Cardiovascular diseases & Dental Management


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Cardiovascular diseases & Dental Management

  1. 1. CARDIOVASCULAR DISEASES Dr.Priyanka Sharma 1st year MDS Dept of Public Health Dentistry 1
  2. 2. CONTENTS 1) Introduction 2) Diagnosis of Cardiovascular diseases 3)Causes of cardiovascular diseases 4) Hypertension 5) Coronary Artery Diseases ( ischemic) 2
  3. 3. 6) Angina pectoris 7) Myocardial Infarction 8) Rheumatic fever 9) Rheumatic heart diseases 10) Heart Failure 11) Cardiac Arrhythmia 12) Oral Health Consideration & Oral Manifestation 13) Oral Procedures & Need For Antibiotic Prophylaxis To Minimise Risk Of Bacterial Endocarditis 3
  4. 4. 14) Pregnancy and cardiovascular diseases 15) Congenital Cardiovascular diseases 16) Studies involving cardiovascular diseases and dentistry 15) Summary & Conclusion 15) References 4
  5. 5. Introduction  Cardiovascular diseases (CVD) comprise of a group of diseases of heart and the vascular system.  30.5% of all deaths takes places globally according to the global and regional estimates for 2008.  Compared with all other countries, India suffers the highest loss, due to dealths from CVD in people aged 35-64 years.  The prevalence of CVD is 2-3 times more in urban than rural. 5
  6. 6. On the Indian subcontinent and in Africa, it is predominantly due to rheumatic fever, whereas calcific aortic valve disease is the most common problem in developed countries.  With over 3 million deaths owing to CVD every year, India is set to be the “ HEART DISEASE CAPITAL OF THE WORLD” in few years, said doctors on the eve of WORLD HEART DAY (Sept. 29th 2010). 6
  7. 7. Prompt recognition of the development of heart disease is limited by two key factors: 1) Firstly, it is often latent. 2) Secondly, the diversity of symptoms attributable to heart disease is limited. 7
  8. 8. CVD Hypertension Coronary Artery Disease Myocardial Infarction Acute coronary Syndrome Rheumatic heart disease & fever Cardiac Arrythmia Angina Pectoris Stroke Congenital CV Disease Congestive Heart Failure 8
  10. 10. SCHEME OF HISTORY TAKING 1) Symptoms and history of presenting illness 2) Past history 3) Family History 4) Personal History 10
  11. 11. SYMPTOMS AND HISTORY OF PRESENTING ILLNESS 1. Dyspnoea 2. Chest Pain 3. Palpitation 4. Syncope 5. Cough With Expectoration And Haemoptysis 6. Cyanosis 11
  12. 12. 7. Right Hypocondrial Pain, Swelling Of Feet And Decrease In The Urine Output 8. Gastrointestinal Symptoms Like Anorexia, Fullness Of Abdomen And Vomiting 9. Fatigability 10. Fever 11. Diabetes Mellitus And Hypertension 12
  13. 13. PAST HISTORY 1. Rheumatic Fever 2. Cyanotic Spells 3. Recurrent Respiratory Infections Since Childhood 4. Detection Of Murmur/Cardiac Lesion At School 5. Recent Dental Extraction, Genitourinary Instrumentations 6. Hypertension, Diabetes Mellitus, Ischaemic Heart Disease Or Any Other Significant Medical Illness 7. Nifedipine- Gingival Hyperplasia 13
  14. 14. FAMILY HISTORY 1. Hypertension 2. Ischaemic Heart Disease 3. Congental Heart Disease 4.Rheumatic Heart Disease 5. Sudden Death 14
  15. 15. PERSONAL HISTORY 1. Appetite 2. Weight Loss 3. Disturbed Sleep 4. Bowel And Bladder Disturbances 5. Habits- Smoking And Alcoholism 6. Exposure To Syphilis 15
  17. 17. ANALYSIS OF PRESENTING SYMPTOMS DEFINITION:-  Abnormal awareness of breathing with discomfort.  Dyspnoea is a significant manifestation of cardiac failure.  Dyspnoea is more commonly due to left-sided cardiac failure than due to right heart failure. 17
  18. 18. SEVERITY (GRADING) : FUNCTIONAL GRADING OF DYSPNOEA GRADE I : No limitationn of any physial activity but dyspnoea occurs on more than ordinary (unoccustomed) exertion. GRADE II: Dyspnoea on ordinary daily activity GRADE III : Dyspnoea on less than ordinary daily activities. GRADE IV : Limitations of all activities( dyspnoea at rest) 18
  19. 19. Mechanism underlying dyspnoea : During Heart Failure  Interstitial pulmonary edema  stimulates the J receptors  reflex  rapid and shallow breathing. Respiratory muscle fatigue Bronchial mucosal edema Increased bronchial mucosal production 19
  20. 20.  Paroxysmal Nocturnal Dyspnoea (PND)  This is an attack of severe shortness of breath and coughing usually occurring at night.  Awakening the patient from sleep.  Persist after sitting upright.  May be due to depression of the respiratory centre at night.  Reduced adrenergic stimulation to the myocardium at night. 20
  21. 21. Definition:  Dyspnoea that occurs usually on lying down/ recumbent position. Characteristic features:  Usually occurs within minutes of assumption of recumbency.  Occurs when a patient is awake.  Indicates the presence of severe left heart failure (pulmonary oedema).  Manifests later than PND. (in slowly progressive left heart disease). 21
  22. 22.  Dyspnoea occurs on sitting (upright) rather than on lying down position.  Example: left atrial myxoma, left atrial ball valve thrombus. 22
  23. 23. Occurs on breathlessness only when lying down in lateral/decubitus position. May be due to ventilation perfusion relationship alteration in certain body position. Occur in patients with pathology of one lung and chronic congestive heart failure. 23
  24. 24. There is severe periods characterised by alternating hypopnoea and hyperpnoea follwed by periods of apnoea sign of severe heart failure. The patient lies motionless for 10-20 seconds and again the cycle is repeated. Conditions associated : HF, Increased intracranial pressure, Uraemia, Severe pneumonia, Chronic hypoxia, Narcotic drug poisoning, Cerebral trauma and haemorrhage, Normal subjects living at high altitudes. 24
  25. 25. 25
