APPROACH TO CHEST PAIN IN ED ( to present).pptx

approach to chest pain

1. APPROACH TO CHEST PAIN IN ED

2. INTRODUCTION > Chest pain is common ED presentation . Hence, the aim is to be able to identify the life threathening conditions. > A good history remains the cornerstone of the diagnosis of the life threatening causes of chest pain > Life threatening conditions: 1/ Acute myocardial infaction 2/ Aortic dissection 3/ Pulmonary embolism 4/ Tension pneumothorax 5/ Oesophageal rupture

3. Important but not life threatening causes of chest pain Cardiac - Stable angina - prinzmetal angina - pericarditis/myocarditis Respiratory - simple pneumothorax - pneumonia with pleurisy Gastrointestinal - Reflux oesophagitis / Oesophageal spasm Referred pain - Gastritis/ PUD - Biliary disease

4. HISTORY Classically, cardiac chest pain is retrosternal in the left anterior chest with crushing, tightness,squeezing or pressure that is often brought on by exertion and relieved with rest. Patients may also complain of dyspnea, diaphoresis, and nausea with pain radiating to the left shoulder, jaw, arm or hand. The onset of symptoms may be sudden or gradual Unstable angina : 10-30min AMI pain : > 30min Cocaine abuse and HIV infection can accelerate atherosclerosis. Location Nature of pain Exacerbating factor/ relieving factor Radiation of pain Duration Associated symptoms

5. Acute coronary syndrome (ACS)

6. Acute coronary syndrome (ACS)

7. Myocardiac InfarctionDiagnosed by:

8. Unstable angina

9. ECG ST elevation in 2 contiguous leads in patient with symptoms of ischaemia Cut-off point for new or presumed new ST elevation (in absence of LVH & LBBB): ≥ 0.1 mV in all leads except V2-V3 In leads V2-V3, cut off point: ≥ 0.25 mV (males < 40yrs) ≥ 0.2 mV (males > 40yrs) ≥ 0.15 mV (females)

10. ECG

11. Serum Cardiac Biomarkers Cardiac troponins (cTnT and cTnI) Creatine kinase-Myocardial Band (CK-MB) Creatine kinase (CK)

12. Management Aim: Pain relief Establishing early reperfusion Treatment of complications - arrhythmias

13. Reperfusion Strategies TIME LOST is equivalent to MYOCARDIUM LOST factors Time from symptom onset to first medical contact Time delay to PCI (time from hospital arrival to balloon dilatation – door to balloon time) Time to hospital fibrinolysis (time from hospital arrival to administration of fibrinolytic therapy – door to needle time) Contraindications to fibrinolytic therapy High risk patients

14. Early presentation (within 3 hours) equally effective except for the following situations where primary PCI is the preferred strategy: - fibrinolytic therapy is contraindicated - in high-risk patients - PCI time delay [(door-to-balloon time) – (door-to-needle time)] is less than 60 minutes Late presentation (3 to 12 hours) Primary PCI is preferred The door to balloon time should be within 90 min if the patient presents at a PCI capable facility If transferred from a center with no PCI facilities, it should be less than 2 hours. (including transfer delay) If the time delay to primary PCI is longer than as mentioned,then fibrinolytic therapy should be given.

15. Very late presentation (> 12 hours) Both primary PCI and fibrinolytic therapy are not routinely recommended in patients who are asymptomatic and haemodynamically stable reperfusion therapy would still be beneficial in patients with persistent ischaemic symptoms, haemodynamic or electricalinstability. In this subgroup, primary PCI is the preferred strategy.

16. High Risk Patients Large Infarct Anterior Infarct Hypotension and cardiogenic shock Significant Arrhythmia Elderly patient Post revascularization (post CABG/PCI) Post infarct angina

17. Fibrinolytic Streptokinase not fibrin specific and is less efficacious than fibrin selective agents lower risk of intracranial haemorrhage The reduction in mortality is less than fibrin specific agent antigenic and promotes the production of antibodies less effective if given again 5 days after the first administration Regimen: 1.5 mega units in 100 ml normal saline or 5% dextrose over 1 hour. .

18. Alteplase fibrin specific and achieves better reperfusion at 90 min as compared to streptokinase higher rate of reocclusion -needs to be given for 48 hours Second generation fibrin specific agents: Tenecteplase Tenecteplase - as efficacious as alteplase slightly lower bleeding risk as compared to alteplase advantage easier to administer (single dose) and do not induce antibody production Rapid reperfusion compared to streptokinase Heparin needs to be given for 48 hours

19. Contraindications to Fibrinolytic therapy Absolute contraindications Risk of Intracranial haemorrhage Any history of intracranial haemorrhage Ischaemic stroke within 3 months Known structural cerebral vascular lesion (e.g. arteriovenousmalformation ) Known intracranial neoplasm Risk of bleeding Active bleeding or bleeding diathesis (excluding menses) Significant head trauma within 3 months Suspected aortic dissection

