VENTILATORY FAILURE
Ventilatory failure is the type of
ventilation-perfusion (V/Q) mismatching
in which perfusion is normal but ventilation is inadequate. Ventilatory failure occurs when the
thoracic pressure cannot be changed
sufficiently to permit appropriate air movement into and out of the lungs. As a
result, insufficient oxygen
reaches the alveoli and carbon dioxide is retained. Both problems lead to hypoxemia.
Ventilatory
failure is usually the result of one or more of the following three mechanisms: a mechanical abnormality of the lungs or
chest wall, a defect in the respiratory control center in the brain, or an impairment in the function of the respiratory muscles. Ventilatory failure is usually
defined by a Paco2 level
above 45 mm Hg in clients who have otherwise healthy lungs.
OXYGENATION FAILURE
In oxygenation failure, thoracic pressure changes are
normal, and the lungs can move air sufficiently but cannot oxygenate the
pulmonary blood properly. Oxygenation failure can result from the type of V/Q mismatch in which
ventilation is normal but
perfusion is decreased.
COMBINED VENTILATORY AND OXYGENATION FAILURE
Combined ventilatory and oxygenation failure involves
insufficient
respiratory movements (hypoventilation). Gas exchange at the
alveolar-capillary membrane is inadequate, so that too little oxygen reaches
the blood and carbon dioxide is retained. The condition
may or may not include poor pulmonary
circulation. When pulmonary circulation is not adequate, V/Q mismatching occurs and both ventilation
and perfusion are inadequate. This
type of respiratory failure results in a more profound hypoxemia than either
ventilatory failure or oxygenation failure alone.
Etiology
VENTILATORY
FAILURE
Numerous diseases and conditions can result in
ventilatory failure. Causes of
ventilatory failure are categorized as either extrapulmonary (involving
nonpulmonary tissues but affecting respiratory function) or intrapulmonary (disorders
of the respiratory tract).
OXYGENATION FAILURE
Many
diseases and disorders of the lung can cause oxygenation failure. Mechanisms
include impaired diffusion of oxygen at the alveolar level, right-to-left shunting of blood in the pulmonary vessels, V/Q mismatching, breathing
air with a low partial
pressure of oxygen (a rare problem), and abnormal hemoglobin that fails to
absorb the oxygen. In one type of V/Q mismatching, areas of the lungs are still being perfused but gas exchange is not able to occur, which leads
to hypoxemia. An extreme example of V/Q mismatching is
a right-to-left shunt. A normal shunt is
less than 5% of cardiac output. With a
right-to-left shunt, increased amounts of venous blood are not oxygenated, and 100% oxygen does not correct the deficiency. A classic cause of such a V/Q mismatch
is acute respiratory distress syndrome (ARDS).
COMBINED VENTILATORY AND OXYGENATION FAILURE
A combination of ventilatory failure and oxygenation
failure occurs in clients who have abnormal lungs, such as those who have any
form of chronic airflow limitation (CAL), such as chronic bronchitis, emphysema,
or asthma). The bronchioles and
alveoli are diseased (causing oxygenation failure), and the work of breathing increases until the
respiratory muscles are unable to
continue (causing ventilatory failure). Acute respiratory failure results. This process can also occur in clients who have
cardiac failure, as well as respiratory failure. This is a very dangerous
situation because the cardiac system cannot compensate
for the decreased oxygen by increasing the cardiac output.
COLLABORATIVE MANAGEMENT
Assessment
The
nurse assesses for dyspnea (difficulty breathing), the hallmark of respiratory failure. With use of a
dyspnea assessment guide, if
one is available, the nurse objectively
evaluates the dyspnea. Depending on the process, nature, and course of the
underlying condition, the client may or
may not be aware of dyspnea. In addition, the client needs to be alert enough to perceive the sensation of
difficult breathing.
Dyspnea tends to be more intense when it develops
rapidly. Slowly progressive respiratory failure
may first manifest as dyspnea on exertion
(DOE) or when lying down. The client notes orthopnea, finding it is
easier to breathe in an upright position.
