1. APPROACH TO CHEST PAIN Dr.Hanan AlBackr 18/10/1429(18/10/2008)

4. APPROACH TO CHEST PAIN  Objectives: 1. Establish a differential diagnosis for chest pain 2. Know what clues to obtain on history to rule-in or out MI, PE, pneumothorax and pericarditis. 3. Identify risk factors for MI and PE 4. Know how to do a focused physical exam, identifying features that would distinguish between MI, PE, pneumothorax, pericarditis, tamponade, pneumonia, and aortic dissection. 5. Identify investigations required in diagnosing MI, PE, pneumothorax and pneumonia and how to interpret results. 6. Outline management strategy in MI, PE, peumothorax and pneumonia

5. Chest Pain Common presentation to A&E Trivial to life-threatening causes Key to diagnosis is history Negative baseline investigations DO NOT ruleout serious conditions

6. Life-threatening Causes of Chest Pain Myocardial infarct Unstable angina Thoracic aortic dissection Pulmonary embolus Tension pneumothorax Oesophageal rupture

7. Other Differentials Costochondritis Herpes Zoster Musculoskeletal Pancreatitis Anxiety

8. CHEST PAIN ASSESSMENT History Vitally Important Pain -Nature Site Severity Radiation Onset Exac/relieving factors Associated features Duration Previous similar pains

9. CHEST PAIN ASSESSMENT RISK FACTORS Family history Smoking Raised BP Raised cholesterol Past Medical History (IHD,diabetes)

10. Initial Approach Assume the worst! 100% Oxygen IV access Monitoring ECG quickly Done in tandem with history taking

11. Chest Pain Assessment Examination General Examination ( sweaty clammy pale cyanosed, anaemic etc pulse BP) Cardiovascular /Respiratory examination ? Failure ( crackles,oedema, raised JVP) Heart Sounds - rate, nature,?quiet ? added heart sounds, ?murmurs

12. CHEST PAIN INVESTIGATIONS 12 Lead ECG Cardiac Enzymes (incl Troponins) CXR

13. Investigations ECG most important 20% of patients having an MI will have a normal ECG initally Negative cardiac enzymes in A&E are not helpful CXR useful to rule out other causes

14. CXR PneumothoraxCXR Pneumothorax

18. Case 1 A 65 year-old male presents with a 2-hour history of central chest pain. He describes it as “though an elephant is sitting on my chest”. He gets similar symptoms when walking 2 blocks and is relieved with rest. Today’s episode began after he walked to the bathroom and was not relieved by rest.

19. 1) What is the most likely diagnosis? What other clues in his history would support the diagnosis? 2) What is the difference between stable angina and unstable angina? The patient’s BP is 140/75 and his HR is 110 and regular. His JVP is at 3 cm ASA, he has no crackles, no murmurs and no peripheral edema. His EKG is EKG #1. 3) How would you manage this patient? 4) Would your management strategy change if he presented with EKG #2?

20. 5) Outline the indications and contraindications to thrombolysis The patient stabilizes and is admitted to the CCU. He develops chest pain again 2 days later but of a different quality. The pain is worse when he is supine and improves when he sits up. 6) What is a possible diagnosis? 7) What clinical and diagnostic clues would help confirm the diagnosis? 8) What is the management? What should you look out for?

23. APPROACH TO CHEST PAIN 1) Myocardial ischemia or infarction History: – - pressure-type of chest pain – - generally involves central to left-sided pain with radiation to jaw or arms – - exacerbated by activity, relieved with rest – - relieved with nitro spray – - associated with nausea, diaphoresis, syncope, shortness of breath – - enquire about cardiac risk factors: age, sex, smoking history, diabetes, hypertension, hyperlipidemia, previous myocardial infarction and family history

24.  Physical exam: - Does the patient look distressed? - ↓BP indicates cardiogenic shock - ↓HR may indicate block or increased vagal tone, ↑HR may indicate an ischemia-related tachyarrhythmia - ↑JVP, pulsatile liver and peripheral edema seen in right-sided heart failure - oxygen desaturation, crackles, S3 seen in left-sided heart failure - new murmurs: mitral regurgitation murmur in papillary muscle dysfunction - Look for other signs of vasculopathy (carotid, abdo, femoral bruits, peripheral pulses)

25.  Investigations: - EKG (should be knee-jerk reflex in chest pain scenario!) – see section on approach to EKG - CXR to look for signs of congestive heart failure - Cardiac enzymes: CK (will begin to rise 6 hours after infarct and remain elevated for 24-48 hours), troponin (will begin to rise 12 hours after infarct and remain elevated for 2 weeks). Need to follow serially if first set negative. - Exercise-stress test, dobutamine stress echo, myocardial perfusion scan: useful to look for inducible ischemia if unsure - Coronary angiography: gold-standard

26.  Management: Morphine for pain Oxygen if hypoxic Nitro spray/drip for pain Aspirin Lasix if in congestive heart failure Inotropes if in cardigenic shock Streptokinase (thrombolysis-TPA or TNK more commonly used) Anticoagulation Also, think of beta-blockers (reduce heart rate and contractility but beware of worsening of CHF). Statins and Ace-inhibitors should be added as indicated. Primary angioplasty may be indicated.

