Abc 2011 2012 respiratory disorders part 2


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Abc 2011 2012 respiratory disorders part 2

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  4. 4. etiology<br />Precipitating conditions<br />Previous PE<br />CVS disease: HF, RV infarction, cardiomyopathy, corpulmonale<br />Surgery: orthopedic, vascular, abdominal<br />Cancer: ovarian, pancreatic, stomach, extrahepatic bile duct system<br />Trauma (injury or burns): lower extremities, pelvis, hips<br />Gynecologic status: pregnancy, postpartum, birth control pills, estrogen replacement therapy<br />
  5. 5. Vascular endothelial injury, stasis, hypercoagulability<br />Detaches and travels<br />Embolus <br />Thrombus formation<br />Occlusion and blockage of a branch of the pulmonary artery<br />Reaches the pulmonary arterial system<br />An area of the lung is not being perfused but is being ventilated<br />hypoxemia<br />vasoconstrictors<br />atelectasis<br />Pulmonary hypertension<br />Pulmonary dead space<br />Compensatory shunting<br />Inflammatory/chemical mediators are released<br />No participation in gas exchange<br />More bronchoconstriction<br />Hypocarbia, hypoxia<br />Increased airway resistance<br />Increase work of breathing<br />Localized bronchoconstriction<br />
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  7. 7. Assessment and diagnosis<br />Impaired gas exchange related to V/Q mismatching or intrapulmonary shunting<br />Acute pain related to transmission and perception of cutaneous, visceral, muscular, or ischemic impulses<br />Powerlessness related to lack of control over current situation or disease progression<br />Deficient knowledge: discharge regimen related to lack of previous exposure to information<br />
  8. 8. Assessment and diagnosis<br />Tachycardia, tachypnea<br />Dyspnea, apprehension, increased pulmonic component of the second heart sound<br />Fever, rales, pleuritic chest pain, cough, evidence of DVT, and hemoptysis<br />Syncope and hemodynamic instability<br />
  9. 9. Assessment and diagnosis<br />ABG<br />D-dimer – a fibrin degradation product that is a small protein present in the blood after the clot has undergone fibrinolysis<br />ECG<br />Chest radiography<br />Echocardiography<br />CT scan<br />V/Q scintigraphy<br />Pulmonary angiogram<br />
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  18. 18. Ventilation scintigraphy is a diagnostic procedure that portrays the regional and global distribution of an inhaled radioactive gas or radioaerosol within the lungs’ broncho-alveolar space.   Perfusion scintigraphy is a diagnostic procedure that portrays the regional and global distribution of pulmonary artery blood flow.    In combination V/Q is a useful procedure for the diagnosis of focal vascular, ventilatory or parenchymal pulmonary lesions.<br />
  19. 19. • The most common indication: to determine the likelihood of pulmonary embolism• Less common indications: -evaluation of lungs transplantation -pre-operative lungs evaluation -evaluation of right-to-left shunt -tracheobronchialmucociliary escalator function and clearance -evaluation of alveolar function and clearance in patients with endothelial injury such as in AIDS, sarcoidosis, pneumonitis, alveolitis, ARDS<br />
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  21. 21. Medical management<br />Prevention of recurrence <br /><ul><li>Administration of unfractionated or low-molecular-weight heparin and warfarin (Coumadin)
  22. 22. Heparin has no effect on existing clot
  23. 23. Heparin should be adjusted to maintian the aPTT in a range of 1.5 to 2.3 times the control
  24. 24. Warfarin should be started at the same time, and when the INR reaches 3.0, the heparin should be discontinued
  25. 25. The patient should remain on warfarin for 3 to 12 months depending on the patient’s risk for thromboembolic disease</li></li></ul><li>Medical management<br />Prevention of recurrence <br /><ul><li>Interruption of the IVC is reserved for patients in whom anticoagulation is contraindicated
  26. 26. The procedure involves placement of a percutaeneous venous filter (e.g., Greenfield filter) into the vena cava, usually below the renal arteries
  27. 27. The filter prevents further thrombotic emboli form migrating into the lungs</li></li></ul><li>
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  29. 29. Medical management<br />Clot dissolution<br /><ul><li>Thrombolytic agents had limited success, and is reserved for the patient with a massive PE and concomitant hemodynamic instability
  30. 30. Either recombinant tissue-type plasminogen activator (rt-PA) or streptokinase may be used
  31. 31. Therapeutic window for thrombolytic therapy is 14 days</li></li></ul><li>Medical management<br />Clot dissolution<br /><ul><li>Pulmonary embolectomy, often considered as a last resort, may be performed to surgically remove the clot
  32. 32. Generally it is performed as an open procedure while the pattern is on cardiopulmonary bypass</li></li></ul><li>Medical management<br />Reversal of pulmonary hypertension<br /><ul><li>Administration of inotropic agents and fluid
  33. 33. Fluids should be administered to increase RV preload, which would stretch the RV and increase contractility, thus overcoming the elevated pulmonary arterial pressures
