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MODULE 5 Respiratory W. P a w l i u k M P H MSNEd RN CEN OXYGEN DELIVERY DEVICES REVIEW Nasal Cannula 1-6 LPM 24-44% FiO2 Simple face mask 5 > 8 Lpm 40-60% FiO2 Venturi mask 4-12 Lpm 24-60% FiO2 Parital nonrebreather mask 6-10 Lpm 40-70% FiO2 Non-rebreather mask > 10 Lpm 60-80% FiO2 Mechanical ventilation FiO2 variable up to 100% OXYGEN ADMINISTRATION Oxygen to treat or prevent hypoxemia Humidification Flow rates > 4 L/min Mechanical ventilation Delivery devices Low flow: nasal cannula High flow: nasal cannula Simple face mask Reservoir systems Venturi or air-entrainment mask Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 3 OXYGEN DELIVERY DEVICES Fraction of delivered oxygen (FiO 2 ) Room air 21% or 0.21 FiO 2 Nasal cannula = 0.24-0.44 FiO 2 High flow cannula = 0.60 -0.90 FiO 2 Simple face mask = 0.30 -0.60 FiO 2 Face masks w/ reservoirs Partial rebreather = 0.35-0.60 FiO 2 Nonrebreather = 0.60-0.80 FiO 2 Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 4 OXYGEN DELIVERY DEVICES (CONTINUED) Air-entrainment mask = varied depending on size of jet orifice Manual resuscitation bags 15 L/min to deliver 1.00 FiO 2 Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. Figure 9-13. Air-entrainment (Venturi) mask with various jet orifices. Each orifice provides a specific delivered FiO2. (Modified from Kacmarek RM, Dimas S, Mack CW. The Essentials of Respiratory Care. 4th ed. St. Louis: Mosby; 2005.) 5 OXYGEN DELIVERY DEVICES (CONTINUED) Figure 9-12. Partial rebreathing and non-rebreathing oxygen masks. (From Kacmarek RM, Dimas S, Mack CW. The Essentials of Respiratory Care. 4th ed. St. Louis: Mosby; 2005.) Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 6 OXYGEN DELIVERY DEVICES (CONTINUED) Figure 9-14. Devices used to apply high-flow, high-humidity oxygen therapy. A, Aerosol mask. B, Face tent. C, Tracheostomy collar. D, Briggs T-piece. (From Kacmarek RM, Dimas S, Mack CW. The Essentials of Respiratory Care. 4th ed. St. Louis: Mosby; 2005.) Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 7 AIRWAY MANAGEMENT Positioning Devices Oral airway Nasopharyngeal airway Endotracheal intubation Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 8 ENDOTRACHEAL INTUBATION Insertion of an endotracheal tube (ETT) through the mouth or nose Orotracheal route preferred to reduce infections Used to: Maintain an airway Remove secretions Prevent aspiration Provide mechanical ventilation Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 9 ENDOTRACHEAL TUBE Figure 9-17. A, Endotracheal tube. B, Hi-Lo Evac endotracheal tube. Note suction port above the cuff for removal of pooled secretions. (From Shilling A, Durbin CG. Airway management. In: Cairo JM, ed. Mosby’s Respiratory Care Equipment. 8th ed. St. Louis: Mosby; 2010.) Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 10 INTUBATION EQUIPMENT Figure 9-18. Equipment used for endotracheal intubation: A, stylet (disposable); B, endotracheal tube with 10-mL syringe for cuff inflation; C, laryngoscope handle with attached curved blade (left) and straight blade (right); D, water-soluble lubricant; E, colorimetric CO2 detector to check tube placement; F, tape or G, commercial device to secure tube; H, Yankauer disposable pharyngeal suction device; I, Magill forceps (optional). Additional equipment, not shown, includes suction source and stethoscope. 