  26. 26.  Bluish dicoloration of skin and mucous membrane.  Resulting from increased amount of reduced haemoglobin.  Cyanosis appearing in infancy indicates the presence of congenital cardiac anomalies with right to left shunt (teratology of fallot).  Cyanosis beginning to appear after 6 weeks of age may be an indication of VSD with slowly progressive right ventricuar outflow obstruction.  History of cyanosis in a suspected patient of congenital heart disease between the age of 5-20 years indicates reversal of left to right shunt (Eisenmeger Syndrome). 26
  27. 27. 27
  28. 28.  Right heart failure causes systemic venous congestion with increased hydrostatic pressure in the lower limb veins. This results in the transudation of fluid causing edema.  Ankle edema is more common in ambulatory patients. Bed-ridden patient develop sacral edema. 28
  29. 29.  This is due to enlarged and congested liver and stretching of its capsule, as in congestive heart failure.  Cardiac pain may occasionally present as upper abdominal pain.  Pain from a dissecting abdominal aortic aneurysm is usually most marked in the back and may originate in the chest and spread down the legs. Other arteries can have aneurysms and bleed. 29
  30. 30.  In the presence of cardiac failure due to decreased cardiac output, renal blood flow decreases with decrease in the glomerular fitration rate, this causes decrease of urine output in patients with cardiac failure.  Transient loss of consciousness with postural collapse.  Expectoration (coughing up) of blood or of blood- stained sputum.  Suggests uncomfortable awareness of heartbeat, which may be unpleasant. 30
  32. 32. 1) General examination 2) External markers of cardiac disease 3) Examination of peripheral cardiovascular system 4) Examination of precordium 5) Examinations including various other signs 6) Examinations of face 7) Examinations of mouth 8) Examinations of ear 9) Examinations of eyes 10)Examinations of fingers 32
  33. 33. GENERAL EXAMINATION 1. Build 2. Nourishment 3.Pallor 4.Cyanosis 5. Clubbing 6. Jaundice 7. Pedal Odema 8. Lymphadenopathy 33
  34. 34. PALLOR  Severe anemia may be associated with: 1. Chronic CCF 2. Infective endocarditis  Severe anemia can itself cause- cardiac failure or aggravate the underlying heart disease.  Patients with cyanotic congenital heart disease may have polycythemia with suffused conjunctiva. 34
  35. 35. CYANOSIS  Central cyanosis occurs in: [Decreased atrial oxygen saturation] 1. Cyanotic congenital heart disease 2. Reversal of left to right shunt (Eisenmenger’s syndrome) 3. Tetralogy of Fallot 4. Pulmonary edema (left heart failure)  Peripheral cyanosis occurs in: [Diminished peripheral blood flow = Reduced Cardiac output] 1. Congenital cardiac failure 2. Peripheral vascular disease 3. Shock 35
  36. 36. Differential cyanosis: • Feet and toes are blue but hands and fingers are not cynosed. • e.g. PDA with pulmonary hypertension with reversal of shunt. Reverse differental cyanosis: • Fingers are more cyanosed than toes. • e.g. Transposition of great vessels with pulmonary hypertension with preductal coarctation with reversed flow through PDA. 36
  37. 37. CLUBBING CARDIAC CAUSES: 1. Cyanotic congenital heart disease 2. Reversal of left to right shunt 3. Infective endocarditis  Clubbing of fingers also known as drumstick fingers and watch-glass nails.  Clubbing develops in five steps: 1) Fluctuation and softening of the nail bed. 2) Loss of the normal <165° angle (Lovibond angle) between the nailbed and the fold (cuticula). 3) Increased convexity of the nail fold. 4) Thickening of the whole distal (end part of the) finger (resembling a drumstick). 5) Shiny aspect and striation of the nail and skin. 37
  38. 38. JAUNDICE Following cardiac conditions may be associated with jaundice: 1. Congestive cardiac failure with congestive hepatomegaly 2. Cardiac cirrhosis 3. Pulmonary infarction 38
  39. 39. PEDAL EDEMA Pitting edema of feet can occur in: 1. congestive cardiac failure 2. constrictive pericarditis 3. tricuspid valve disease LYMPHADENPATHY  Condition associated with generalized lymphadenopathy may involve the cardiovascular system.  e.g. lymphoma, SLE etc. 39
  40. 40. EXTERNAL MARKERS OF CARDIAC DISEASE VITAL SIGNS • Pulse • Blood Pressure • Respiratory Rate • Temperature RADIAL PULSE • Rate • Rythm • Volume • Character 40
  41. 41. EXAMINATION OF • The Carotids & Jugular Venous Pulse And Pressure • Peripheral Signs Of Infective Endocarditis • Peripheral Signs Of Rheumatic Fever 41
  42. 42. Jugular Venous Pulse 42
  43. 43. 43
  44. 44. 44
  45. 45. EXAMINATION OF THE PRECORDIUM INSPECTION 1. Precordial Bulge • Position Of Apical Impulse Pulsations In The:- A. Left Parasternal Region B. 2nd Left Intercostal Space C. 2nd Right Intercostal Space D. Epigastric Pulsation E. Suprasternal Pulsation F. Engorged Veins Over The Chest G. Spine(kyphoscoliosis) 45
  46. 46. PALPATION • PERCUSSION 1) Right Cardiac Border 2) Left Cardiac Border 3) Left And Right 2nd Intercostal Space. 46
  47. 47. AUSCULTATION • Mitral, Tricuspid, Aortic, Pulmonary And Other Additional Areas For:- A) 1st And 2nd Heart Sounds B) Additional Sounds C) Murmurs 47
  48. 48. EXAMINATION OF FACE Following Features May Be Indicative Of Underlying Cardiac Abnormality While Examination Of Face : ABNORMALITIES CLINICAL MANIFESTATIONS CONDITIONS ASSOCIATED ELFIN FACIES Receding jaws, Flared nostrils, Pointed ears Supraventricular aortic stenosis HIGH ARCHED PALATE Marfan syndrome MITRAL FACIES Malar flush and pinkish purple patches over the cheek Mitral stenosis with decreased cardiac output and Systemic vasoconstriction 48
  50. 50. Acute macroglossia: The tongue is diffusely enlarged and bright red along its lateral portion. The patient had bleeding into the tongue while on anticoagulants. Acute macroglossia Due to Enalapril: this 75-year-old Black female developed acute swelling of tongue and lips after being on enalapril for 2 days. She was unable to talk or swallow (upper photo). In lower photo, 2 days after stopping enalapril, the tongue and lips have returned to their normal size. EXAMINATION OF MOUTH 50
