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Cardiac diseases mi-chf egh-nsg.forum-palestine.com

  1. 2. Cardiac Diseases Prepared by Abed Shagora In-service Education EGH
  2. 4. Stroke Volume <ul><li>The amount of blood ejected by the left ventricle each beat. </li></ul><ul><li>Preload </li></ul><ul><ul><li>The amount of stretch placed on the cardiac muscle just prior to systole </li></ul></ul><ul><ul><li>Starling ’ s Law </li></ul></ul><ul><li>Afterload </li></ul><ul><ul><li>The force or pressure at which the blood is ejected from the ventricle </li></ul></ul><ul><ul><li>Equated with systemic vascular resistance (SVR) </li></ul></ul><ul><li>Contractility </li></ul>
  3. 5. Cardiac Output/Index <ul><li>Cardiac output </li></ul><ul><ul><li>CO = HR (beats/minute) X SV (liters/beat) </li></ul></ul><ul><ul><li>Normal adult: 4-8 liters/minute </li></ul></ul><ul><li>Cardiac index </li></ul><ul><ul><li>CI = CO(liter/minute)/Body surface area (m 2 ) </li></ul></ul><ul><ul><li>Normal adult: 2.8-4.2 liter/minute/m 2 </li></ul></ul><ul><ul><li>Normalizes liter flow to body size </li></ul></ul>
  4. 6. <ul><li>Myocardial Infarction </li></ul>
  5. 7. <ul><li>Myocardial infarction (MI) refers to a dynamic process which one or more regions of the heart muscle experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood flow; subsequently, necrosis or &quot;death&quot; to the myocardial tissue occurs. </li></ul><ul><li>The onset of the myocardial infarction process may be sudden gradual, and the progression of the event to completion takes approximately 3 to 6 hours. </li></ul>
  6. 8. Pathophysiology and Etiology <ul><li>1. Acute coronary thrombosis (partial or total) -associate with 90% of MIs. </li></ul><ul><li>a. Severe coronary artery disease (greater than 70% narowing of the artery) precipitates thrombus formation </li></ul><ul><li>b. Intramural hemorrhage into atheromatous plaque causes the lesion to enlarge and occlude the vessles </li></ul><ul><li>c. The plaque ruptures into the vessel lumen, and a thrombus forms on top of the ulcerated lesion, with resultant vessel occlusion. </li></ul>
  7. 10. <ul><li>2. Other etiologic factors include coronary artery spasm, coronary artery embolism, infectious diseases causing arterial inflammation, hypoxia, anemia, and severe exertion or stress on the heart in the presence of significant coronary artery disease (ie, surgical procedures). </li></ul>
  8. 11. <ul><ul><li>3. Different degrees of damage occur to the heart muscle </li></ul></ul><ul><ul><li>a. Zone of necrosis-death to the heart muscle caused by extensive and complete oxygen deprivation; _irreversible damage </li></ul></ul><ul><ul><li>b. Zone of injury-region of the heart muscle surrounding the area of necrosis; inflamed and injured, but still viable if adequate oxygenation can be restored' </li></ul></ul><ul><ul><li>c. Zone of ischemia-region of the heart muscle surrounding the area of injury, which is ischemic and viable; not endangered unless extension of the infarction occurs </li></ul></ul>
  9. 12. <ul><ul><li>4. According to the layers of the heart muscle involved, MIs can be classified as: </li></ul></ul><ul><ul><li>Transmural (Q wave) infarction-area of necrosis occurs throughout the entire thickness of the heart muscle. </li></ul></ul><ul><ul><li>B. Subendocardial (nontransmural/non-Q) infarction- area of necrosis is confined to the innermost layer of the heart lining the chambers. </li></ul></ul>
