Abc 2011 2012 respiratory disorders


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Abc 2011 2012 respiratory disorders

  1. 1. Respiratory disorders<br />
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  3. 3. Difference of a child’s airway anatomy from an adult<br />The back of the head of a child is slightly larger, so positioning requires more care<br />The tongue is proportionately larger and more anterior in the mouth<br />The trachea is smaller in diameter and more flexible<br />The airway itself is lower and narrower <br />
  4. 4. Acute respiratory failure<br />
  5. 5. Acute respiratory Failure<br />A clinical condition in which the pulmonary system fails to maintain adequate gas exchange<br />Most common organ failure in the ICU<br />Mortality rate: 22% to 75%<br />Results from a deficiency in the performance of the pulmonary system<br />Usually occurs secondary to another disorder that has altered the normal function of the pulmonary system in such a way as to decrease the ventilatory drive, decrease muscle strength, decrease chest wall elasticity, decrease lung’s capacity for gas exchange, increase airway resistance, or increase metabolic O2 requirements<br />
  6. 6. Etiology - extrapulmonary<br />Brain – drug overdose, brain trauma or lesion, post-op anesthesia depression<br />Spinal cord – Guillain-Barre syndrome, poliomyelitis, spinal cord trauma or lesion<br />Neuromuscular system – Myasthenia gravis, Multiple sclerosis, neuromuscular-blocking agents, organophosphate poisoning<br />Thorax – massive obesity, chest trauma<br />Pleura – pleural effusion, pneumothorax<br />Upper airways – sleep apnea, tracheal obstruction, epiglottitis<br />
  7. 7. Etiology - intrapulmonary<br />Lower airways and alveoli – COPD, asthma, bronchiolitis,pneumonia<br />Pulmonary circulation – pulmomary emboli<br />Alveolar-capillary membrane – acute lung injury, inhalation of toxic gases, near-drowning<br />
  8. 8. Extrapulmonary and intrapulmonary disorders<br />Blood passes through alveoli that are underventilated<br />Blood reaches the arterial system without participating in gas exchange<br />Insufficient oxygen to meet metabolic demands<br />Alveolar hypoventilation<br />V/Q mismatch<br />Mixing of unoxygenated and oxygenated blood<br />Hypercapnia<br />Blood passes through a portion of a lung that is not ventilated<br />Intrapulmonary shunting<br />Acidosis <br />Hypoxemia <br />
  9. 9. Assessment and diagnosis<br />Clinical manifestations are related to the development of hypoxemia, hypercapnia, and acidosis<br />Clinical manifestations are so varied that they considered unreliable in predicting the degree of hypoxemia or hypercapnia or the severity<br />ABG: PaO2 less than 60 mm Hg and the PaCO2 is greater than 45 mm Hg<br />Bronchoscopy, chest X-ray, thoracic CT<br />
  10. 10. Nursing diagnosis priorities<br />Impaired gas exchange related to alveolar hypoventilation<br />Impaired gas exchange related to ventilation/perfusion mismatching or intrapulmonary shunting<br />Ineffective breathing pattern related to musculoskeletal fatigue or neuromuscular impairment<br />
  11. 11. Medical management<br />Aimed at treating the underlying cause, promoting adequate gas exchange, correcting acidosis, initiating nutrition support, and preventing complications<br />Medical interventions to promote gas exchange are aimed at improving oxygenation and ventilation<br />
  12. 12. 1. Oxygenation<br />Purpose is to correct hypoxemia – aim is to keep the arterial hemoglobin oxygen saturation greater than 90%<br />Goal is to keep the tissues’ needs satisfied but not produce hypercapnia or oxygen toxicity<br />Supplemental oxygenation administration is effective in treating hypoxemia related to alveolar hypoventilation and V/Q mismatching<br />Positive pressure is necessary when there is intrapulmonary shunting (to open collapsed alveoli) can be delivered via nasal or oronasal mask (to avoid intubation)<br />
  13. 13. 2. ventilation<br />Depending on the underlying cause and severity, the patient may be initially treated with noninvasive ventilation<br />Mechanical ventilation<br />PEEP – positive end expiratory pressure<br />
  14. 14. PEEP<br />Opens collapsed alveoli<br />Stabilizes flooded alveoli<br />Increases FRC<br />However,<br />Decreases cardiac output, decreasing venous return secondary to increased intrathoracic pressure<br />Barotrauma, as a result of gas escaping into the surrounding spaces secondary to alveolar rupture<br />