  51. 51. GUM HYPERPLASIA Due to dilantin. similar findings may be seen in patients on nifedipine TANGIER DISEASE OF THE TONSILS: The tonsils are enlarged with bright orange yellow streaks (“tiger stripes”) (premature cad). 51
  52. 52. EXAMINATION OF EYES: • Exopthalmus: associated with thyroid artery disease. • Blue sclera: Osteogenesis imperfecta with aortic regulation. • Opthalmic fundus: looks for a. Arteriosclerotic changes b. Hypertensive retinopathy c. Roth’s spots( of infective endocarditis) d. Cork screw arteries- coarctation of aorta. BLUE SCLERA ROTHS SPOT 52
  56. 56. 1. MYOCARDIAL A. Overload Secondary To Hypertenson Or Valve Disease B. Coronary( Ischaemic) Heart Disease C. Cardiomyopathies 2. ENDOCARDIAL A. Rheumatic Heart Disease B. Congenital Anomalies C. Infective Endocarditis 3. PERICARDIAL A. Pericarditis B. Pericardial Effusion C. Functional Disorders 56
  57. 57.  DUE TO HYPERTENSION  DUE TO ABNORMALITIES IN HEART RATE A. Tachycardia B. Bradicardia C. Other Dysrthymias  CHANGES IN CIRCULATORY VOLUME A. Hypovoloemia (Shock Syndrome) B. Hypervolaemia ( Circulatory Overload) C. Others  CONGENITAL ABNORMALITIES : 1) Patent ductus arteriosus 2) Ventricular septal defect 3) Arterial septal defect 4) Tetralogy of Fallot , etc. 57
  58. 58. NYHA CLASSIFIACTION FUNCTIONAL CAPACITY OBJECTIVE ASSESSMENT CLASS I. Patients With Cardiac Disease But Without Resulting Limitation Of Physical Activity. Ordinary Physical Activity Does Not Cause Undue Fatigue, Palpitation, Dyspnea, Or Anginal Pain. A. No Objective Evidence Of Cardiovascular Disease. CLASS II. Patients With Cardiac Disease Resulting In Slight Limitation Of Physical Activity. They Are Comfortable At Rest. Ordinary Physical Activity Results In Fatigue, Palpitation, Dyspnea, Or Anginal Pain. B. Objective Evidence Of Minimal Cardiovascular Disease. CLASS III. Patients With Cardiac Disease Resulting In Marked Limitation Of Physical Activity. They Are Comfortable At Rest. Less Than Ordinary Activity Causes Fatigue, Palpitation, Dyspnea, Or Anginal Pain. C. Objective Evidence Of Moderately Severe Cardiovascular Disease. CLASS IV. Patients With Cardiac Disease Resulting In Inability To Carry On Any Physical Activity Without Discomfort. Symptoms Of Heart Failure Or The Anginal Syndrome May Be Present Even At Rest. If Any Physical Activity Is Undertaken, Discomfort Is Increased. D. Objective Evidence Of Severe Cardiovascular Disease. 58
  59. 59. HYPERTENSION 59
  60. 60. CONTENTS OF HYPERTENSION  Definition  Classification  Types  Other risk factors  Effects of hypertension  Complications  Symptoms  Oral manifestations  Diagnosis  White coat hypertension  Dental management  Treatment of hypertension  Oral medications used  Conclusion 60
  61. 61. HYPERTENSION Hypertension is known as Silent Killer of mankind. Most of the sufferers (85 %) are asymptomatic and hence early diagnosis is a problem.  Normal or optimal blood pressure (BP) is defined as the level above which minimal vascular damage occurs. There is a continuous, consistent, and independent relationship between elevated BP and risk of cardiovascular events. 61
  62. 62. Definition • Hypertension is usually defined by the presence of a chronic elevation of systemic arterial pressure above a certain threshold value.* • According to Davidson : • Hypertension is defined as having systolic blood pressure (SBP) >/= 140mm of Hg . (or) Diastolic blood pressure (DBP) >/= 90mm of Hg. (or) As having to use antihypertensive medications. * Thomas D. Giles et al.Definition and Classification of Hypertension: An Update ; Emerging concept : 2009, 11:611–614. 62
  63. 63. CLASSIFICATION The Seventh Joint National Committee Criteria (JNC VII) classifies hypertension for adults aged 18 years and older into following stages: Blood Pressure Classification SBP(mm Hg) DBP(mmHg) •Normal <120 & <90 •Pre hypertension 120-139 & 80-89 •Stage I hypertension 140-159 & 90-99 •Stage II hypertension >/=160 & >/=100 •Isolated Systolic hptn. >140 & <90 63
  64. 64. • “For individuals 40-70 years of age, each increment of 20 mmHg in systolic BP or 10 mmHg in diastolic BP doubles the risk of CVD across the entire BP range from 115/75 to 185/115 mmHg”. [JNC VII. JAMA 2003;289:2560-2572 ] Classification according to WHO • Grade I: Hypertension without damages to the end organ. • Grade II: Hypertension with damages to the end organ (e.g.. fundus hypertonicus (Grade I and II), plaque formation in the larger blood vessels) • Grade III: Hypertension with manifest cardiovascular secondary diseases (e.g. angina pectoris,heart attack, stroke) 64
  65. 65. TYPES PRIMARY (or) ESSENTIAL HYPERTENSION • Which develops gradually over many years & has no underlying cause. • 90% of people have this type of hypertension SECONDARY HYPERTENSION • Which has an underlying cause such as renal disorders, endocrinal disturbances, neurologic causes etc. • 10% of people have this type of hypertension. 65
  66. 66. Other Risk Factor of Hypertension •Lack of exercise •Increased salt intake •Family history •Too little potassium •Alcohol •Smoking •Stress & •Age 66
  67. 67. Effect of Hypertension The common target organs damaged by long standing hypertension are: •Brain •Heart •Kidneys •Eyes & •Peripheral arteries. 67
  68. 68. Complications of hypertension Left ventricular hypertrophy Heart failure Cerebral hemorrhage Renal insufficiency Aortic dissection Atherosclerotic disease 68
  69. 69. Symptoms Symptoms due to hypertension: 1. Headache - usually in morning hours. 2. Dizziness 3. Epistaxis Symptoms due to affect over target organs: 1. CVS: a. Dyspnea on exertion b. Anginal chest pain c. Palpitations 69
  70. 70. 2. Kidneys: Hematuria , nocturia , polyuria . 3.CNS: a. Transient ischemic attacks ( TIA or Stroke) b. Hypertensive encephalopathy(headache , vomiting etc.) c. Dizziness, Tinnitus & syncope. 4. Retina: a. Blurred vision or b. sudden blindness. 70