11 Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. ENDOTRACHEAL INTUBATION Right size tube 7.5 to 8.0 mm female; 8.0 to 9.0 mm male Check balloon on tube for leak Stylet Lubricate tube Laryngoscope and blade Sniffing position Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. Premedicate prn Topical anesthetic/ paralytic medication Ventilate patient Suction oropharynx Intubate within 30 sec Inflate balloon Verify placement 12 VERIFY PLACEMENT Auscultate epigastric area Auscultate bilateral breath sounds ETCO 2 detector Esophageal detector device Chest x-ray—3 to 4 cm above carina Secure tube when placement is verified Record cm at the lip line for reference Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 13 STRATEGIES FOR SECURING ETT Figure 9-20. Two methods for securing the endotracheal tube: tape (A) and harness device (B). Harness device shown is the SecureEasy Endotracheal Tube Holder. Nonelastic headgear reduces the risk of self-extubation. A soft bite block prevents tube occlusion. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 14 PNEUMOTHORAX Types of pneumothorax Closed pneumothorax Open pneumothorax Spontaneous pneumothorax Tension pneumothorax Hemothorax PNEUMOTHORAX Fig. 28-4 Fig. 28-5 PNEUMOTHORAX (CONT'D) Clinical manifestations Collaborative care CONDITIONS CAUSED BY PULMONARY DISEASE OR INJURY Chest wall restriction Compromised chest wall Deformation, immobilization, and/or obesity Flail chest Instability of a portion of the chest wall FLAIL CHEST ACUTE RESPIRATORY FAILURE Results from inadequate gas exchange Insufficient O 2 transferred to the blood Hypoxemia Inadequate CO 2 removal Hypercapnia GAS EXCHANGE UNIT ACUTE RESPIRATORY FAILURE Not a disease but a condition Result of one or more diseases involving the lungs or other body systems ACUTE RESPIRATORY FAILURE (CONT’D) Classification Hypoxemic respiratory failure Hypercapnic respiratory failure CLASSIFICATION OF RESPIRATORY FAILURE ACUTE RESPIRATORY FAILURE Hypoxemic respiratory failure PaO 2 <60 mm Hg on inspired O 2 concentration >60% ACUTE RESPIRATORY FAILURE (CONT’D) Hypercapnic respiratory failure PaCO 2 above normal ( >45 mm Hg) Acidemia (pH <7.35) HYPOXEMIC RESPIRATORY FAILURE ETIOLOGY AND PATHOPHYSIOLOGY Causes Ventilation-perfusion (V/Q) mismatch COPD Pneumonia Asthma Atelectasis Pulmonary embolus RANGE OF V/Q RELATIONSHIPS HYPOXEMIC RESPIRATORY FAILURE ETIOLOGY AND PATHOPHYSIOLOGY (CONT’D) Causes Shunt Anatomic shunt Intrapulmonary shunt HYPOXEMIC RESPIRATORY FAILURE ETIOLOGY AND PATHOPHYSIOLOGY (CONT’D) Causes Diffusion limitation Severe emphysema Recurrent pulmonary emboli Pulmonary fibrosis Hypoxemia present during exercise DIFFUSION LIMITATION HYPOXEMIC RESPIRATORY FAILURE ETIOLOGY AND PATHOPHYSIOLOGY Causes Alveolar hypoventilation Restrictive lung disease CNS disease Chest wall dysfunction Neuromuscular disease HYPERCAPNIC RESPIRATORY FAILURE ETIOLOGY AND PATHOPHYSIOLOGY (CONT’D) Airways and alveoli Asthma Emphysema Chronic bronchitis Cystic fibrosis HYPERCAPNIC RESPIRATORY FAILURE ETIOLOGY AND PATHOPHYSIOLOGY (CONT’D) Central nervous system Drug overdose Brainstem infarction Spinal cord injuries HYPERCAPNIC RESPIRATORY FAILURE ETIOLOGY AND PATHOPHYSIOLOGY (CONT’D) Chest wall Flail chest Fractures Mechanical restriction Muscle spasm HYPERCAPNIC RESPIRATORY FAILURE ETIOLOGY AND PATHOPHYSIOLOGY (CONT’D) Neuromuscular conditions Muscular dystrophy Multiple sclerosis RESPIRATORY FAILURE TISSUE ORGAN NEEDS Major threat is the inability of the lungs to meet the oxygen demands of the tissues RESPIRATORY FAILURE CLINICAL MANIFESTATIONS Sudden or gradual onset A sudden decrease in PaO2 or rapid increase in PaCO2 indicates a serious condition RESPIRATORY FAILURE CLINICAL MANIFESTATIONS (CONT’D) When compensatory mechanisms fail, respiratory failure occurs Signs may be specific or nonspecific RESPIRATORY FAILURE CLINICAL MANIFESTATIONS (CONT’D) Severe morning headache Cyanosis Late sign Tachycardia and mild hypertension Early signs RESPIRATORY FAILURE CLINICAL MANIFESTATIONS (CONT’D) Consequences of