Adult Noninvasive Positive

Pressure Ventilation
in the Acute Care Setting

Self-learning Packet

* See SWIFT for list of qualifying boards for continuing education hours.
Table of Contents

Introduction ...................................................................................................................................................... 4

Regulation of Breathing .................................................................................................................................. 4

Sleep Disordered Breathing............................................................................................................................ 6

Acute Respiratory Failure ............................................................................................................................... 8

Hypoxemic Respiratory Failure (Hypoxemia) ............................................................................................... 8
Hypercapnic Respiratory Failure (Hypercapnia)......................................................................................... 10

Indications/Contraindications for Noninvasive Ventilation....................................................................... 12

Advantages of NPPV .................................................................................................................................. 13
Disadvantages of NPPV.............................................................................................................................. 13
Advantages of Invasive Mechanical Ventilation.......................................................................................... 13
Disadvantages of Invasive Mechanical Ventilation..................................................................................... 13

Application of the Mask Interface................................................................................................................. 14

Troubleshooting .......................................................................................................................................... 16

Noninvasive Positive Pressure Ventilation (NPPV).................................................................................... 17

Ventilator Settings ......................................................................................................................................... 17

Modes of Ventilation ...................................................................................................................................... 19

Nursing Care................................................................................................................................................... 21

Weaning .......................................................................................................................................................... 21

Summary ......................................................................................................................................................... 22

Appendix A: Muscles of Ventilation............................................................................................................ 23

Diaphragm................................................................................................................................................... 23
Accessory Muscles of Ventilation ............................................................................................................... 24

Appendix B: Management of Snoring......................................................................................................... 25

Appendix C: Treatment for Sleep Apnea .................................................................................................... 26

Appendix D: APACHE Scoring System ...................................................................................................... 28

Glossary .......................................................................................................................................................... 29

Abbreviations ................................................................................................................................................. 30

Internet Resources......................................................................................................................................... 31

Post-Test ......................................................................................................................................................... 33

References ...................................................................................................................................................... 35

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Purpose
The purpose of this self-learning packet is to educate patient care providers on the function and care
of the adult patient utilizing non-invasive ventilation.
Orlando Health is an Approved Provider of continuing nursing education by Florida Board of
Nursing (Provider No. FBN 2459) and the North Carolina Nurses Association, an accredited
approver by the American Nurses Credentialing Center’s Commission on Accreditation (AP 085).

Objectives
After completing this packet, the learner will be able to:
1. Discuss regulation of breathing.
2. Differentiate between the three types of sleep apneas; obstructive, central and mixed.
3. Discriminate between hypercapnic and hypoxemic respiratory failure.
4. Define noninvasive positive pressure ventilation.
5. Discuss indications and contra-indications for noninvasive positive pressure ventilation.
6. Identify the complications of noninvasive positive pressure ventilation.
7. Discuss application of noninvasive positive pressure ventilation (NPPV) and continuous
positive airway pressure (CPAP) in the acute care setting.
8. Analyze the efficacy of mask application and patient tolerance for nasal and/or full-face masks
during noninvasive positive pressure ventilation.
9. Discuss the techniques for practical application of NPPV equipment.
10. Compare and contrast ventilatory modes available with noninvasive positive pressure
ventilation (NPPV).
11. Select appropriate interventions for a patient on noninvasive positive pressure ventilation
(NPPV) based on clinical findings.

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Instructions
In order to receive 2.0 contact hours, you must:
 complete the posttest at the end of this packet
 achieve an 84% on the posttest
For Non-Orlando Health employees: Complete the test using the bubble sheet provided. Be sure
to complete all the information at the top of the answer sheet. You will be notified if you do not
pass, and you will be asked to retake the posttest.
Return to: Orlando Health, Education & Development, MP14, 1414 Kuhl Ave, Orlando, FL 32806

For Orlando Health Team Member: Please complete testing via Online Testing Center. Log
on to: SWIFT Departments E-Learning Testing Center. Use your Orlando Health Network
Login and password. Select “SLP” under type of test; choose correct SLP Title. Payroll
authorization is required to download test.

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Introduction
The first noninvasive ventilators were used in the 1940’s with the outbreak of Polio. The iron lung applied a
negative pressure to the thorax which created a vacuum. The application of this negative pressure drew air
into the lungs. The iron lung demanded that the patient’s entire body be encased in the machine. The iron
lung was replaced by positive pressure ventilators that used an invasive endotracheal tube to deliver air into
the lungs, removing the need for the patient to be enclosed inside the ventilator. Because these ventilators
were invasive, their use was limited to critical care or specially equipped long-term care settings.
Modern noninvasive ventilators push air into the lungs under positive pressure and use a face mask rather
than an invasive tube. The advent of noninvasive positive pressure ventilation has taken mechanical
ventilation out of the critical care unit and introduced it to the acute care unit and the home care setting as
well. This packet will focus on the use of noninvasive ventilators in the acute care setting.
Noninvasive ventilation is a supportive therapy used to maintain adequate oxygenation and ventilation in
patients who cannot maintain these functions independently. A noninvasive ventilator is a machine that uses
a noninvasive facial interface (mask) to provide temporary ventilatory assistance. This type of system is
intended to aid the ventilation of a spontaneously breathing patient. It is not intended for extended continuous
use or to provide the total ventilatory requirements of the patient; invasive ventilators are more appropriate
for those situations. Information in this packet refers to the BiPAP Vision™ Ventilatory Support System.

Regulation of Breathing
Breathing (ventilation) is regulated by a combination of chemoreceptors located in the brain, aorta and
carotid arteries. The peripheral chemoreceptors are located in the aortic and carotid bodies and primarily
sense PO2 levels, though they also can sense PCO2 and pH. Central receptors are located in the medulla (part
of the brainstem) and respond to the PCO2 and hydrogen levels of the cerebral spinal fluid (CSF). The
brainstem integrates information received from the cerebral cortex and then generates a respiratory rhythm
sending messages to the respiratory muscles (inspiratory and expiratory). The brainstem responds to low PO2
or high PCO2 levels by increasing the rate and depth of breathing. Emotional states can also alter ventilation.

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To ventilate the lungs effectively, the respiratory muscle pump must have the capacity to sustain ventilation
against a given load.

Capacity
Capacity is the sum of two or more volumes (eg. Total Lung Capacity (TLC) = Vital Capacity (VC) +.
Reserve Volume), see illustration below. Impairment in capacity may be reversible or irreversible. It is
affected by structural deformities and/or respiratory muscle strength and drive. Capacity changes on a minute
to minute basis based on these variables.
Capacity is greatly decreased in skeletal deformity and neuromuscular disease. It is only slightly decreased in
obesity. NPPV helps restore capacity by resting fatigued respiratory muscles. Capacity is increased in COPD.

Total
Lung
Capacity

IRV (Inspiratory
Reserve Volume)
Vital
Capacity
Tidal Volume

Expiratory
Reserve Volume

Reserve Functional
Volume Residual
Capacity

Drive
Changes in the drive to breathe can be structural or metabolic in nature.
Slight decrease in drive occurs with skeletal deformity, neuromuscular disease, obesity, and COPD. In CNS
abnormalities the drive can be greatly reduced. Medications that can decrease drive include narcotics,
hypnotics, sedatives and barbiturate drugs.

Resistance
Changes in resistance can be reversible or irreversible. Causes of increased resistance include sputum, fluid
retention, small or large airway obstruction, and decreased upper airway muscle tone.
Primary abnormalities in skeletal deformities, COPD, and obesity also greatly increase resistance. In
neuromuscular disease resistance is increased slightly.

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The chart below reflects the changes that can occur in capacity, drive and resistance with physiologic
changes.

