Intensive Course Phase 1 2010a


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My lecture notes in pdf during MMed (Emergency Medicine) Phase I Conjoint Board Intensive Course in Universiti Malaya, 22 February 2010

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Intensive Course Phase 1 2010a

  1. 1. Intensive Course For Emergency Medicine Phase I (MMed Professional Exam 2010) KS Chew School of Medical Sciences Universiti Sains Malaysia
  2. 2. Cardiovascular Physiology Review: Cardiac Output
  3. 3. • Stroke volume = End diastolic volume – End systolic volume = 135 – 65 = 70 ml • At rate of 70 beats/min, CO = 70 * 70 = 4900 ml • Ejection fraction (EF) is the ratio of stroke volume to end-diastolic volume (EDV), expressed as a percentage: • EF = (SV/EDV) * 100
  4. 4. Schematic Representation Of The Frog- heart Preparation Used By Otto Frank
  5. 5. Frank-Starling Law
  6. 6. Effects On Stroke Volume Of Stimulating The Sympathetic Nerves To The Heart
  7. 7. The pressure-volume cycle of the human left ventricle. The area bounded by the pressure-volume curve gives the stroke work of the heart. The lower confine of the pressure-volume loop shown by the dotted line is defined by the passive stretch of the relaxed ventricular muscle by the returning blood.
  8. 8. Increased Preload Increased Increased Afterload Contractility
  9. 9. Vascular Function and Cardiac Function Curve
  10. 10. Vascular Function and Cardiac Function Curve
  11. 11. Relationship Between End-diastolic Ventricular Volume and Stroke Volume
  12. 12. Pathophysiology of Acute Coronary Syndrome
  13. 13. Onset of STEMI Hospital Management Modified from Libby. Circulation 2001;104:365, - Prehospital issues - Medications Hamm et al. The Lancet 2001;358:1533 and - Initial recognition and management - Arrhythmias Davies. Heart 2000;83:361. in the Emergency Department (ED) - Complications - Reperfusion - Preparation for discharge Secondary Prevention/ Management Long-Term Management Before STEMI Chronology of the interface between the 1 2 3 4 5 6 patient and the clinician 4 through the progression of plaque formation and the onset of Presentation Ischemic Discomfort Working Dx Acute Coronary Syndrome complications of ECG No ST Elevation UA NSTEMI ST Elevation STEMI. Cardiac Biomarker Final Dx Unstable NQMI QwMI Angina Myocardial Infarction
  14. 14. Pathophysiology of ACS Large One example of atherothrombotic fissure disease progression Occlusive thrombus Lipid pool (Q-wave MI) Macrophages Small Stress, tensile, fissure internal Mural thrombus Shear forces, Fissure (unstable angina/ external non-Q-wave MI) Atherosclerotic Plaque Thrombus plaque disruption Fuster V et al NEJM 1992;326:310–318 Davies MJ et al Circulation 1990;82(Suppl II):II–38, II–46
  15. 15. Atherothrombosis: a Generalized and Progressive Process Plaque Unstable Fatty Fibrous Athero- rupture/ sclerotic fissure & angina MI }ACS Normal streak plaque plaque thrombosis Ischemic stroke/TIA Critical leg Clinically silent ischemia Stable angina Cardiovascular Intermittent claudication death Increasing age ACS, acute coronary syndrome; TIA, transient ischemic attack
  16. 16. Platelet Inhibition With GP IIb/IIIa Inhibitors Reproduced with permission from Yeghiazarians Y, Braunstein JB, Askari A, et al. Unstable angina pectoris. N Engl J Med. 2000;342:101-114. Copyright © 2000, Massachusetts Medical Society. All rights reserved.
  17. 17. Mechanism of Action of Aspirin in Acute Coronary Syndrome Prostacyclin is produced by endothelial cells and thromboxane A2 by platelets from their common precursor arachidonic acid via the cyclooxygenase pathway. Thromboxane A2 promotes platelet aggregation and vasoconstriction, whereas prostacyclin inhibits platelet aggregation and promotes vasodilation. The balance between platelet thromboxane A2 and prostacyclin fosters localized platelet aggregation and consequent clot formation while preventing excessive extension of the clot and maintaining blood flow around it.
  18. 18. Mechanism of Action of Aspirin in Acute Coronary Syndrome The thromboxane A2–prostacyclin balance can be shifted toward prostacyclin by administration of low doses of aspirin. Aspirin produces irreversible inhibition of cyclooxygenase. Although this reduces production of both thromboxane A2 and prostacyclin, endothelial cells produce new cyclooxygenase in a matter of hours whereas platelets cannot manufacture the enzyme, and the level rises only as new platelets enter the circulation. This is a slow process because platelets have a half- life of about 4 days.
  19. 19. The thrombus in STEMI is RBC & fibrin rich and often called a red clot or red thrombus Unstable angina and NSTEMI often precedes STEMI (preinfarction angina). During this phase blood flow in the coronary artery becomes sluggish gradually, and therefore the platelets get trapped within the plaque. Hence in NSTEMI, thrombus is predominantly a white thrombus (platelet rich). Often, a central platelet core is seen over which fibrin clot may also be formed.
  20. 20. Fibrinolytics • Why is streptokinase not used in treating UA/ NSTEMI? • All available thrombolytic agents act basically as a fibrinolytic agents, therefore it is difficult to lyse the platelet rich clot. • There is also a risk of these agents lysing the fibrin cap and exposing underlying platelet core and trigger a fresh thrombus (TIMI IIIb trial)
  21. 21. STEMI, NSTEMI and UA • STEMI - occlusive thrombus - ST elevation (and Q waves) - Cardiac Enzyme elevation - Fibrinolytics beneficial • NSTEMI - non-occlusive thrombus - NO ST/Q - Cardiac Enzyme elevation present - Fibrinolytics not beneficial • UA - non-occlusive thrombus - NO ST/Q - Cardiac Enzyme elevation absent - Fibrinolytics not beneficial
  22. 22. Electrophysiological Changes During Cardiac Ischemia • Ischemia/hypoxia causes an elevation in extracellular K+. This occurs because K+ leaks out through K+ - ATP channels and because of decreased activity of the Na+/K+-ATPase pump
  23. 23. Pathophysiology of Asthma and COPD
  24. 24. • A chronic inflammatory disorder of the airways • Many cells and cellular elements play a role • Characterized by airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing • Widespread, variable, and often reversible airflow limitation
  25. 25. ASTHMA COPD Allergens Cigarette smoke YY Y Ep cells Mast cell Alv macrophage cells Ep CD4+ cell Eosinophil CD8+ cell Neutrophil (Th2) (Tc1) Bronchoconstriction Small airway narrowing AHR Alveolar destruction Airflow Limitation Reversible Irreversible Source: Peter J. Barnes, MD