Cardiac cycle

1. CARDIOVASCULAR SYSTEM

2. CONTENTS INTRODUCTION LAYERS OF THE HEART WALL PROPERTIES OF CARDIAC MUSCLE CARDIAC CYCLE HEART SOUNDS AND MURMURS ECG APPLIED ASPECTS RELATED ARTICLES CONCLUSION REFERENCES

3. INTRODUCTION The heart is a chambered muscular organ that pumps blood received from the veins into the arteries, thereby maintaining the flow of blood through the entire circulatory system. Somewhat pyramid shaped and lies between two lungs in the mediastinum .

4. LAYERS OF THE HEART WALL

5. PERICARDIUM

6. PERICARDIUM 2parts – outer fibrous inner serous Outer fibrous – continues as tunica adventitia of large blood vessels and attached to diaphragm below Inner serous – parietal vicseral In between the above two – pericardial space / cavity

7. MYOCARDIUM Formed by cardiac muscles. Mainly three : Muscles which form contractile unit of heart Those which form the pacemaker Those which form the conductive system

8. THE MUSCLE FIBRES FORMING CONTRACTILE UNIT Striated Similar to skeletal muscles but involuntary Bound by sarcolemma Centrally placed nucleus Myofibrils embedded in sarcoplasm Sarcomere contains all muscle proteins

9. INTERCALATED DISC Cardiac muscle fibres are branched Point of union of branches – membrane of both muscles fuse together – Tough structure called intercalated disc

10. INTERCALATED DISC

11. SYNCYTIUM All muscles act like a single unit Gap junctions – permeable to ions Facilitates rapid conduction of electrical activity

12. THE MUSCLE FIBERS FORMING PACE MAKER Muscle fibers modified Specialized structure with lesser striations Generates impulses for heart beat Formed by pacemaker cells SA node is situated in posterior wall of Right atrium near opening of Superior vena cava.

13. THE MUSCLE FIBRES FORMING CONDUCTIVE SYSTEM Modified cardiac muscle fibres Specialized cells - conduct impulses from SA node to ventricles Junctional tissues Atria – directly Vetricles - various tissues

14. ELECTRICAL SYSTEM OF THE HEART

15. ENDOCARDIUM Inner most layer Thin,smooth , glistening membrane Single layer of endothelial cells Continues as endothelium of blood vessels

16. SEPTAE OF THE HEART

17. VALVES OF THE HEART Pulmonary semilunar valve Aortic semilunar valve Left AV (bicuspid) valve Right AV (tricuspid) valve Chordai tendineae Papillary muscle

18. Heart valves ensure unidirectional blood flow through the heart Composed of an endocardium with a connective tissue core. Two major types Atrioventricular valves Semilunar valves

19. Semilunar valves prevent backflow of blood into the ventricles Have no chordae tendinae attachments Aortic semilunar valve lies between the left ventricle and the aorta Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk Heart sounds (“ lub -dup”) due to valves closing “ Lub ” - closing of atrioventricular valves “Dub”- closing of semilunar valves

20. ARTERIAL SUPPLY The arterial supply of the heart is provided by the right and left coronary arteries, which arise from the ascending aorta immediately above the aortic valve.

21. PROPERTIES OF CARIAC MUSCLES EXCITABILITY RHYTHMICITY CONDUCTIVITY CONTRACTILITY

22. EXCITABILITY Ability of a tissue to give response to a stimulus . Muscles respond by development of an action potential.

23. ELECTRIC POTENTIAL IN CARDIAC MUSCLE RAPID DEPOLARIZATION INITIAL RAPID REPOLARIZATION PLATEAU PHASE SLOW REPOLARIZATION

24. Ionic basis of Action potential

25. SPREAD OF ACTION POTENTIAL Spreads very rapidly Gap junctions- allows free movement of ions Cardiac muscles act like a syncytium

26. RHYTHMICITY Ability of a tissue to produce its own impulses regularly. Autorythmicity / Self excitation SA node – discharge impulses rapidly – spreads to other parts of the heart

27. PACEMAKER Part of the heart from which impulses for heart beat are produced SA node – modified cardiac muscle Superior part of lateral wall of right atrium. Below opening of Superior Venacava . Do not have contractile elements Continuous with fibers of atria Maximum number of impulses

28. Spread of impulses

29. CONDUCTIVITY Three groups of fibres Anterior internodal Bachman Middle internodal Wenkebach Posterior internodal Thorel All these converge towards AV node

30. CONTRACTILITY Ability of a tissue to shorten in length after receiving a stimulus. All or none law Staircase phenomenon Summation of subliminal stimuli Refractory period

31. Stimulus applied- whatever may be the strength- maximum response/ no response. Subthreshold stimuli- no response. Threshold stimulus- weakest stimulus that evokes a response All or none law

32. Staircase phenomenon

33. Summation of subliminal stimuli Stimulus with subliminal strength – no response Repeated subliminal stimuli- contraction- summation.

