cardiac disruptions alterations in oxygenation


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  • Are friable – easily break off  emboli
  • Petechiae Splinter hemorrhages? Roth’s spots Jane Ways lesions
  • Abnormal humoral and cell-mediated response seen sometimes in people who have a strep B URI, appears about 2-3 weeks after that infection Seen more frequently in underdeveloped countries, in poor living conditions – genetic factor?
  • dilated: all 4 ventricles affected but ventricles dilate s/s heart has globular shape b. Idiopathic????? Growth is asymmetric, no dilation of ventricles
  • Rare typed
  • cardiac disruptions alterations in oxygenation

    1. 1. Alterations In Oxygenation Cardiac Disruptions
    2. 2. Cross Section of the Heart
    3. 3. Coronary Arteries & Veins
    4. 4. Blood Flow Through the Heart
    5. 5. Conduction System of the Heart
    6. 6. I. Overview of alterations in the cardiac systemA. Lack of blood supply 1. Consequences of decreased flow Coronary arteries perfuse heart to meet O2 & nutritional needs Ischemia Stable angina pectoris Acute coronary Syndrome Myocardial infarction
    7. 7. 2. Conditions which cause this type of cardiac disruptionCan be either: increased O2 demand decreased O2 supplya) atherosclerosis of the coronary arteriesb) thrombus within the coronary arteriesc) vasospasm of the coronary arteriesd) hypovolemia
    8. 8. Occlusion/Collateral CirculationVessel Occlusion with Collateral CirculationA.Open, functioning coronary arteryB.Partial coronary artery closure with collateral circulation being establishedC.Total coronary artery occlusion with collateral circulation bypassing theocclusion to supply the myocardium
    9. 9. B. Infections of the heart1. Consequences Inflammation of the endocardium2. Example of infectious conditions of the heart a) Infective endocarditis
    10. 10. a) Infective endocarditis Most common causative agents are bacterial Must be:  endothelial damage  microorganisms invade and colonize structures - cause inflammation  vegetations - damage valves  interfere with valve function and predispose to embolus formation
    11. 11. Bacterial Endocarditismitral/bicuspid valve – destructive vegetations
    12. 12. C. Immune mediated inflammatory conditions 1. Consequences  Immune attack on individual’s own tissue  Can damage many tissues & organs -including the heart
    13. 13. 2. Example of immune mediated inflammatory conditiona) Rheumatic heart disease Diffuse, inflammatory disease caused by delayed immune response to infection by group A beta- hemolytic strep Antibodies directed against self tissues Acute rheumatic fever is febrile illness - inflammation of joints, skin, nervous system, heart. Untreated, causes scarring & deformity of cardiac structures  rheumatic heart disease (10% occurrence)  Primary lesion usually is at the mitral/bicuspid valves
    14. 14. Valve DiseaseDisease of the aortic valve as viewed from the aortaA.Stenosis of the valve openingB.An incompetent or regurgitant valve that is unable to close completely
    15. 15. Rheumatic ValvulitisChronic rheumatic valvulitis. A view of the mitral valve from the left atrium showsrigid, thickened, and fused leaflets with a narrow orifice, creating thecharacteristic “fish mouth” appearance of the rheumatic mitral stenosis.