hypoxemia and hypoxia Metabolic acidosis and cell death Decreased cardiac output Impaired renal function RESPIRATORY FAILURE CLINICAL MANIFESTATIONS (CONT’D) Specific clinical manifestations Rapid, shallow breathing pattern Dyspnea RESPIRATORY FAILURE CLINICAL MANIFESTATIONS (CONT’D) Specific clinical manifestations Pursed-lip breathing Retractions RESPIRATORY FAILURE DIAGNOSTIC STUDIES History and physical assessment ABG analysis Chest x-ray CBC, sputum/blood cultures, electrolyte ECG V/Q lung scan Pulmonary artery catheter (severe cases) ACUTE RESPIRATORY FAILURE NURSING AND COLLABORATIVE MANAGEMENT Nursing Assessment Health information Health history Medications Surgery Functional health patterns Health perception–health management Nutritional-metabolic Activity-exercise Sleep-rest Cognitive-perceptual Coping–stress tolerance ACUTE RESPIRATORY FAILURE NURSING AND COLLABORATIVE MANAGEMENT (CONT’D) Nursing Assessment Physical assessment General Integumentary Respiratory Cardiovascular Gastrointestinal Neurologic Laboratory findings ACUTE RESPIRATORY FAILURE NURSING AND COLLABORATIVE MANAGEMENT (CONT’D) Nursing Diagnoses Impaired gas exchange Ineffective airway clearance Ineffective breathing pattern Risk for fluid volume imbalance Anxiety Imbalanced nutrition: Less than body requirements ACUTE RESPIRATORY FAILURE NURSING AND COLLABORATIVE MANAGEMENT (CONT’D) Planning: Overall goals ABG values within patient’s baseline Breath sounds within patient’s baseline No dyspnea or breathing patterns within patient’s baseline Effective cough and ability to clear secretions ACUTE RESPIRATORY FAILURE NURSING AND COLLABORATIVE MANAGEMENT (CONT’D) Respiratory therapy Oxygen therapy: Delivery system should Be tolerated by the patient Maintain PaO2 at 55 to 60 mm Hg or more and SaO2 at 90% or more at the lowest O2 concentration possible ACUTE RESPIRATORY FAILURE NURSING AND COLLABORATIVE MANAGEMENT (CONT’D) Respiratory therapy Mobilization of secretions Hydration and humidification Chest physical therapy Airway suctioning Effective coughing and positioning ACUTE RESPIRATORY FAILURE NURSING AND COLLABORATIVE MANAGEMENT (CONT’D) Respiratory therapy Positive pressure ventilation (PPV) Noninvasive PPV BiPAP CPAP ACUTE RESPIRATORY FAILURE NURSING AND COLLABORATIVE MANAGEMENT (CONT’D) Drug Therapy Relief of bronchospasm Bronchodilators Reduction of airway inflammation Corticosteroids Reduction of pulmonary congestion Diuretics, nitrates if heart failure present ACUTE RESPIRATORY FAILURE NURSING AND COLLABORATIVE MANAGEMENT (CONT’D) Drug Therapy Treatment of pulmonary infections IV antibiotics Reduction of severe anxiety, pain, and agitation Benzodiazepines Narcotics ACUTE RESPIRATORY FAILURE NURSING AND COLLABORATIVE MANAGEMENT (CONT’D) Nutritional Therapy Maintain protein and energy stores Enteral or parenteral nutrition Nutritional supplements ACUTE RESPIRATORY FAILURE NURSING AND COLLABORATIVE MANAGEMENT (CONT’D) Medical Supportive Therapy Treat the underlying cause Maintain adequate cardiac output and hemoglobin concentration ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) Sudden progressive form of acute respiratory failure Alveolar capillary membrane becomes damaged and more permeable to intravascular fluid Alveoli fill with fluid STAGES OF EDEMA FORMATION IN ARDS A, Normal alveolus and pulmonary capillary B, Interstitial edema occurs with increased flow of fluid into the interstitial space Fig. 68-8 C, Alveolar edema occurs when the fluid crosses the blood-gas barrier ARDS Results Severe dyspnea Hypoxia Decreased lung compliance Diffuse pulmonary infiltrates 150,000 causes annually 50% mortality rate ETIOLOGY AND PATHOPHYSIOLOGY Develops from a variety of direct or indirect lung