Diseases of the Heart

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Diseases of the Heart
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  1. What is Congestive Heart Failure?
    A clinical syndrome resulting from deficient cardiac stroke volume with inability of the cardiac output to keep up with the venous return.

    Resulting in:

    Inadequate perfusion of the tissues from insufficient cardiac output.
  2. What are the top four causes for L-CHF?
    • 1. Ischemic heart disease
    • 2. Hypertension
    • 3. Valvular disease (aortic stenosis or mitral regurgitation) - (NOT mitral valve stenosis)
    • 4. Primary myocardial disease
  3. What is forward Failure? Backward Failure?
    Forward Failure is heart failure secondary to: decreased Cardiac Output.

    Backward Failure is heart failure secondary to: increased workload and/or increased pressure load and/or increased blood volume.
  4. Are the following Forward failure or Backward failure?
    1. Ischemic heart disease ___________
    2. Hypertension ___________
    3. Valvular disease __________
    4. Primary myocardial disease __________
    • 1. Forward
    • 2. Backward
    • 3. Backward
    • 4. Forward
  5. What are the gross morphologic changes with L-CHF?
    Left ventricular hypertrophy and dilation (increased volume).
  6. What organs are affected by L-CHF?
    Primarily Lungs, Brain, and kidney.
  7. What are some symptoms that the lungs have been affected by L-CHF?
    • 1. Chronic passive congestion and pulmonary edema (predisposes for pneumonia)
    • 2. "Heart failure cells" - hemosiderin laden macrophages - and brown induration of lungs
  8. What are some clinical manifestations that the Lungs have been affected by L-CHF?
    • Clinically:
    • 1. Dyspnea (difficulty breathing) - most common
    • 2. Orthopnea (difficulty breathing lying down)
    • 3. Paroxysmal nocturnal dyspnea
    • 4. Cough
    • 5. Cyanosis
  9. If the brain is affected by L-CHF, what happens?
    • Cerebral hypoxia resulting in:
    • 1. Irritability
    • 2. restlessness
    • 3. stupor
    • 4. coma (perhaps - extreme)
  10. If the kidneys are affected by L-CHF, what happens?
    • Reduced renal perfusion results in:
    • 1. fluid retention
    • 2. peripheral edema
  11. What are the top five causes of R-CHF? (in order)
    • 1. L-CHF
    • 2. Valvular disease - pulmonic stenosis or tricuspid regurgitation
    • 3. Congenital left-to-right shunts
    • 4. Intrinsic lung diseases
    • 5. Cardiomyopathy or myocarditis
  12. Are the following backward or forward failure?
    1. L-CHF
    2. Valvular disease - pulmonic stenosis or tricuspid regurgitation
    3. Congenital left-to-right shunts
    4. Intrinsic lung diseases
    5. Cardiomyopathy or myocarditis
    • 1. Backward
    • 2. Backward
    • 3. Backward
    • 4. Backward
    • 5. Forward
  13. What other organs could be affected by R-CHF?
    • 1. Liver (nutmeg liver) (scarring around central vein)
    • 2. Spleen (congestive splenomegaly)
    • 3. Kidney (fluid retention)
    • 4. Brain (congestion and hypoxia)
    • 5. Subcutaneous tissues (peripheral edema and possible anasarca)
    • 6. Portal system (hypertension; maybe ascites)
  14. During your initial assessment of a patient you will get a comprehensive health history, what would that include?
    • 1. Medications
    • 2. Hospitalizations
    • 3. Changes in health status
    • 4. Exercise tolerance and fatiguability
    • 5. Dyspnea
  15. Dental management of a patient with congestive heart failure would include:
    • 1. Make sure pt has taken meds on day of appointment
    • 2. Consider orthopnea and orthostatic hypotension
    • 3. Stress reduction protocol
    • 4. Baseline vitals at start of appointment
    • 5. Monitor vitals during procedure (don't dismiss until vitals are with 10-20% of baseline)
  16. What is Ischemic Heart Disease (or Coronary Heart Disease)?
    Heart disease featuring an imbalance between supply and demand for oxygen to the myocardium.
  17. What are four patterns of coronary heart disease? Which is most common?
    • 1. Angina pectoris (AP)
    • 2. Myocardial Infarction (MI)
    • 3. Sudden Cardiac death (SCD)
    • 4. Chronic Ischemic Heart Disease (CIHD) - Most common
  18. How many deaths in the U.S. is Coronary heart disease responsible for?
    One third to one fourth!
  19. Is the pathogenesis the same for all four patterns of ischemic heart disease?
    Yes
  20. Remember with coronary heart disease there is an imbalance of between supply and demand of oxygen to the myocardium.