  71. 71. Diagnosis • Physical Examination • Laboratory and Additional Testing – it includes Routine laboratory procedures like hemoglobin, urinalysis, routine blood chemistries and fasting lipid profile. • Electrocardiography & Electroencephaloghy • Ambulatory BP Monitoring • Plasma renin activity testing • Radiologic testing 71
  72. 72. WHITE COAT HYPERTENSION ‘’White coat hypertension’’ is a phenomenon in which individuals present with persistent elevated BP in a clinical setting but present with non-elevated BP in an ambulatory setting. •20% of mild hypertensive individuals may present with white coat hypertension. 72
  73. 73. Dental Management • Measure and record BP at initial visit 73
  74. 74. Recheck :- •Every 2 yrs for patient with BP <120/80 mm Hg. •Every 1 yr for patient with BP 120-139/80-89 mm Hg. •Every visit for patient with BP >140/90 mm Hg. •Every visit for patient with established coronary artery disease, diabetes mellitus or chronic renal disease with BP >135/85 mm Hg. •Every visit for patient with established hypertension. Before initiating dental care: •Assess presence of hypertension •Determine presence of target organ disease •Determine dental treatment modifications 74
  75. 75. 1. Asymptomatic BP <159/99 mm Hg, no history of target organ disease • No modifications needed • Can safely be treated in dental setting 2. Asymptomatic BP 160-179/100-109 mm Hg, no history of target organ disease • Assessment on an individual basis with regard to type of dental procedure BP>180/110 mm Hg, no history of target organ disease • No elective dental care until BP is controlled. 3. Presence of target organ disease or poorly controlled diabetes mellitus • No elective dental care until BP is controlled , preferable below 140-90 mm Hg. 75
  76. 76. TREATMENT OF HYPERTENSION Non Pharmacological Treatment Lifestyle Modifications 1. Salt restriction 2. Weight reduction 3. Stop smoking 4. Diet modifications such as: • Reduce intake of Cholesterol & Saturated fat. • Adequate intake of Calcium & Magnesium. 76
  77. 77. 77 5.Avoid / Limit of alcohol intake 6. Relaxation such as yoga, psychotherapy etc. 7. Regular exercise.
  78. 78. ORAL MEDICATIONS USED FOR TREATMENT OF HYPERTENSION •Diuretics •Beta-Adrenergic Blockers •Central Acting Inhibitors •Peripheral Acting Inhibitors •Non-Selective alpha & beta Adrenergic Inhibitors •Vasodilators •Angiotensin Converting Enzyme ACE Inhibitors 78
  79. 79. ORAL MANIFESTATION OF HYPERTENSION There are no recognized manifestations of hypertension but anti-hypertensive drugs can often cause side affects ,such as: •Xerostomia, •Gingival overgrowth, •Salivary gland swelling or pain, •Lichenoid drug reactions, •Erythema multiforme, •Taste sense alteration, •Paresthesia. 79
  80. 80. CONCLUSION • HYPERTENSION has no cure, but it can be controlled with proper diet, lifestyle changes, and if necessary medications. • Get regular health check ups. Think about the consequences of untreated high blood pressure. • Do not take chances with the disease that can be controlled. • Lastly, Hypertension is a silent disease, but its silence is not golden. 80
  82. 82. Coronary artery diseases 1) Etiopathogenesis 2) Risk factors 3) Diagnosis 4) Management 5) Dental aspects 82
  83. 83. • Atherosclerosis is the most common cause of CAD ETIOPATHOGENESIS Various risk factors include: 1. lipids (especially HDL) 2. hypertension 3. diabetes mellitus & glucose intolerance 4. cigarette smoking 5. lifestyle & dietary factors 6. exercise 7. obesity 83
  84. 84. 8. plasma fibrinogen 9. endothelial dysfunction 10. antioxidants 11. estrogen deficiency 84
  85. 85. RISK FACTORS Induce variety of pathological processes Interaction & disruption of vascular endothelium Plaque formation Effective arterial luminal area compromised Myocardial ischaemia acute plaque rupture thrombus formation angina M I 85
  86. 86. 86
  87. 87. 87
  88. 88. DIAGNOSIS 1) Based on clinical presentation :  chest tightness  Jaw discomfort  Left arm pain  Dyspnea  Epigastric distress 2) E.C.G. 3) Exercise E.C.G. 4) Coronary Angiography 5) P.C.I.(Percutaneous Coronary Intervention) 6) In case of complications like stroke/ shock – EEG 7) Recent development : One minute angiogram 88
  89. 89. MANAGEMENT Management of CAD depends on: • Extent and severity of ischemia • Exercise capacity • Prognosis based on exercise testing • Overall LV function • Associated features such as diabetes mellitus  Patients with a small ischemic burden, normal exercise tolerance, and normal LV function may be safely treated with pharmacologic therapy.  Selected use of aspirin, β-blockers, ACEIs, and HMG CoA reductase inhibitors.  Nitrates and calcium channel blockers may be added to primary agents to relieve symptoms of ischemia in selected patients. 89
  90. 90. • SURGICAL MANAGEMENT:  Percutaneous coronary intervention (PCI) with percutaneous transluminal coronary angioplasty (PTCA) and intra coronary stenting relieves symptoms in chronic ishchemia. 90
  91. 91. • Patient with complex multivessel CAD require PCI with medical therapy of surgical revascularization. • Patients with reduced LV function and severe ischemia, often associated with left main or multivessel CAD, are best served by coronary artery bypass graft (CABG) surgery. 91
  92. 92. DENTAL ASPECTS • STRESS, ANXIETY, EXERTION or PAIN can provoke angina. • Short, minimally stressful dental appointments. • Late morning appointments. • Excessive dose of LA containing adrenaline to be avoided in patients taking beta blockers. • More Common - severe dental caries and periodontal disease in pts of IHD. 92
  93. 93. Angina pectoris 93
  94. 94. • Name given to paroxysms of severe chest pain CLINICAL FEATURES 1) 40 TO 60 years , M > F 2) Pain often described as sense of Strangling, choking , Tightness, Heaviness ,Compression, or Constriction of chest. 3) PAIN MAY RADIATE TO JAW or left arm. 4) Rarely pain in mandible, teeth or other tissues. PRECIPITATING FACTORS • Physical exertion(main) particularly in cold weather • Emotion(anger or anxiety) & stress caused by fear or pain  TYPICALLY RELEIVED BY REST 94
