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1. DISORDERS OF CARDIOVASCULAR SYSTEM REVISION OF BASIC CARDIOVASCULAR ANATOMY AND PHYSIOLOGY

2. Gross Anatomy of the heart

3. Gross anatomy cont

4. GREAT VESSELS

5. Valvular anatomy

6. Epicridiac Coronary Arteries

7. Coronary vessels cont

8. THE ELECTRICAL CONDUCTION SYSTEM OF THE HEART

9. THE ELECTRICAL CONDUCTION SYSTEM OF THE HEART There is a hierarchy of automaticity within the tissue of the heart The tissue that possesses the greatest degree of automaticity (e.g., has the fastest rate of spontaneous depolarization) functions as the dominant pacemaker

10. PHASES OF ACTION POTENTIAL (VENTRICLES, ATRIA , BUNDLE OF HIS, BUNDLE BRANCHES AND THE PURKINJE SYSTEM) P0 : is the up stroke of the action potential and is caused by a transient increase in Na+ conductance P1 : is a brief period of in i tial depolarization and is as a result of movement of K+ ions out of the cell and a decreased Na+ conductance. P2 : is the plateau of the action potential and is generated by a balance of repolarizing potassium currents and depolarizing calcium current . P3 : repolarization (Ca2+ conductance decreases and K+ conductance increases) P4 : the resting membrane potential (inward and out ward currents are equal)

11. PHASES OF ACTION POTENTIAL (SA- AND AV- NODE ) Phase 0 : is the upstroke of the action potential and is caused by an increase in Ca2+ conductance. Phase 3 : is repolarization and is caused by increased K+ conductance. Phase 4 : is slow depolarization and accounts for the pace maker activity of the SA node (is caused by increased Na+ conductance) Phase 1 and 2 : absent

12. DEFINITIONS OF CHRONOTROPIC AND DROMOTROPIC EFFECTS Cronotropic effect : change in heart rate A negative chronotropic effect es HR by ing the firing rate of the SA node A positive chronotropic effect causes the opposite Dromotropic effect : produce changes in conduction velocity in the AV node

13. Cellular Basis of Cardiac Contraction

14. STEPS IN EX CI TATION- CONTRACTION COUPLING The action potential spreads from the cell membrane into the T tubles During plateau of the action potential, Ca 2+ conductance is increased and Ca 2+ enters the cell from the extracellular fluid This Ca 2+ entry triggers the release of even more Ca 2+ from the SR (Ca 2+ -induced-Ca 2+ release) Ca 2+ binds to troponin C , and tropomyosin is moved out of the way, removing the inhibition of actin and myosin binding

15. Cellular Basis of Cardiac Contraction

16. STEPS IN EXITATION- CONTRACTION COUPLING Actin and myosin bind, the thick and thin filaments slide past each other, and the myocardial cells contract The magnitude of the tension that develops is proportional to the intracellular concentration of Ca 2+ Lowering of cytosolic [Ca 2+ ] by the sarcoplasmic reticulum (SR) cause this ion to dissociate from troponin and relaxes the heart

17. CARDIAC MUSCLE CONTRACTILITY It is the intrinsic ability of the cardiac muscles to develop force at a given muscle length. It is also called inotropism It is related to the intracellular Ca 2+ concentration It can be estimated by the ejection fraction

18. POSITIVE INOTROPISM Increased heart rate Sympathetic stimulation Cardiac glycosides (inhibits the N + ,K + -ATPase)

19. NEGATIVE INOTROPISM Parasympathetic stimulation Decreases the force of contraction in the atria by decreasing the inward Ca 2+ current during the pleatu of the cardiac action potential .

20. DETERMINANTS OF STROKE VOLUME PRELOAD AFTERLOAD MYOCARDIAL CONTRACTILITY

21. PRELOAD It is equivalent to t he length of the muscle at the onset of contraction It determines the length of the sarcomeres at the onset of contraction It also regulates the extent of activation of the contractile system, i.e., its sensitivity to Ca 2+ This relationship forms the basis of Starling's law of the heart within limits, the force of ventricular contraction depends on the end-diastolic length of the cardiac muscle; in the intact heart the latter relates closely to the ventricular end-diastolic volume .