20. Relative contraindications Risk of intracranial haemorrhage Severe uncontrolled hypertension on presentation (BP > 180/110mm Hg)* Ischaemic stroke more than 3 months ago History of chronic, severe uncontrolled hypertension Risk of Bleeding Current use of anticoagulation in therapeutic doses (INR > 2) Recent major surgery < 3 weeks Traumatic or prolonged CPR >10 minutes Recent internal bleeding (e.g. gastrointestinal or urinary tract haemorrhage ) within 4 weeks Non-compressible vascular puncture Active peptic ulcer

21. Indicators of Successful Reperfusion resolution of chest pain (may be confounded by the use of narcotic analgesics). early return of ST segment elevation to isoelectric line or a decrease in the height of the ST elevation by 50% in the lead that records the highest ST elevation therapy within 60-90mins of initiation of fibrinolytic therapy. early peaking of CK and CK-MB levels. restoration and/or maintenance of haemodynamic and/or electrical stability

22. PULMONARY EMBOLISM Complication of venous thromboembolism Most PE’s occur when a portion of a venous clot breaks off, travel through the venous system through the right side of the heart, and subsequently enters pulmonary artery

23. Clinical presentation “ PE is TACHY ” - T achycardia, A cute dyspnea , C hest pain, H ypoxia , s Y ncope Physical examination : - tachycardia, tachypneic - low grade fever - Loud P2 - signs of RV strain: JVP elevated, right parasternal heave - haemodynamic instability/ syncope - Signs of DVT ECG changes : non specific , normal ECG in about ~ 6% of the patients - S1Q3T3 ( classical , only present in 12% of massive PE) - sinus tachycardia - RBBB - non specific T inversion in lead V1-V4

24. Wells score Clinical Characteristic Score Previous pulmonary embolism or deep vein thrombosis + 1.5 Heart rate >100 beats per minute + 1.5 Recent surgery or immobilization (within the last 4/52 + 1.5 Clinical signs of DVT + 3 Alternative diagnosis less likely than PE + 3 Hemoptysis + 1 Cancer/malignancy + 1 Clinical Probability of Pulmonary Embolism Score Low 0-1 (3.4%) Intermediate 2-6 (27.8%) High >6 (78.4)

25. Diagnostic test for PE D-Dimer CT Angiography V/Q lung scan Pulmonary Angiography

26. CHEST XRAY Normal (~40%) Hampton’s hump Westermark sign Small pleural effusion Atelectesis Raised diaphragm Localised infiltration Consolidation ‘plump’ pulmonary arteries in massive PE

27. Hampton’s hump (wedge shape opacity in the periphery of the lung with its base against the pleural surface-d/t pul . Infarction) Fleischner sign (a prominent dilated central pulmonary artery on chest x-ray, associated with massive embolus enlarging the luminal diameter of the proximal artery acutely; or pulmonary hypertension in the subacute to chronic setting.

28. Westermark sign chest x-ray finding of oligaemia (clarified area) distal to a large vessel that is occluded by a pulmonary embolus. The focal area of increased translucency due to oligaemia is caused by impaired vascularisation of the lung due to primary mechanical obstruction or reflex vasoconstriction.

29. CTPA   will show filling defects within the pulmonary vasculature with acute pulmonary emboli. When the artery is viewed in its axial plane the central filling defect from the thrombus is surrounded by a thin rim of contrast, which has been called the polo mint sign

30. Classification : 1. Massive PE:   Acute PE with sustained hypotension (systolic blood pressure < 90 mm Hg) for at least 15 minutes or requiring vasopressor support, or with persistent profound bradycardia (heart rate < 40 beats/min) with signs/symptoms of shock.  2. Submassive PE:   PE without systemic hypotension but with right ventricular (RV) dysfunction 3. Low-risk PE:   Acute PE associated with normal blood pressure, no evidence of RV dysfunction, and normal biomarkers .

31. Management Haemodynamic and respiratory support Hypoxaemia is one of the features of severe PE, and is mostly due to the mismatch between ventilation and perfusion. Patients with RV failure are frequently hypotensive or are highly susceptible to the development of severe hypotension during induction of anaesthesia , intubation, and positive-pressure ventilation. Consequently, intubation should be performed only if the patient is unable to tolerate or cope with non-invasive ventilation. When feasible, non-invasive ventilation or oxygenation through a high-flow nasal cannula should be preferred. If mechanical ventilation is used, care should be taken to limit its adverse hemodynamics effects. In particular, positive intrathoracic pressure induced by mechanical ventilation may reduce venous return and worsen low CO due to RV failure in patients with high-risk PE. Treatment of acute RV failure in high-risk PE patients 1/ Cautious volume loading If the central venous pressure is low, modest (<_500 mL) fluid challenge can be used as it may increase the cardiac index in patients with acute PE. However, volume loading has the potential to overdistend the RV and ultimately cause a reduction in systemic CO. Experimental studies suggest that aggressive volume expansion is of no benefit and may even worsen RV function 2/ Use of vasopressors Use of vasopressors is often necessary, in parallel with (or while waiting for) pharmacological, surgical, or interventional reperfusion treatment. Norepinephrine Increases RV inotropy and systemic BP, promotes positive ventricular interactions, and restores coronary perfusion gradient 3/ Use of ECMO