  95. 95. Dental aspects  Preoprerative glyceryl trinitrate & oral sedation advised sometimes.  Dental care carried with minimal anxiety & oxygen saturation  Monitor pulse & B.P.  POST ANGIOPLASTY elective dental care deffered for 6 months , emergency dental care in a hospital setting.  Patients with BYPASS GRAFTS – anti biotic cover against infective endocarditis . - LA containing adrenaline is contraindicated (may ppt dysrhythmia) 95
  96. 96. Patients with vascular stents – no antibiotic cover except during 1st 6 week postop for emergency dental care.  DRUGS used in t/t of angina may cause oral adverse effects like : -lichenoid reaction Ca channel - gingival swelling blockers - ulcers (nicorandil) 96
  97. 97. Gingival hyperplasia in patient consuming Ca channel blockers 97
  98. 98. Myocardial Infarction 98
  99. 99. • Synonyms – coronary thrombosis or heart attack CLINICAL FEATURES 1. Clinical picture is variable 2. More than 50% patients are symptomless 3. MI may be preceded by angina often felt as indigestion like pain 4. any anginal attack lasting longer than 30 minutes is considered MI 5. Tachycardia &irregular pulse 6. Nausea, vomitting, sweating ,restlessness, facial pallor 7. Breathlessness, cough 8. Loss of conciousness, shock & even death 9. Many pts die within 1st hour to few days after attack. Thus, MI is a MEDICAL EMERGENCY. 99
  100. 100. 100
  101. 101. DIAGNOSIS I. Based on clinical features II. Elevated TLC & ESR during 1st wk III.ECG changes IV.Rise in serum “cardiac” enzymes ( CPK) V. Rise in troponin T within 4-8 hours VI.Echocardiography 101
  102. 102. General Precautions during Dental Procedures • Dental clinic should have advanced cardiac life support or at least basic cardiac life support. • Use of pulse oximeter to determine the level oxygenation. • Automatic external defibrillator. • Determination of vital signs prior to dental care. • BP & pulse rate & rhythm should be recorded & any abnormal findings should be addressed. • Premedication with antianxiety drugs and inhalation nitrous oxide in anxious patients. • Elective procedures esp those requiring GA should be avoided for atleast 4 wks aftr MI. consult pt’s physician prior to dental therapy 102
  103. 103. Management on dental chair 1. Terminate all dental treatment 2. Position pt in semirecline position 3. Give nitroglycerin(TNG) (abt 0.4 mg) tablet or spray 4. Administer oxygen 5. Check pulse & B.P. Discomfort relieved Discomfort continues 3 mins after 2nd TNG 6. Assume angina pectoris is 6. give 2nd TNG dose present 7. monitor vital signs. 7. Slowly taper oxygen over 5 mins 8. Modify t/t to prevent recurrence discomfort discomfort continues relieved 3 mins after TNG 103
  104. 104. 8. give 3rd TNG dose 9. Monitor vitals 10. Call for medical assistance Discomfort relieved discomfort continues 3 mins after 3rd TNG dose 11. Refer pt for medical 12.assume MI is in progress evaluation before 13. start i.v. line with drip of a crystalloid solution further dental care at 30 mL/ hr 14. If discomfort severe titrate morfine sulphate 2mg s/c or i/v every 3 mins until relief is obtained 15. Transport to emergency care. Administer Basic Life Support ,if necessary. 104
  105. 105. Anticoagulation Therapy & Dental Care • Anticoagulant therapy is used both to treat & to prevent throboembolism. • 2 major types : 1. antiplatelet medications 2. antithrombin medications • Acetylsalicylic acid (ASA) + clopidogrel ( anticoagulant) given for 4 weeks after stent implantation. • daily aspirin typically continued lifelong. • May increase risk of oral bleeding following surgical procedures. • Associated conditions which predispose patient to uncontrolled hemostasis : uraemia or liver diseases or use of NSAIDS. • If emergency surgery needs to be done,DDAVP(1- desamino-8-D-arginine vasopressin) is administered{0.3 micro kg/body wt parenterally} within 1 hr of surgery. 105
  106. 106. • Antithrombin medications are dicumarols ( eg. Warfarin), it inhibits biosynthesis of vit. – K dependent coagulations protein. - Efficacy monitored by prothrombin time or the international normalized ratio (INR), which is calculated on the basis of international sensitivity index (ISI). - INR ranges from 2.0 – 3.5 & it should be performed within 24 hrs of surgery. - If INR is < 3.5, anticoagulation therapy should be discontinued before minor surgical procedures. 106
  107. 107.  3 different protocols used to treat patients with elevated INR : • Ist protocol – warfarin not discontinued (minimizes thromboembolic events & increases risk of bleeding after surgery). • IInd protocol – warfarin discontinued (drug should be discontinued 2-3 days prior to surgery, during this period patient is at risk of developing thromboembolic event but not bleeding). • IIIrd protocol – warfarin discontinued & patient placed on alternative anticoagulant therapy (thromboembolic event minimized). 107
  108. 108. Rheumatic Fever 108
  109. 109. • Rheumatic fever is an inflammatory disease that may develop two to three weeks after a Group A streptococcal infection (such as strep throat or scarlet fever). It is believed to be caused by antibody cross-reactivity and can involve the heart, joints, skin, and Brain . • Acute rheumatic fever commonly appears in children ages 5 through 15, with only 20% of first time attacks occurring in adults. 109
  110. 110. 110
  111. 111. • What are the symptoms of strep throat? • Sudden onset of sore throat (streptococcal oropharyngitis) • Pain on swallowing • Fever, usually 101–104°F • Headache • Red and edematous soft palate and oropharynx. • Areas of tonsillar ulceration and exudation. • Abdominal pain, nausea and vomiting may also occur, especially in children. 111