  10. 13. <ul><li>5. Location of MI is identified as the location of the damaged heart muscle within the left ventricle: inferior, anterior, lateral, and posterior or right ventricle. </li></ul><ul><li>a. Left ventricle is the most common and dangerous location for an MI, because it is the main pumping' chamber of the heart. </li></ul><ul><li>b. Right ventricular infarctions commonly occur in conjunction with damage to the inferior and/or posterior wall of the left ventricle. </li></ul>
  11. 14. <ul><li>6. Region of the heart muscle that becomes damaged- determined by the coronary artery that becomes obstructed . </li></ul><ul><li>7. The amount of heart muscle damage and the location of the MI-determine prognosis. </li></ul>
  12. 15. Clinical Manifestations <ul><li>1. Chest pain </li></ul><ul><li>a. Severe, diffuse steady substernal pain of a crushing and squeezing nature </li></ul><ul><li>b. Not relieved by rest or sublingual vasodilator therapy, but requires narcotics </li></ul><ul><li>c. May radiate to the arms (commonly the left), shoulders, neck, back, and/or jaw </li></ul><ul><li>d. Continues for more than 15 minutes </li></ul><ul><li>e. May produce anxiety and fear, resulting in an in- crease in heart rate, blood pressure, and respiratory rate </li></ul><ul><li>2. Diaphoresis, cool clammy skin, facial pallor </li></ul>
  13. 16. <ul><li>3. Hypertension or hypotension </li></ul><ul><li>4. Bradycardia or tachycardia </li></ul><ul><li>5. Premature ventricular and/or atrial beats </li></ul><ul><li>6. Palpitations, severe anxiety, dyspnea </li></ul><ul><li>7. Disorientation, confusion, restlessness </li></ul><ul><li>8. Fainting, marked weakness . </li></ul><ul><li>9. Nausea, vomiting, hiccups </li></ul><ul><li>10. Atypical symptoms: epigastric or abdominal distress, dull aching or tingling sensations, shortness of breath, extreme fatigue </li></ul>
  14. 17. Diagnostic Evaluation <ul><li>ECG Changes </li></ul><ul><ul><li>1. Generally occur within 2 to 12 hours, but may take 72 to 96 hours. </li></ul></ul><ul><ul><li>2. Necrotic, injured, and ischemic tissue alters ventricular depolarization and repolarisation. </li></ul></ul><ul><ul><li>a. S-T segment depression and T wave inversion indicate a pattern of ischemia. </li></ul></ul><ul><ul><li>b. S- T elevation indicates an injury pattern. </li></ul></ul><ul><ul><li>c. Q waves indicate tissue necrosis and are permanent. </li></ul></ul>
  15. 20. Elevation of-Serum Enzymes and Isoenzymes <ul><li>1. Enzymes are drawn in a serial pattern, usually on ad- mission and every 6 to 24 hours until three samples are obtained; enzyme activity then is correlated to the ex- tent of heart muscle damage. </li></ul><ul><li>2. Enzymes commonly evaluated include creatinine kinase (CK), lactic dehydrogenase (LDH), and aspartate amino- transferase (AST). </li></ul>
  16. 21. <ul><li>3. CK and LDH can be broken down further into isoenzymes, which are more organ specific. </li></ul><ul><ul><li>a. CK-MB is specific to heart muscle and thus the most sensitive enzyme for determining heart muscle damage. </li></ul></ul><ul><ul><li>b. LDH enzymes are specific to heart muscle and they elevated </li></ul></ul>
  17. 22. Other Findings <ul><li>1. Elevated cardiac troponins </li></ul><ul><li>2. Elevated myoglobin </li></ul><ul><li>3. White blood cell count and sedimentation rate elevation due to inflammatory process associated with the damaged heart muscle. </li></ul><ul><li>4. Radionuclide imaging allows recognition of areas of decreased perfusion. </li></ul><ul><li>5. PET determines the presence of reversible heart muscle injury and irreversible or necrotic tissue. </li></ul><ul><li>6. Cardiac muscle dysfunction noted on echocardiograph </li></ul>
