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