ABNORMALITIES CAPACITY DRIVE RESISTANCE

Skeletal Deformity Largely decreased Very slightly decreased Largely increased

Neuromuscular Diseases Greatly decreased Very slightly decreased Very slightly increased

COPD Increased Very slightly decreased Largely increased

Obesity Decreased Very slightly decreased Largely increased

Central No change Greatly decreased No change

Sleep Disordered Breathing

Many patients have abnormal breathing during sleep, and
some of these problems are treated with noninvasive positive Obstructive Sleep Apnea
pressure ventilation. Sleep disordered breathing (sleep apnea, Clinical Presentation
hypopneas, and hypoventilation) can develop into or
 snoring
exacerbate ventilatory insufficiency and can complicate other
pulmonary diseases.  hypersomnolence
Sleep apnea is defined as absence of air flow through the  increased upper airway resistance
nose or mouth for at least 10 seconds during sleep-
interrupting the sleep cycle.  disturbed sleep pattern

Obstructive sleep apnea (OSA) occurs when air stops  obesity

flowing through the nose and mouth, interrupting nocturnal  older adult; men > women (except
sleep 30 or more times during a 7-hour period, and the throat postmenopausal)
and abdominal breathing efforts are uninterrupted. Several
conditions that reduce the size of the airway are associated  hypothyroidism
with obstructive sleep apnea. They include obesity, a short
thick neck, and reduction in muscle tone of the soft palate,
uvula and pharynx. The upper airway may be narrowed by enlarged tonsils or adenoids, a deviated nasal
septum, nasal polyps, or congenital abnormalities.
The snoring that results is produced when the upper rear of the mouth (the soft palate and the cone-shaped
tissue—the uvula—that descends from it) relaxes and vibrates as air passes in and out. This sets up an air
current between the palate and the base of the tongue, resulting in snoring. Typically, the individual will
wake up, emit a vigorous snort or grunt while gasping for air, then immediately fall back to sleep, only to
repeat the cycle. Hypersomnia sleep apnea (HSA) syndrome is the result of obstruction in the upper airway;
HSA patients experience hundreds of apneic episodes each night. The repeated hypoxic stimulation can
desensitize the central nervous system to low arterial oxygen levels and may result in central apnea.
Central apnea is the result of altered chemosensitivity and brainstem respiratory control. Both oral breathing
and throat and abdominal breathing efforts are simultaneously interrupted.
Mixed apnea results from a combination of central and obstructive causes.
At high altitudes sleep disruption may occur because of low oxygen concentration.

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Complications associated with untreated sleep apnea include hypertension, arrhythmias, abnormal blood
levels of oxygen and carbon dioxide, and peripheral edema. Other complications include sleepwalking,
blackouts, automatic robot-like behavior, intellectual deterioration, hallucinations, anxiety, irritability,
aggressiveness, jealousy, suspiciousness, and irrational behavior. Loss of interest in sex, morning headaches,
and bedwetting may also occur with time.
Diagnosing sleep apnea is done using the technique of polysomnography or sleep study. This test is
performed in a sleep lab and records the number and duration of apneic episodes, determines the stage of
sleep, oxygen saturation and observes the patient during arousal. Other diagnostic tests may be indicated
including imaging of the face, jaw, and throat structures.
Treatment is based upon the diagnosis and patient complaints. Mild OSA is often treated with nasal
decongestant and weight reduction if indicated. Intra-oral devices to open the airway may be used to position
the tongue and mandible to keep the airway open. More serious sleep apnea can be treated with continuous
positive airway pressure (CPAP). CPAP regulates air pressure within the upper airway to keep the nasal and
oropharyngeal passages open. The amount of pressure needed is determined by the polysomnography
diagnostic test. It takes time for the patient to adjust to the equipment interface before they can settle down to
a more normal sleeping pattern. The equipment is portable and can travel with the person if needed. Surgery
may be indicated for the small number of patients with OSA who do not experience relief with CPAP. The
surgical procedure called uvulopalatopharyngoplasty (UPPP) opens up more air space by removing part of
the soft palate and tissue at the back of the throat.
If the underlying diagnosis is related to obesity-hypoventilation or neuromuscular disease rather than
obstruction, CPAP will not improve the ventilatory impairment. This packet will not focus on the use of
NPPV in the home setting, but the concept of CPAP will be discussed further.

Clinical Application
Sedatives, hypnotic medications and alcoholic beverages may be harmful for people with sleep
apnea; they should not be taken if the condition is suspected.

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Acute Respiratory Failure

Acute respiratory failure is defined as an acute onset of severely impaired gas exchange. The onset may
occur over several hours or several days. Diagnosis is based upon clinical presentation and arterial blood gas
values. Patients with acute respiratory failure typically present with dyspnea or increased work of breathing.
Other common symptoms include increased pulmonary secretions, neurologic changes, and tachycardia.
Specific manifestations will depend on the cause and the patient’s underlying disease process. There are two
types of acute respiratory failure: hypoxemic and hypercapnic (ventilatory). Patients may present with one or
a mixture of both types.
Regardless of the cause, patients with acute respiratory failure often require mechanical ventilation until the
underlying pathology can be resolved. If the underlying cause can be resolved rapidly, noninvasive
mechanical ventilation may be used.

Hypoxemic Respiratory Failure (Hypoxemia)

Hypoxemia is defined as an acute reduction in PaO2 of
10% or more over a period ranging from several Signs & Symptoms of Hypoxemia
minutes to several hours. Emergent treatment should be  Asymptomatic
initiated when the PaO2 is less than 60mm Hg
indicating a rapid decline in the oxygen content of  Headache
blood and subsequent tissue hypoxia. If there is not a  Cognitive deficits
shift of the oxyhemoglobin dissociation curve, a PaO2
of 60mm Hg is roughly equivalent to a pulse oximetry  Tachypnea
reading (SpO2) of 92% in Caucasians without any  Tachy or bradydsyrhythmias
cardiac involvement. Because of the potential for
inaccurate pulse oximetry measurements, SpO2  Hypotension
readings alone are insufficient to diagnose hypoxemia.  Central cyanosis – late sign
Contributing factors that may cause inaccurate
oximetry readings are: poor perfusion, dark skin
pigmentation, motion artifact, bright lights, dyes
(methylene blue), abnormal hemoglobin, nail polish/acrylic nails and hypothermia. After making sure a good
quality waveform is present on the pulse oximeter the SpO2 reading should be correlated to the SaO2 from the
arterial blood gas and then used as a tool to trend the patient’s progress.

PaO2  SaO2
Diagnosis
Diagnosis of hypoxemic respiratory failure is made on the basis of the PaO2. The other components of the
blood gas are not used to make this diagnosis. Treatment is focused on immediate stabilization and
supportive care. An assessment of the appropriate oxygen delivery system, cardiac rhythm and
hemodynamics are rapidly performed and correlated to the physical assessment. If supplemental oxygen and
appropriate drug therapy is insufficient to rapidly resolve the patient’s hypoxemia and respiratory distress,
mechanical ventilation may be required.

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Etiology
The causes and contributing factors of hypoxemia are listed in the following table.

Causes Contributing Factors

Low FiO2  Supplemental oxygen device removed or maladjusted
 Lack of oxygen in ambient air (high altitude)
Hypoventilation  Low respiratory rate (<12 breaths per minute)
 Medications (sedative, opioid, paralytic)
 Adverse neurological event
Ventilation/Perfusion (V/Q) mismatch  Narrowed airway due to bronchospasm, bronchial
Deadspace secretions, or edema
 Impaired pulmonary circulation due to pulmonary embolus

Pulmonary shunt  Lung parenchymal injury – e.g. lung infections, near

drowning, chemical or smoke inhalation (carbon monoxide
poisoning), and liquid aspiration
 Alveoli are filled with edema, blood or exudate
 Severe atelectasis
 Pneumothorax
 Cardiac septal defects
Low mixed venous oxygen saturation  Decrease in cardiac output (CO) superimposed on diseased
(SVO2) lungs
Procedures/Nursing Interventions  Patient positioning
 Chest physiotherapy
 Tracheal suction
 Dialysis
 Thoracentesis
 Moderate to deep sedation
 Bronchoscopy/Endoscopy

Diagnoses associated with hypoxemic respiratory failure include cardiogenic pulmonary edema, pneumonia,
post-traumatic respiratory failure, ARDS and weaning difficulties.

Treatment
Treatment for hypoxemia is based on restoring adequate oxygenation to prevent life-threatening
complications. Diagnostic procedures to evaluate treatment are performed as needed in addition to
continuous monitoring of pulse oximetry and capnography. Diagnostic procedures may include chest x-ray,
ABG measurement, bronchoscopy, V/Q scanning and CT scan.