injuries Most common cause is sepsis Exact cause for damage to alveolar -capillary membrane not known Pathophysiologic changes of ARDS thought to be due to stimulation of inflammatory and immune systems PATHOPHYSIOLOGY OF ARDS Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved. ETIOLOGY AND PATHOPHYSIOLOGY Neutrophils are attracted and release mediators producing changes in lungs ↑ Pulmonary capillary membrane permeability Destruction of elastin and collagen Formation of pulmonary microemboli Pulmonary artery vasoconstriction ETIOLOGY AND PATHOPHYSIOLOGY (CONT’D) Injury or exudative phase 1 - 7 days after direct lung injury or host insult Neutrophils adhere to pulmonary microcirculation Damage to vascular endothelium ↑ Capillary permeability Etiology and Pathophysiology (Cont’d) Injury or exudative phase (cont’d) Engorgement of peribronchial and perivascular interstitial space Fluid crosses into alveolar space Intrapulmonary shunt develops as alveoli fill with fluid and blood passing through cannot be oxygenated Etiology and Pathophysiology (Cont’d) Injury or exudative phase (cont’d) Alveolar cells type 1 and 2 are damaged Surfactant dysfunction → atelectasis Hyaline membranes line alveoli Contribute to atelectasis and fibrosis Etiology and Pathophysiology (Cont’d) Injury or exudative phase (cont’d) Severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia Unresponsive to increasing O2 concentrations Lungs become less compliant Increased airway pressures must be generated Etiology and Pathophysiology (Cont’d) Injury or exudative phase: Summary Interstitial and alveolar edema (noncardiogenic pulmonary edema) Atelectasis resulting in V/Q mismatch Shunting of pulmonary capillary blood Hypoxemia unresponsive to increasing concentrations of O2 (refractory hypoxemia) Etiology and Pathophysiology (Cont’d) Reparative or proliferative phase 1 to 2 weeks after initial lung injury Influx of neutrophils, monocytes, and lymphocytes Fibroblast proliferation Lung becomes dense and fibrous Lung compliance continues to ↓ Etiology and Pathophysiology (Cont’d) Reparative or proliferative phase (cont’d) Hypoxemia worsens Thickened alveolar membrane Diffusion limitation and shunting If reparative phase persists, widespread fibrosis results If phase is arrested, lesions resolve Etiology and Pathophysiology (Cont’d) Fibrotic or chronic/late phase 2 to 3 weeks after initial lung injury Lung is completely remodeled by sparsely collagenous and fibrous tissues Etiology and Pathophysiology (Cont’d) Fibrotic or chronic/late phase (cont’d) ↓ Lung compliance ↓ Area for gas exchange Pulmonary hypertension Results from pulmonary vascular destruction and fibrosis CLINICAL PROGRESSION Some persons survive acute phase of lung injury Pulmonary edema resolves Complete recovery CLINICAL PROGRESSION (CONT’D) Survival chances are poor for those who enter fibrotic phase Require long-term mechanical ventilation CLINICAL MANIFESTATIONS: EARLY Dyspnea, tachypnea, cough, restlessness Chest auscultation may be normal or reveal fine, scattered crackles ABGs Mild hypoxemia and respiratory alkalosis caused by hyperventilation CLINICAL MANIFESTATIONS: EARLY (CONT’D) Chest x-ray may be normal or show minimal scattered interstitial infiltrates Edema may not show until 30% increase in lung fluid content CLINICAL MANIFESTATIONS: LATE Symptoms worsen with progression of fluid accumulation and decreased lung compliance Pulmonary function tests reveal decreased compliance and lung volume Evident discomfort and increased WOB CLINICAL MANIFESTATIONS: LATE (CONT’D) Suprasternal retractions Tachycardia, diaphoresis, changes in sensorium with decreased mentation, cyanosis, and pallor Hypoxemia and a PaO2/FIO2 ratio <200 despite