  18. 23. Management <ul><li>Therapy is aimed at the protection of ischemic and injury of heart tissue to preserve muscle function, reduce the infarction size, and prevent death. Innovative modalities provide early restoration of coronary blood flow, and the use pharmacologic agents improves oxygen supply and demand, reduces and/or prevents dysrhythmias, and inhibit the progression of coronary artery disease. </li></ul><ul><li>Oxygen Therapy </li></ul><ul><ul><li>Improves oxygenation to ischemic heart muscle. </li></ul></ul>
  19. 24. Management <ul><li>Pain Control </li></ul><ul><li>Endogenous catecholamine release during pain imposes increased workload on the heart muscle, thus causing increase in oxygen demand. </li></ul><ul><li>1. Opiate analgesic therapy </li></ul><ul><li>a. Morphine is used to relieve pain, to improve heart Hemodynamic by reducing preload and afterload and to provide anxiety relief. </li></ul>
  20. 25. <ul><li>b. Meperidine (Demerol) is useful for pain management in those patients allergic to morphine or sensitive( respiratory depression. </li></ul><ul><li>2. Vasodilator therapy </li></ul><ul><li>a. Nitroglycerin (sublingual, IV, paste) promotes venous (low-dose) and arterial (high-dose) relaxation as well as relaxation of coronary vessels and prevention of coronary spasm </li></ul>
  21. 26. <ul><li>b. Myocardial oxygen demand is reduced with subsequent pain relief. c. Persistent chest pain requires prompt action (IV nitroglycerin) </li></ul><ul><li>3. Anxiolytic therapy </li></ul><ul><ul><li>a. Benzodiazepines are used with analgesics when anxiety complicates chest pain and its relief. </li></ul></ul>
  22. 27. Pharmacologic Therapy <ul><li>1. Thrombolytic agents, such as tissue plasminogen activator (Activase), streptokinase (Streptase), and reteplase (Retavase), reestablish blood flow in coronary vessels by dissolving obstructing thrombus. </li></ul><ul><li>a. No effect on the underlying stenosis that precipitated the thrombus to form. </li></ul><ul><li>b. Administered IV or intracoronary. </li></ul><ul><li>2. Adjunctive therapy aimed to prevent platelet activation, aspirin. </li></ul>
  23. 28. <ul><li>3. Anticoagulation therapy is useful as an adjunct to thrombolytic therapy. Also used in situations of prolonged bed rest, pulmonary embolism, deep vein thrombosis, mural thrombi, cardiogenic shock, and patients with atrial fibrillation. </li></ul>
  24. 29. <ul><li>4. Beta-adrenergic blocking agents improve oxygen supply and demand, decrease sympathetic stimulation to the heart, promote blood flow in the small vessels of the heart, and have antidysrhythmic effects. </li></ul><ul><li>a. Appears to lower mortality and decrease chance of reinfarction and sudden death post-MI. </li></ul>
  25. 30. <ul><li>5. Antidysrhythmic therapy-lidocaine (Xylocaine) decreases ventricular irritability, which commonly occurs after MI. </li></ul><ul><li>6. Calcium channel blockers improve the balance between oxygen supply and demand by decreasing heart rate, blood pressure, and dilating coronary vessels. </li></ul><ul><li>a. Diltiazem has been shown to decrease the incidence of reinfarction in patients with non-Q-wave MIs and is currently the only calcium blocker proven to be beneficial. </li></ul>
  26. 31. Complications <ul><li>1. Rhythm disturbances </li></ul><ul><li>2. Cardiac failure </li></ul><ul><ul><li>a. Infarct expansion (thinning and dilation of the necrotic zone) </li></ul></ul><ul><ul><li>b. Infarct extension (additional heart muscle necrosis occurring after 24 hours of acute infarction) </li></ul></ul><ul><ul><li>c. CHF (with 20% to 35% left ventricle damage) </li></ul></ul><ul><ul><li>d. Cardiogenic shock . </li></ul></ul><ul><ul><li>f. Reinfarction </li></ul></ul><ul><ul><li>g. Ischemic cardiomyopathy – </li></ul></ul>