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Hypercapnic Respiratory Failure (Hypercapnia)

Ventilatory respiratory failure (hypercapnia) is
diagnosed by a PaCO2 > 50mm Hg. The other Signs & Symptoms of Hypercapnia
components of the blood gas are not used to make
this diagnosis. For patients with chronic  Headache
hypercapnia, an increase in PaCO2 above baseline  Dizziness
is used for diagnosis.
 Change in level of consciousness
Etiology  Asterixis (abnormal muscle twitching)
Causes of hypercapnic respiratory failure are:  Miosis (abnormal contraction of the pupils)
 Decreased Respiratory Drive  Papilledema
Causes of decreased respiratory drive leading  Hypertension
to hypercapnia include: medications (opiods,
alcohol, tricyclic antidepressants, barbiturates,  Diaphoresis
propofol or other sedative drugs),
hypothyroidism, metabolic alkalosis, structural
lesion(s) in the central nervous system, infections of the central nervous system, alveolar hypoventilation
and idiopathic causes.
 Inability to generate effective ventilatory muscle contraction
Causes of an inability to generate effective respiratory muscle contraction include: medications
(neuromuscular blockade drugs), tetanus, myasthenia gravis, Guillain-Barre syndrome, amyotropic
lateral sclerosis, poliomyelitis, cervical cord injury (C-4 or higher), muscular dystrophy, electrolyte
abnormalities (hyper/hypokalemia, hypophosphatemia, hypermagnesemia), malnutrition and
diaphragmatic fatigue.
 Obstructive and restrictive pulmonary disorders
Examples include: chronic obstructive lung disease (COPD), acute respiratory distress syndrome (ARDS),
near drowning, severe pneumonia, liquid aspiration, pulmonary embolism, pulmonary edema, cancer, acute
airway obstruction (acute epiglottitis, secretions), status asthmaticus, smoke inhalation/chemical inhalation,
laryngospasm, emphysema, severe kyphoscoliosis and morbid obesity.

Treatment
Hypercapnia is treated by increasing the amount of air moving in and out of the alveoli thus increasing
ventilation. Immediate stabilization is achieved by ensuring an open airway and augmenting spontaneous
breathing with manual ventilation. After the patient has been stabilized, treatment specific to the underlying
cause of hypercapnia will be provided. If hypoventilation cannot be rapidly corrected, mechanical ventilation
may be required.

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Clinical Application
Mechanical Ventilation & Obstructive Airway Disease
A severe exacerbation of obstructive airway disease, like that seen in status asthmaticus, results in
hypercapnia. Treatment includes supplemental oxygen, inhaled bronchodilators, intravenous
glucocorticosteroids, and antibiotics (if infection is suspected). Although supplemental oxygen is part of
the treatment plan, it will not be effective without the other components. The problem in this disease state
is that not enough air is moving in and out of the lungs. Oxygen alone cannot correct the problem.
Bronchodilators and corticosteroids function to open the airways, allowing improved ventilation. If these
interventions are not successful, invasive mechanical ventilation may be required.

Ventilatory Impairment
Ventilatory impairment is defined as ventilatory insufficiency or ventilatory muscle fatigue. Ventilatory
insufficiency occurs when inadequate amounts of air are able to move through the airways resulting in an
accumulation of CO2 (hypercapnia). Causes include mucus plugs, bronchospasms, bronchial edema, CNS
pathology and masses. Muscle weakness can also contribute to ventilatory insufficiency. Patients with
ventilatory insufficiency and an SpO2 less than 92% are at high risk of ventilatory failure without
intervention.

Clinical Application
Decreased Ventilatory Response to Hypercapnia Occurs with:
 Medications such as calcium channel blockers, aminoglycosides, and benzodiazepines decrease
the ventilatory response to hypercapnia and hypoxia and exacerbate hypoventilation.
 Beta blockers can increase airway resistance by inducing bronchospasm.
 Malnutrition, acidosis, electrolyte disturbances, infection, result in fatigue that can exacerbate
ventilatory insufficiency.
 Sleep decreases the ventilatory response to blood gases, cough reflex, and accessory inspiratory
muscle recruitment. Increase in upper airway resistance and an increase in PaCO2 are noted
during sleep.
 Oxygen administration.

Ventilatory muscle fatigue occurs when the inspiratory and expiratory muscles are unable to sustain adequate
ventilation. This can occur due to neuromuscular dysfunction (ALS, MS), sustained increased work of
breathing (asthma, COPD, trauma), drugs (sedatives, neuromuscular drugs, anesthetics), and severe
metabolic imbalances (acidosis, malnutrition).
Ventilatory insufficiency and ventilatory muscle fatigue often coexist, and the presence of both increases the
risk that the patient will develop respiratory failure. They are also both worsened in the sleeping patient. This
is because sleep dulls the drive to breathe and recumbent position places the weight of the abdominal
contents against the diaphragm causing increased work of breathing. This sleep-induced exacerbation means
that sometimes patients require mechanical ventilation while asleep even if they are maintaining adequate

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ventilation while awake. Presence of a compensatory metabolic alkalosis will depress the hypoxic and
hypercapnic drives to breathe, and increases the risk of severe hypercapnia, coma and/or respiratory arrest.

Indications/Contraindications for Noninvasive Ventilation

Appropriate patient selection is important to the success of noninvasive positive pressure ventilation (NPPV).
Ultimately it becomes a clinical judgment based on the physician’s experience and knowledge of NPPV. As
more attention is focused on the negative side effects of invasive ventilation, noninvasive ventilation is being
used with increased frequency. Some experts feel that noninvasive ventilation should be considered for any
patient requiring mechanical ventilation that does not have a specific contraindication to NPPV.
INDICATIONS
The primary indication for noninvasive mechanical ventilation in the acute care setting is to quickly reverse
hypercapnia and/or hypoxemia associated with respiratory insufficiency or failure. The ventilatory support
provided by NPPV “buys time” for other therapeutic modalities to reverse the underlying cause. NPPV is
best used for short-term treatment of patients whose underlying pathology can be rapidly corrected. It is also
used for patients with chronic respiratory pathology who are experiencing an acute exacerbation or who
require support during sleep. In addition, patients who do not wish to be intubated may find temporary NPPV
an acceptable alternative when mechanical ventilation is required.
Specific acute indications include exacerbated chronic obstructive pulmonary disease (COPD), severe
asthma, severe pneumonia, pulmonary edema, and patients for whom invasive mechanical ventilation is not
desirable or who do not wish to be intubated. NPPV can also be used as a bridge to spontaneous breathing for
patients who cannot tolerate a full 24 hours without ventilatory support and in whom reintubation is not
indicated or desired. The use of NPPV for sleep apnea is a chronic indication and will not be extensively
discussed.
CONTRAINDICATIONS
Relative contraindications include extreme anxiety, massive obesity, copious secretions and the need for
continuous ventilatory assistance. The nature of the mask interface makes NPPV very difficult for anxious
patients to tolerate. Morbidly obese patients present challenges with mask fitting and increased chest wall
resistance due to the excess weight. Patients who require continuous ventilatory assistance may be better
served by the more secure airway provided by traditional invasive ventilatory techniques.
ADDITIONAL CONSIDERATIONS
There are other contraindications to NPPV. Some practitioners feel these are absolute contraindications while
others feel they may be relative. Uncooperative, intolerant, or agitated patients may have trouble tolerating
the mask and are likely to attempt to remove it. Patients who cannot protect their own airway (including
those with impaired swallowing and cough) are at high risk for aspiration if NPPV is used. Coma or
obtundation present a similar risk for aspiration and NPPV is not as effective in patients whose respiratory
drive is compromised. Respiratory arrest may require high levels of ventilatory support, and is usually treated
with invasive ventilation. Hemodynamic instability may be exacerbated by any form of positive pressure
ventilation, and hemodynamically unstable patients may be better candidates for invasive techniques. NPPV
is poorly suited to patients with an acute abdominal process because of the large amounts of air that tend to
enter the GI tract. Any injury or malformation of the face may prevent secure fitting of the mask interface.
Long term contraindications include use of heavy sedation, high levels of supplemental oxygen, SpO2 that
cannot be maintained > 92%, uncontrollable seizures, and substance abuse.
Invasive and noninvasive ventilation each have unique advantages and disadvantages. The decision to use
one over another will depend on the patient’s diagnosis, co-morbidities, and clinical condition. The
discussion below reviews some of the pros and cons of each type of ventilation.

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Advantages of NPPV
The mask interface for NPPV is easy to remove and reapply. The freedom to do this allows patients to have
the ventilator removed for periods of time. During the time the ventilator is off, the patient can eat and drink.
Because the interface is a mask, patients can speak during NPPV, allowing them to express their wishes and
preserving their autonomy. Because of its noninvasive nature, NPPV is better tolerated by many patients and
lessens the need for sedative or paralytic drugs. The fact that there is no invasive tube into the trachea helps
prevent nosocomial pneumonia as well.

