An Approach to Chest Pain

Transcription

1 Oesophageal Spasm Acute Coronary Syndrome Pneumothorax An Approach to Chest Pain Musculoskeletal Pulmonary Embolism Aortic Dissection Ema Pitts Cardiology Registrar Basic Trainee

2 Pain S Site O Onset C Character R Radiation A Associates Symptoms T Timing E Exacerbating/Relieving Factors S Severity O Onset L Location D Duration C Character A Associated/Aggravating/Alleviating R Radiation S Severity

3 Background Chest Pain accounts for 5% of all presentations to the Emergency Department Of these presentations 15% AMI 25-30% Unstable Angina 15-35% Other Conditions Atypical Presentations are Common

4 Aetiology of Acute Chest Pain Cardiovascular Acute Coronary Syndrome Aortic Dissection Pericarditis Aortic Stenosis Chest Wall Pain Costochondritis Musculoskeletal Radicular nerve pain Herpes Zoster Pulmonary Pulmonary Embolism Pneumothorax Pneumonia Gastrointestinal GORD Oesophageal Spasm or Rupture Peptic Ulcer Disease Pancreatitis Cholecystitis

5 Case #1 Mr. DG, 64 year old male He presents to the Emergency Department with pain in his chest It came on suddenly in the centre of his chest earlier today at work The pain was getting worse so one of his colleagues called an Ambulance The pain got a little better when he was given some tablets under his tongue by one of the Ambulance drivers What else do we want to know about his pain?

6 Taking a Pain History (1) Onset What was he doing at the time? rest pain vs exertional pain time of onset Character of the Pain Pleuritic? Sharp or Dull? Positional? Reproducible with palpation? Radiation Ischaemic pain is usually diffuse and poorly localised. Pain that is well localised is more likely to be musculoskeletal rather than pleural, visceral or vascular

7 Taking a Pain History (2) Associated Features Nausea or vomiting? Diaphoresis? Syncope? Shortness of Breath? Timing The onset of ischaemic pain is usually gradual with increasing intensity over time Chest pain that lasts only seconds is rarely due to ischaemia Exacerbating and Reliving Factors Ischaemic Pain is often exacerbated with exertion, emotional stress, cold weather and meals Pain that is relieved by nitroglycerin is frequently attributed to cardiac aetiology (but may also be due to oesophageal spasm) Severity Not a good indicator of cardiac pain beware the diabetic patient with a silent infarct.

8 Mr DG The pain came on suddenly at 10:00 while he was sitting at his computer at work Dull, central chest pain that radiated to his left shoulder. He felt short of breath and sweaty when the pain started and he felt nauseated. The pain gradually got worse over minutes, and was relieved with GTN. What else would you like to know about Mr AG s history to confirm your diagnosis?

9 Is it Cardiac Pain?

10 Past Medical History Mr. DG tells you he has had this same pain off an on in the past, but it has usually come on when he has been walking, and goes away with rest. It has never been this bad. He was diagnoesd with reflux last time he visited his GP - 5 years ago. He takes no regular medications and has no allergies. He tells you he is healthy You take note of Mr. DG s Blood Pressure on the monitor in ED What else do we need to know?

11 Social and Family History Social History Mr. DG works as an office manager for an interstate delivery company He has a 30 pack year smoking history Family History Mr. DG s tells you his brother had an AMI last year at the age of 54 You review Mr. DG's Investigations

12 Examination and Investigations Clinical examination is unremarkable. Routine FBE and UEC are normal. No obvious consolidation or effusion on CXR ECG:

13 Risk Factors for CAD Age >65 Smoker Diabetes Hypertension Dyslipidaemia Family History What is wrong with Mr DG?

14 Acute Coronary Syndrome NSTEMI

15 Managemet of ACS Immediate Management Aspirin 300mg Glyceryl Trinitrate mcg Repeat every 5 minutes, for a maximum of 3 doses as long as BP >90mmHg Morphine 2-4 mg (IV) Oxygen Only give if the patient is hypoxic (sats <94%) The AVOID Study showed hyperoxia to be harmful Larger infarct size More recurrent AMI More major arrhythmias

16 AVOID Study

17 Management of ACS Second Antiplatelet Clopidogrel - 300mg initially (then 75mg daily) Ticagrelor - 180mg initially (then 90mg BD) Antithrombotic Therapy Therapeutic Enoxaparin 1mg/kg BD (more predictable) Heparin (requires frequent adjustment depending on APTT, but better if time to angiography uncertain)

18 Risk Stratification of Chest Pain Risk Features Management High Intermediate Low Unlikely to be ACS Ongoing Chest Pain Recent history of effort angina Deterioration of previously stable angina or pain similar to previous UA/AMI New ECG changes Haemodynamic compromise Features suggestive of other life threatening condition No high risk features Known IHD previous MI, previous revascularisation (stents/cabg), known stenosis >50% on previous coronary angiography >3 risk factors for CAD Pain resolved in last 8hrs No intermediate or high risk features No high or intermediate risk features Clincally unlikely to be ACS Immediate management Acute Admission Clinical judgement Treat as either low or high risk Further Ix required Consider hs-tnt Mx depends on hs-tnt hs-tnt not recommended

19 Back to Mr DG You decide Mr. DG's presentation is high risk and he needs to be admitted to hospital for further investigations You explain to Mr. DG he will most likely need an angiogram in the morning You leave your intern to complete his admission paperwork and return to the ward.