  15. 15. 3. pharmacology<br />Bronchodilators – Beta-agonists and antocholinergic agents<br />Steroids<br />Sedation can be used to comfort the patient and decrease the work of breathing, particularly if the patient is fighting the ventilator<br />Analgesics for pain control<br />Methylxanthines and mucolytics are no longer used because of their negative side effects<br />
  16. 16. 4. Acidosis - treatment<br />Once the patient is adequately oxygenated and ventilated, the acidosis should correct itself<br />Use of sodium bicarbonate has been shown to be of minimal benefit and is no longer recommended, even in the presence of severe acidosis<br />
  17. 17. 5. Nutrition support<br />Goals are to meet the overall nutritional needs of the patient, while avoiding overfeeding, to prevent nutrition delivery-related complications and to improve patient outcomes<br />The enteral route is the preferred method of nutrition administration<br />Parenteral nutrition for those who cannot tolerate enteral feedings or cannot receive enough nutrients enterally<br />
  18. 18. 6. Complications - treatment<br />Maintaining oxygenation, normalizing electrolytes, and monitoring drug levels will facilitate the prevention and treatment of encephalopathy and dysrhythmias<br />Venous thromboembolism can be prevented by using compression stockings and low-dose unfractionated heparin or low-molecular weight heparin<br />GIT bleeding can be prevented through the use of histamine-2 antagonists, cytoprotective agents, or gastric proton pump inhibitors<br />Patient is at risk of developing complications associated with artificial airway, mechanical ventilation, enteral and parenteral nutrition, and peripheral cannulation<br />
  19. 19. Guideline Values for estimating Fio2 with low flow o2 devices<br />
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  34. 34. Nursing management <br />Optimizing oxygenation and ventilation<br />Providing comfort and emotional support<br />Maintaining surveillance for complications <br />Providing patient education<br />
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  36. 36. 1. Optimizing oxygenation and ventilation<br />Positioning – the goal is to place the least affected area of the affected lung in the most dependent position <br />– gravity normally facilitates preferential ventilation and perfusion to the dependent areas of the lungs<br />- the best gas exchange would take place in the dependent areas of the lungs<br />
  37. 37. 1. Optimizing oxygenation and ventilation<br />Positioning<br />Patients with diffuse lung disease may benefit from being positioned with the right lung down, because it is larger and more vascular than the left lung<br />For those with alveolar hypoventilation, a nonrecumbent position (sitting or semierect) may be beneficial<br />Semirecumbency position can help prevent aspiration and inhibit the development of hospital-associated pneumonia<br />Frequent positioning (at least every 2 hours) is beneficial in optimizing the patient’s ventilatory pattern and V/Q matching<br />
  38. 38. 1. Optimizing oxygenation and ventilation<br />Preventing desaturation – performing procedures as needed: oxygenating before suctioning, providing adequate rest and recovery time between various procedures, and minimizing oxygen consumption <br />Promoting secretion clearance – providing adequate systemic hydration, humidifying supplemental oxygen, coughing, and suctioning<br />Note: postural drainage and chest percussion and vibration have been found to be of little benefit in the critically ill patient; to facilitate breathing, the thorax should be maintained in alignment and the head of the bed elevated 30 to 45 degrees<br />
  39. 39. 2. Patient education<br />Pathophysiology of the disease<br />Specific etiology<br />Precipitating factor modification<br />Importance of taking medications<br />Breathing techniques (e.g., pursed-lip breathing diaphragmatic breathing)<br />Energy conservation techniques<br />
  40. 40. 2. Patient education<br />Measures to prevent pulmonary infections (e.g., proper nutrition, hand washing, immunization against S. pneumoniae and influenza viruses)<br />Signs and symptoms of pulmonary infections (e.g., sputum color change, shortness of breath, fever)<br />Cough enhancement techniques<br />
