Transcript Module 5

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
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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
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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.)
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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.
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ENDOTRACHEAL INTUBATION
 Insertion of an endotracheal tube (ETT) through the mouth or
nose
 Orotracheal route preferred to reduce infections
 Used to:
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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.
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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
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VERIFY PLACEMENT
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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
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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
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Restrictive lung disease
CNS disease
Chest wall dysfunction
Neuromuscular disease
HYPERCAPNIC RESPIRATORY FAILURE
ETIOLOGY AND PATHOPHYSIOLOGY
(CONT’D)
 Airways and alveoli
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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
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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
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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
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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
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General
Integumentary
Respiratory
Cardiovascular
Gastrointestinal
Neurologic
 Laboratory findings
ACUTE RESPIRATORY FAILURE
NURSING AND COLLABORATIVE MANAGEMENT
(CONT’D)
 Nursing Diagnoses
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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
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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
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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
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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
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↑ 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
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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
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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
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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
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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
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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
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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
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