In the client with chronic respiratory problems, a minor increase in dyspnea from the baseline
condition may represent severe gas
exchange abnormalities.
The nurse assesses for a change in the client's
respiratory rate or pattern, a change in lung sounds, and the signs and
symptoms of hypoxemia and hypercapnia. Pulse oximetry may
indicate decreased oxygen saturation, but an
arterial blood gas (ABG) analysis is needed for adequate assessment of oxygenation status. The health care
provider reviews the ABG studies to
identify the degree of hypercapnia and
hypoxemia.
Interventions
The physician orders oxygen therapy for the client
with acute respiratory failure to keep the partial pressure of arterial oxygen (Pao2) level above 60 mm Hg while treating the underlying cause of the respiratory failure. If
supplemental oxygen cannot maintain
acceptable Pao2 levels, the physician may order mechanical ventilation.
The nurse or assistive nursing personnel helps the client find a position of comfort that allows easier
breathing. To decrease the anxiety commonly associated with dyspnea,
the nurse assists with interventions such as
relaxation, guided imagery, and
diversion. Energy-conserving measures, such as minimal self-care and no
unnecessary procedures, are instituted. The physician
may order pulmonary medications administered
systemically or by metered dose inhaler (MDI) to open the bronchioles and
promote gas exchange. The client is instructed
about the use of the inhaler and about the medications. Deep breathing and
other breathing exercises are encouraged.
ACUTE RESPIRATORY
DISTRESS SYNDROME
OVERVIEW
Acute respiratory distress syndrome (ARDS) is a
form of acute respiratory
failure characterized by the following:
Refractory hypoxemia
Decreased pulmonary compliance
Dyspnea
Noncardiogenic bilateral pulmonary edema
Dense pulmonary infiltrates (ground-glass appearance)
ARDS usually occurs after an acute catastrophic event in people with no previous pulmonary disease. The
mortality rate remains at 50% to 60% despite
continuing research. Terminology for ARDS
includes the current term noncardiogenic pulmonary edema and the former
term shock lung.
Pathophysiology
Despite diverse causes leading to injury of the
lung in ARDS, no common pathway has
been found in its development, although the principal clinical manifestations
are similar. In some forms of
ARDS, the pathophysiologic mechanism is understood; in many others, it is not. The major site of
injury in the lung is the
alveolar-capillary membrane, which is normally permeable to only small molecules. The
alveolar-capillary membrane can be injured intrinsically (caused by
conditions happening within the client, such as sepsis, pulmonary embolism, or
shock) or extrinsically (caused by conditions from the outside, such as
aspiration or inhalation injury). The interstitium
of the lung normally remains relatively dry, but in clients with ARDS, increased extravascular lung fluid contains a high concentration of proteins.
Other significant changes occur in the alveoli and
respiratory bronchioles.
The type II pneumocyte is responsible for producing surfactant, a substance that maintains the
elasticity of lung tissue and
prevents alveolar collapse on expiration. Surfactant activity is reduced in
ARDS either because of destruction
of the type II pneumocyte or inactivation or dilution of surfactant.
Consequently, the alveoli become unstable and tend to collapse unless they are filled with fluid
from the interstitial space.
These alveoli can no longer participate in gas exchange. As a result,
interstitial edema forms around terminal airways, which are compressed and
obliterated. Lung volume
is further reduced, and there is even less compliance (elasticity). As the leak expands, fluid,
protein, and blood cells collect
in the interstitium and alveoli. Lymph channels are compressed and ineffective.
Poorly ventilated alveoli receive
blood. Thus the shunt fraction increases, and hypoxemia and ventilation-perfusion (V/Q) mismatching
result.
Etiology
ARDS
is associated with a number of causative factors. Some causes involve direct injury to lung tissue; others do not
directly involve the respiratory system. Serious
nervous system injury, such as trauma, strokes, tumors, and sudden increases in cerebrospinal fluid pressure, may cause massive sympathetic discharge.
Systemic vasoconstriction results,
with redistribution of large volumes of blood into the pulmonary
circuit. The marked elevation of hydrostatic pressure, then, probably causes
lung injury. Processes that produce cerebral
hypoxia, such as shock and ascent to high altitudes, may operate by a
similar mechanism.