20 Mr. DG You are not long gone from the Emergency Department when you are urgently called back to review Mr. DG. He has had recurrent chest pain and the nurse presents you with the following ECG What has happened to Mr DG? What is your diagnosis now?

21 STEMI (Anterior Leads LAD territory)

22 Managemet of STEMI URGENT REPERFUSION Mr. DG is rushed to the cath lab. He undergoes successful PCI and stenting of his LAD.

23 Case #2 Mrs CT, 43F presents to the Emergency Department with left sided chest pain and central chest heaviness. She tells you the pain woke her up at 2am. She felt cold and clammy at the time and her heart was racing. She still has chest pain and feels short of breath when you review her in the Emergency Department 7 hours later. What next?

24 Pain History The pain is poorly localised to the lateral left chest and is worse with deep inspiration It does not radiate or change with position The pain did not respond to GTN administered in ED She has never had this pain before

25 Medical and Family History Mrs CT is slightly overweight She was recently diagnosed with hypothyroidism for which she takes thyroxine 100mcg daily She reports a family history of Factor V Leiden but no personal or family history of DVT or PE. What should we do next?

26 Investigations

27 D-Dimer Measures fibrin degradation product after a blood clot is degraded by fibrinolysis A level >500ng/mL is considered positive Great Test... If its negative! If your clinical suspicion of DVT/PE is either low anyway Other Causes of a Raised D-Dimer Infection Heart Failure Pregnancy Malignancy Trauma Or if its positive and you strongly suspected DVT/PE in the first place (Well's Criteria)

28 Wells Criteria Active Cancer (1) Bedridden Recently >3 days or major surgery within 4 weeks (1) Calf swelling >3cm compared with the other leg (1) Collateral superficial veins present (1) Entire leg swollen (1) Localised tenderness along the deep venous system (1) Pitting oedema, confined to the symptomatic leg (1) Paralysis, paresis, or recent plaster immobisilation of the lower extremity (1) Previous documented DVT (1) Alternative Diagnosis as likely or more likely (-2) SCORE 0 = Low Risk, 1-2 = Moderate Risk, 3 = High Risk for DVT

29 CTPA Large saddle PE

30 Acute Management of PE Anticoagulation Therapeutic Enoxaparin 1.5mg/kg daily or 1mg/kg BD Then switch to oral anticoagulation Warfarin to target therapeutic INR ( ) DOAC (need adjustment in renal impairment avoid if CrCl <30ml/min) Rivaroxaban 15-20mg daily (direct Xa inhibitor) Apixaban mg BD (direct Xa inhibitor) Dabigatran mg BD (direct thrombin inhibitor) Provoked PE 3 to 6 months treatment Unprovoked PE lifelong anticoagulation

31 Chest Pain Summary Aetiology Quality Location Radiation Duration Associated Sx Onset Unstable Angina Visceral Retrosternal Neck, jaw, shoulder, arm <15 minutes Nausea, vomiting, diaphoresis, dyspnoea Gradual AMI Visceral Retrosternal Neck, jaw, shoulder, arm >15minutes Nausea, vomiting, diaphoresis, dyspnoea Variable Aortic Dissection Severe Retrosternal Interscapular tearing Constant Diaphoresis, Dyspnoea, Nausea Sudden PE Pleuritic Lateral Constant Dyspnoea Sudden PTX Pleuritic Lateral Neck, back Constant Dyspnoea Sudden

32 References Westvic.healthpathways.org.au AVOID Study, Supplemental O2 in STEMI Study. Stub D, et al. Circulation. 2015;131: ECG Findings in Pulmonary Embolism Chan TC, Vilke GM, et al. Electrocardiographic manifestations: pulmonary embolism. J Emerg Med. 2003; 21(3):

33 Questions

34 The ECG in Chest Pain In patients with chest pain and a Normal ECG 1% have a final diagnosis of AMI 4% have a final diagnosis of UA Non-specific ST and T Wave Changes Found in 3-4% of all patients with AMI Found in 20% of all patients with NSTEMI/UA Of ALL patients with ACS, 20% will show a normal or non-specific ECG

35 ECG points Approximately 50% of patients with an AMI will have a diagnostic ECG at the time of presentation (ST-elevation or ST-depression) ST-elevation is important for revascularisation therapy Thrombolysis Emergency PCI Widespread ST-elevation correlates with increased mortality It is important to recognise other causes of ST elevation to avoid unwarranted thrombolysis

36 Investigations Troponin and CK Troponin: - Comprised of 3 proteins (Troponin C, I and T). Attached to tropomyosin found in the grooves between actin filaments in skeletal and cardiac (but not smooth) muscle tissue - Troponin T and I are excellent markers for myocardial infarction - Serum Troponin I rises within 4-8 hours after the onset of chest pain, peak within 12-16hrs and return to baseline within 5-9 days CKMB: - Found in heart muscle, skeletal muscle and in brain - increased in over 90% of AMI, but also elevated in muscle trauma, physical exertion and post-surgery - Begins to rise in 4-6hrs, peaks at 24hrs and returns to normal in 2 days.

37 Cardiac Enzymes First Detectable Peak Duration Troponin I 2-4h 10-24h 5-10 days Troponin T 2-4h 10-24h 5-14 days CK-MB 3-4h 10-24h 2-4 days LDH 6-12h 24-48h 6-8 days Higher negative predictive value Reduces the troponin blind period 4% absolute risk increase and 20% relative risk increase for the detection of type 1 AMI

38 Non-Cardiac Causes of Raised Troponin