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
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.
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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:
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
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.
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