  34. 34. Inotropic agents also cane be sued to increase contractility to facilitate an increase in CO</li></li></ul><li>Nursing management<br />Optimizing oxygenation<br />Monitoring bleeding<br />Patient education<br />
  35. 35. Collaborative management<br />Administer oxygen therapy<br />Intubate patient<br />Initiate mechanical ventilation<br />Administer medications: thrombolytics, anticoagulants, bronchodilators, inotropic agents, sedatives, analgesics<br />Administer fluids<br />Position patient to optimize V/Q matching<br />Maintain surveillance for complications: bleeding and acute lung injury<br />Provide comfort and emotional support<br />
  36. 36. Patient education<br />Pathophysiology of the disease<br />Specific etiology<br />Precipitating factor modification<br />Measures to prevent DVT<br />Signs and symptoms of DVT<br />Importance of taking medications<br />Signs and symptoms of anticoagulant complications<br />Measures to prevent bleeding<br />
  37. 37. Status asthmaticus<br />
  38. 38. Status asthmaticus<br />Asthma – a COPD that is characterized by partially reversible airflow obstruction, airway inflammation, and hyperresponsiveness to a variety of stimuli<br />Status asthmaticus – a severe asthma attack that fails to respond to conventional therapy with bronchodilators, which may result in acute respiratory failure<br />
  39. 39. etiology<br />URTI<br />Allergen exposure<br />Decreased in antiinflammatory medications<br />Overreliance on bronchodilators<br />Environmental pollutants<br />Lack of access to health care<br />Failure to identify worsening airflow obstruction<br />Non-compliance with the health care regimen<br />
  40. 40. First exposure to allergens (pollen, dust)<br />Absorbed into the tissues <br />Immune cells are triggerred<br />IgE antibodies are produced<br />IgE attach to mast cells, which gather in the lungs<br />
  41. 41. Second exposure to the same allergen<br />Allergens attach to IgE antibodies<br />Mast cells degranulate<br />Increase capillary permeability<br />Inflammatory mediators (histamine) are released<br />Bronchial smooth muscles contract<br />Edema and inflammation of the bronchial walls<br />Increase mucus secretion<br />Bronchospasm <br />Wheezing and dyspnea<br />Obstruction<br />
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  44. 44. Assessment and diagnosis<br />Impaired gas exchange related to alveolar hypoventilation<br />Ineffective breathing pattern related to musculoskeletal fatigue or neuromuscular impairment<br />Ineffective airway clearance related to excessive secretions or abnormal viscosity of mucus<br />Anxiety related to threat of biologic, psychologic, and/or social integrity<br />Deficient knowledge: discharge regimen related to lack of previous exposure to information<br />
  45. 45. Assessment and diagnosis<br />Cough, wheezing and dyspnea<br />As the attack continues, the patient develops tachypnea, tachycardia, diaphoresis, increased accessory muscle use, and pulsusparadoxus greater than 25 mm Hg<br />Decreased LOC, increasing inability to speak, significantly diminished or absent breath sounds, and inability to lie supine herald the onset of acute respiratory failure<br />
  46. 46. Assessment and diagnosis<br />ABG indicate hypocapnia and respiratory alkalosis caused by hyperventilation<br />Hypoxemia and hypercapnia develops as the patient starts to fatigue<br />Lactic acidosis may also occur<br />Deterioration of PFT despite aggressive bronchodilator therapy is diagnostic of status asthmaticus<br />
  47. 47. Assessment and diagnosis<br />A PEFR less than 40% of predicted or an FEV1 (maximum volume of gas that the patient can exhale in 1 second) less than 20% of predicted indicates severe airflow obstruction, and the need for intubation with mechanical ventilation may be imminent<br />
  48. 48. Medical management<br />Bronchodilators – Beta2-agonists and anticholinergics<br />Systemic corticosteroids<br />Oxygen therapy<br />Intubation and mechanical ventilation<br />
  49. 49. Bronchodilators – B2-agonists<br />Can be administered by nebulizer or metered-dose inhaler (MDI)<br />Usually a larger and more frequent doses are given, and the drug is titrated to the patient’s response<br />Xanthines are not recommended<br />Studies are being focused on the bronchodilating abilities of magnesium<br />Magnesium is still inferior to B2-agonists, but may be beneficial to patients who are refractory to conventional therapy<br />A bolus of 1 to 4g of IV Mg given over 10 to 40 minutes has been reported to produce desirable effects<br />
  50. 50. anticholinergics<br />Not very effective by themselves<br />Used in conjunction with Beta-agonists (synergistic effect)<br />Studies are evaluating the effects of leukotriene inhibitors (zafirlukast, montelukast, and zileuton) in the treatment of status asthmaticus<br />Studies have shown that leukotriene inhibitors may be beneficial in those patients who are refractory to B2-agonists<br />
  51. 51. Systemic corticosteroids<br />IV or oral<br />Limit iflammation, decrease mucus production, and potentiate B2-agonists<br />Usually takes 6 to 8 hours for the effects to become evident<br />