increased FIO2 CLINICAL MANIFESTATIONS As ARDS progresses, profound respiratory distress requires endotracheal intubation and positive pressure ventilation CLINICAL MANIFESTATIONS (CONT’D) Chest x-ray termed whiteout or white lung because of consolidation and widespread infiltrates throughout lungs CHEST X-RAY OF PERSON WITH ARDS CLINICAL MANIFESTATIONS If prompt therapy not initiated, severe hypoxemia, hypercapnia, and metabolic acidosis may ensue ARDS Complications of treatment Hospital-acquired pneumonia Barotrauma Volu-pressure trauma High risk for stress ulcers Renal failure COMPLICATIONS Hospital-acquired pneumonia Strategies for prevention of ventilator-associated pneumonia Strict infection control measures Elevate HOB 45 degrees or more to prevent aspiration COMPLICATIONS (CONT’D) Barotrauma Rupture of overdistended alveoli during mechanical ventilation To avoid, ventilate with smaller tidal volumes Higher PaCO2 Permissive hypercapnia COMPLICATIONS (CONT’D) Volu-pressure trauma Occurs when large tidal volumes used to ventilate noncompliant lungs Alveolar fractures and movement of fluids and proteins into alveolar spaces Avoid by using smaller tidal volumes or pressure ventilation COMPLICATIONS (CONT’D) Stress ulcers Bleeding from stress ulcers occurs in 30% of patients with ARDS on mechanical ventilation Management strategies Correction of predisposing conditions Prophylactic antiulcer agents Early initiation of enteral nutrition COMPLICATIONS (CONT’D) Renal failure Occurs from decreased renal tissue oxygenation from hypotension, hypoxemia, or hypercapnia May also be caused from nephrotoxic drugs used for infections associated with ARDS NURSING ASSESSMENT Similar to ARF (Acute Respiratory Failure) NURSING DIAGNOSES Inef fective airway clearance Inef fective breathing pattern Risk for fluid volume imbalance Anxiety Impaired gas exchange Imbalanced nutrition: Less than body requirements PLANNING Following recovery PaO2 within normal limits or at baseline SaO2 > 90% Clear lungs or auscultation RESPIRATORY THERAPY Oxygen High flow systems used to maximize O2 delivery SaO2 continuously monitored Give lowest concentration that results in PaO2 60 mm Hg or greater RESPIRATORY THERAPY (CONT’D) Risk for O2 toxicity increases when FIO2 exceeds 60% for more than 48 hours Patients will commonly need intubation with mechanical ventilation because PaO2 cannot be maintained at acceptable levels RESPIRATORY THERAPY (CONT’D) Mechanical ventilation PEEP at 5 cm H2O compensates for loss of glottic formation Opens collapsed alveoli RESPIRATORY THERAPY (CONT’D) Mechanical ventilation Higher levels of PEEP are often needed to maintain PaO2 at 60 mm Hg or greater High levels of PEEP can compromise venous return ↓ Preload, CO, and BP RESPIRATORY THERAPY (CONT’D) Alternative modes of mechanical ventilation if hypoxemia persists Pressure support ventilation Pressure release ventilation Pressure control ventilation Inverse ratio ventilation High-frequency ventilation Permissive hypercapnia RESPIRATORY THERAPY (CONT’D) Positioning strategies Mediastinal and heart contents place more pressure on lungs when in supine position than when in prone Predisposes to atelectasis Turn from supine to prone position May be sufficient to reduce inspired O2 or PEEP Fluid pools in dependent regions of lung INTERVENTIONS ET intubation, conventional mechanical ventilation with PEEP or CPAP Drug and fluid therapy Nutrition therapy ENDOTRACHEAL TUBE VERIFYING TUBE PLACEMENT End-tidal carbon dioxide levels Chest x-ray Assess for breath sounds bilaterally, symmetrical chest movement, air emerging from ET tube ENDOTRACHEAL TUBES: NURSING CARE Assess tube placement, minimal cuf f leak, breath sounds, chest wall