing. • Criteria: -Age < 50 -Pulse < 100 -SaO2 > 94% -No unilateral LE swelling -No recent trauma or surgery -No hemoptysis -No prior DVT or PE -No hormone use Am J Emerg Med 2008; 26:181-5 J Thromb Haemost 2004; 2:1247-55

42. Pulmonary Embolus • Diagnostic studies • D-dimer • Sensitive, but not specific • Helpful in low risk patients • V/Q scan • PIOPED probabilities • CT • May miss small peripheral emboli • Most commonly used imaging test • Pulmonary Angiography • The Gold Standard, but rarely done

43. Pulmonary Embolus • Treatment • Anticoagulation (Heparin or LMWH) • IVC filter if anticoagulation contraindicated • Thrombolytics if hemodynamic instability • Surgical embolectomy if contraindicated NEJM 2008;358:1037-52

44. Case #4 • 44 yo M presents with 10 hours of constant, sharp, pleuritic, sub-sternal chest pain that is exacerbated by lying supine. • Vitals: 992F 18 102 112/78

45. Diagnosis?

46. Pericarditis

47. Pericarditis: Diagnosis • History • Sharp pleuritic pain, worse when supine • Exam • Pericardial friction rub • EKG • Diffuse ST elevation and PR depression • Echo

48. Pericarditis • Many etiologies • Idiopathic most common • Infectious • Neoplastic • Post MI / Post CABG • Autoimmune • Uremic

49. Pericarditis: Treatment • Treatment depends on cause • NSAIDS • Antimicrobials • Dialysis

50. Case 4 (continued) • The patient becomes hypotensive (80/38) • Repeat EKG • Electrical alternans • What diagnostic and therapeutic steps would you consider?