  27. 32. Complications <ul><li>3. Cardiac rupture </li></ul><ul><li>4. Ventricular mural thrombus </li></ul><ul><li>5. Thromboemboli </li></ul><ul><li>6. Ventricular aneurysm </li></ul><ul><li>7. Cardiac tamponade </li></ul><ul><li>8. Pericarditis (2 to 3 days after MI) </li></ul><ul><li>9. Psychiatric problems-depression, personality </li></ul><ul><li>changes </li></ul>
  28. 33. Nursing Assessment <ul><li>1. Gather information regarding the chest pain: </li></ul><ul><li>a. Nature and intensity-describe the pain in patient's own words and compare it with pain experienced in the past. </li></ul><ul><li>b. Onset and duration-exact time pain occurred, as well as the time pain relieved or diminished . </li></ul><ul><li>c. Location and radiation-point to the area where the pain is located and to other areas where the pain seems to travel. </li></ul><ul><li>d. Precipitating and aggravating factors-describe the activity performed just before the onset of pain . </li></ul>
  29. 34. <ul><li>2. Ask patient about other symptoms experienced associated with the pain. Observe patient for diaphoresis, facial pallor, dyspnea, guarding behaviors, rigid body posture, extreme weakness, confusion. </li></ul><ul><li>3. Evaluate cognitive, behavioral, and emotional status. </li></ul><ul><li>4. Ask patient regarding prior health status with emphasis on current medications, allergies (opiate analgesics, iodine, shellfish), recent trauma or surgery, aspirin ingestion, peptic ulcers, fainting, drug and alcohol use. </li></ul>
  30. 35. <ul><li>5. Analyze information for contraindications for thrombolytic therapy and/or PTCA. </li></ul><ul><li>6. Gather information on presence or absence of cardiac risk factors. </li></ul><ul><li>7. Identify patient's social support system and potential caregivers. </li></ul><ul><li>8. Identify significant other's reaction to the crisis situation. </li></ul>
  31. 36. Nursing Interventions <ul><li>Reducing Pain </li></ul><ul><li>1. Handle patient carefully while providing initial care, starting IV infusion, obtaining baseline vital signs, and attaching electrodes for continuous ECG monitoring. </li></ul><ul><li>2. Administer oxygen by nasal cannula if prescribed, and encourage patient to take deep breaths-may decrease incidence of dysrhythmias by allowing the heart to be less ischemic and less irritable; may reduce infarct size, decrease anxiety, and resolve chest pain. </li></ul>
  32. 37. Nursing Interventions <ul><li>3. Offer support and reassurance to patient that relief of pain is apriority. </li></ul><ul><li>4. Administer sublingual nitroglycerin as directed; recheck blood pressure (BP), heart rate (HR), and respiratory rate </li></ul>
  33. 38. Nursing Interventions <ul><li>5. Discuss with patient and family member the anticipate nursing and medical regimen. </li></ul><ul><li>a. Explain visiting hours and need to limit number of visitors at one time. </li></ul><ul><li>b. Offer family members preferred times to phone to check on patient's status. </li></ul>
  34. 39. <ul><li>6. Observe for autonomic signs of anxiety such as increases in heart rate, BP, respiratory rate. </li></ul><ul><li>7. Administer antianxiety agents as prescribed. </li></ul><ul><li>a. Explain to patient the reason for sedation: und anxiety can make the heart more irritable and require more oxygen. </li></ul><ul><li>b. Assure patient that the goal of sedation is to promote comfort and, therefore, should be requested anxious, excitable. </li></ul>