    What is the primary cause?
    Severe coronary atherosclerosis with stenosing plaques.
  21. What is a critical stenosis?
    A plaque that obstructs 70% o 80% of the coronary artery lumen, but usually asymptomatic unless there is an increased demand.
  22. What is a fixed stenosis?
    A stenosing plaque that occludes approximately 90% of the lumen causing symptoms at rest.
  23. Another major influencing factor contributing to the four patterns of coronary heart disease would include:
    Intraluminal thrombosis overlying a ruptured or fissured plaque (often resulting in coronary crisis).
  24. What is angina pectoris? (one of the four major patterns of coronary heart disease)
    Paroxysmal attacks of substernal or precordial chest pain or discomfort caused by myocardial ischemia that falls precariously short of inducing infarction.
  25. Where would you experience pain with Angina Pectoris? and why?
    Left shoulder or arm, even jaws.

    Pain is due to a transient reversible myocardial hypoxia.
  26. What are the three patterns of angina pectoris?
    • 1. Typical Angina (stable angina)
    • 2. Prinzmetal Angina
    • 3. Unstable Angina
  27. What is typical angina?
    Ischemia due to stenosing atherosclerosis compounded with increased myocardial demand.

    Attacks are brought on by exertion/stress and are relieved by rest.
  28. What is prinzmetal angina?
    Attacks attributed to vasospasm (sudden constriction of b.v.) which may be superimposed on a fixed stenosis.

    Attacks may appear even at rest and are relieved by vasodilators such as nitroglycerin.
  29. What is unstable angina?
    A change in the usual pattern of attacks (freq, duration) brought about by multiple mechanisms.

    Attacks forewarn imminent danger of a subsequent acute MI!
  30. What are some dental precautions for Angina Pectoris?
    • 1. Know health history
    • 2. Have pt's meds handy (Nitroglycerine)
    • 3. Stress reduction protocol
  31. What is a Myocardial Infarction (MI)?
    Ischemic (hypoxic) necrosis of the myocardium.
  32. Some epidemiology of MI:
    • 1. Single most frequent cause of death in U.S.
    • 2. 1.5 million suffer from MI per year and 1/3rd of them die.
    • 3. Men are more likely to suffer an MI, especially at 50 year old range.
  33. What two types of MI are there?
    • 1. Transmural
    • 2. Subendothelial
  34. What is a transmural MI?
    When ischemic necrosis involves the full thickness of the ventricular wall. (most common/serious, usually left ventricle)
  35. What is a subendothelial MI?
    Necrosis involves not more than the inner one third to half of the thickness of the wall.
  36. What is the pathogensis for MI? (remember it's the same for all four patterns)
    Primarily its the severe coronary narrowing/stenosis from atherosclerotic plaques.
  37. What are other contributing factors to the pathogenesis of MI?
    Thrombosis - initiated by plaque fissure, rupture, or intraplaque hemorrhage.

    For transmural infarcts, 90-95% of cases have superimposed thrombosis.

    Also: platelet activation, vasospasm, hypotensive episode, increased myocardial demand.
  38. What is the sequence of biomechanical and morphologic changes during an MI? (know bold)
    • 1-2 minutes - Loss of contractility
    • 10 minutes - 50% depletion of ATP
    • 20-40 minutes - Irreversible cell injury
    • 8-12 hours - Gross pallor
    • End of first week - Soft yellow lesion has red rim
    • 7-10 days - Lesion maximally soft and weak (susceptible to rupture)
    • 7th week - Lesion completely healed by scarring
  39. What are possible morphologic complications of Transmural Myocardial Infarction?
    • 1. infarction of papillary muscle
    • 2. Rupture of infarcted papillary muscle - usually lethal
    • 3. Fibrinous pericarditis - scar tissue adhesions between pericardium and pericardial sac results in loss of mobility
    • 4. Mural thrombosis with risk of embolization - forms over area of infarction on wall of heart
    • 5. Rupture of infarct may cause cardiac tomponade - occurs 7 to 10 days after infarct
    • 6. Ventricular aneurysm - disrupts the "electrical conduction system" causing arythmias
  40. What is a diagnosis of MI based on?
    • 1. Symptoms
    • 2. ECG changes
    • 3. Elevations of specific serum enzymes
  41. Discuss symptoms of MI
    • Symptoms may be
    • 1. Prodromal
    • 2. concurrent
    • 3. asymptomatic
  42. What are some prodromal symptoms of a MI?
    • Symptoms may occur days or weeks ahead and can include:
    • 1. fatigue
    • 2. dyspnea
    • 3. change in angina pattern
  43. What are some symptoms that can occur with the MI?
    • 1. Sweating (diaphoresis)
    • 2. Nausea and vomiting
    • 3. Breathlessness
  44. What are the clinical outcomes for patients who've had a MI?
    10 to 20% are uncomplicated with a complete recovery