Some factors produce ARDS by direct injury to
the lung. For example, aspiration of gastric contents leads to mechanical
obstruction or produces an acid burn to the airway when the pH of the gastric contents is less than 2.5. In
such a direct injury, rapid
necrosis of the alveolar type I pneumocyte occurs. The injured capillary endothelium allows
protein and cellular
elements to escape from the intravascular space. Radiation, near-drowning, and
inhalation of toxic gases similarly injure the
alveolar and capillary endothelium. In addition,
trauma, sepsis, drowning, and burns cause the release of
thromboplastins, which form fibrin clots in the peripheral blood.
The clots, together with platelets and leukocytes, are filtered out in the
lung. In many cases of ARDS, especially after
trauma, production of plasminogen activation inhibitors by the liver is
enhanced. Fibrinolysis (clot breakdown) is prevented, and small emboli
remain in the lung. Disseminated intravascular
coagulation (DIC) plays a role in some clients.
Incidence/Prevalence
Because of varying definitions, the incidence of ARDS
is unknown, although a 1995 estimate suggested that 150,000
to 250,000 cases
of ARDS occur yearly in the United
States. Its high
rank on the list of common diseases may be a result of the improved treatment of other catastrophic illnesses.
A major goal in the prevention of ARDS is early
recognition of clients at
high risk for the syndrome. Because clients with aspiration of gastric contents
are at great risk, the nurse closely assesses and
monitors older clients receiving tube feeding
and those with neurologic deficits and altered swallowing and gag reflexes. All personnel
meticulously follow all infection
control guidelines, including handwashing, invasive catheter and wound care,
and body substance precautions. In addition,
the nurse carefully observes clients who are being treated for any of the
diseases or disorders associated with ARDS.
COLLABORATIVE MANAGEMENT
Assessment
The nurse assesses the client's respirations and notes
whether increased work of
breathing is evident, as indicated by hyperpnea, grunting respiration, cyanosis, pallor, and
retraction intercostally (between the ribs) or suprasternally (above
the ribs). The presence
of diaphoresis and any change in mental status is documented. No abnormal lung sounds are
present on auscultation because
the edema of acute respiratory distress syndrome (ARDS) occurs first in the interstitial
spaces and not in the airways. Vital signs are monitored at least hourly to assess for hypotension, tachycardia, and
dysrhythmias.
The primary laboratory study for establishing the
diagnosis of ARDS is a lowered partial pressure of arterial oxygen (Pao2) value, determined by arterial
blood gas (ABG) measurements.
Because a widening alveolar oxygen gradient (increased fraction of inspired oxygen [Fio2]
does not yield corresponding increased Pao2 levels) develops with
increased shunting of blood, the client has a progressive need for higher
concentrations of oxygen. However, the client with ARDS is poorly responsive to high concentrations of
oxygen (refractory
hypoxemia) and invariably
requires intubation and mechanical ventilation. A large difference between the
predicted and actual alveolar
oxygen tension indicates shunting. The physician orders sputum cultures to isolate any
organisms causing an infection
that must be treated. Because decreased mortality depends on aggressive therapy, sputum may be
obtained through bronchoscopy with protective brushings
and by transtracheal aspiration.
The chest x-ray film shows the diagnostic
diffuse haziness or
"whited-out" (ground-glass) appearance of the lung. An electrocardiogram rules out cardiac
abnormalities and usually reveals
no specific changes. The placement of a Swan-Ganz hemodynamic monitoring
catheter is a diagnostic tool: in the client with ARDS, the pulmonary capillary
wedge pressure (PCWP) is
usually low to normal. This pressure differs from that in the client with cardiogenic pulmonary edema,
in whom the PCWP is higher than 15 mm Hg.
