4. etiology Precipitating conditions Previous PE CVS disease: HF, RV infarction, cardiomyopathy, corpulmonale Surgery: orthopedic, vascular, abdominal Cancer: ovarian, pancreatic, stomach, extrahepatic bile duct system Trauma (injury or burns): lower extremities, pelvis, hips Gynecologic status: pregnancy, postpartum, birth control pills, estrogen replacement therapy

5. Vascular endothelial injury, stasis, hypercoagulability Detaches and travels Embolus Thrombus formation Occlusion and blockage of a branch of the pulmonary artery Reaches the pulmonary arterial system An area of the lung is not being perfused but is being ventilated hypoxemia vasoconstrictors atelectasis Pulmonary hypertension Pulmonary dead space Compensatory shunting Inflammatory/chemical mediators are released No participation in gas exchange More bronchoconstriction Hypocarbia, hypoxia Increased airway resistance Increase work of breathing Localized bronchoconstriction

7. Assessment and diagnosis Impaired gas exchange related to V/Q mismatching or intrapulmonary shunting Acute pain related to transmission and perception of cutaneous, visceral, muscular, or ischemic impulses Powerlessness related to lack of control over current situation or disease progression Deficient knowledge: discharge regimen related to lack of previous exposure to information

8. Assessment and diagnosis Tachycardia, tachypnea Dyspnea, apprehension, increased pulmonic component of the second heart sound Fever, rales, pleuritic chest pain, cough, evidence of DVT, and hemoptysis Syncope and hemodynamic instability

9. Assessment and diagnosis ABG D-dimer – a fibrin degradation product that is a small protein present in the blood after the clot has undergone fibrinolysis ECG Chest radiography Echocardiography CT scan V/Q scintigraphy Pulmonary angiogram

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.

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

22. Heparin has no effect on existing clot

23. Heparin should be adjusted to maintian the aPTT in a range of 1.5 to 2.3 times the control

24. Warfarin should be started at the same time, and when the INR reaches 3.0, the heparin should be discontinued

26. The procedure involves placement of a percutaeneous venous filter (e.g., Greenfield filter) into the vena cava, usually below the renal arteries

30. Either recombinant tissue-type plasminogen activator (rt-PA) or streptokinase may be used

33. Fluids should be administered to increase RV preload, which would stretch the RV and increase contractility, thus overcoming the elevated pulmonary arterial pressures

35. Collaborative management Administer oxygen therapy Intubate patient Initiate mechanical ventilation Administer medications: thrombolytics, anticoagulants, bronchodilators, inotropic agents, sedatives, analgesics Administer fluids Position patient to optimize V/Q matching Maintain surveillance for complications: bleeding and acute lung injury Provide comfort and emotional support

36. Patient education Pathophysiology of the disease Specific etiology Precipitating factor modification Measures to prevent DVT Signs and symptoms of DVT Importance of taking medications Signs and symptoms of anticoagulant complications Measures to prevent bleeding

37. Status asthmaticus

38. Status asthmaticus Asthma – a COPD that is characterized by partially reversible airflow obstruction, airway inflammation, and hyperresponsiveness to a variety of stimuli Status asthmaticus – a severe asthma attack that fails to respond to conventional therapy with bronchodilators, which may result in acute respiratory failure

39. etiology URTI Allergen exposure Decreased in antiinflammatory medications Overreliance on bronchodilators Environmental pollutants Lack of access to health care Failure to identify worsening airflow obstruction Non-compliance with the health care regimen

40. First exposure to allergens (pollen, dust) Absorbed into the tissues Immune cells are triggerred IgE antibodies are produced IgE attach to mast cells, which gather in the lungs

41. Second exposure to the same allergen Allergens attach to IgE antibodies Mast cells degranulate Increase capillary permeability Inflammatory mediators (histamine) are released Bronchial smooth muscles contract Edema and inflammation of the bronchial walls Increase mucus secretion Bronchospasm Wheezing and dyspnea Obstruction

44. Assessment and diagnosis Impaired gas exchange related to alveolar hypoventilation Ineffective breathing pattern related to musculoskeletal fatigue or neuromuscular impairment Ineffective airway clearance related to excessive secretions or abnormal viscosity of mucus Anxiety related to threat of biologic, psychologic, and/or social integrity Deficient knowledge: discharge regimen related to lack of previous exposure to information

45. Assessment and diagnosis Cough, wheezing and dyspnea As the attack continues, the patient develops tachypnea, tachycardia, diaphoresis, increased accessory muscle use, and pulsusparadoxus greater than 25 mm Hg Decreased LOC, increasing inability to speak, significantly diminished or absent breath sounds, and inability to lie supine herald the onset of acute respiratory failure

46. Assessment and diagnosis ABG indicate hypocapnia and respiratory alkalosis caused by hyperventilation Hypoxemia and hypercapnia develops as the patient starts to fatigue Lactic acidosis may also occur Deterioration of PFT despite aggressive bronchodilator therapy is diagnostic of status asthmaticus