    80 to 90% develop complications
  45. For patients developing complications from MI, what are they, and is their onset early or late?
    • 1. Arrhythmias (majority) (early)
    • 2. Cardiogenic shock (death) (early)
    • 3. Rupture of wall, septum, or papillary muscle (early)
    • 4. Embolism of a mural thrombus (early)
    • 5. Development of Left ventricular CHF (late)
  46. Say something regarding the prognosis of patients with MI
    • * 50% die before reaching the hospital
    • * of those reaching the hospital more than 10% die
    • * 30% still die within first year
  47. What can be done to prevent a Myocardial Infarction?
    • 1. Coronary bypass surgery
    • 2. Angioplasty (balloon)
    • 3. Cardiac stents (metal stent)
    • 4. Anticoagulant/ antiplatelet meds (Coumadin, Aspirin/Plavix)
    • 5. Lifestyle - Important - Don't smoke, eat well, exercise
  48. What is Sudden Cardiac Death (SCD)?
    Unexpected death from cardiac causes within 1 hour of the onset of acute symptoms.
  49. How many deaths are caused by SCD, per year, in the U.S.?
    300,000
  50. To what can we contribute 75-90% of SCD's?
    Ischemic Heart Disease
  51. What is the pathogenesis of SCD?
    1. Marked stenosing atherosclerosis of at least one coronary artery...

    2. The ultimate mechanism: development of a lethal arrhythmia (asystole, ventricular fibrillation)
  52. How do you treat one who is having a ventricular fibrillation?
    AED, install pacemaker
  53. What is Chronic Ischemic Heart Disease (aka coronary cardiomyopathy)?
    Appears insidiously in older people developing ECG changes and congestive heart failure as a consequence of long-term, progressive ischemic myocardial damage.
  54. What morphologic changes occur with CIHD?
    Heart may be normal weight or smaller, and dark brown.

    Microscopically one will see myocardial atrophy, lipofuscin deposits in the myocytes, and diffuse fibrosis around vessels.
  55. Briefly describe the clinical course of chronic ischemic heart disease
    • * May be asymptomatic until CHF develops
    • * Years prior to CHF - angina or MI
    • * Scarring of conduction system may cause arrhythmias
    • * Most die of unrelated causes
  56. What is Hypertensive Heart disease?
    Diagnosis is based on left ventricular hypertrophy and the absence of other cardiac changes.
  57. Whats so bad about hypertensive heart disease?
    Hypertension predisposes to atherosclerosis. While CO is maintained, the hypertrophied heart eventually fails!
  58. What is Cor Pulmonale?
    Affected lung structure or function --> increased resistance to blood flow through lungs --> pulmonary hypertension --> right ventricular enlargement
  59. What is acute cor pulmonale?
    Temporary right ventricular dilation without hypertrophy.
  60. What is Chronic cor pulmonale? (TEST)
    Characterized by right ventricular hypertrophy without ventricular dilation!
  61. Describe Congenital Heart Disease
    A category of disease characterized by cardiac malformations present at birth (not always recognized).
  62. What is the most common clinical sign of a congenital heart defect?
    A heart murmur.
  63. What are the functional categories of congenital cardiac anomalies?
    • 1. Left-to-right shunt: late cyanosis
    • 2. Right-to-left shunt: early cyanosis
    • 3. Obstruction without cyanosis
  64. Clinically, what does a left-to-right shunt look like?
    • 1. Normal color at first
    • 2. Over time, right heart pressure overloads left pressure leading to a reversal of flow
    • 3. Unoxygenated blood is then circulated causing cyanosis
  65. Clinically, what does a right-to-left shunt look like?
    • 1. Cyanosis from the outset
    • 2. allow for paradoxical emboli to enter systemic circulation
  66. What is an example of obstruction to flow without cyanosis?
    • 1. Coarctation of the aorta
    • 2. Aortic stenosis
    • 3. Pulmonic stenosis
  67. What are the three most common congenital heart defects resulting in L-to-R shunts? (know their defining characteristics and severity)
    • 1. Ventricular Septal defect (VSD)
    • 2. Atrial Septal defect (ASD)
    • 3. Patent Ductus Arteriosus
  68. What is the single most common congenital heart defect?
    Ventricular septal defect
  69. Whats happening with a ventricular septal defect?
    There is a hole present in the ventricular septum, with 90% occuring in the thin membranous portion just below the aortic valve.
  70. Relate size with severity for a ventricular septal defect.
    • * Very small (<.5 cm) may close spontaneously.
    • * Small to medium may produce jet lesions that predispose to IE
    • * Large holes produce sever shunting with consequent cyanosis and pulmonary complications.
  71. What (where) is an atrial septal defect?
    A hole in the atrial septum above the level of the valves.
  72. What are the characteristics and severity of an ASD?
    Symptoms may not develop for years, larger lesions can cause heart failure from severe pulmonary HTN.
  73. What is the third Left-to-right shunt?
    Patent Ductus Arteriosus
  74. Describe Patent Ductus Arteriosus
    A congenital heart defect that occurs when the ductus joining the pulmonary artery to the aorta fails to close at birth.
  75. Briefly describe clinical signs of patent ductus arteriosus.
    • * Machine-like murmur and systolic thrill.
    • * L-2-R flow becomes R-2-L flow resulting in late onset cyanosis.
  76. What are the two R-to-L cyanotic shunts?
    • 1. Tetralogy of Fallot
    • 2. Transposition of the Great Vessels
  77. What four components are required to be tetralogy?
    • 1. Ventricular septal defect
    • 2. Dextraposed aorta that overrides the ventricular septal defect
    • 3. Obstruction of right ventricular outflow
    • 4. Right ventricular hypertrophy
  78. Severity of clinical signs is directly related to what? (For tetralogy of fallot)
    Degree of obstruction of right ventricular outflow.
  79. Pertaining to tetralogy of fallot:
    Mild pulmonic stenosis with a large septal defect produces what?
    Left-to-right shunting without cyanosis.
  80. Pertaining to tetralogy of fallot:
    With more severe obstruction, shunting is:
    right-to-left with cyanosis and pulmonary HTN
  81. Describe transposition of the Great vessels:
    Reversed position of the pulmonary artery and aorta.
  82. Describe corrected transposition of the great vessels:
    There is a reversed position of the pulmonary artery and aorta, as well as venous input being transposed.
  83. What is the prognosis for transposition of the Great Vessels?
    It is the most lethal heart shunt, prognosis is bad! With the corrected, a patient can live, but they have weaker cardiac function.
  84. What is an obstructive noncyanotic congenital anomaly?
    Coarctation of the Aorta - a constriction within the aorta.
  85. Moving on to Endocardial and Valvular disease...

