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Pathophysiology & Clinical Presentations

Acute Coronary Syndromes. GAP. Pathophysiology & Clinical Presentations. San Juan : Hotel Intercontinental, Dec. 12, 2006 - Jorge Ortega Gil, MD Mayagüez : Casa del Médico, Dec. 13, 2006 – Marcos Velázquez, MD Ponce : Casa del Médico, Dec. 14, 2006 – José Acevedo, MD.

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Pathophysiology & Clinical Presentations

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  1. Acute Coronary Syndromes GAP Pathophysiology & Clinical Presentations San Juan : Hotel Intercontinental, Dec. 12, 2006 - Jorge Ortega Gil, MD Mayagüez : Casa del Médico, Dec. 13, 2006 – Marcos Velázquez, MD Ponce : Casa del Médico, Dec. 14, 2006 – José Acevedo, MD

  2. Ischemic Heart Disease - Overview Parameters Anatomy: Atheroma / Atherothrombosis Subjective: Angina Objective: EKG T wave ST seg changes Chemistry: Cardiac serum biomarkers: CPK, CK-MB, Troponins Pathophysiology Atherosclerosis Epicardial & Microvascular Spam Atherothrombosis Silent ischemia Acute Coronary Syndromes Stable angina Prevalence & severity of stenosis Clinical Presentations

  3. Events During Atherogenesis

  4. P x r 2h Wall Stress =

  5. ISCHEMIC CASCADE TIME FROM ONSET OF ISCHEMIA • Flow Maldistribution Predictable sequence of pathophysiologic events post myocardial supply/demand imbalance • Biochemical metabolic actions • Hypoperfusion Nuclear • Compliance • (S4) • LVEDP • (Rales) Echo • Contractility • EF EKG ±45 sec. Angina / SI

  6. Effect of Fixed Stenosis on Myocardial Blood Flow

  7. Progression of coronary plaque over time Clinical Findings Acute Coronary Syndromes Sudden Cardiac Death Acute silent occlusive process Angina pectoris Endothelial dysfunction Atherogenic risk factors Thrombogenic risk factors Age 60 years 20 years

  8. IHD – Clinical Spectrum Chronic • Stable Angina • Silent Ischemia • Mixed Angina • Microvascular Angina (Syndrome X) • Stunned & Hibernating Acute • Unstable Angina • Acute Myocardial Infarction (NSTEMI, STEMI) • Sudden Cardiac Death Prinzmetal Angina

  9. Clinical Classification of Chest Pain Canadian Cardiovascular Society Classification ( CCSC) Typical angina (define) • Substernal chest discomfort with a characteristic quality and duration that is • Provoked by exertion or emotional stress and • Relieved by rest or nitroglycerin Atypical angina ( probable) Meets 2 of the above characteristics Noncardiac chest pain Meets one or none of the typical angina characteristics DIFFERENTIAL DIAGNOSIS OF CHEST PAIN • Cardiovascular: Pericarditis, Aortic Valve Disease, Aortic Dissection, Pulmonary Embolism, Mitral Valve Prolapse • Gastrointestinal: Esophageal, Biliary, Peptic ulcer, Pancreatitis • Pulmonary: Pneumothorax, Pneumonia, Pleuritis • Chest Wall: Costochondritis, Rib fracture, Herpes zoster • Psychological: Anxiety disorders *CHRONIC STABLE ANGINA – 2 TO 10 Min & CCSC I – II ACUTE CORONARY SYNDROMES > 15 Min. – Hours & CCSC III - IV

  10. CAD - Clinical Spectrum • Chronic ischemic heart disease Ischemia precipitated by increased myocardial oxygen demand in the setting of a fixed, not vulnerable atherosclerotic lesion. It is called Stable Angina when the clinical characteristics (Angina attacks) do not change in frequency, duration, precipitating causes, or easy with the angina is relieved, for at least 60 days. -Silent Ischemia, -Mixed Angina -Syndome X -Stunning & Hibernating. • Acute Coronary Syndromes (ACS) Ischemia or infarction are caused from a primary reduction in coronary flow, precipitated by plaque disruption and subsequent thrombus formation: Unstable Angina, NSTEMI, STEMI Prinzmetal Angina

  11. Stable Plaque Vulnerable Plaque

  12. Plaque Disruption UA NSTEMI STEMI + S. Markers

  13. Distinguishing Features of Acute Coronary Syndromes

  14. Acute Coronary Syndromes Coronary Atherothrombosis

  15. -RCA, 1yr. Before of the acute MI (B)

  16. Acute MI • Typical rise and gradual fall (troponin) or more rapid rise and fall of CK-MB, markers of myocardial necrosis, with at least one of the following: • Ischemic symptoms • EKG changes indicative of ischemia (ST-seg elevation or depression)

  17. T Wave – ST seg. changes Lateral T-wave ∆ ST-seg ∆ Zone of ischemia Path. Q waves Zone of injury Zone of necrosis >0.03 seconds >1/3 the total of QRS Anterior Septal Inferior

  18. “ Time is muscle” Myocardial Infarction is a true emergency in cardiac care.

  19. If the clinical picture is consistent with acute STEMI (including True Posterior MI) or new left bundle branch block (LBBB) is present in EKG, select and implement reperfusion therapy, Fibrinolysis or PCI as quickly as possible within 12 hours of symptoms onset to obtain and sustain optimal flow in the infarct-related artery (IRA). Do not wait for serum cardiac biomarkers result before implementing reperfusion strategy !

  20. ACS Treatment • Revascularization • Mechanical: PCI, CABG • Pharmacologic: Thrombolytics • Stabilization of Vulnerable Plaque Aspirin • Antithrombotics • Beta-Blockers • ACE-Inhibitors • Lipid-Lowering Agents (+stantins) • Antioxidants • Aggressive Risk Factors Modifications

  21. Complications of Ml

  22. COMPLICATIONS OF INFARCTION Papillary Muscle Rupture Left Ventricular Thrombus Ventricular Septal Rupture Ventricular Free Wall Rupture

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