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Chest pain structured approach

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by Dr. Anas Babiker, Consulant Cardiologist, Alzaytouna Hospital …

by Dr. Anas Babiker, Consulant Cardiologist, Alzaytouna Hospital
& Academic Secretary of the Sudan Heart Society

Published in: Health & Medicine

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  • 1. Chest pain- structured approach challenges with ST segment (MI and its mimics) Dr Anas Albadawi Babiker Assoc. Prof of Medicine – UMSTInterventional cardiologist – Alzaytouna Specialist Hospital MBBS, MRCPI, MRCP (UK) MSc Med Sci (Ireland), MSc interv card (Madrid) CSCST cardiology / interv card (Ireland)
  • 2. • 7 million visits in USA every year to ER with chest pain, only 15-25% are ACS• Retrospective study of patients with confirmed MI, 47% did not present with chest pain especially females and older patients• Associated sweating and vomiting were found to be strong predictor of ACS pain
  • 3. Chest pain presenting to PHC service
  • 4. Causes of chest painMI, Pericarditis, myocarditis, endocarditis, aorticdissection, MVPPneumonia, pleurisy , PE, tension pneumothoraxTrauma, fracture ribs, metastasesGastritis, oesphagitis, PUD, oesphageal rupture,cholecystitis, pancreatitisMuscular pain, arthritis, radiculopathy,
  • 5. Systemic approach is needed Detailed History Focused physical examination Relevant investigations
  • 6. HISTORY
  • 7. • Central, crushing ? • Sharp? Character • Tearing radiating to the back • Exertional , relieved by rest and nitrates Aggravating / • Worse with food? • Worse with inspiration?relieving factors • Worse when lying back and relieved by sitting forward Associated • Sweating, nausea, vomiting symptoms Age, smoking, DM, HTN, Obesity, DL, Risk factors gender…etc,
  • 8. Other points in the history• History of IHD• Use of cocaine in young people• Detailed drug history• Response to nitroglycerine has no diagnostic role (sensitivity 35% specificity 59%)• Neither response to antiacids
  • 9. EXAMINATION
  • 10. Pulse and BP Eyes,Lungs face Exam HEART Abdomen
  • 11. INVESTIGATIONS
  • 12. • ST changes,new LBBB, new Qs, ECG (<10 min) arrhythmias • Pneumonia, pneumothorax, pleural CXR effusion • RWMA, pericardial effusion Echocardiogram • At first assessment and repeat in 3- 6 Cardiac biomarkers hours • CBC, RFT, LFTs, D-dimersGeneral investigations • TMET, CT cors, Coronary angiography, More advanced CT aortogram, CTPA
  • 13. 3RD UNIVERSAL DEFINITION OF MI 2012 Arise or a fall in troponin with at lease one reading above upper limit of normal Identification Imaging ofSymptoms New evidence of ST-T changes or intracoronary of pathologiical Q new loss of a new LBBB thrombus byischaemia waves viable angiography or myocardium autopsy
  • 14. Where is the ST segment?
  • 15. ST ELEVATION
  • 16. STEMI Pericarditis LV aneurysmMyocarditis CVA PE Persistent Early LVH/ RVH jeuvenile repolarization pattern Electrolyte Hypothermia disturbance
  • 17. How to measure ST elevation?
  • 18. Sequence of ST changes in STEMI•ST elevation at the J-point in two contiguous leads with the cut-off points:≥0.1 mV (mm) in all leads except V2 and V3•In V2 and V3:  ≥ 0.25 mV (2.5mm) for men <40 yrs  ≥ 2.0 mV (2 mm) for men ≥ 40 yrs, and  ≥ 1.5 mV (>1.5 mm) for women
  • 19. ST changes of pericarditis•Stage I  wide spread concave ST elevation with PR depression•Stage IIPseudonormalization•Stage III inverted T wave•Stage IVNormalization
  • 20. myocarditis•Acute myocarditis causes nonspecific ST segment changes. These can beaccompanied by supraventricular and ventricular rhythm disturbances and T-wave abnormalities.
  • 21. Hypothermia•Sinus bradycardia•Prolonged QTc-interval•ST segment elevation (inferior and left precordial leads)•Osborn-waves (slow deflections at the end of the QRS-complex)
  • 22. Early repolarization• Is a term used for ST segment elevation without underlying disease.• It is commonly seen in young men.• Characteristics of early repolarization are:[7] – an upward concave elevation of the RS-T segment with distinct or "embryonic" J waves – slurred downstroke of R waves or distinct J points or both – RS-T segment elevation commonly encountered in the precordial leads – persistence of these characteristics for many years – absence of reciprocal ST depression – large symmetrical T waves
  • 23. ST elevation due to early repolarization
  • 24. ST DEPRESSION
  • 25. LBBB/ RBBB NSTEMI Hypokalemia/LVH with strain Hypomagnesemia Acute neurological Digoxin effect event
  • 26. ST changes in LBBB/ RBBB
  • 27. ECG changes in NSTEMINew horizontal or down-sloping ST depression >0.05 mV (1/2mm) in two contiguous leads; and/or T inversion ≥0.1 mV(1mm) in two contiguous leads
  • 28. Types of ST depression
  • 29. LVH with strain pattern •Sokolow-Lyon criteria: R in V5 or V6 + S in V1 >35 mm •The criteria is not available for those under 40 •ECG sensitivy for LVH is 27%
  • 30. Hyperkalemia •P-waves are widened and of low amplitude due to slowing of conduction •QRS complex: QRS widening fusion of QRS-T loss of the ST segment •Tall tented T waves
  • 31. Digoxin toxicity Oddly shapped, scooped out concavity
  • 32. Hypokalemia •ST depression and flattening of the T wave • Negative T-wave •U wave might be seen
  • 33. Acute neurological conditions •Can happen in SAH, brain tumours, CVA, Gullina Barre, epilepsy, migraine oQ waves oST segment elevations oST segment depressions oT wave changes. Large negative T waves over the precordial leads are observed frequently. oProlonged QT-interval. oProminent u-waves.ECG from a patient with SAH
  • 34. Take Home Messages• Never take chest pain lightly• ECG should always be interpreted in the context of clinical conditions THANKS