  52. 52. Oxygen therapy<br />Supplemental oxygen for initial treatment of hypoxemia<br />High-flow oxygen therapy to keep the patient’s SpO2 greater than 92%<br />
  53. 53. Intubation and mechanical ventilation<br />Indications for mechanical ventilation:<br />Cardiac or respiratory arrest<br />Disorientation<br />Failure to respond to bronchodilator therapy<br />Exhaustion<br />Avoid high inflation pressures because they can result in barotrauma<br />PEEP monitoring is important because the patient is prone to air trapping<br />Patient-ventilator asynchrony also can occur and can be a major problem<br />Sedation and neuromuscular paralysis may be necessary to allow for adequate ventilation <br />
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  57. 57. Nursing management<br />Optimizing oxygenation and ventilation<br />Providing comfort and emotional support<br />Maintaining surveillance for complications<br />
  58. 58. Patient education<br />Pathophysiology of the disease<br />Specific etiology<br />Early warning signs of worsening airflow obstruction<br /> treatment of attacks<br />Importance of taking prescribed medications and avoidance of OTC asthma medications<br />Correct use of an inhaler (with and without spacer)<br />
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  62. 62. Patient education<br />Correct use of peak flow meter<br />Removal or avoidance of environmental triggers<br />Measures to prevent pulmonary infections<br />Signs and symptoms of pulmonary infections<br />Importance of participating in pulmonary rehabilitation program<br />
  63. 63. Acute respiratory distress syndrome<br />
  64. 64. ards<br /><ul><li>A form of pulmonary edema that can quickly lead to acute respiratory failure
  65. 65. Also known as shock or stiff, white or Da Nang lung
  66. 66. Difficult to diagnose and can be fatal within 48 hours
  67. 67. Severe form of Acute Lung Injury</li></li></ul><li>Phase 1<br />Phase 2<br />Phase 3<br />Phase 4<br />Phase 5<br />Phase 6<br />
  68. 68. H5N1 and A(H1N1)<br />H – hemagglutinin<br />N - enzyme on the surface of influenza viruses that enables the virus to be released from the host cell. <br />Drugs that inhibit neuraminidase are used to treat influenza. <br />
  69. 69. Phase 1 – injury reduces normal blood flow to the lungs<br />Platelets aggregate<br />Release of histamine, serotonin and bradykinin<br />Interstitial osmotic pressure increases<br />Phase 2 – inflammation of alveolocapillary membrane<br />Phase 3 - Leakage of protein and more fluids<br />Fluid shifts from intravascular space into the interstitial space<br />Capillary membrane permeability is increased<br />
  70. 70. Pulmonary edema<br />Interstitial osmotic pressure increases<br />Phase 4 - decrease blood flow to the lungs<br />Decreasing lung compliance<br />Increase fluid in the alveoli<br />Impeding gas exchange<br />Surfactant is damaged<br />Alveoli collapse<br />Impairs type 2 pneumocytes to produce more surfactant<br />
  71. 71. Decreasing lung compliance<br />Phase 5 – oxygen cannot cross the alveolocapillary membrane but carbon dioxide can<br />Phase 6 – pulmonary edema worsens<br />Carbon dioxide is lost through exhalation<br />Fibrosis <br />Oxygen and carbon dioxide levels decrease in the blood<br />
  72. 72. Causes of ARDS<br />Shock<br />Sepsis<br />Trauma<br />Trauma-related factors: fat emboli, pulmonary contusions, and multiple transfusions may increase the likelihood that microemboli will develop<br />
  73. 73. Assessment and diagnosis<br />Impaired gas exchange related to V/Q mismatching or intrapulmonary shunting<br />Decreased cardiac output related to alterations in preload<br />Imbalanced nutrition: less than body requirements related to lack of exogenous nutrients or increased metabolic demand<br />Anxiety related to threat to biologic, psychologic, and/or social integrity<br />Compromised family coping related to critically ill family member<br />
  74. 74. Assessment and diagnosis<br />Tachypnea, restlessness, apprehension, and moderate increase in accessory muscle use – exudativepahse<br />Agitation, dyspnea, fatigue, excessive accessory muscle use, and fine crackles as respiratory failure – fibrinolytic phase<br />ABG<br />Low PaO2 despite increases in supplemental O2 (refractory hypoxemia)<br />Low PaCO2 initially, but eventually increases as the patient fatigues<br />The pH is high initially but decreases as respiratory acidosis develops<br />
  75. 75. Assessment and diagnosis<br />Chest x-ray<br />Initially, it is normal<br />After 48 hours: diffuse patchy interstitial and alveolar infiltrates appear<br />Progression to multifocal consolidation of the lungs, which as a “white out” on the chest x-ray film<br />
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  78. 78. Management<br />A – antibiotics<br />R – respiratory support<br />D – diuretics<br />S – situate in the prone position<br />
  79. 79. Medical management<br />Ventilation <br />Low tidal volume<br />Permissive hypercapnia<br />Pressure control ventilation<br />Inverse ratio ventilation<br />Oxygen therapy<br />PEEP<br />Tissue perfusion<br />
  80. 80. Nursing management<br />Optimizing oxygenation and ventilation<br />Providing comfort and emotional support<br />Maintaining surveillance for complications<br />