47. Assessment and diagnosis 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

48. Medical management Bronchodilators – Beta2-agonists and anticholinergics Systemic corticosteroids Oxygen therapy Intubation and mechanical ventilation

49. Bronchodilators – B2-agonists Can be administered by nebulizer or metered-dose inhaler (MDI) Usually a larger and more frequent doses are given, and the drug is titrated to the patient’s response Xanthines are not recommended Studies are being focused on the bronchodilating abilities of magnesium Magnesium is still inferior to B2-agonists, but may be beneficial to patients who are refractory to conventional therapy A bolus of 1 to 4g of IV Mg given over 10 to 40 minutes has been reported to produce desirable effects

50. anticholinergics Not very effective by themselves Used in conjunction with Beta-agonists (synergistic effect) Studies are evaluating the effects of leukotriene inhibitors (zafirlukast, montelukast, and zileuton) in the treatment of status asthmaticus Studies have shown that leukotriene inhibitors may be beneficial in those patients who are refractory to B2-agonists

51. Systemic corticosteroids IV or oral Limit iflammation, decrease mucus production, and potentiate B2-agonists Usually takes 6 to 8 hours for the effects to become evident

52. Oxygen therapy Supplemental oxygen for initial treatment of hypoxemia High-flow oxygen therapy to keep the patient’s SpO2 greater than 92%

53. Intubation and mechanical ventilation Indications for mechanical ventilation: Cardiac or respiratory arrest Disorientation Failure to respond to bronchodilator therapy Exhaustion Avoid high inflation pressures because they can result in barotrauma PEEP monitoring is important because the patient is prone to air trapping Patient-ventilator asynchrony also can occur and can be a major problem Sedation and neuromuscular paralysis may be necessary to allow for adequate ventilation

57. Nursing management Optimizing oxygenation and ventilation Providing comfort and emotional support Maintaining surveillance for complications

58. Patient education Pathophysiology of the disease Specific etiology Early warning signs of worsening airflow obstruction treatment of attacks Importance of taking prescribed medications and avoidance of OTC asthma medications Correct use of an inhaler (with and without spacer)

62. Patient education Correct use of peak flow meter Removal or avoidance of environmental triggers Measures to prevent pulmonary infections Signs and symptoms of pulmonary infections Importance of participating in pulmonary rehabilitation program

63. Acute respiratory distress syndrome

65. Also known as shock or stiff, white or Da Nang lung

66. Difficult to diagnose and can be fatal within 48 hours

68. H5N1 and A(H1N1) H – hemagglutinin N - enzyme on the surface of influenza viruses that enables the virus to be released from the host cell. Drugs that inhibit neuraminidase are used to treat influenza.

69. Phase 1 – injury reduces normal blood flow to the lungs Platelets aggregate Release of histamine, serotonin and bradykinin Interstitial osmotic pressure increases Phase 2 – inflammation of alveolocapillary membrane Phase 3 - Leakage of protein and more fluids Fluid shifts from intravascular space into the interstitial space Capillary membrane permeability is increased

70. Pulmonary edema Interstitial osmotic pressure increases Phase 4 - decrease blood flow to the lungs Decreasing lung compliance Increase fluid in the alveoli Impeding gas exchange Surfactant is damaged Alveoli collapse Impairs type 2 pneumocytes to produce more surfactant

71. Decreasing lung compliance Phase 5 – oxygen cannot cross the alveolocapillary membrane but carbon dioxide can Phase 6 – pulmonary edema worsens Carbon dioxide is lost through exhalation Fibrosis Oxygen and carbon dioxide levels decrease in the blood

72. Causes of ARDS Shock Sepsis Trauma Trauma-related factors: fat emboli, pulmonary contusions, and multiple transfusions may increase the likelihood that microemboli will develop

73. Assessment and diagnosis Impaired gas exchange related to V/Q mismatching or intrapulmonary shunting Decreased cardiac output related to alterations in preload Imbalanced nutrition: less than body requirements related to lack of exogenous nutrients or increased metabolic demand Anxiety related to threat to biologic, psychologic, and/or social integrity Compromised family coping related to critically ill family member

74. Assessment and diagnosis Tachypnea, restlessness, apprehension, and moderate increase in accessory muscle use – exudativepahse Agitation, dyspnea, fatigue, excessive accessory muscle use, and fine crackles as respiratory failure – fibrinolytic phase ABG Low PaO2 despite increases in supplemental O2 (refractory hypoxemia) Low PaCO2 initially, but eventually increases as the patient fatigues The pH is high initially but decreases as respiratory acidosis develops

75. Assessment and diagnosis Chest x-ray Initially, it is normal After 48 hours: diffuse patchy interstitial and alveolar infiltrates appear Progression to multifocal consolidation of the lungs, which as a “white out” on the chest x-ray film

78. Management A – antibiotics R – respiratory support D – diuretics S – situate in the prone position

79. Medical management Ventilation Low tidal volume Permissive hypercapnia Pressure control ventilation Inverse ratio ventilation Oxygen therapy PEEP Tissue perfusion

80. Nursing management Optimizing oxygenation and ventilation Providing comfort and emotional support Maintaining surveillance for complications