    16. 16. D. Cardiomyopathy Group of diseases that affect myocardium structure and function Can be primary or secondary Caused by many things  Cardiotoxic agents  HTN  Endomyocardial fibrosis  Not necessarily related to CAD
    17. 17. 1. Consequences of Cardiomyopathy 3 different types Each type has own pathogenesis, clinical presentation, and treatment protocols Regardless of type - often leads to heart failure and death
    18. 18. 2. Types of Cardiomyopathya. Dilated - most common form. Cardiomegaly w/ventricular dilation Impaired systolic function Atrial enlargement Stasis of blood in LV. Heart: globular shape
    19. 19. 2. Types of Cardiomyopathyb. Hypertrophic - 4 main characteristics: Massive ventricular hypertrophy Rapid, forceful contraction of LV Impaired relaxation  as ventricles become noncompliant Obstruction of aortic outflow (not always) Growth is asymmetric No dilation of ventricles
    20. 20. 2. Types of Cardiomyopathyc. Restrictive - least frequent.Impairs diastolic filling & stretch.Systolic function remains unaffected.Heart becomes infiltrated by various substances,resulting in severe fibrosis – can’t stretch.(Amyloidosis: protein deposits)
    21. 21. II. Angina PectorisA. Definition/description Pain (angina) in chest (pectoris) Ischemia related to supply and demand Usually transient - about 3 to 5 minutes Subsides when precipitating factor relieved If blood flow restored, no permanent damage
    22. 22. B. Causes of myocardial ischemia: Supply: decreased O2 supply Develops if flow of O2 content of coronary blood insufficient to meet metabolic needs of myocardial cells or conditions exist that increase hearts O2 demands Usually caused by atherosclerosis and almost always by obstruction of major coronary artery
    23. 23. B. Causes of myocardial ischemia: Demand – increased O2 need High systolic BP Increased ventricular volume Increased thickness of myocardium Increased HR
    24. 24. Angina Pectoris: Risk FactorsModifiable UnmodifiableCigarette smoking AgeHypertension SexAbnormal lipid profile HeredityObesity Race and ethnicityHyperglycemiaPhysical inactivityStress
    25. 25. C. Types of Angina Pectoris Chronic stable angina Unstable angina (pre-infarction) Printzmetal’s angina (variant) Silent ischemia
    26. 26. Types of Coronary Heart Disease
    27. 27. 1. Stable angina1. Stable angina Caused by narrowing & hardening of arterial walls – the 4 E’s  Exertion  Extremes in temperature – vasoconstriction  Emotions – SNS stimulation  Excessive eating – blood diverted to GI tract Affected vessels can’t dilate Pain usually relieved by rest & nitrates
    28. 28. 2. Variant or Prinzmental’s angina Chest pain caused by transmural ischemia of myocardium Occurs unpredictably & almost exclusively at rest Pain caused by vasospasm of one or more coronary arteries Pain frequent during rest and at night Rare type of angina, not precipitated by exertion, etc. Treated with nitrates and Ca++ channel blockers
    29. 29. 3. Unstable angina (Pre-infarction) Angina that is new in onset, occurs at rest, or has a worsening pattern Seldom predictable Often associated with deterioration of stable atherosclerotic plaque May mean impending infarction
    30. 30. 4. Silent Ischemia May only be detected on routine EKG Lack of pain or discomfort Increases risk of myocardial infarction May precede a sudden & severe MI without warning Largely associated with HTN
    31. 31. D. Clinical manifestations & related pathogenesis Substernal chest discomfort May radiate to neck, lower jaw, left arm, left shoulder, or back  LT arm most common  But may also radiate to RT arm Often mistaken for indigestion May be accompanied by severe apprehension & feeling of impending deathMyocardial cells are viable for 20 minutesEventually revert to anaerobic metabolism  lactic acid  pain
    32. 32. Locations of Chest Pain During Angina or MI
    33. 33. Angina Pain Areas
    34. 34. E. Potential medical complications1. Myocardial infarction Worst case scenario2. Arrhythmias/Dysrhythmias Affects myocardial cell’s sensitivity to nerve impulsesInitially, BP rises, then eventually as heart stops pumping effectively & F/F response wears off, CO drops & BP drops
    35. 35. Tissue Destruction After MI
    36. 36. Acute MIX-section of ventricles of a man who died a few days after onset of severe chest pain.Transmural infarct & septal regions of the left ventricle.The necrotic/infarcted myocardium is soft, yellowish, and sharply demarcated.