Disadvantages of NPPV
If NPPV is attempted and poorly tolerated for a long period, ventilatory muscle fatigue may result in a
prolonged period of intubation once invasive ventilation is instituted. Complications related to the mask
interface include facial skin necrosis and large mask leaks. The fact that the positive-pressure air is applied to
the whole oropharynx can result in significant gastric insufflation. It has also been noted that NPPV may
require a longer period of recovery and increases myocardial ischemia. Other complications include dry
mouth, eye irritation from air leakage, nasal congestion
and dripping, sinusitis, nose bleeding, gum discomfort Gastric Insufflation
and receding from nasal interface or lipseal pressure. Normally the gastroesophageal sphincter can
withstand peak airway pressures up to 25
Advantages of Invasive Mechanical cmH20 without stomach dilation.
Ventilation
Invasive mechanical ventilation provides a secure airway that is protected from aspiration. By introducing
the positive pressure air only into the trachea, invasive ventilation avoids gastric insufflation. In addition,
invasive ventilation provides the ability to completely control ventilation if needed. Invasive ventilation is
the preferred type of ventilation for patients who cannot protect the airway, who are comatose, or who have
minimal to no respiratory drive. Invasive ventilation is required if there is significant upper airway
obstruction, facial trauma or facial malformation that precludes use of a mask interface.

Disadvantages of Invasive Mechanical Ventilation

As with any invasive therapy, invasive ventilation increases the risk of infection. Infection can occur during
insertion of the endotracheal tube, during endotracheal suctioning, and anytime during the period of
intubation. The likelihood of pneumonia in an intubated patient is great because the mucociliary elevator is
interrupted by the tube, and the area above the cuff of the tube acts as a reservoir for bacterial growth. Oral
care is difficult in intubated patients, adding to the risk. Ventilator associated pneumonias increase mortality,
length-of-stay, and healthcare costs. There is also potential for aspiration of gastric contents during insertion
and removal of the invasive airway. Invasive airways are uncomfortable for the patient. They preclude
expectoration, eating and speech, increasing patient frustration and increasing the need for sedative,
analgesic, and paralytic medications.

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Predictors of Success for NPPV

There are several predictors of success with the use of NPPV: ability of the patient to understand and
cooperate with the application of the mask and ventilator, ability of the patient to protect their airway, good
mask fit, minimal secretions, overall health of the patient, and patient response within the first 2 hours of
therapy.
Overall patient health is evaluated by the physician. The
ABG’s of the likely candidate for NPPV reflect an initial Effectiveness of NPPV
PaCO2 > 50 mm Hg, and a pH < 7.30. The final predictor  Patient selection
is the initial response to NPPV in the first 1 – 2 hours of
application as demonstrated by an improvement in ABG  Patient cooperative / anxiety level
(increase in pH, decrease in PaCO2) and decrease in  Patient/ventilatory synchrony
respiratory rate. The key to the success of noninvasive
ventilation is early intervention and appropriate patient  Technical aspects
selection. o Mask
If NPPV is utilized in DNR (do not resuscitate) patients, o Ventilator settings
the clinician must understand that this is a form of life
support. If the patient cannot be successfully weaned o Monitoring
from the ventilator, paperwork for removal of life support
will be needed before the ventilator is removed. Prior to
initiation of ventilation the family must be informed that it is considered life support, that it may be
uncomfortable to the patient, may prolong the dying process and will increase the cost of care. The primary
determinant for whether or not to apply NPPV must be the patient’s wishes. If the patient’s wishes are
unclear, NPPV may allow a few extra hours or days for the family to finalize affairs.
Complications and side effects of NPPV include: air leak, skin necrosis (usually over bridge of nose),
retention of pulmonary secretions, gastric distension, failure to ventilate, sleep fragmentation, and upper
airway obstruction.

Application of the Mask Interface

The interface between the ventilator and the patient in NPPV is the mask. Selection of the type and size of
the mask and securing the mask are critical to successful NPPV. There is no single mask that works for all
patients; and even the best-fitting mask will not be successful if it is not applied correctly. Optimal results are
also enhanced when the patient and family are well-educated about the mask, its purpose and its fit.
Most masks are triangular in shape with a soft material around the flanges to obtain an air seal and a circular
port for tube connection. For the acute care setting there are nasal masks, oronasal masks and full face masks
that are used to interface with NPPV. Mouth pieces and lip seal devices are reserved for chronic use of
NPPV.
Patients should be offered a variety of masks and allowed to choose with guidance from a licensed
professional who knows NPPV well. No one can predict which interface will provide the best seal and have
the least insufflation leakage or which one the patient will be the most comfortable with. It may be necessary
to try several masks before the optimal one is identified.

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Nasal Mask
The nasal mask is available in three sizes. This lightweight mask has forehead
support and thin cushioning for patient comfort. The noninvasive circuit has a 360
rotating swivel, providing freedom of movement.
Advantages of the nasal mask include allowing for oral feedings and decreasing the
risk of aspiration by allowing the patient to clear oral secretions. Because it is small,
it decreases the sense of claustrophobia associated with larger masks. The nasal
mask is easier to fit in a male patient with facial hair. Because patients can exhale
through the mouth, the amount of rebreathed CO2 is reduced.
Disadvantages are that approximately 50 %(11) of the total airway resistance resides
in the nasal passages. Because of this increased resistance, the pressure support displayed on the machine
may exceed the amount actually in the lung. Patients with narrow or collapsed airways may require a face
mask for NPPV. Mask ventilation may also be required in the immediate post op patient due to collapsed
airways. Nasal masks may also cause significant drying of the nasal mucosa.
Overall, the nasal mask is better tolerated, but better minute ventilation and PaCO2 are achieved with the
oronasal mask. The nasal mask is preferred for chronic treatment of patients with sleep apnea.

Oronasal Mask
The oronasal mask can help eliminate mouth leaks. In the acute care setting the oronasal
mask is the preferred choice. The oronasal mask is available in four sizes, with or
without head straps. Advanced cushion design provides an effective seal without
excessive strap tightening. It has an air entrainment valve that provides quiet air flow.
The Quick Clip™ allows easy disconnection and reconnection of the head strap without
refitting the mask.
This mask provides more reliable ventilation and CO2 control than the nasal mask does.
Because it is larger and covers the mouth, there is an increased risk of aspiration and
patients may feel confined. In patients with no teeth or presence of facial hair, this may prevent a good seal
resulting in air leakage. Disadvantages include large leaks that increase the risk of complications such as eye
irritation and nasal skin necrosis secondary to tightening of the mask. Patients with large tongues may
obstruct the oral pharynx with the delivered pressure to the lungs. If the patient has large amount of
secretions the full face mask needs to be opened for the patient to expectorate frequently. The CO2 level
should also be monitored as the patient is rebreathing more expired CO2.

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Full Face Mask

The full face mask is selected in patients that have tried and failed using the nasal or
oronasal masks. Despite its fearsome appearance, the full face mask produces less
claustrophobia for patients. It has a larger, less obstructed viewing area, and decreases
the amount of direct pressure on the face. Both of these characteristics tend to reduce
anxiety. The faceplate also eliminates pressure on the bridge of the nose. The full face
mask provides a fast effective seal with no fitting. The straps also include a quick
release head strap (red strap) in case of emergency.
If the patient has large amount of secretions the full face mask needs to be opened for
the patient to expectorate frequently. The CO2 level should be monitored as the
patient is rebreathing more expired CO2. Complications from the previous use of
nasal or oronasal mask (as stated above) may continue with the use of NPPV.

Mouthpiece
This is the last option to be considered for delivery of NPPV in the acute care setting. Lipseal retention
devices may also be used to decrease the insufflation leakage out of the mouth when a nasal mask is used.