  35. 40. <ul><li>c. Observe for adverse effects of sedation such as lethargy, confusion, and/or increased agitation. </li></ul><ul><li>8. Maintain consistency of care with one or two nurse regularly assisting patient, especially if severe anxiety is present. </li></ul><ul><li>9. Offer back massage to promote relaxation, decrease muscle tension, and improve skin integrity. </li></ul><ul><li>10. Use techniques such as guided imagery to relieve tension and anxiety. </li></ul>
  36. 41. Nursing Interventions <ul><li>Maintaining Hemodynamic Stability </li></ul><ul><li>1. Monitor BP every 2 hours or as directed-hypertension increases afterload of the heart, elevating oxygen demand; hypotension causes reduced coronary an tissue perfusion. </li></ul><ul><li>2. Monitor respirations and lung fields every 2 to 4 hours or as prescribed. </li></ul><ul><li>a. Auscultate for normal and abnormal breath sound (crackles may indicate left ventricular failure; diffuse crackles indicate pulmonary edema). </li></ul>
  37. 42. Congestive Heart Failure
  38. 43. Basic Definition <ul><li>Heart failure is a medical term that describes an inability of the heart to keep up its work load of pumping blood to the lungs and to the rest of the body. </li></ul>
  39. 44. Statistic <ul><li>It is estimated that as many as two million Americans suffer from congestive heart failure and that up to 29, 000 die annually from this chronic disorder. </li></ul>
  40. 45. Symptoms (involving gravity/exhaustion of heart) <ul><li>Swelling of the ankles, legs, and hands </li></ul><ul><li>Orthopnea, or the shortness of breath when lying flat </li></ul><ul><li>Shortness of breath during exertion </li></ul>
  41. 46. Symptoms (involving circulation) <ul><li>Cyanosis, or a bluish color that is seen in the lips and fingernails from a lack of oxygen </li></ul><ul><li>Fatigue or weakness </li></ul><ul><li>Rapid or irregular heart beat </li></ul><ul><li>Changes of behavior such as restlessness, confusion, and decreased attention span </li></ul>
  42. 47. Symptoms (involving congestion) <ul><li>Unexplained or unintentional weight gain </li></ul><ul><li>Chronic cough </li></ul><ul><li>Increased urination </li></ul><ul><li>Distended neck veins </li></ul><ul><li>Loss of appetite or indigestion </li></ul>
  43. 48. Congestive heart failure is a syndrome that can be caused by multiple underlying diseases such as: <ul><li>Congenital heart disease </li></ul><ul><li>Atherosclerosis </li></ul><ul><li>Rheumatic fever </li></ul><ul><li>Cardiomyopathy </li></ul><ul><li>Valve disorders </li></ul><ul><li>Ventricular failure </li></ul><ul><li>Left or right-sided failure </li></ul><ul><li>Hypertension </li></ul><ul><li>Prolonged alcohol or drug addiction </li></ul><ul><li>Previous heart attack </li></ul><ul><li>Diabetes </li></ul><ul><li>Chronic rapid heartbeats </li></ul>
  44. 49. Cardiomyopathy <ul><li>Cardiomyopathy is the stretching and enlarging of the heart cavity that occurs making the heart weak so it does not pump correctly </li></ul>
  45. 50. Ventricular Failure <ul><li>Ventricular failure occurs when there are weak spots in the ventricular walls causing a bulge, or an aneurysm. </li></ul>
  46. 51. Atherosclerosis <ul><li>Atherosclerosis is the gradual clogging of the arteries by fatty, fibrous deposits. A tiny lump of fibrous tissue grows as the artery tries to repair the damage. Cholesterol accumulates and more tissue builds up. </li></ul><ul><li>The arteries are thickened and hardened making a loss of elasticity causing congestion. </li></ul>
  47. 52. Left-sided/Right-sided Failure <ul><li>Blood backs up causing congestion and thus swelling of extremities and internal organs </li></ul>