movement Prevent movement of tube by patient Check pilot balloon Soft wrist restraints Mechanical sedation VENTILATOR SETTINGS FiO 2 Tidal Volume (V T ) 6 to 8 mL/kg (ideal weight) Adjusted according to peak and plateau pressures Respiratory rate 14-20 breaths initially I:E ratio; normal 1:2 Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 102 VENTILATOR SETTINGS Positive end-expiratory pressure (PEEP) 5-20 cm H 2 O Increases FRC to improve oxygenation Can cause reduced cardiac output if high and impedes venous return 103 POSITIVE END-EXPIRATORY PRESSURE (PEEP) Figure 9-25. Effect of application of positive end-expiratory pressure (PEEP) on the alveoli. (Modified from Pierce LNB. Management of the Mechanically Ventilated Patient. Philadelphia: Saunders; 2007.) 104 VOLUME ASSIST/CONTROL VENTILATION (V-A/C) Preset number of breaths at preset V T Patient may trigger additional breaths V T does not vary Ventilator performs most of the WOB Useful in normal respiratory drive but weak or unable to exert WOB Risk of hyperventilation and respiratory alkalosis , 105 VOLUME ASSIST/CONTROL (V-A/C) Figure 9-26A. Waveforms of volume-controlled ventilator modes. A, Volume assist/control (V–A/C) ventilation. The patient may trigger additional breaths above the set rate. The ventilator delivers the same volume for ventilatortriggered and patient-triggered (assisted) breaths. B, Synchronized intermittent mandatory ventilation (SIMV). Both spontaneous and mandatory breaths are graphed. Mandatory breaths receive the set tidal volume (V T). V T of spontaneous breaths depends on work patient is capable of generating, lung compliance, and airway resistance. 106 SYNCHRONIZED INTERMITTENT MANDATORY VENTILATION (SIMV) Preset V T at a preset respiratory rate In between “mandatory” (preset) breaths, the patient may initiate spontaneous breaths V T of spontaneous breaths varies Helps to prevent respiratory muscle weakness because patient contributes more WOB Risk of hypoventilation 107 SIMV Figure 9-26B. Waveforms of volume-controlled ventilator modes. A, Volume assist/control (V–A/C) ventilation. The patient may trigger additional breaths above the set rate. The ventilator delivers the same volume for ventilator-triggered and patient-triggered (assisted) breaths. B, Synchronized intermittent mandatory ventilation (SIMV). Both spontaneous and mandatory breaths are graphed. Mandatory breaths receive the set tidal volume (V T). V T of spontaneous breaths depends on work patient is capable of generating, lung compliance, and airway resistance. c. 108 CPAP Continuous positive airway pressure throughout respiratory cycle to patient who is spontaneously breathing Similar to PEEP Via ventilator or nasal or face mask Option for patients with sleep apnea May facilitate weaning Can also be used to prevent re -intubation Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 109 CPAP Figure 9-27. Continuous positive airway pressure (CPAP) is a spontaneous breathing mode. Positive pressure at end expiration splints alveoli and supports oxygenation. Note that the pressure does not fall to zero, indicating the level of CPAP. E, Expiration; I, inspiration. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc. 110 YOUTUBE VIDEOS OF http://www.youtube.com/watc h? v =0yqxfDgJ0Dc http://www.youtube.com/watc h? v =rhSMCvYW8wE http://www.youtube.com/watc h? v =7_X9PDctWh8 http://www.youtube.com/watc h? v =HbCuqpvx2EU http://www.youtube.com/watc h? v =hQlt57AyQmg http://www.youtube.com/watc h? v =tVy5KH3jjUM I N T E R E S T ( C U T - N - PA S T E ) http://www.youtube.com/wa tch?v=1JME24q8Yvs http://www.youtube.com/wa tch?v=cVCvYxVxSt4 http://www.youtube.com/wa tch?v=aXjaxvL6y7I http://www.youtube.com/wa tch?v=6nERo9g5sBU