Troubleshooting
Problem Cause Troubleshooting
1. Mask uncomfortable to  Improper mask  Check for correct mask size, refit mask or try
wear size a different size mask
 Improper mask  Check head gear adjustments and reposition
adjustments
2. Significant air leak  Improper mask fit  Check for correct mask sizing, refit mask or
around the mask try a different size mask
 Improper mask  Check the head gear adjustments and refit to
adjustments patient
3. Skin redness due to mask  Improper mask fit  Refit mask or try a different size mask
 Improper mask  Rinse mask after cleaning to remove residue
cleaning
 Irritation or  Use a barrier between the skin and the mask;
allergic reaction if irritation continues, consider alternative
interfaces
4. Runny nose or nasal  Airflow reaction  Consider the use of a humidifier in the
congestion patient circuit
5. Dryness in throat or nose  Dry air  Consider the use of a humidifier in the
patient circuit
6. Nasal, sinus, or ear pain  Sinus or ear  Notify the physician
infection

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Noninvasive Positive Pressure Ventilation (NPPV)

Noninvasive positive pressure ventilation refers to continuous positive airway pressure (CPAP) as well as to
intermittent positive pressure ventilation (IPPV) and a combination of positive inspiratory pressure (PIP)
otherwise known as inspiratory positive airway pressure (IPAP) and a positive end-expiratory pressure
(PEEP) otherwise known as expiratory positive airway pressure
(EPAP).
Theoretically NPPV works by recruiting atelectic lung and
improving chest wall compliance by stretching the chest wall with
positive pressure ventilation.
Therapies such as bronchodilators, diuretics, antibiotics and
intensive airway secretion clearance take time to improve the
patient’s respiratory function. NPPV can be used as a bridge to
avoid invasive mechanical ventilation, while other therapies are
initiated.

Ventilator Settings

IPAP
Inspiratory positive airway pressure is the amount of pressure the ventilator applies to the airways during
inspiration. IPAP increases capacity and lessens resistance by pushing air into the lung when the patient
initiates a breath. The higher the IPAP, the more air is exchanged and the more CO2 is removed from the
lung. IPAP is usually adjusted in response to the patient’s CO2 level.
Increasing IPAP will increase the mean airway pressure. A secondary effect of IPAP is improved
oxygenation. Increased mean airway pressures also increase intrathoracic pressures. Increased intrathoracic
pressures affect the cardiovascular system by
decreasing preload (venous return) that may
result in changes of cardiac output and blood
pressure.

EPAP
Expiratory positive airway pressure is the
amount of pressure applied during expiration,
and during the pause between expiration and
inspiration. EPAP is always lower than IPAP
so expiration can occur. EPAP is similar to
PEEP, discussed more fully below.

PEEP
The normal airway pressure at the end of
expiration and before inspiration is zero.
Application of pressure by the ventilator at
this stage of the ventilatory cycle is called
positive end-expiratory pressure (PEEP). PEEP aids in propping open alveoli that would otherwise collapse
during the expiratory phase. It is a very effective treatment modality for V/Q mismatching (refer to glossary)
caused by atelectatic processes. PEEP enhances oxygenation by increasing the number of available gas
exchange units and is adjusted in response to measures of oxygenation. Use of PEEP allows lower FiO2

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levels, which are safer for the patient. PEEP also improves functional residual capacity (FRC) because more
of the lung is expanded.
PEEP is measured at the bedside by noting the airway pressure reading at the end of expiration. If the reading
is greater than zero, PEEP is present. A PEEP setting of 5 cm H2O is considered equivalent to the effect of
the closed glottis, and is called physiologic PEEP.
The beneficial effects of PEEP take up to an hour or two to be fully effective and are lost immediately when
the pressure is removed. Each time the mask seal is broken, PEEP is lost. Patients who are highly dependent
on PEEP to maintain oxygenation will not tolerate frequent mask removals.

CPAP
CPAP is physiologically the same as PEEP. The term CPAP is used when PEEP is applied without any other
ventilator modality such as IPAP or a ventilator rate during spontaneous breathing. Continuous positive
airway pressure (CPAP) can be used to compensate for air leaks in NPPV. The typical amount used in NPPV
is 5 – 10 cm H2O. CPAP also aids in keeping the oropharynx from collapsing before the onset of inspiration
making it very beneficial for the treatment of OSAs.

Auto-CPAP (Auto-PEEP)
Auto-CPAP occurs when the expiratory time is not sufficient for the lung to empty before the patient takes
the next breath. It is also referred to as breath stacking. Patients with emphysema or severe tachypnea are at
high risk. Auto-CPAP is also sometimes called breath stacking. With each breath, the pressure within the
alveoli increases. The alveolar pressure will be greater than the baseline at the end-expiration. If pressure
continues to build in this manner, delivered tidal volumes will drop, work of breathing will increase, and the
patient will experience acute discomfort until the extra volume producing the pressure is released. Two
interventions that can correct auto CPAP are the reduction in airway obstruction or increased expiratory time.

Pressure Support
Pressure support is sometimes referred to as PSV (pressure support ventilation), though this is not a precise
term. Pressure support works by responding to a patient’s inspiratory effort with a positive pressure breath
delivered at a set pressure. When used in NPPV, pressure support is calculated by subtracting the EPAP from
the IPAP (PSV = IPAP – EPAP). The volume of a pressure support breath will vary from breath to breath in
proportion to the patient’s inspiratory effort.
Pressure support is used to increase ventilation, decrease load, and compensate for increased airway
resistance. Pressure support enhances spontaneous tidal volumes, and is adjusted in response to CO2 levels.
Pressure support typically ranges from 5 – 30 cm H2O.

Rate
The set ventilatory rate is the minimum number of breaths the ventilator will deliver to the patient each
minute. Rate is a determinant of ventilation, and is adjusted to in response to the patient’s CO2 levels. In
noninvasive positive pressure ventilation rate is used only as a backup in the event of apnea. The rate is set
below the patient’s spontaneous rate to permit the ventilator to trigger in the event of detected apnea. Normal
backup breath rates used in NPPV are between 4 to 6 breaths per minute.

Oxygen Percentage
The fraction of inspired oxygen (FiO2) is the amount of oxygen delivered to the patient. FiO2 can be
expressed as a decimal fraction or a percentage. Oxygen concentrations of greater than 0.50 (50%) increase
the risk of oxygen toxicity if delivered for more than 24 hours. Supplemental oxygen is administered in
response to low PaO2, SpO2, or indicators of tissue hypoxia.
There are a few causes of tissue hypoxia that are unresponsive to treatment with supplemental oxygen.

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 Anemia is associated with high oxygen saturation but limited oxygen carrying capacity; additional
oxygen will not improve oxygen delivery to the tissues under these circumstances. The only effective
treatment for tissue hypoxia related to anemia is to increase the hemoglobin level.
 Right to left shunt occurs when a proportion of the circulated blood passes through the pulmonary
circulation without coming into contact with any functional gas exchange units. This phenomenon can
occur with congenital heart defects and severe atelectasis, pneumonia or pulmonary edema. Increasing
the amount of delivered oxygen will not help in this case, because the blood would still not come into
contact with the extra oxygen.
 Hypoxia related to insufficient perfusion does not improve with supplemental oxygen either. The
problem here is lack of delivery from a dysfunctional cardiovascular system. To correct hypoxia due to
this cause adequate circulation must be restored.
 Tissue dysoxia occurs when a toxin prevents the cells from utilizing delivered oxygen. Dysoxia is
associated with cyanide toxicity and severe sepsis. The only correction is to reverse the effects of the
toxin.
Tidal Volume
Tidal volume (VT) is the volume of gas delivered to the patient with each breath. The normal tidal volume is
approximately 6 – 8 ml/kg body weight. The tidal volume is closely related to ventilation, and often
manipulated in response to abnormal levels of CO2.

Flow
With NPPV, ventilatory support results from the cyclic application of an airway pressure that generates a
desired amount of air flow. This pressure is selected to compensate for intermittent leaks, provide flow
sufficient to meet the patient’s demands, and to avoid over pressurizing the airway. The ventilation achieved
from a set airway pressure is dynamic and varies with patient effort and the mechanical characteristics of the
patient’s respiratory system (compliance, resistance, and the presence or absence of auto-PEEP). Inspiratory
flow ends when IPAP cycles to EPAP. Patients who are exhibiting air hunger on NPPV may have inadequate
flow to meet their respiratory demand.

Initial Ventilator Settings

Usually settings begin at an IPAP of 10cm H2O, EPAP of 5cm H2O and a FiO2 equivalent to any
supplemental oxygen the patient was already receiving. Adjustments are made in the IPAP by increasing it in
small increments based upon the desired tidal volume (6-8 ml/kg), respiratory rate and ABG results. The
IPAP is increased in small increments (keeping it at least 4 cm H2O above EPAP) to the maximum pressure
the patient can tolerate without discomfort and major air leaks. IPAP is titrated to achieve a respiratory rate
less than 25 breaths per minute and a tidal volume (Vt) > 7 ml/kg. FiO2 and EPAP are titrated to achieve an
oxygen saturation of 90%.