  112. 112.  What are the symptoms/clinical features of rheumatic fever? Symptoms may include: • fever • painful, tender, red swollen joints • pain in one joint that migrates to another one • heart palpitations • chest pain • shortness of breath • skin rashes • fatigue • small, painless nodules under the skin 112
  113. 113. 113
  114. 114. • Minor criteria • Fever • Arthralgia • Laboratory abnormalities: increased Erythrocyte sedimentation rate • Electrocardiogram abnormalities • Evidence of Group A Strep infection: elevated or rising Antistreptolysin O titre. 114
  115. 115. LAB INVESTIGATIONS • Raised ESR • Culture studies of throat swabs is always negative in RF. • High anti sterptolysin o(ASO)titre-300 micro units • Chest radiograph- enlargement of heart • ECG-prolonged PR interval • Echocardiogram-confirms ventricular dilatation n pericardial effusion 115
  116. 116. • TREATMENT : • Oral phenoxymthyl penicillin 500 mg until age of 20 yrs. • Allergic to penicillin,sulfadimidine by mouth. • Aspirin for fever and pain 50mg/kg in 4 hrly doses • Corticosteroids 60-80mg prednisolone • Digoxin and diuretics for heart failure • Ballon valvuloplasty,using inoue balloon,if mitral valves damage. 116
  117. 117. DENTAL CONSIDERATION • Dental extractions and local anesthesia in consent with physician. • The prophylactic use of antibiotics prior to a dental procedure is now recommended ONLY for those patients with the highest risk of adverse outcome resulting from endocarditis. • GA should be avoided if essential must be given in hospital. 117
  118. 118. Rheumatic Heart Disease 118
  119. 119. Rheumatic heart disease : • History of rheumatic fever during childhood or adolescence can act as a predisposing factor for RHD after several years. • Common signs-murmur due to valvular damage n later enlargement of heart. 119
  120. 120. 120
  121. 121. ORAL MANIFESTATIONS • Most prominent during acute phase • Pharyngitis • Inc oral temperature • Distended neck veins and a bluish color of the skin. 121
  122. 122. DENTAL CONSIDERATIONS • To prevent complication of infective endocarditis ,all dental procedures should be carried under antibiotic cover. • Amoxicillin prophylaxis-1 hour before and 6 hours after the initial dose. • Good oral hygiene measures ,fluoride treatment, chlorhexidine rinses and routine cleanings to reduce harmful bacteremias. 122
  123. 123. • Proper history should be taken to identify history of rheumatic fever during childhood. • Suspicious cases should be referred to cardiologist for cardiac evaluation prior to dental procedures. • Clindamycin or erythromycin prophylaxis during dental treatment. • Elective dental treatment under physician consultation. 123
  124. 124. Heart failure 124
  125. 125. HEART FAILURE • Heart failure (HF) is a condition in which a problem with the structure or function of the heart impairs its ability to supply sufficient blood flow to meet the body's needs . • Common causes of heart failure – • ischemic heart diseases • Hypertension • Valvular diseases 125
  126. 126. Left-sided failure(MORE COMMON) • Failure of the left ventricle causes congestion of the pulmonary vasculature, and so the symptoms are predominantly respiratory in nature. The patient will have dyspnea (shortness of breath) on exertion and in severe cases, dyspnea at rest. Increasing breathlessness on lying flat, called orthopnea. • Another symptom of heart failure is paroxysma nocturnal dyspnea also known as "cardiac asthma", a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep. • Inadequate cerebral oxygenation leads to loss of concentration,restlessness and irritability. 126
  127. 127. Right-sided failure • Failure of the right ventricle leads to congestion of systemic capillaries. This helps to generate excess fluid accumulation in the body. This causes swelling under the skin (termed peripheral edema or anasarca) • If occurs with Mitral stenosis is called congestive heart failure. 127
  128. 128. • Biventricular failure ,faiure of one side of heart leads to failure of other. CLINICAL FEATURES • Pedal edema • Dyspnea • Congestion of neck veins • Cynosis • Fatigue 128
  129. 129. DIAGNOSIS • Imaging Echocardiography • Electrophysiology electrocardiogram (ECG/EKG) • Blood tests • Angiography • Monitoring 129
  130. 130. TREATMENT MODALITIES • Diet and lifestyle measures • Weight reduction • Monitor weight • Sodium restriction -excessive sodium intake may precipitate or exacerbate heart failure • Fluid restriction – patients with CHF have a diminished ability to excrete free water load. • stress reduction,rest • Stop smoking 130
  131. 131. Pharmacological management • Diuretic • Loop diuretics (e.g. furosemide, bumetanide) • ACE inhibitor/ Angiotensin II receptor antagonist Positive inotropes • Digoxin • Beta blockers • Alternative vasodilators • The combination of isosorbid dinitrate/hydralazine 131
  132. 132. ORAL MANIFESTATIONS • Distention of the external jugular viens. • Compensatory polycythemia –ruddy complexion and bleeding tendencies. • Abnormal production of clotting factors • Bleeding can be spontaneous or extravasational. 132
  133. 133. DENTAL ASPECTS • The dental chair should be kept in partially reclining or erect position and patient should be raised slowly in upright position. • Emergency dental care should be conservative, principally with analgesics and antibiotics. • Appointments should be short • Non stressful appointments • Patients are best treated in late morning because of epinephrine levels peak in early morning. 133
  134. 134. • Bupivacaine should be avoided as it is cardiotoxic. • An aspirating syringe should be used to give local anesthetic • Epinephrine containing LA should be not given in large doses to patients taking beta blockers. • Gingival retraction cords containing epinephrine should be avoided 134