    37. 37. F. ManagementPrimary aim – Reduce myocardial O2 consumption1. Diagnostic studies a. EKG/ECG – Electrocardiography May have normal EKG when no pain, so requires EKG during attack Can indicate which coronary artery is involved Treatment:  A.  B.  C.  D. diet & diabetes management  E. education & exercise
    38. 38. b. Serum enzyme level testsCreatine Kinase (CK) – 3 isoenzymes CK-MB: present in heart muscle CK-MM: present in skeletal muscle CK-BB: present in brain tissue CK-MB found only in cardiac cells - rises only when damage to cells Always increases in MI:  Rises 4-6 hours after onset  Peaks at 18-24  Returns to normal in 3-4 days (0-6%)
    39. 39. Troponin myocardial protein released into circulation after injury Greater specificity: specific MI indicator  Rises 2-12 hours after MI  Peaks at 24-48 hours  Returns to normal in 5-14 days (remain elevated for 2 weeks)
    40. 40. Myoglobin O2 carrying protein present in cardiac and skeletal muscle Released quickly from infarcted myocardial tissue Not cardiac specific Rapidly excreted from urine
    41. 41. Albumin Colbalt-binding test Measures how much cobalt is bound to albumin Changes in structure of albumin occur with MI Used in conjunction with EKG & troponin test
    42. 42. c. Serum lipid level tests Triglycerides Total Cholesterol Cholesterol fractionation Not used for MI diagnostic purposes, but reveals if high-risk
    43. 43. c. Serum lipid level tests C-Reactive Protein (CRP)  Appears in blood 6-10 hours after acute inflammatory process and tissue destruction  Peaks at 48-72 hours after MI N High Sensitivity C- Reactive Protein (hs CRP) - highly sensitive test for detecting risk of cardiovascular and peripheral vascular diseases. Frequently done with cholesterol screening
    44. 44. d. Exercise stress test Reveals heart function during exercise Attach patient to EKG & BP cuff Useful to differentiate angina from other types of chest pain Can be done with a scan as well Patients who can’t walk may use a bike
    45. 45. e. Nuclear Cardiology Imaging Several tests use radionuclides to visualize distribution of:  Blood flow  Ventricular structures  “cold spots” in infarcted zone – no accumulation of radionuclides  Perfusion or metabolism of myocardium
    46. 46. f. Coronary angiography Diagnostic radiography of heart & blood vessels using radiopaque contrast media Used to evaluate coronary arteries and collateral circulation Helps determine anatomic extent of CAD
    47. 47. Non-pharmacologic Treatment Education R – Rest E – Exercise S – Stop smoking C – Count cholesterol & calories U – Unwind  reduce stress E – Education
    48. 48. Nitrate Therapy First line of defense – prevention/prophylaxis and treatment Relax smooth muscles in the blood vessel walls Improve blood delivery to the heart by dilating blood vessels Improve blood delivery to the heart by decreasing the workload of the heart Ineffective in sclerosed vessels, effective if collateral vessels in place
    49. 49. 2. Pharmacologic therapya. In acute attacks i) Nitroglycerine SL Actions - increases coronary blood flow by dilating coronary arteries & improving collateral flowDestruction by GI tractMust dissolve sublingually, patient shouldn’t swallow saliva while dissolving
    50. 50. i) Nitroglycerine SLNI: Give sublingually. Teach patient: keep tongue still keep med with you at all times very unstable - capped, dark, glass bottle inactivated by heat, moisture, air, light, time. Should have burning sensation Replace every 6months Not fixed dose - patient regulates usage
    51. 51. Nitroglycerine SL - continued maximum of 3 tablets in 15 minutes - 5 minutes apart transient side effects – hypotension, headache, facial flushing lie down to prevent falling carry medic-alert information journal all attacks  precipitating factors, duration, pills taken, etc.