Modes of Ventilation

Pressure limited ventilation

Pressure-limited ventilation will deliver air until a preset pressure is reached. It is a cyclic application of
airway pressure or flow (IPAP & EPAP). Not every patient achieves the desired ventilatory effect from set
pressures or flow. Variability in tidal volume is the result of patient effort and the mechanical characteristics
of the patient’s respiratory system related to the ongoing pathology present. Patient demand must be met with
IPAP & EPAP. Adjustments in settings are required to achieve synchrony in the ventilatory cycle.

Volume limited ventilation

Volume-limited ventilation means the ventilator will deliver air until a set volume has been given with each
breath. It is used to assist the patient that requires high tidal volumes (10 – 15ml/kg) to compensate for an air
leak. Patients that utilize this mode include obese patients (need high inflation pressure); patients with
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neuromuscular diseases (need high tidal volumes) and those with chest wall deformities (need high inflation
pressure).

Proportional Assist Ventilation (PAV)

This mode responds rapidly to the patient’s ventilatory efforts. Adjusting the gain on the flow and volume
signals selects the proportion of breathing work that is to be assisted. This is a newer mode of ventilation.

Patient Examples:
Patient #1:
Mr. Smith is on NPPV settings of: IPAP 15 cm H2O, EPAP 5 cm H2O, and FiO2 0.40
ABG reveals pH 7.28, PCO2 62, PO2 49, HCO3 24
ABG interpretation reveals that the patient is in respiratory acidosis with hypoxemia.
Vital Signs: BP 120/75, HR 116, RR 30, Spontaneous Tidal Volume (VT) 300.
The patient is hemodynamically stable. NPPV is still indicated. NPPV settings need to be adjusted based on
the data above. The priority will be to first increase the FiO2 to 0.50 in an effort to correct the hypoxemia.
The second priority will be to increase the IPAP to 20 cm H2O to improve the tidal volume and correct the
elevated CO2. To maintain the PSV of 10 cm H2O, the EPAP will also need to be increased to 10 cm H2O.

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Patient #2:
Mrs. Brown is a 52 year-old female with a history of COPD and CHF. She currently has pulmonary edema.
Her physician has ordered NPPV. Current settings are IPAP 25 cm H2O, EPAP 10 cm H2O, and FiO2 of 0.50.
Her SpO2 is 99%.
Current ABG reveals: pH 7.48, PCO2 31, PO2 90, HCO3 26
ABG interpretation: Respiratory Alkalosis uncompensated.
Vital Signs: RR 24, Spontaneous tidal volume (VT) 700 ml, HR 115, BP 150/86
The patient is hemodynamically stable. NPPV is still indicated. Adjustments need to be made in the NPPV
settings based upon the data above. The elevated pH and low PaCO2 indicate hyperventilation, and the PaO2
is needlessly high, increasing her risk of oxygen toxicity. The IPAP should be decreased to 20 cm H2O to
reduce the tidal volume – this should correct the respiratory alkalosis. The FiO2 should be decreased to 0.40
to lessen the risk of O2 toxicity. The PSV on the new settings is now reduced to 10 from the original 15,
which should reduce the tidal volume. Continual assessment of patient’s respiratory rate and use of accessory
muscles and spontaneous tidal volume (VT) should occur to detect how the patient is responding to the
setting changes.

Nursing Care
Nursing care is focused on preventing the complications of noninvasive ventilation – skin necrosis, gastric
insufflation, drying/thickening of oral and nasal secretions, nasal congestion, and barotraumas while
monitoring for other system complications. A resuscitator bag and mask must always be with the patient in
the event of an emergency. To try and prevent skin necrosis tincture of benzoin and a skin patch (such as
Duoderm) may be applied to the bridge of the nose. Adequate humidification of air, proper hydration, and
frequent mouth care is necessary to prevent drying and thickening of oral secretions. Nasal congestion may
require a physicians order for a nasal decongestant, corticosteroids or antibiotics as needed. Occasionally air
leaks around the nasal area may cause eye irritation. Adjusting the mask or changing to a different interface
may decrease the air leak. The physician may also consider ordering eye drops.
Documentation of settings (FiO2, RR, PSV, minute ventilation, IPAP, EPAP) and volumes are placed on the
interdisciplinary flowsheet by the respiratory therapist every four hours and with any changes. Coordination
of care is needed between the nurse and respiratory therapist for administration of oral medications and/or
other procedures to assess the patient’s tolerance without NPPV.

Weaning
A patient is considered ready for weaning when the underlying disease process that necessitated mechanical
ventilation begins to resolve and the patient is no longer requiring increases in pressures or FiO2. At this
point the pressures and/or FiO2 will be decreased in small increments while the patient is closely monitored.
If the patient tolerates the changes well, another incremental decrease is attempted. If the patient does not
tolerate the decreased settings as evidenced by increased respiratory rate, use of accessory muscles or
desaturation, the settings are increased and the patient allowed to rest for a few hours. The process then
begins anew. The speed of weaning will depend on how well the underlying disease process has resolved the
overall health of the patient, and the clinician’s judgment. Weaning may take place over a period of a few
hours to a few days.
Once the FiO2 and pressure settings are at minimal levels, the patient will begin to spend more time off the
ventilator. Time off NPPV allows for oral intake of foods, fluids and medication, takes pressure off the facial
skin, and allows the patient to expectorate and perform oral hygiene. At this time activity levels will also be
gradually increased and aggressive pulmonary toilet continues. Close monitoring of the patient continues
during this phase, and the same indicators of weaning tolerance are used.
NPPV can be reapplied if the patient does not successfully wean. If NPPV has been prolonged or if the
patient’s hemodynamic status deteriorates, invasive mechanical ventilation can be instituted. If the patient
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fails weaning and the patient or family desires that the ventilator be removed, follow your hospital’s
procedures for discontinuation of life support.

Summary
Noninvasive mechanical ventilation is available to assist patients to breathe in the event of exacerbated
pulmonary pathology in the acute care setting. Patients need to be offered this therapy as an adjunct to
invasive mechanical ventilation listing the benefits and risks to both. Success of NPPV is highly dependent
upon the inclusion/exclusion criteria and understanding of the nurse, respiratory therapist and physician to
provide education to the patient as to the effectiveness of the therapy.

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Appendix A: Muscles of Ventilation

Diaphragm
The diaphragm is the major muscle of ventilation. It is a dome-shaped musculofibrous partition located
between the thoracic and abdominal cavities. It is composed of two muscles: the right and left
hemidiaphragms. The diaphragm allows the esophagus, the aorta, several nerves, and the inferior vena cava
to exit through it. The phrenic nerve exits the central nervous system between cervical vertebrae 3 – 5 and
extends down to innervate the diaphragm assisting in controlling ventilation.

© Ciba Geigy

Muscles of Inspiration (I) Muscles of Expiration (E)

Scalene muscles Rectus abdominis muscles
Sternocleidomastoid muscles External abdominal obliqus muscles
Pectoralis major muscles Internal abdominis obliquus muscles
Trapezius muscles Transversus abdominis muscles
External intercostal muscles Internal intercostal muscles

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Accessory Muscles of Ventilation

Scalene Muscle (I) St l id t id l (I)

Pectoralis major muscle (I)

Rectus Abdominis (E)

E t l Obli (E)

Internal
intercostal
muscles (E)

Trapezius
muscle (I) External
intercostal
muscle (I)

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Appendix B: Management of Snoring

1. Lifestyle modifications – weight loss, overweight obese BMI > 30, no alcohol ingestion, avoid sedative,
hypnotic and muscle relaxant medications, and stop smoking.
2. Positional Training – prevention of snoring – not to lie on back
3. Medications – none to cure snoring – if nasal congestion – nasal decongestants
4. Nasal Dilators – nozovent, or Breathe Right strips
5. CPAP – nasal mainstay of treatment for sleep apnea (overkill for snoring)
6. Oral appliances – preference for non-apneic snoring – two dozen types of oral appliances focuses in two
categories
a. Tongue-retaining devices (TRD)
b. Mandibular advancement appliances (MAA)
1. Fixed
2. Adjustable
7. Surgical treatment
a. Nasal surgery
b. Pharyngeal surgery – non-laser or laser

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Appendix C: Treatment for Sleep Apnea

Snoring is the most common symptom of sleep apnea.
Direct:
Stimulate upper airway muscle activity
Modulate central respiratory control
Alter sleep patterns (suppress REM sleep, arousals)
Indirect:
Anti-obesity agents
Enlarge upper airway
Treatment complications:
Alterations in sleep patterns cause daytime sleepiness
Oxygen-induced respiratory drive depression
(if supplemental oxygen is used to treat apnea-induced hypoxemia)