  135. 135. • Supplemental O2 should be available • Rubber dam is contraindicated when it contributes to breathing difficulty. • NSAIDS other than aspirin should be avoided in pts taking ACE inhibitors (renal damage). • Erythromycin and tetracycline to be avoided as they may induce digitalis toxicity 135
  136. 136. • GA is contraindicated in cardiac failure.until under control (venous thrombosis and pulmonary embolism) • ACE inhibitors can sometimes cause erythema multiforme, angioedema or burning mouth. • Antibiotic prophylaxis required for dental care. • History of recent MI ,required delay of elective dental care for 6 months. 136
  137. 137. Cardiac arrhythmia 137
  138. 138. CARDIAC ARRHYTHMIA : • Cardiac arrhythmia (also dysrhythmia) is a term for any of a large and heterogeneous group of conditions in which there is abnormal electrical activity in the heart. • The heart beat may be too fast or too slow, and may be regular or irregular . • Accordingly there are 2 types : 1) Atrial arrhythmia 2) Ventricular arrhythmia 138
  139. 139. • TACHYCARDIA : Any heart rate faster than 100 beats/minute is labelled tachycardia. • BRADYCARDIAS :A slow rhythm, (less than 60 beats/min), can lead to syncope. • HEART BLOCK :Blockage of cardiac impulse anywhere in the conduction system. 139
  140. 140. 140
  141. 141. TREATMENT AA : • Digoxin • Propanolol • Quinidine sulphate • Anticoagulant such as warfarin VA : • Procainamide • Phenytoin • Dispyramide • Propanolol 141
  142. 142. • Physical maneuvers • Antiarrhythmic drugs • Electricity • Electrical cautery 142
  143. 143. ORAL MANIFESTATIONS • Procainamide can cause agranulocytosis,oral ulcerations. • Quinidine-infrequent oral ulcerations. • Disopyramide is anticholinergic agent capable of producing xerostomia. • verapamil,enalapril can cause gingival hyperplasia. 143
  144. 144. DENTAL CONSIDERATIONS • A proper history to be taken. • Stress and anxiety be minimized. • Short appointments • Use of epinephrine to be minimized. • Proper chair position is important, SUPINE. • At end of appointment chair should be raised slowly to minimize orthostatic hypotension. 144
  145. 145. • Use of vasoconstrictors should be minimized in pts taking digitalis glycosides. • The equipments like pulp testers ,ultrasonic scalers ,electrosurgical units ,should not be in close proximity. • Prophylactic antibiotics before and after treatment in recently placed pacemaker patients. • Pts who report palpitations or skipped beats must be evaluated by physician. 145
  146. 146. • Sustained sinus tachycardia above 100 beats/min in resting position is indicative of sinus tachycardia. • Dental treatment shd not be carried out in patients with irregular pulse. • Long use of procainamide can cause a lupus like syndrome. • Drug like quinidine can cause erythema multiforme. • CA may be induced by general anesthesia and vagal reflex. 146
  148. 148. • Valvular heart disease that compromises cardiac output produces signs of hypoxemia. • Cyanosis of lips and oral mucosa is the most prominent oral sign of tissue hypoxia. According to American heart association guidelines: • Antibiotic prophylaxis should be administered to patients who have undergone mitral or aortic valve repair or replacement. • Patients with a prior history of infective endocarditis. • Patients with mitral or aortic regurgigation or stenosis. • Patients with mitral valvular prolapse with valvular regurgigation. 148
  149. 149. • Prosthetic heart valves. • Previous bacterial endocarditis. • Acquired valvular dysfunction. • Complex cyanotic congenital heart disease. • Surgically constructed systemic pulmonary shunts. 149
  150. 150. ORAL PROCEDURES & NEED FOR ANTIBIOTIC PROPHYLAXIS TO MINIMISE RISK OF BACTERIAL ENDOCARDITIS • Extractions. • Periodontal procedures including surgery,subgingival,placement of antibiotic fibers or Strips,scaling &root planning. • Implant placement. • Tooth reimplantation. • Placement of orthodontic bands(not brackets). • Endodontic instrumentation. • Intra ligamentary injection. • Prophylatic cleaning of teeth where bleeding is anticipated. • Other procedure in which significant bleeding is anticipated. 150
  151. 151. STANDARD REGIMENS FOR PROPHYLAXIS TO MINIMISE RISK OF BACTERIAL ENDOCARDITIS • Oral medication. • Adults & children not allergic to penicillin-amoxicillin. • Adults & children allergic to penicillin-clindamycin. • Non oral medication. • Adults & Childrens not allergic to penicillin-iv or im ampicillin. • Adults & children alergic to penicillin-iv clindamycin. 151
  152. 152. 152
  153. 153. 153
  155. 155. • Diagnosis of congenital cardiac malformations can be made as early as 13 weeks, and, in families with heart disease. • Early examination in pregnancy allows parents to consider all options, including termination of pregnancy, if there are major malformations. • Hypertensive disorders during pregnancy occur in women with pre-existing primary or secondary chronic hypertension, and in women who develop new-onset hypertension in the second half of pregnancy. 155
  156. 156. 156
  157. 157. 157
  159. 159. • Congenital heart disease usually manifests in childhood but may pass unrecognised and not present until adult life. • The fetus has only a small flow of blood through the lungs, as it does not breathe in utero. The fetal circulation allows oxygenated blood from the placenta to pass directly to the left side of the heart through the foramen ovale without having to flow through the lungs. 159
  160. 160. Persistent Ductus Arteriosus • During fetal life, before the lungs begin to function, most of the blood from the pulmonary artery passes through the ductus arteriosus into the aorta. • Normally, the ductus closes soon after birth but sometimes fails to do so. • Since the pressure in the aorta is higher than that in the pulmonary artery, there will be a continuous arteriovenous shunt. 160
  161. 161. 161