32. Initial anticoagulation START ANTICOAGULATION EARLY > In patients with high or intermediate clinical probability of PE ( while awaiting for results) LMWH and fondaparinux are preferred over UFH for initial anticoagulation in PE, as they carry a lower risk of inducing major bleeding and heparin-induced thrombocytopenia. Use of UFH is nowadays largely restricted to patients with overt haemodynamic instability or imminent haemodynamic decompensation in whom primary reperfusion treatment will be necessary. UFH is also recommended for patients with serious renal impairment [creatinine clearance ( CrCl ) <_30 mL/min] or severe obesity Transition to oral anticoagulation 1/ Non-vitamin K antagonist oral anticoagulants (NOAC) NOACs are small molecules that directly inhibit one activated coagulation factor, which is thrombin for dabigatran and factor Xa for apixaban, edoxaban , and rivaroxaban. Recommended over vitamin K antagonist (VKAs) NOAC regimens include: Dabigatran : initial parenteral for ≥ 5 days, then 150mg twice daily Rivaroxaban: 15mg twice daily for 3/52, then 20mg once daily Apixaban : 10mg twice daily for 7 days, then 5mg twice daily Edoxaban : LMWH/UFH ≥ 5days, then 60mg once daily ( or 30mg if CrCl 30-50mL/min or weight < 60kg) 2/ VKAs When VKAs are used, anticoagulation with UFH, LMWH, or fondaparinux should be continued in parallel with the oral anticoagulant for >_5 days and until the international normalized ratio (INR) value has been 2.03.0 for 2 consecutive days. Warfarin may be started at a dose of 10 mg in younger (e.g. aged <60 years) otherwise healthy patients and at a dose <_5 mg in older patients.

33. Reperfusion therapy In high‑risk PE —marked by hemodynamic instability— systemic thrombolysis is the first-line reperfusion treatment The greatest benefit is observed when treatment is initiated within 48 h of symptom onset, but thrombolysis can still be useful in patients who have had symptoms for 6-14 days. Unsuccessful thrombolysis, as judged by persistent clinical instability and unchanged RV dysfunction on echocardiography after 36 h, has been reported in 8% of high-risk PE patients. If thrombolysis is contraindicated or unsuccessful, consider surgical embolectomy or percutaneous catheter‑directed treatments , based on resource availability and expertise

34. Aortic dissection

35. History and presentation Sudden, severe,tearing chest pain/upper abdominal pain radiating to back, maximal at the outset Migratory pain from chest to the abdomen to the lower limbs Difference in SBP in both arms (>20mmHg) or BP in the upper limbs > than lower limbs Radio-radial / radio-femoral delay

36. Investigation CXR 1) Widen mediastenum (>8cm PA) 2) Extension of aortic shadow > 5cm beyond calcified wall ’eggshell’, due to acute dissection 3) Obliteration aortic knob/localized bulge 4) Aortic enlargement 5) Double density of aorta 6) New pleura effusion 7) Apical pleural cap-localized haemothorax 8) Depression of left main stem bronchus to more than 140’ 9) Shift and elevation of the right main stem bronchus 10) Trachea deviate to the right 11) Widening of paravertebral stripe 12) Loss of space between aorta and pulmonary artery

37. OTHER INVESTIGATIONS : >> CT angiogram >> ECG >> Echocardiogram >> FBC,RP,Coagulation profile,GXM,cardiac enzyme

38. Management Supplemental oxygen 2 large bore IVL Analgesia-iv morphine Urinary catheter Antihypertensive-reduction of SBP to 100-120mmHg, provided urine output >30mls/hr Iv labetolol 20mg bolus then infusion 2mg/hr up to 8mg/hr Iv propanolol Iv esmolol

39. If hypotensive, start fluid resuscitation Surgical repair Stanford type A Type b with complication Uncontrolled HPT Progression of dissection

40. Esophageal Rupture ( Boerhaave’s syndrome) Often present with sudden onset, sharp substernal chest pain that follows an episode of forceful vomiting. Patients are normally very ill, with tachycardia, fever, dyspnea and diaphoresis Physical examination may reveal crepitus in the neck or chest from subcutaneous emphysema, while audible crepitus on cardiac auscultation (Hamman’s crunch) - rare finding CXR may be normal or demonstrate a pleural effusion ( left more common), pneumothorax, pneumomediastinum, pneumoperitoneum or subcutaneous air.

41. PNEUMOTHORAX

42. HEART SCORE : predicts 6-week risk of major adverse cardiac events in patients with chest pain.

43. HEART PATHWAY : identifies patients with low risk for acute coronary syndrome (ACS) to enable safe, early discharge from the emergency department (ED)

44. THANK YOU References ; 1/ Tintinalli 2/ shirley ooi 3/ CPG MI 4/ ESC guideline for PE