27. Case 2 A 78 year-old woman presents with sudden- onset, sharp right-sided chest pain. She has been coughing since the onset of her pain and has noted that she is dyspneic. Her pain significantly worsens with inspiration.

28. 1) What diagnoses are you considering? 2) What clinical clues can help? She reports some hemoptysis and has a documented fever. Her CXR shows some changes likely consistent with atelectasis in the right lower lung field. 3) What is your next step? On further questioning you get a history of calf tenderness just prior to the onset of chest pain. 4) What test would you order? 5) What is your management strategy?

29. 2) Pulmonary Embolus  History: - Sudden-onset sharp chest pain - exacerbated by inspiratory effort - can be associated with hemoptysis, sycope, dyspnea, calf swelling/pain from DVT - risk factors: immobilization, fracture of a limb, post-operative complications, hypercoagulable states (underlying carcinoma, high-dose exogenous estrogen administration, pregnancy, inherited deficiencies of antithrombin III, activated protein C, S, lupus anticoagulant, prior history of DVT/PE [Virchow’s triad]  Physical: - Anxious patient, sense of impending doom - Tachycardia, tachypnea, hypoxia - If severe, can get hypotension, syncope, and RV failure (↑JVP, RV heave and loud/palpable P2)

30.  Investigations: - ↓PaO 2 and ↓PaCO 2 from increase in overall minute ventilation - Increased A-a gradient - D-dimer is sensitive but has a low specificity. Do NOT order it to rule-in a PE! - CXR: – a. Frequently normal – b. Often non-specific (atelectasis, pleural effusion) – c. May see Hampton’s hump (area of infarction), Westermark’s sign (area of oligemia/decreased vascular markings) - EKG: sinus tachycardia most common, S1Q3invertedT3 with large embolus (classic, but rare!), look for right-axis deviation - Echo: if large embolus, can see signs of right-sided compromise - V/Q scan very sensitive but not specific - Spiral CT with contrast show large, central emboli - Pulmonary angiogram is gold standard but carries risk - Consider Doppler U/S of legs

31.  Management: - Anticoagulation to prevent further thrombus (heparin initially and then coumadin with therapeutic INR level of 2-3 for 6 months – length of therapy still controversial) - Thrombolysis if hemodynamically unstable - Supportive treatment with oxygen, and fluids

32. Case 3 A 23 year-old man with Marfanoid appearance presents to the ER with acute onset of sharp right-sided chest pain and SOB. His BP is 80/60 and he has decreased breath sounds on the right side.

33. 1) What is the most likely diagnosis? 2) What is your next step? The patient is appropriately managed but continues to be hypotensive. On further questioning he remarks that his chest pain radiates to his back between his shoulder blades. 3) What additional diagnoses should be considered now? 4) What investigations would help confirm the diagnosis? 5) How would you manage this patient?

34.  3) Pneumothorax  History: - can be asymptomatic or present with acute pleuritic chest pain and dyspnea - primary pneumothorax predominantly in healthy young tall males - secondary – a. due to trauma (MVA accidents – associated with rib fractures, iatrogenic – during line placement, thoracentesis) – b. increased alveolar pressure from asthma or barotraumas (BiPAP, ventilator-associated) – c. rupture of bleb in COPD patients – d. necrosis of tissue in pneumonia, empyema, cancers

35.  Physical: - decreased expansion of chest, decreased breath sounds and decreased tactile/vocal fremitus on side of pneumothorax - hyperresonant percussion note - In tension pneumothorax, where pleural injury produces a one-way valve, increased positive pressure can cause tracheal deviation away from the side of the pneumothorax, mediatinal shift with compression of contralateral lung, decreased venous return and CO and BP. This is an emergency.

36.  Investigations: - CXR: fine line of visceral pleural detached from parietal pleura seen on ipsilateral side - In large pneumoathoraces, mediastinal shift and contralateral compression of lung can be seen  Management: - watchful wait for small pneumothoraces – repeat CXR - chest tube insertion for large, hemodynamically unstable pneumothoraces - In emergent situation, insert large bore needle in 2 nd ICS, midclavicular line, followed then by chest tube insertion