    What is mitral valve prolapse?
    Also known as floppy valve syndrome, the valve leaflets prolapse, ballooning backward toward the left atrium during systole.
  86. What is unique about mitral valve prolapse? (think epidemiology)
    It is the most common cardiac valve disease in the US
  87. What age group does mitral valve prolapse target?
    20-40 year old females.
  88. What are some clinical consequences of mitral valve prolapse?
    • * Mild cases have no untoward consequences
    • * Mitral valve regurgitation
    • * With regurgitation - Infective Endocarditis
  89. What is Rheumatic heart disease? (Rheumatic fever)
    An acute febrile, immune-mediated inflammatory disease, affecting mostly children, that follows shortly after an infection with group A B-hemolytic strep!
  90. Is rheumatic fever an active infection?
    No, is is a post-streptococcal response.
  91. Describe the pathogenesis of rheumatic fever in 3 concise steps:
    • 1. M protein of strep evokes antibodies that are reactive with human epitopes
    • 2. The antibodies stimulate the immune system to produce acute systemic disease
    • 3. After dz subsides, there may be permanent damage to tissues, specifically heart valves.
  92. What is pathognomonic of RF?
    Aschoff body
  93. What pericarditis is common with RF?
    Fibrinous (bread-and-butter) pericarditis.
  94. Describe what happens to the valves with RF:
    Valves develop vegetations along leaflet edges, which become fibrotic and then calcified. Stenosis and regurgitation follows.
  95. How long after a strep infection does RF occur? (3% chance to occur)
    2-3 weeks after
  96. What are some clinical S/S of RF?
    • * Joint pain/swelling
    • * Skin rash
    • * Heart murmur
  97. What are the risks of heart involvement with RF?
    • 1st time = 66%
    • 2nd time = 100%
  98. What is Infective Endocarditis?
    Colonization or invasion of the heart valves by microbiologic agents, leading to local formation of thrombotic masses laden with organisms - infective vegetations.
  99. What heart tissue is affected by I.E.?
    All heart tissue if affected, but especially heart valve leaflets.
  100. What three factors must be present for IE to occur?
    • 1. Microorganisms in
    • 2. Circulating blood in a
    • 3. Susceptible host
  101. What strains of bacteria cause subacute bacterial endocarditis? (with example)
    alpha strep, Strep viridans (dental related)
  102. What is the most common cause of acute IE?
    S. aureus
  103. List six portals of entry to the circulation (which may cause bacteremia):
    • 1. IV drug use
    • 2. Dental procedures
    • 3. Surgical procedures
    • 4. Urinary tract catheterization
    • 5. IV catheterization
    • 6. Respiratory and skin infections
  104. List three factors that increase risk for IE:
    • 1. Cardiac abnormalities
    • 2. Prosthetic heart valves
    • 3. Intravenous drug use
  105. Cardiac abnormalities increase risk for IE and are usually accompanied by a heart murmur. List some examples:
    • 1. Rheumatic heart disease
    • 2. Congenital heart defects
    • 3. Mitral valve prolapse with regurgitation
    • 4. SLE
    • 5. Previous use of phen-fen
  106. We previously mentioned that alpha strep causes SBE, what is a more generic way to describe what causes SBE?
    low virulence organisms
  107. Briefly describe subacute infective endocarditis:
    Gradual onset with fever, malaise and weight loss. Clubbing of digits is common. Course is over weeks to months.
  108. What generic organisms cause acute infective endocarditis? (besides s aureus)