34. REFRACTORY PERIOD Period when muscles do not show any response to a stimulus Cardiac muscles have long refractory period Absolute – 0.27 s- throughout contraction Relative – 0.26 s- first half of relaxation

35. CARDIAC CYCLE Defined as the succession of coordinated activities which take place in every heart beat. 2 major steps – systole – 0.27 s diastole – 0.53 s Duration- 0.8 s when heart rate is 72/min

36. SYSTOLE Isometric contraction – 0.05s Ejection period – 0.22s

37. DIASTOLE Protodiastole – 0.04s Isometric relaxation – 0.08s Rapid filling – 0.11s Slow filling – 0.19s Atrial systole – 0.11s

38. ATRIAL SYSTOLE Also called presystole End of ventricular diastole 10% blood forced into ventricles from atria. 0.11 sec

39. ISOMETRIC CONTRACTION Lasts for 0.05s Starts immediately after atrial systole AV valves close – increased pressure in ventricles No change in volume or length of muscle fibres - only tension

40. EJECTION PERIOD Due to opening of semilunar valves 2 stages Rapid ejection Slow ejection 0.22 sec

41. PROTODIASTOLE Pressure in ventricles drop Pressure in aorta and pulmonary artery increase Semilunar valves close again Indicates end of systole 0.04 sec

42. ISOMETRIC RELAXATION Once again all valves are closed Both ventricles relax – with no change in volume or length of muscle Fall in intraventricular pressure When pressure goes less than atria – AV valves open Leading to filling of ventricles 0.08 sec

43. RAPID FILLING Av valves open Blood accumulates in atria – atrial diastole Sudden rush into ventricles – 70% of filling 0.11 sec

44. SLOW FILLING/DIASTASIS Ventricular filling slows down 20 % filling takes place 0.19 sec atrial systole/last rapid filling phase and the cycle repeats, 10% filling.

45. HEART SOUNDS Four sounds Fisrt and second – more prominent – resemble ‘LUBB DUBB’ respectively Heard – stethoscope 3 rd - mild – microphone – children and athelets 4 th – inaudible – graphic registration- phonocardiogram

46. First sound – simultaneous closure of both AV valves Second – closure of semilunar valves Third – rapid filling Fourth – atrial systole

47. CARDIAC MURMURS Abnormal heart sounds or bruits Turbulence in blood flow Ventricular diseases / abnormal conditions

48. CLASSIFICATION CARDIAC MURMURS SYSTOLIC MURMURS DIASTOLIC MURMURS CONTINUOUS MURMURS INCOMPETENT AV STENOSIS OF AV VALVES PDA VALVES INCOMPETENCE OF S V STENOSIS OF S V

49. ELECTROCARDIOGRAM Electrocardiography – technique Electrocardiograph – instrument Electrocardiogram – graphical registration Introduced in 1901 – Dutch physiologist – Willem Einthoven

50. ECG INDICATIONS

51. APPLIED ASPECTS CONGENITAL HEART DISEASES Acyanotic Cyanotic ACQUIRED HEART DISEASES Rheumatic fever Infective endocarditis

52. CONGENITAL HEART DISEASE Incidence – 9 in 1000 births Maybe abberant embryonic development Maternal rubella / chronic maternal alcohol abuse

53. ACYANOTIC CONGENITAL HEART DISEASES Minimal or no cyanosis Left to right shunting of blood Ventricular septal defect Atrial septal defect

54. CYANOTIC Right to left shunting Cyanosis even during minor exertion Tetralogy of Fallot Pulmonary stenosis Tricuspid atresia Transposition of great vessels

55. ATRIAL SEPTAL DEFECT

56. Most common More frequent in females Dyspnea ,chest infections Fixed splitting of second heart sound Chest radiograph – enlarged heart Echo shows clear defect with ventricular dilatation and hypertrophy and PA dilatation

57. MANAGEMENT Closure – cardiac catheterization Implantable closure devices

58. VENTRICULAR SEPTAL DEFECT

59. Congenital VSD – incomplete separation of ventricles Left to right shunting 1 in 500 live births Murmur heard at the left sternal edge. Occurs as acute failure in infants Chest x ray and ECG – ventricular hypertrophy Mary S. Minette , MD; David J. Sahn , MD, Ventricular Septal Defects Circulation. 2006;114:2190-2197.)

60. MANAGEMENT Small VSD – no treatment – prophylaxis is must Large defects – initially treated with medications – digoxin ,diuretics Persistent failure – surgical repair

61. PATENT DUCTUS ARTERIOSUS Ductus arteriosus – present in fetal life Normally closes after birth Sometimes may persist – defect Since pressure in aorta greater than PA – continuous AV shunt.