    52. 52. b. For chronic anginal prophylaxisi) Nitroglyercin ointment - topical - rotate sites to prevent skin irritation - remove old patch/paper - dose may be increased to highest does that doesn’t cause hypotension - apply only with measuring applicator - don’t allow contact with your skinDON’T SHAVE an area. This will create small abrasions. Clip hair
    53. 53. ii) Transdermal nitratesTransderm-Nitro, Nitro-Dur, Nitrodisc apply to hairless site remove all previous patches apply firm pressure waterproof - not affected by bathing do not cut or trim patches remove before cardioversion or defibrillation to prevent burns
    54. 54. iii) Long-acting nitrates Extended release capsules  Nitrocap T.D., Nitrogly, Nitrolin, Nitrospan Extended release tablets  Nitrong Taken every 8 to 12 hours
    55. 55. iv) SL nitroglycerine prior to activity Can be used to prevent or minimize anginal attacks before stressful events Will increase tolerance for exercise & stress Best to take before pain develops
    56. 56. Case Study A 60 year old male was shoveling snow after a heavy snowstorm and experienced chest pain. He has a history of angina and has SL nitroglycerin in the house. He keeps it on his windowsill in a clear plastic pillbox.
    57. 57. Questions: What type of angina is he experiencing? What should he do to treat this episode? After taking the maximum tablets, his pain has not subsided. What should he do? What patient teaching is indicated in this situation?
    58. 58. v) Beta-adrenergic blockersPropanolol (Inderal)Action: Decreases CO and reduces sympathetic vasoconstrictor tone. Decreases renin secretion by kidney. Decreases HR, BP, & myocardial contractility.
    59. 59. vi) Calcium channel blockersAction - inhibits transport of calcium into myocardial & vascular smooth muscle cells, resulting in inhibition of excitation- contraction coupling & subsequent contractionNifedipine (Procardia), verapamil (Calan)
    60. 60. Calcium MovementCa2+ channel blocker:mechanism of actionA.During muscle relaxation,K+ inside muscle cell, Ca++ &Na+ outside muscle cell.A.For muscle contraction tooccur, K+ efflux, Na+ & Ca2+influx through openmembrane channels.A.When Ca2+ channels areblocked by drug molecules,muscle contraction decreasesbecause Ca2+ can’t movethrough cell membrane intomuscle cell.
    61. 61. vii) Antithrombotic therapy . . . Aspirin (ASA)Action - in low doses, appears to impede clotting by blocking prostaglandin synthesis, which prevents formation of platelet-aggregation81 mg(325 mg Rx)
    62. 62. 3. Invasive & surgical treatmentsa. Percutaneous transluminal coronary angioplasty (PTCA) Improve blood flow - crack plaque or atheroma that has built up & interfering with circulationDone more frequently than CABG
    63. 63. b. Intracoronary stents PTCA with intravascular stent over balloon When balloon is deflated, stent remains in artery & holds it open. Eventually endothelium covers stent & incorporates into wall
    64. 64. c. Laser angioplasty Catheter with small laser introduced into peripheral artery then diseased coronary artery Vaporizes plaque
    65. 65. d. Atherectomy Plaque is shaved off using rotational blade Removes atheromas
    66. 66. e. Coronary artery bypass grafting (CABG) Blood vessel from another part of body (saphenous vein, left internal mammary artery) is grafted distal to coronary artery lesion - “bypassing” obstruction MIDCABG – newer procedure; limited use
    67. 67. Coronary Artery Revascularization
    68. 68. 4. Prehospital emergency care of chest pain (from AHA)For person with unknown CHD: recognize symptoms - chest pain, sweating, nausea, SOB, weakness stop activity and sit or lie down if pain persists for 5 minutes or more, activate the EMS
    69. 69. 4. Prehospital emergency care of chest pain (From AHA)For person with known CHD: recognize symptoms - chest pain, sweating, nausea, SOB, weakness stop activity - sit or lie down place one NTG tablet under tongue. Repeat at 5 minute intervals up to 3 times if symptoms persist, activate the EMS