Obstructive Sleep Apnea

Pharmacologic
Beneficial:
 Tricyclic Antidepressants – (Imipramine, Protriptyline) decrease REM Sleep
 Serotonergic Agents – SSRI’s (Fluoxetine) – decreases apnea hypopnea index during non-REM
sleep improving upper airway stability
 Sex Steroids – Estrogen/Progesterone replacement – increases muscle activity – genioglossus
muscle of the upper airway. There is no effect on apnea events
 Theophylline – increases diaphragm contractility. Blockade of ventilatory depressant – acts on
endogenous neuromodulator adenosine.
 Octreotide – used for hypothyroidism/acromegaly –– decreases central sleep apnea episodes
Harmful effects:
 Antihypertensive agents – ACE – (cilazapril), beta-blockers (metoprolol) Calcium Channel
blockers– decreases ventilatory response to hypercapnia and hypoxia and exacerbate
hypoventilation especially during sleep. Beta blockers can also increase airway resistance.
 Nicotine – disturbs sleep
 Benzodiazepines – decreases ventilatory response to hypercapnia and hypoxia

Central Sleep Apnea

Harmful effects
 Acetazolamide – induces metabolic acidosis – in turn stimulates respiratory drive

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 Theophylline –avoid use of Theophylline in patients with CHF, hypertension, arrhythmias and/or
right heart failure. The decreased clearance of Theophylline in these patients causes hypercarbia.
 Other – oxygen therapy related to heart failure, Benzodiazepines – decreases elevated ventilatory
drive

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Appendix D: APACHE Scoring System

The APACHE (Acute Physiology And Chronic Health Evaluation) is a system for classifying patients in the
intensive care unit. Patients are evaluated by physiologic scores and evaluation of chronic health status.
Physiologic scores correlate with severity of illness. Results of the evaluation can be used to estimate the
mortality rate for patients in the ICU and during the hospitalization.

Visit http://www.sfar.org/scores2/apache22.html for more information.

References:

Knaus WA; Zimmerman JE; et al. APACHE - acute physiology and chronic health evaluation: a
physiologically based classification system. Crit Care Med. 1981; 9: 591-597.

Knaus WA; et al. APACHE II: A severity of disease classification system. Crit Care Med. 1985; 13:
818-29.

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Glossary
ABG: Arterial blood gas. A test which analyzes arterial blood for oxygen, carbon dioxide and bicarbonate
content in addition to blood pH. It is utilized to test the effectiveness of ventilation and oxygenation.
Acidosis: A pathologic state characterized by an increase in the concentration of hydrogen ions in the arterial
blood above the normal level. May be caused by an accumulation of carbon dioxide or acidic products of
metabolism or a by a decrease in the concentration of alkaline compounds.
Adrenergic: Relating to drugs that mimic the actions of the sympathetic nervous system
Alkalosis: A state characterized by a decrease in the hydrogen ion concentration of arterial blood below
normal level. The condition may be caused by an increase in the concentration of alkaline compounds, or by
decrease in the concentration of acidic compounds or carbon dioxide.
Alveoli: Plural of Alveolus. Terminal air spaces that contain numerous capillaries in their speta, which serves
as sites for gas exchange.
Alveolus: A small cell, cavity or socket. In the lung it is the acinus which is a gas exchange unit.
Agonist: A drug capable of combining with receptors to initiate drug actions; it possesses affinity and
intrinsic activity.
Anticholinergic: Antagonistic to the action of parasympathetic or other cholinergic nerve fibers.
Apnea: Cessation of airflow for 10 seconds or more and hypopneas as reductions in normal tidal volumes by
more than 30%.
Asthma: A disease process that is characterized by paradoxical narrowing of the bronchi (lung passageways)
making breathing difficult.
Bronchodilator: A medication that acts to expand or increase the lumen of the airway to allow the
unrestricted passage of air. These medications are commonly given to asthma patients who manifest
wheezing.
Bronchospasm: An abnormal constriction of the smooth muscle of the bronchi resulting in an acute
narrowing and obstruction of the respiratory airway. A cough with generalized wheezing usually indicates
this condition. The most common cause of bronchospasm is asthma.
Capnogram: A continuous record of the carbon dioxide content of expired air.
Capnography: Continuous measurement and graphical display of the carbon dioxide (CO2) level of a
patient’s exhaled breath.
Capnometry: Measurement of CO2 in proximal airway during inspiration and expiration.
Chemoreceptor: Any cell that is activated by a change in its chemical milieu and results in a nerve impulse.
Chronic obstruction pulmonary disease (COPD): a disease process involving chronic inflammation of the
airways, including chronic bronchitis (disease in the large airways) and emphysema (disease located in
smaller airways and alveolar regions). The obstruction is generally permanent and progressive over time.
Compliance: A measure of distensibility of a chamber expressed as a change in volume per unit change in
pressure.
Corticosteroids: Any of various adrenal-cortex steroids (such as corticosterone, cortisone, and aldosterone)
used especially as anti-inflammatory agents.
Cyanosis: A dark bluish or purplish discoloration of the skin and mucous membrane due to deficient
oxygenation of the blood.
Dead space: Area in which there is ventilation but no perfusion.
Diaphragm: The musculomembranous partition between the abdominal and thoracic cavities.
Diffusion: The random movement of molecules or ions or small particles in solution or suspension under the
influence of thermal motion toward a uniform distribution throughout the available volume.
Hypercapnia: An excess of carbon dioxide in the blood
Hypocapnia: A deficiency of carbon dioxide in the blood
Hypoxemia: Below-normal oxygen content in arterial blood due to deficient oxygenation of the blood and
resulting in hypoxia.
Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the
tissue by blood.
Hypoperfusion: Decreased blood flow through an organ.

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Hyperventilation: A state in which there is an increased amount of air entering the pulmonary alveoli
(increased alveolar ventilation), resulting in reduction of carbon dioxide tension and eventually leading to
alkalosis.
Hypoventilation: A state in which there is a reduced amount of air entering the pulmonary alveoli.
Lactate: A salt or ester of lactic acid. Lactic acid is a byproduct of anaerobic oxidation, metabolism of sugar.
Leukotriene: Product of eicosanoid metabolism with postulated physiologic activity such as mediators of
inflammation and roles in allergic reactions.
Mechanoreceptor: A receptor which responds to mechanical pressure or distortion.
Mucolytic: Capable of dissolving, digesting or liquefaction of mucous.
Noninvasive: Descriptive of diagnostic procedures which do not involve the insertion of needles, cannulas,
or other devices that require penetration of the skin/body.
Oxygenation: The process of supplying, treating or mixing with oxygen.
Oxygen delivery system: A device used to deliver oxygen concentrations above ambient air to the lungs
through the upper airway.
Oxyhemoglobin: Hemoglobin in combination with oxygen.
Peak Expiratory Flow Rate (PEFR): Measurement of the maximum rate of airflow attained during a forced
vital capacity determination.
Perfusion: The passage of fluid (usually blood) through out the body (organs and tissues).
Pneumothorax: An abnormal state characterized by the presence of gas (as air) in the pleural space.
Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and
conveying unaerated blood to the lungs.
Pulmonary Embolism: The lodgment of a blood clot or fat globulin the lumen of a pulmonary artery,
causing a severe dysfunction in respiratory function.
Pulse Oximetry: Determination of arterial saturation of hemoglobin: the absorption of light by blood is
measured spectrophotometrically.
Resistance: Impedance to flow in a tube or conduit; quantified as a ration of the difference in pressure
between the two points along a tube length divided by the volumetric flow of the fluid per unit time.
Respiration: Gas exchange, specifically the exchange by a living organism of carbon dioxide (CO2), a waste
product formed during the oxidation of food molecules, for oxygen (02), which the organism needs to
continue oxidizing its food.
Respiratory insufficiency: The inability of the body to provide adequate arterial oxygenation.
Spacer: A device used to improve aerosol delivery by stabilizing particle size and reducing the need for
breath/actuation coordination.
Spectrophotometry Equipment: Devices that measure emission or absorption of light as a function of
wavelength.
Surfactant: Lung lining fluid that reduces surface tensions
Tachypnea: An abnormally rapid (usually shallow) respiratory rate. The normal resting adult respiratory rate
is 12 – 20 breaths/minute.
Ventilation: Movement of gas(es) into and out of the lungs(breathing)
Volume: Space occupied by matter measured in milliliters or liters
V/Q ratio: The ratio of ventilation (V) to perfusion (Q).
V/Q Mismatch: Ventilation/Perfusion mismatch – an imbalance between ventilation compared to perfusion.
Extremes are shunt perfusion and dead space ventilation.

