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Acs gpmeeting-110912161748-phpapp02
- 1. Chest pain ofrecent onset and ACS few highlights GP - meeting at NNUH 13 September 2011 Toomas Särev Consultant Cardiologist NNUH-JPUH 1
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- 3. Challenges - Chestpain + ECG & Lab 3
- 4. Concept of Supply- Demand O2 supply O2 demand Coronary anatomy Diastolic BP Heart Rate Characteristics of blood O2-extraction •Hb •PaO2 Heart Rate Preload Afterload Contractility 4
- 5. Pathophysiology Clinical Diagnosis UNSTABLEANGINA ASYMPTOMATIC/ SYMPTOMATIC CHRONIC ACUTESTEMI Markersof myocardial injury (TnI, CK-Mb) ECG RISK PLAQUE RUPTURE INTRACORONARY THROMBUS DECREASED FLOW MYOCARDIAL HYPOXIA ISCHAEMIA IN MYOCYTES → 5
- 6. 6 Rupture of aplaque 6
- 7. The spectrum ofACS DiagnosticChallenges 7
- 8. diagnostic challenges? • riskassessment • individuals without clear symptoms or ECG features • atypical presentations (dyspnea, syncope, abdominal pain) • older patients (> 75 y) • women • diabetes, chronic renal failure, dementia 8
- 9. How to identifyhigh risk patients? 9
- 10. ECG - when shouldyou be concerned? 10
- 11. • collateral circulation •“double” supply • preconditioning Grade of ischaemia in EGG depends on • normal ECG does not rule out ACS • negative T waves indicate open vessel 11
- 12. This patient developed cardiogenic shock shortlyafter debut of his chest pain LM normal RCA The patient died despite initial success with PPCI Occlusion in the LEFT MAIN STEM: deep ST-depressions and negative T waves in inferolateral and antero-septal leads 12
- 13. Culprit in theproximal LAD (before the take-off of a Diagonal branch) - no protection LAD Diagonal Intermediate ST elevations in I, aVL andV2-V5 13
- 14. RCAa 100% RCA POST-PTCA Occlusionin the proximal RCA: ST-elevaton in in II, III, aVF +V1 & V4R 14
- 15. The spectrum ofACS DiagnosticChallenges 15
- 16. Abnormal Troponin possible causes •chronic or acute renal dysfunction • severe congestive heart failure - acute and chronic • hypertensive crisis • tachy- or bradyarrhythmias • pulmonary embolism, PAH • myocarditis • acute neurological disease, stroke, SAH 16
- 17. ACS in the elderly •clinical presentation might be different (dyspnea) • more extensive and severe CAD, • more comorbidities, level of frailty very individual • worse prognosis • different benefit/risk ratio with usual therapies • higher rate of secondary effects and complications © Gary Larson 2002 17
- 18. How to manage? Whento refer? © Gary Larson 2002 18
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- 20. Targets for Management O2supply O2 demand Revascularisation (PCI, CABG) Antithrombotic therapy •Antiplatelet therapy •Anticoagulation Preventive and plaque stabilising •Statins •ACEi Optimal hemodynamics (anti- ishcaemic therapy) •Beta blockers •Nitrates Optimise PaO2 Optimise Hb Optimal hemodynamics •Beta blockers •Nitrates •Ivabradine Respiratory support (CPAP) Painkillers Sedation GUIDELINES 20
- 21. Revascularisation • medical therapyif no critical coronary lesions if no options for revascularisation • PCI with stenting of the cuprit lesion • individualised decision in multivessel disease • staged PCI or all at once • PCI at first and then CABG • CABG 21
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- 23. Thank You! this presentationcan be downloaded from: www.slideshare.net/ kardiostar comments: kardostar@mac.com © Gary Larson 2002 23