    Virulent organisms.
  109. Briefly describe acute infective endocarditis:
    Rapid onset and may be explosive. Symptoms may include high fever, shaking chills, and weakness.
  110. What two clinical signs are common to both subacute and acute endocarditis?
    • 1. changing heart murmur
    • 2. enlarged spleen
  111. What complications go along with IE?
    • 1. Valve damage
    • 2. Cardiogenic shock
    • 3. Septic emboli - hemorrhages of skin and mucosa, splinter hemorrhages of nails
    • 4. Fibrinous pericarditis
  112. How do you treat IE
    Start with I.V. broad spectrum antibiotics. Then do aggressive antimicrobial therapy aimed at the specific organism cultured from patient.
  113. What screening steps must a dentist take to determine correct preventative measures for IE?
    • 1. Review pt's health history to determine if a pt is at risk for IE
    • 2. Determine if pt at risk falls in AHA guideline for IE prophylaxis
    • 3. Pre-medicate only those with greatest risk of adverse outcomes if they were to get IE
  114. The 2007 AHA guidelines for prevention (prophylaxis) of IE fall under two major categories, what are they?
    • 1. Cardiac conditions associated with the highest risk of adverse outcome from endocarditis.
    • 2. Dental procedures for which prophylaxis is recommended
  115. What four cardiac conditions should prophylaxis with dental procedures be used?
    • 1. prosthetic cardiac valve
    • 2. Previous IE
    • 3. Congenital heart disease
    • 4. Cardiac transplant recipients who develop cardiac valvulopathy
  116. What congenital heart disease situations should you use prophylaxis?
    • 1. Unrepaired cyanotic CHD
    • 2. Completely repaired congenital heart defect with prosthetic material within the last 6 months
    • 3. Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic device
  117. For which dental procedures is endocarditis prophylaxis recommended?
    Those that involve manipulation of the gingival tissue or the periapical region of teeth or perforation of the oral mucosa.
  118. Premedication protocols: What is the drug of choice? How much? When?
    Amoxicillin, 2 gm by mouth, 1 hour before dental appointment
  119. If a pt is allergic to penicillin, how many alternative options are there? Would you give all of them?
    There are five alternate regimens. Two include cephalosporins which wouldn't be given because of potential cross-reactivity. So No, there are really three.
  120. What are the three antibiotic regimen given to pts allergic to penicillin?
    • 1. Clindamycin - 600 mg by mouth - one hour prior
    • 2. Azithromycin - 500 mg by mouth - one hour prior
    • 3. Clarithromycin - 500 mg by mouth - one hour prior
  121. What is myocarditis?
    Myocardial inflammation, primarily bc of infection, sufficient to cause clinical manifestations.
  122. What is cardiomyopathy?
    Non-inflammatory myocardial disease that is not attributable to pressure or volume overload, usually caused by myocardial abnormalities or dysfunction.
  123. Pericardial disease:

    There are three types of fluid that can collect in the pericardial sac, what are they?
    • 1. Effusions - non-inflammatory
    • 2. Exudates - inflammatory
    • 3. Blood - due to rupture or trauma - rapid accumulation results in cardiac tamponade
  124. What is pericarditis?
    Inflammation involving the pericardial surface of the heart.
  125. What is the primary cause of pericarditis?
    Almost always viral
  126. What is the most common type of pericarditis?
    Fibrinous

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