    70. 70. III. Congestive Heart FailureA. DefinitionAbnormal condition involving impaired cardiac pumpingAssociated with numerous types of heart disease - esp. long-standing HTN and CAD
    71. 71. Characterized by: ventricular dysfunction reduced exercise tolerance diminished quality of life shortened life expectancy
    72. 72. Can be:Systolic Failure Results from inability of heart to pump blood. Caused by:  impaired contractile function  increased afterload  Cardiomyopathy  mechanical abnormalities Decreased CO
    73. 73. Can be:Diastolic Failure Impaired ability of ventricles to fill Results in decreased stroke volume Decreased COMixed systolic and diastolic failure
    74. 74. B. Compensatory MechanismsOverloaded heart tries to compensate to maintain adequate CO1. Ventricular dilation Chambers enlarge when pressure elevated over time Muscle fibers stretch and increase contractile force
    75. 75. 2. Ventricular hypertrophy Heart hypertrophies in response to overwork Will lead to increased CO
    76. 76. 3. Sympathetic nervous system activation Inadequate stroke volume and CO caused sympathetic nerve activation Results in increased HR, myocardial contractility, and peripheral vascular constriction Initially increase in HR and contractility improve CO, but detrimental over time
    77. 77. 4. Neurohormonal responses Decrease blood flow to kidneys causes release of renin Renin caused conversion of angiotension I to II – which caused adrenal cortex to release aldosterone (increased sodium retention & ↑ peripheral vasoconstriction Posterior pituitary secretes ADH – ↑ water reabsorption in renal tubels
    78. 78. C. Types of CHF1. Left-sided heart failurea. Pathogenesis Left ventricle fails - unable to pump adequate blood coming to it from lungs Increases pressure in pulmonary circulation - causes fluid to be forced into pulmonary tissues
    79. 79. Left-Sided Heart Failure
    80. 80. 2. Right-sided failurea. PathogenesisVenous congestion in systemic circulation results in: peripheral edema hepatomegaly splenomegaly vascular congestion of GI tract jugular venous distention
    81. 81. Right-Sided Heart Failure
    82. 82. 3. Clinical manifestationsa. Fluid retention and edema Edema Nocturia
    83. 83. b. Respiratory manifestations Pulmonary edema Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Cough
    84. 84. c. Fatigue & limited exercise tolerance  Fatigue  Tachycardia  Anxiety and restlessness
    85. 85. d. Cachexia Weight loss Malnutrition
    86. 86. e. Cyanosis Skin changes
    87. 87. 4. Complicationsa. Pleural effusionsb. Arrhythmiasc. Left ventricular thrombusd. Hepatomegaly
    88. 88. E. Management1. Diagnostic studies a. CXR b. EKG c. Echocardiogram d. Radionuclide angiography e. Labs
    89. 89. Normal EKG
    90. 90. 2. Pharmacologic Therapya. ACE inhibitors (Angiotension Converting Vasotec Prevents production of Angiotension II by blocking it’s conversion to the active form - results in systemic vasodilation Decreases preload & afterload in patients with CHF
    91. 91. Angiotensin Conversion
    92. 92. b. InotropicsDigoxinIncreases force of myocardial contraction, decreases conduction through SA and AV nodes, slows heart rate and increases diastolic filing timeIncreases CO, slows heart rateNI - Take AP for one minute. Hold & notify MD if below 60
    93. 93. c. DiureticsPromotes excretion of edema fluid and helps sustain cardiac output and tissue perfusion by reducing preloadReview notes on Thiazides, loop diuretics, and K+ sparing diuretics
    94. 94. d. Vasodilator drugsNitrates Reduces circulating volume by decreasing preload and also increases coronary artery circulation by dilating coronary arteries
    95. 95. e. Beta adrenergic blockers Becoming more important in management of CHF Block sympathetic nervous system’s negative effects on the failing heart - such as increased heart rate
    96. 96. 3. Supportivea. Supplemental oxygenb. Restc. Daily weightsc. Sodium restricted diet