Interventions
The
client with ARDS usually requires endotracheal intubation and mechanical
ventilation with positive end-expiratory pressure (PEEP) or continuous positive airway pressure
(CPAP). Sedation and paralysis may be necessary for
adequate ventilation and for reducing
oxygen requirements. Because one of the side effects of PEEP is tension
pneumothorax, the nurse assesses lung sounds frequently and maintains a
patent airway with suctioning. Positioning may be important in promoting gas exchange.
DRUG AND FLUID
THERAPY.
Corticosteroids are seldom
used in the treatment of ARDS, although they may help decrease
neutrophil mobilization and stabilize the capillary membrane. Their effectiveness, however, has not been determined.
Antibiotics are used to treat infections with organisms identified by culture.
Many interventions are under investigation, but none
has been shown to be effective in decreasing mortality. Some of these
interventions include mediators (vitamins Ń and E, interleukin, prostacyclin,
aspirin), nitric oxide, surfactant replacement, and prone positioning.
The optimal type of fluid therapy for the client with ARDS remains unknown. A colloidal solution may
be effective for intravascular
volume expansion. Fluid volume should be titrated to
maintain adequate cardiac output and tissue perfusion. Induced diuresis may
help decrease lung edema, but care should
be taken to prevent overall dehydration and hypotension.
NUTRITION THERAPY. The client with ARDS is at risk for malnutrition, which further compromises the
respiratory system. An altered immune response, as well as an altered
ventilatory response to hypoxemia, may occur with undernourished clients.
Diaphragm function is also altered. Therefore enteral nutrition in the form of tube feeding or
parenteral nutrition in the form of hyperalimentation is instituted as soon as
possible.
CASE MANAGEMENT. Case management of the client with ARDS focuses on the phases of ARDS rather
than day-to-day care. The
course of ARDS and its management are divided into four phases:
Phase 1. This phase includes
early changes with the client
exhibiting dyspnea and tachypnea. Early interventions
focus on supporting the client and providing oxygen.
Phase 2. Patchy infiltrates
form from increasing pulmonary
edema. Interventions include mechanical ventilation and prevention of complications.
Phase 3. This phase occurs
over days 2 to 10, and the client exhibits
progressive refractory hypoxemia. Interventions
focus on maintaining adequate oxygen transport, preventing complications, and supporting the failing lung until
it has had time to heal.
Phase 4. Pulmonary fibrosis
pneumonia with progression occurs after 10 days. This phase
is irreversible and is frequently
referred to as "late" or "chronic" ARDS. Interventions
focus on preventing sepsis, pneumonia, and multiple organ dysfunction syndrome (MODS), as well as weaning the client from the ventilator. The client
in this phase may be ventilator dependent for weeks to months. He or she may be cared for in specialized
units or facilities that
focus on rehabilitation and long-term weaning. Some clients may not be weanable and go home ventilator dependent.
THE CLIENT REQUIRING INTUBATION
AND VENTILATION
OVERVIEW
Through the use of mechanical ventilation, the client
who has severe problems of
gas exchange may be supported until the underlying process has resolved or has been adequately
treated. Thus mechanical
ventilation is nearly always a temporary life support technique. The need for
ventilatory support may, however, be lifelong, especially for those clients with chronic, progressive neuromuscular diseases
that preclude effective spontaneous ventilation.
Mechanical ventilation is most commonly used for clients
with hypoxemia and progressive
alveolar hypoventilation with
respiratory acidosis. The hypoxemia is usually due to intrapulmonary shunting of blood when external devices
cannot provide a sufficiently high fraction
of inspired oxygen (FIO2). Mechanical ventilation is also indicated
for clients who need respiratory support after surgery, who are barely maintaining adequate gas exchange at the cost of
expending energy with the high work of breathing, or who require general
anesthesia or heavy sedation to allow diagnostic or therapeutic interventions.
COLLABORATIVE MANAGEMENT
Assessment
The
nurse assesses the client about to undergo intubation in the same way as for other respiratory problems.
Once mechanical ventilation has been initiated, the respiratory system is
assessed on an ongoing basis. The nurse monitors and assesses for complications related to the
artificial airway or ventilator, as
well as for those related to mechanical ventilation.