Abbreviations
APAP – Auto-Positive Airway Pressure
CPAP – Continuous Positive Airway Pressure
EPAP – Expiratory Positive Airway Pressure
IPAP – Inspiratory Positive Airway Pressure

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Internet Resources
Auscultation Assistant – Breath Sounds
http://www.wilkes.med.ucla.edu/lungintro.htm
The R.A.L.E. Repository
http://www.rale.ca/Repository.htm

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Post Test

Directions: In order to receive 2.0 contact hours, you must:

 complete the posttest at the end of this packet
 achieve an 84% on the posttest
For Non-Orlando Health employees: Complete the test using the bubble sheet provided. Be sure to
complete all the information at the top of the answer sheet. You will be notified if you do not pass, and you
will be asked to retake the posttest.
Return to: Orlando Health, Education & Development, MP14, 1414 Kuhl Ave, Orlando, FL 32806

For Orlando Health Team Member: Please complete testing via Online Testing Center. Log on to:
SWIFT Departments E-Learning Testing Center. Use your Orlando Health Network Login and
password. Select “SLP” under type of test; choose correct SLP Title. Payroll authorization is required to
download test.

1. The primary chemoreceptor that senses a low PCO2 is located in the:

A. aortic arch
B. carotid body
C. medulla
D. cerebrum

2. The primary symptom of obstructive sleep apnea is:

A. coughing
B. abdominal breathing
C. hiccups
D. snoring

3. Diagnosis of hypoxemic respiratory failure is made on the basis of:

A. SpO2
B. PaO2
C. ETCO2
D. PaCO2
4. Symptoms of hypercapnic respiratory failure (hypercapnia) include:
A. hyperpnea
B. hypotension
C. diaphoresis
D. cyanosis

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5. Select the patient that is the most appropriate candidate for non-invasive positive pressure ventilation:
A. morbidly obese, in acute respiratory failure
B. agitated, restless hypoxemic respiratory failure
C. CHF with pulmonary edema
D. 50% facial/neck burns

6. Select the most appropriate interface for the patient with hypoxemic respiratory failure:
A. nasal mask
B. lipseal mouthpiece
C. oronasal mask
D. the type the patient is most comfortable with

7. Noninvasive positive pressure ventilation:

A. improves ventilation by supplying supplemental oxygen
B. provides continuous positive airway pressure to aid oxygenation and ventilation
C. requires use of a definitive invasive artificial airway
D. prevents a patient from receiving nutritional support

8. Gastric insufflation is a common complication of NPPV because the:

A. gastroesophageal sphincter can only withstand peak airway pressures up to 25 cm H2O
B. ileocecal junction relaxes to allow movement of air through the bowel that can lead to an ileus
C. bulbocavernous muscles contract to allow passage of gas
D. face mask is not secured properly

9. The use of CPAP in noninvasive mechanical ventilation is indicated for:

A. increasing tidal volume
B. compensation of air leakage
C. improving minute ventilation
D. decreasing secretions

10. Pressure support ventilation is utilized to:

A. improve functional residual capacity (FRC)
B. stabilize the V/Q mismatching
C. compensate for increased airway resistance
D. improve chest wall compliance by stretching the chest wall

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11. Select the patient that is the best candidate for a nasal mask.
A. patient with facial fractures
B. male patient with facial hair
C. female patient with deviated nasal septum
D. elderly patient with depressed gag reflex

12. The full face mask is selected for patients that have:
A. dentures
B. full heavy beards
C. facial fractures
D. claustrophobia

13. Application of the interface for noninvasive positive pressure ventilation involves:
A. respiratory therapy, speech therapist
B. clinical technician, physician
C. respiratory therapist, nurse, physician
D. respiratory therapist, nurse, speech therapist

14. Calculate the amount of pressure support (PSV) with the following ventilator settings. IPAP 25, EPAP
15, FiO2 .35
A. 5
B. 10
C. 15
D. 20

15. Mr. J is admitted for elective orthopedic surgery with a history of sleep apnea that requires noninvasive
mechanical ventilation. His immediate post operative course requires the use of noninvasive positive
pressure ventilation at the following settings: IPAP 15, EPAP 5 FiO2 0.30. 12 noon vital signs BP 120/70
HR 90, RR 18, SpO2 sat of 94% clear bilateral breath sounds. At 1800 your assessment findings are:
vital signs BP 130/68 HR 112, RR 28, SpO2 88% breath sounds diminished in bases. You notify the
respiratory therapist and physician, and it is determined that adjustments are required with the NPPV.
Based on the most recent assessment data, the initial change in NPPV would be to increase:
A. IPAP to 20
B. FiO2 to 0.40
C. EPAP to 10
D. IPAP to 30, EPAP to 10

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References
Ahya, S. N., Flood K., & Paranjothi, S. (2001). The Washington Manual of Medical Therapeutics 30th Ed.
Philadelphia: Lippincott Williams & Wilkins.
Bach, J. R (2002). Noninvasive Mechanical Ventilation. Philadelphia: Hanley & Belfus, Inc.
Branson, R. D., Hess, D. R., & Chatburn, R. L. (1999). Respiratory Care Equipment 2nd Ed. Philadelphia:
Lippincott Williams & Wilkins.
Caples, S. M. & Gay, P. C. (2005). Noninvasive positive pressure ventilation in the intensive care unit: A
concise review. Critical Care Medicine, 33(11) 2651-2658.
Des Jardins, T. (2002). Cardiopulmonary Anatomy & Physiology 4th Ed. Albany, New York: Delmar
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Gavaghan, S. R., & Jeffries, M. (2006). Your patient’s receiving noninvasive positive-pressure ventilation:
Learn to assist his breathing without the need for intubation. Nursing 2006, 36(5), 46-47.
Gay, P. C. (2004). Chronic Obstructive Pulmonary Disease and Sleep. Respiratory Care 49(1) 39-51.
Gay, P. C. (2009). Complications of noninvasive ventilation in acute care. Respiratory Care 54(2) 246-258.
Hess, DR, MacIntyre, NR, Mishoe, SC, Galvin, WF, Adams, AB, Saposnick, AB (2002). Repsiratory Care
Principles and Practice. Philadelphia: W.B. Saunders Company.
Kacmarek, R. M. (2009). Should noninvasive ventilation be used with the do-not-intubate patient?
Respiratory Care 54(2), 223-231
Kallet, R. H. & Diaz, J. V. (2009). The physiologic effects of noninvasive ventilation. Respiratory Care
54(1), 102-115.
Lanken, P. N., (2001). The Intensive Care Unit Manual. Philadelphia: W.B. Saunders Company.
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Company.
MacIntyre, N. R., Branson, R. D. (2001). Mechanical Ventilation. W.B. Saunders Company: Philadelphia.
Netter, FH (1989). Atlas of Human Anatomy. Summit, New Jersey: Ciba-Geigy Corporation.
Penuelas, O., Frutos-Vivar, F., & Esteban, A. (2007). Noninvasive positive-pressure ventilation in acute
respiratory failure. CMAJ 177(10), 1211-1218.
Rau, Jr., J. L. (2002). Respiratory Care Pharmaclogy 6th Ed. St. Louis, Missouri: Mosby.
Scala, R., Naldi, M., Archinucci, I., Coniglio, G., Nava, S. (2005). Noninvasive positive pressure ventilation
in patients with acute exacerbations of COPD and varying levels of consciousness. Chest 128(3),
1657-1666.
Schettino, G., Altobelli, N., & Kacmarek, R. M. (2005). Noninvasive positive pressure ventilation reverses
acute respiratory failure in select “do-not-resuscitate” patients. Critical Care Medicine 33(9), 1976-
1982.
St. John, R. E. (2006). Airway and ventilatory management. In Chulay & Burns (Eds.), AACN Essentials of
critical care nursing (pp. 111-144). New York: McGraw-Hill.
Thompson, JM, McFarland, GK, Hirsch, JE, Tucker, SM (2002). Mosby’s Clinical Nursing 5th Edition. St.
Louis, Missouri: Mosby.
Tobin, MJ (1994). Principles and Practice of Mechanical Ventilation. McGraw-Hill: New York.
Urden, LD, Stacy, KM, Lough ME (2002). Thelan’s Critical Care Nursing Diagnosis and Management. St.
Louis: Missouri Mosby.

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