  41. 41. Collaborative management<br />Identify and treat underlying cause<br />Administer oxygen therapy<br />Intubate patient<br />Administer medications<br />Position patient to optimize ventilation/perfusion matching<br />Suction as needed<br />
  42. 42. Collaborative management<br />Provide adequate rest and recovery time between various procedures<br />Correct acidosis<br />Initiate nutritional support<br />Maintain surveillance for complications: encephalopathy, dysrhythmias, venous thromboembolism, GI bleeding<br />Provide comfort and emotional support<br />
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  44. 44. Pneumonia<br />
  45. 45. pneumonia<br />An acute inflammation of the lung parenchyma that is caused by an infectious agent that can lead to alveolar consolidation<br />CAP – community acquired pneumonia<br />HAP – hospital acquired pneumonia<br />VAP – ventilator-associated pneumonia<br />
  46. 46. Precipitating conditions of pneumonia<br />
  47. 47. Precipitating conditions of pneumonia<br />
  48. 48. Microorganisms/noninfectious agents<br />Inhalation/aspiration<br />Lower airways<br />Loss of cough reflex, damage to cilia of the respiratory tract, impaired host defenses<br />Colonization of the lower respiratory tract<br />Lung tissue attempts to undergo healing<br />Hepatization<br />Release of histamine and other vasoactive chemical mediators <br />Stage of fibrosis<br />Lung tissue reacts to accumulating exudates and microorganisms<br />Vasodilation<br />Pulmonary function impaired<br />More and more exudates accumulate<br />Stage of congestion<br />Clinical manifestations <br />
  49. 49. Etiology<br />Severe CAP – S. pneumoniae, Legionella species, H. influenzae, S. aureus, M. pneumoniae, respiratory viruses, Chlamydia pneumoniae, and P. aerugionosa<br />HAP – S. aureus, S. pneumoniae, P. aeruginosa, Acinetobacterbaumannii, Klebsiella species, Proteus species, Serratia species, fungi, and respiratory viruses<br />
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  51. 51. Assessment and Diagnosis<br />Ineffective airway clearance related to excessive secretions or abnormal viscosity of mucus<br />Impaired gas exchange related to ventilatory/perfusion mismatching or intrapulmonary shunting<br />Risk for infection, risk factor: invasive monitoring devices<br />Powerlessness related to lack of control over current situation or disease progression<br />
  52. 52. Assessment and diagnosis<br />Chest radiograph<br />Sputum Gram stain and culture<br />Diagnostic bronchoscopy<br />CBC with differential count<br />Chemistry panel<br />Blood cultures<br />ABG<br />
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  59. 59. Medical management<br />Antibiotic therapy<br />Oxygen therapy<br />Fluid management<br />Nutritional support<br />Treatment of associated medical problems and complications<br />Therapeutic bronchoscopy may be necessary in patients who have difficulty mobilizing secretions<br />
  60. 60. Nursing management<br />Optimizing oxygenation and ventilation<br />Preventing the spread of infection<br />Providing comfort and emotional support<br />Maintaining surveillance for complications<br />
  61. 61. Collaborative management<br />Administer oxygen therapy<br />Initiate mechanical ventilation as required<br />Administer medications: antibiotics, bronchodilators<br />Position patient to optimize ventilation/perfusion matching<br />Suction as needed<br />Provide adequate rest and recovery time between various procedures<br />Maintain surveillance for complications: acute respiratory failure<br />Provide comfort and emotional support<br />
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  67. 67. Pulmonary embolism<br />
  68. 68. Pulmonary embolism (PE)<br />Occurs when a clot (thrombotic emboli) or other matter (nonthrombotic emboli) lodges in the pulmonary arterial system, disrupting the blood flow to a region of the lungs<br />Majority come form the deep leg veins, particularly the iliac, femoral, and popliteal veins<br />Other sources: RV, the upper extremities, and the pelvic veins<br />Nonthrombotic emboli: fat, tumors, amniotic fluid, air, and foreign bodies<br />
  69. 69. etiology<br />Three predisposing factors: hypercoagulability, injury to the vascular endothelium and venous stasis (Virchow’s triad)<br />Venous stasis: AF, decreased CO, immobility<br />Injury to the vascular endothelium: local vessel injury, infection, incision, atherosclerosis<br />Hypercoagulability: polycythemia<br />