62. Small shunts – no symptoms Large shunts- growth retardation Dyspnea eventually cardiac failure Machinery murmur- second left intercostal space below clavicle Accompanied by thrill ECG usually normal

63. MANAGEMENT Cardiac catheterization May be done in infancy Smaller shunts – delayed to childhood Prostaglandin synthetase inhibitors – Indomethacin ,Ibuprofen – 1 st week – induce closure

64. PERSISTENT DUCTUS WITH REVERSE SHUNTING Pulmonary Artery pressure rises to exceed aortic pressure Shunt may reverse Central cyanosis – Eisenmenger’s Syndrome ECG – ventricular hypertrophy

65. TETRALOGY OF FALLOT Pulmonary stenosis Overiding aorta VSD Right ventricular hypertrophy Elevated right ventricular pressure Right to left shunting

66. “ FALLOT SPELLS ” Cyanosis Syncope Brain injury Death

67. MANAGEMENT Definitive management – total correction of defect Surgical relief of pulmonary stenosis Closure of VSD

68. AQUIRED HEART DISEASES INFECTIVE ENDOCARDITIS RHEUMATIC FEVER

69. INFECTIVE ENDOCARDITIS

70. CAUSATIVE ORGANISMS Staphylococcus Group A streptococcus pnemonococcus

71. 2 forms – acute , subacute Subacute – viridans stretococci Vegetations – fibrous exudate and microorganisms

72. CLINICAL FEATURES Low irregular fever Sweating Malaise Arthralgia Weight loss Anorexia Murmurs Painful fingers and toes ,skin lesions

73. LABORATORY FINDINGS Leukocytosis Neutrophilia Normocytic normochromic anemia ESR is rapid

74. PROPHYLAXIS SINGLE DOSE 30-60mins BEFORE PROCEDURE ORAL AMOXICILLIN ADULTS 2g CHILDREN 50mg/kg UNABLE TO TAKE ORALLY AMPICILLIN OR CEFAZOLIN OR CEFTRIAXONE 2g IM/IV 1g IM/IV 50mg/kg 50mg/kg ALLERGIC TO PENICILLIN ORAL CEPHALEXIN OR CLINDAMYCIN OR AZITHROMYCIN/ CLARITHROMYCIN 2g 600mg 500mg 50mg/kg 20mg/kg 15mg/kg UNABLE TO TAKE ORALLY – ALLERGIC TO PENICILLIN CEFAZOLIN OR CEFTRIAXONE OR CLINDAMYCIN 1g IM/IV 600mg IM/IV 50mg/kg 20mg/kg

75. Cardiac conditions associated with highest risk of adverse outcome from endocarditis for which prophylaxis with dental procedure is reasonable Prosthetic cardiac valve or prosthetic material used for cardiac valve repair Previous infective endocarditis Congenital heart disease Unrepaired cyanotic CHD Crieghton M, Dental care for the pediatric cardiac patient .Journal of Canadian Dental Association 1992 March;58(3):201-2

76. Prophylaxis recommended: Management of gingival tissues or periapical regions of teeth Perforations of oral mucosa(extractions)

77. Not recommended Anesthetic injections through noninfected tissues Taking dental radiographs Placement of orthodontic or prosthodontic appliances Shedding of decidious teeth Bleeding following trauma to the lips and oral mucosa Arnold S. Bayer et al . Diagnosis and Management of Infective Endocarditis and Its Complications;Circulation . 1998;98:2936-2948

78. Completely repaired CH defect with prosthetic material or device, whether placed by surgery or by catheter intervention , during first 6 months after procedure Repaired CHD with residual defects at the site or adjacent to the site of prosthetic patch or device Cardiac transplantation recipients

79. RHEUMATIC HEART DISEASES children of age group 5-15 years, inflammation of heart Streptococcus bacteria- sore throat (strep throat) and fever called rheumatic fever shortness of breath and chest pain with high fever.

80. Management valvuloplasty or have a valve replacement  long term penicillin prophylaxis

81. Dental care: Special attention to oral health may be recommended for people with heart disease and heart conditions. Wait a minimum of six months after cardiac surgery or heart attack before undergoing any dental treatments.

82. CARDIAC SURGERY PATIENTS Complete dental evaluation prior Preventive dental programme – prevent IE Dental radiographs Consultation with cardiologist – to plan the treatment Treatment – within 3-4weeks of surgery

83. CONCLUSION The heart is the life-giving, ever-beating muscle  The primary function of the heart is to pump blood through the arteries, capillaries, and veins. Heart defects present at birth are called congenital heart defects. Slightly less than 1% of all newborn infants have congenital heart disease.

84. REFERENCES N.A Boon , Cardiovascular System , Davidson’s Principles and Practise of Medicine.19 th edition.Elsevier 2002;357-483 Ralph E.McDonald . Dental problems in children with disabilities.Dentistry for children and adolescents.9 th edition.Elsevier 2010 K.Sembulingam .Cardiovascular System.Essentials of Medical Physiology.2 nd edition.Jaypee 2002

85. Mary S. Minette , MD; David J. Sahn , MD, Ventricular Septal Defects; Circulation. 2006;114:2190-2197 Crieghton M, Dental care for the pediatric cardiac patient .Journal of Canadian Dental Association 1992 March;58(3):201-2 Arnold S. Bayer et al . Diagnosis and Management of Infective Endocarditis and Its Complications;Circulation . 1998;98:2936-2948