  48. 53. Other Contributors <ul><li>Hypertension </li></ul><ul><li>Prolonged Alcohol or Drug Addiction </li></ul><ul><li>Previous Heart Attack </li></ul><ul><li>Diabetes </li></ul><ul><li>Chronic Rapid Heart Beats </li></ul>
  49. 54. Treatment <ul><li>When a treatable underlying cause of </li></ul><ul><li>congestive heart failure exists, </li></ul><ul><li>correcting the cause may resolve, or at </li></ul><ul><li>least greatly improve, the degree of </li></ul><ul><li>heart failure </li></ul>
  50. 55. Valve Surgery <ul><li>If a defective heart valve is </li></ul><ul><li>responsible for heart failure, it may </li></ul><ul><li>be treated by heart valve surgery </li></ul>
  51. 56. Angioplasty <ul><li>Angioplasty, which is catheterization using a balloon to flatten fatty deposits, can be used to treat atherosclerosis or other conditions with blocked arteries. </li></ul><ul><li>An artery of an arm or leg is used to guide the catheter through to the blocked artery. </li></ul><ul><li>An uninflated balloon on the top of a smaller tube is threaded through the larger tube and centered in the plaque narrowed area. </li></ul><ul><li>The balloon inflates compressing the plaque against the walls and increasing the open area. </li></ul>
  52. 57. Drugs <ul><li>Digitalis-strengthen the heart ’ s contractions increasing blood flow </li></ul><ul><li>Diuretic-increase the output of salt and water in urine </li></ul><ul><li>Vasodilators-relax blood vessels which lowers the resistance to blood flow. More blood reaches the tissues and the heart works no harder than before. </li></ul>
  53. 58. In conclusion, congestive heart failure is often assumed to be a disease when in fact it is a syndrome caused by multiple disorders.
  54. 59. <ul><li>Cardiogenic Shock </li></ul>
  55. 60. <ul><li>Systemic hypoperfusion secondary to severe depression of cardiac output and sustained systolic arterial hypotension despite elevated filling pressures. </li></ul><ul><li>Cardiac output is inadequate to meet tissue demands </li></ul>
  56. 61. Etiologies <ul><li>Acute myocardial infarction/ischemia   </li></ul><ul><li>LV failure   </li></ul><ul><li>VSR   </li></ul><ul><li>Severe mitral regurgitation (MR) </li></ul><ul><li>Cardiac Tamponade   </li></ul>
  57. 62. Clinical Findings <ul><li>Physical Exam: elevated JVP, +S3, rales, oliguria, acute pulmonary edema </li></ul><ul><li>Hemodynamics: CO, SVR, SvO2 </li></ul><ul><li>Initial evaluation: hemodynamics (PA catheter), echocardiography, angiography </li></ul>
  58. 63. <90 mmHg <2.2 li/min.m2 >15 mmHg
  59. 64. Management <ul><li>Pressors </li></ul><ul><li>Intra-aortic Balloon Pump (IABP) </li></ul><ul><li>Fibrinolytics </li></ul><ul><li>Revascularization: CABG/PCI </li></ul><ul><li>Refractory shock: ventricular assist device, cardiac transplantation </li></ul>
  60. 65. Pressors <ul><li>Dopamine </li></ul><ul><ul><li><2 renal vascular dilation </li></ul></ul><ul><ul><li><2-10 +chronotropic/inotropic (beta effects) </li></ul></ul><ul><ul><li>>10 vasoconstriction (alpha effects) </li></ul></ul><ul><li>Dobutamine – positive inotrope, vasodilates, arrhythmogenic at higher doses </li></ul><ul><li>Norepinephrine (Levophed): vasoconstriction, inotropic stimulant. Should only be used for refractory hypotension with dec SVR. </li></ul><ul><li>Vasopression – vasoconstriction </li></ul><ul><li>VASO and LEVO should only be used as a last resort </li></ul>
  61. 66. IABP is a temporizing measure <ul><li>Augments coronary blood flow in diastole </li></ul><ul><li>Balloon collapse in systole creates a vacuum effect  decreases afterload </li></ul><ul><li>Decrease myocardial oxygen demand </li></ul>
  62. 67. <ul><li>THANK YOU </li></ul>

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