  162. 162. Management : • A patent ductus is closed at cardiac catheterisation with an implantable occlusive device. • When the ductus is structurally intact, a prostaglandin synthetase inhibitor (indometacin or ibuprofen) may be used in the first week of life and also improving oxygenation to induce closure. 162
  163. 163. Coarctation of the aorta • Narrowing of the aorta occurs in the region where the ductus arteriosus joins the aorta, i.e. at the isthmus just below the origin of the left subclavian artery. • Management : In untreated cases, death may occur from left ventricular failure, dissection of the aorta or cerebral haemorrhage. 163
  164. 164. Atrial septal defect • ‘Ostium primum’ defects result from a defect in the atrioventricular septum and are associated with a ‘cleft mitral valve’ (split anterior leaflet). • As a result there is gradual enlargement of the right side of the heart and of the pulmonary arteries. 164
  165. 165. 165
  166. 166. • Management : Closure can also be accomplished at cardiac catheterisation using implantable closure devices. • Severe pulmonary hypertension and shunt reversal are both contraindications to surgery 166
  167. 167. Ventricular septal defect • Congenital ventricular septal defect occurs as a result of incomplete septation of the ventricles. • Management : Small ventricular septal defects require no specific treatment. Cardiac failure in infancy is initially treated medically with digoxin and diuretics. Persisting failure is an indication for surgical repair of the defect. Percutaneous closure devices are under development. 167
  168. 168. 168
  169. 169. Tetralogy Of Fallot 169
  170. 170. 170
  171. 171. 171
  173. 173. Periodontal infections and cardiovascular disease.The heart of the matter • Journal :The Journal of the American Dental Association (October 2006) 137, 14S-20S. • Author :Ryan T. Demmer • Conclusions. Evidence continues to support an association among periodontal infections, atherosclerosis and vascular disease. Ongoing observational and focused pilot intervention studies may inform the design of large-scale clinical intervention studies. Recommending periodontal treatment for the prevention of atherosclerotic CVD is not warranted based on scientific evidence. Periodontal treatment must be recommended on the basis of the value of its benefits for the oral health of patients, recognizing that patients are not healthy without good oral health. However, the emergence of periodontal infections as a potential risk factor for CVD is leading to a convergence in oral and medical care that can only benefit the patients and public health. 173
  174. 174. Association between dental health and acute myocardial infarction. • Journal : BMJ 2009;298:779. • Authors: K. J. Mattila et al. • Abstract Known risk factors for coronary heart disease do not explain all of the clinical and epidemiological features of the disease. To examine the role of chronic bacterial infections as risk factors for the disease the association between poor dental health and acute myocardial infarction was investigated in two separate case-control studies of a total of 100 patients with acute myocardial infarction and 102 controls selected from the community at random. Dental health was graded by using two indexes, one of which was assessed blind. Based on these indexes dental health was significantly worse in patients with acute myocardial infarction than in controls. The association remained valid after adjustment for age, social class, smoking, serum lipid concentrations, and the presence of diabetes. Further prospective studies are required in different populations to confirm the association and to elucidate its nature. 174
  175. 175. SUMMARY 175
  176. 176. 176
  177. 177. CONCLUSION • Cardiovascular problems are non-communicable diseases which are growing in India and other parts of the world very fast. • The dental considerations for such cases are required with proper investigations and medications. LETS JOIN HANDS FOR SAVING THE HEARTS OF THE NATION! 177
  178. 178. REFERENCES • Davidson’s Principle and Practice of Medicine – 21st Edition • Burket’s Book of Oral Medicine – 11th Edition • Emerging risk factors for cardiovascular diseases:Indian context. Sushil et al. Indian Journal of Endocrinology and Metabolism / Sep-Oct 2013 / Vol 17 | Issue 5 • Heart Disease and Stroke Statistics--2010 Update: A Report From the American Heart Association 178
  179. 179. • Oral Health, Atherosclerosis, And Cardiovascular Disease. Jukka H. Meurman Et Al. Crit Rev Oral Biol Med; 15(6):403-413 (2004). • 2007 Guidelines For The Management Of Arterial Hypertension. European Heart Journal (2007) 28, 1462–1536. • Dental Disease And Risk Ofcoronary Heart Disease And Mortality. Frank Destefano Et Al. Bmj Volume 306 13 March 1993. 179
  180. 180. • Coronary Artery Disease. Munther K. Homoud. Seminar By Md Of Tufts-new England Medical Center Spring 2008. • Hypertension In Pregnancy:the Management Of Hypertensive Disorders During Pregnancy. Royal College Of Obstetricians And Gynaecologists. National Collaborating Centre For Women’s And Children’s Health.Aug 2010. • Relationship Between Oral Health Lars Frithiof Et Al. J Clin Periodontol 2001; 28: 762–768. 180
  181. 181. • Definition And Classification Of Hypertension: An Update. Emerging Concept. Thomas D. Giles Et Al. The Journal Of Clinical Hypertension. Vol. 11 No. 11 November 2009. • Prevention Of Infective Endocarditis: Guidelines From The American Heart Association. A Guideline From The American Heart Association. • Dental Considerations In Patients With Heart Disease. Marta Cruz-pamplona Et Al. J Clin Exp Dent. 2011;3(2):e97-105. 181
  182. 182. • Hypertension Guidelines: Revisiting The JNC 7 Recommendations. The Journal Of Lancaster General Hospital • Fall 2008 • Vol. 3 – No. 3. • ESC Guidelines On The Management Of Cardiovascular Diseases During Pregnancy. European Heart Journal (2011) 32, 3147–3197. • Peripheral Signs Of Endocarditis. Frank L. Urbano. Hospital Physician May 2000. 182
  183. 183. THANK YOU 183