22. FACTORS AFFECTING PRELOAD

23. AFTERLOAD It is t he tension that the muscle is called upon to develop during contraction It is the load that opposes fiber shortening It is determined by the aortic pressure as well as by the volume and thickness of the ventricular cavity

24. Factors affecting afterload

25. Myocardial contractility

26. Cardiac metabolism Consumes 15 % of the total body O2 supply Most ATP production depends on the oxidation of glucose and free fatty acids (FFAs) In the fasting , resting state: circulating FFA s are the principal sources of energy (~70%) In the fed state : glucose oxidation

27. Epidemiology of Cardiovascular disorders

28. GLOBAL BURDEN OF CARDIOVASCULAR DISEASES 3 % of all deaths (world wide) 1 million deaths each year 40% and 28% of deaths in high and low income countries respectively in 2010 Cardiovascular disease are highly prevalent- 80 million adults, 35% of the adult population

29. GLOBAL BURDEN OF CARDIOVASCULAR DISEASES Epidemiologic Transition Economic development determines health status and disease profile of a human society Transition can occur with in a specific disease category

30. Stages of epidemiologic transition

31. ABERA BALCHA, MD 2014

32. ABERA BALCHA, MD 2014

33. Cardiac symptoms The symptoms caused by heart disease result most commonly from : M yocardial ischemia D isturbance of the contraction and/or relaxation of the myocardium O bstruction to blood flow A n abnormal cardiac rhythm or rate

34. CARDIAC SYMPTOMS Dyspnea Cough Orthopnea PND Body swelling Fatigue Cyanosis Chest discomfort Angina equivalents Syncope Palpitation Hemoptysis

35. Investigstion of cardiovsascular disorders

36. ELECTROCARDIOGRAPHY The electrocardiogram (ECG or EKG) is a graphic recording of electric potentials generated by the heart The signals are detected by means of metal electrodes attached to the extremities and chest wall and are then amplified and recorded by the electrocardiograph ECG leads actually display the instantaneous differences in potential between these electrodes

37. CLINICAL USES OF ECG Arrythmia Conduction disturbance Ischemia Life threatening metabolic disturbances Chamber enlargement or hypertrophy I ncreased susceptibility to sudden cardiac death (e.g. QT prolongation syndromes) Guide reperfusion therapy

38. ELECTRICAL DIPOL

39. Principles_ depolarization Depolarization 2012

40. Principles cont Repolarization

41. ECG grid 0.2 sec 0.04 sec Time Voltage 0. 1mv Paper speed 25mm/sec

42. The leads Ordinary ECG has 12 leads 6 limb leads 3 bipolar I, II,III 3 unipolar aVR, aVL and aVF 6 precordial leads V1-V6

43. The leads cont

44. The limb leads ABERA BALCHA, MD 2012

45. The limb leads ABERA BALCHA, MD 2012

46. Chest leads

47. The Normal ECG

48. P wave Atrial depolarization Duration _ <120ms Amplitude_ <0.25mv Terminal negative deflection _<0.1mv in precordial leads Axis _positive in lead II negative in aVR & biphasic in V1

49. PR interval Conduction delay in the AV node Duration 0.12_0.20s

50. THE QRS COMPLEX ABERA BALCHA, MD 2012

51. QRS complex Ventricular depolarization Patterns: Duration <0.12ms Amplitude

52. ST segment Begins with J point Usually isoelectric and has upward concavity

53. T wave Vent repolarization Polarity similar to preceding QRS

54. QT interval Total ventricular activity 40% of cardiac cycle QT c= < 0.44s

55. U wave < o.1 mv Usu seen in right precordial leads V2-V4 ??? repolarization of the His-Purkinje system, ABERA BALCHA, MD 2012

56. The normal ECG cont…

57. CHEST RADIOGRAPHY (PA)

58. CHEST RADIOGRAPHY (LEFT LATTERAL)

59. CHEST RADIOGRAPHY (LEFT LATERAL)

60. ECHOCARDIOGRAPHY

61. Echocardiography

62. Nuclear cardiology CT MRI Nuclear cardiology CT MRI

63. SELECTION OF NON-INVASIVE IMAGING MODALITIES

64. OTHERS Stress ECG Holter Monitor Event recorder Cardiac catheterization and coronary Angiography

65. The complete cardiac diagnosis 1. The underlying etiology 2. Anatomic abnormalities 3. Physiologic disturbances 4. Functional disability