Interventions
ENDOTRACHEAL
INTUBATION. The client
who needs mechanical
ventilation requires an artificial airway. The most common type of artificial airway for establishing and
maintaining the airway
on a short-term basis is the endotracheal (ET) tube. If the client requires an
artificial airway for longer than a specified period, usually longer than 10 to 14 days,
the physician considers a tracheostomy to avoid mucosal and vocal cord damage.
The goals of intubation include maintaining a
patent airway, reducing the
work of breathing, providing a means to remove secretions, and providing ventilation and oxygen.
ENDOTRACHEAL TUBE. An ET tube is a long polyvinyl chloride tube that is passed through the mouth or nose and into the trachea. When
properly positioned, the tip of the ET tube rests
approximately 0.8 to 1.2 inches (2 to 3 cm) above the carina (where the trachea divides
into the right and left
mainstem bronchi). Oral intubation is the easiest
and quickest method of establishing an airway; therefore it is also performed
as an emergency procedure. The nasal route
is reserved for elective intubation, for some facial or oral traumas and surgeries, and when oral
intubation is not possible. This
route is contraindicated if the client has a blood dyscrasia. An experienced, specially trained
professional, such as an
anesthesiologist, nurse anesthetist, or pulmonologist (physician), performs the
intubation.
An ET tube has several parts. The
shaft of the tube contains a radiopaque vertical
line for the length of the tube, which permits demonstration of correct placement by chest x-ray examination. Short horizontal
lines (depth markings) are used to designate correct placement of the tube at the nares or mouth (at the incisor
tooth) and to identify how far the tube has been inserted.
The cuff at the distal end of the tube, with
proper inflation, produces a seal between the trachea and the cuff. The seal
ensures delivery of a set tidal volume when mechanical ventilation is used. When the cuff is inflated to an
adequate sealing volume, no air can pass through the cuff to the vocal cords, nose, or mouth; therefore the client is not able
to talk when the cuff is inflated. The cuff should be
inflated to a pressure of 20 to 25 cm H2O using minimal-leak or no-leak
techniques.
The pilot balloon with a one-way valve permits air to
be inserted into the cuff
and yet prevents air from escaping. This balloon is used as a general guideline for determining
the absence or presence of air in the cuff, although it will not show how much or how little air is present.
The
universal adaptor, which is 15 mm
in diameter, enables attachment to
ventilator tubing or other types of oxygen delivery systems. The tubing size is indicated on the adaptor or
the shaft of the tube. Adult tube sizes range from 5 to 10 mm. Sizes used are 8.0 to 9.0 for large adults, 7.0 to
8.0 for medium-size adults,
and 6.0 to 7.0 for small adults.
PREPARING FOR
INTUBATION. The nurse and assistive nursing personnel know
the proper procedure for summoning intubation personnel to the bedside in an
emergency situation. The
nurse explains the procedure to the client as clearly as possible under the circumstances. Basic life
support measures, such as the
establishment of a patent airway and the administration of 100% oxygen via a resuscitation (Ambu) bag with a
face mask, are crucial to the client's survival until help arrives. The
coordination for resuscitation with a bag and mask device can be cumbersome; therefore practice is
necessary.
In an emergency the nurse or assistive personnel
brings the code (or
"crash") cart, respiratory equipment box, and suction equipment
(which is often already on the code cart) to the bedside. The nurse maintains
a patent airway through positioning and the insertion of an oral airway until
the client is intubated. During
intubation the nurse continuously monitors for changes in vital signs, signs of hypoxia or hypoxemia,
dysrhythmias, and aspiration. The
nurse also ensures that each intubation attempt lasts no longer than 30 seconds,
preferably less than 15 seconds. After 30 seconds,
oxygen is provided by means of a mask
and manual resuscitation bag to prevent hypoxia and potential cardiac arrest. Suctioning is performed as
necessary.
VERIFYING TUBE PLACEMENT. Immediately after an ET tube is inserted, its placement must be
verified. The most accurate way of verifying placement is by checking end-tidal carbon
dioxide concentration, if available. The nurse assesses for bilateral equal breath sounds,
bilateral equal chest excursion, and air emerging from the ET tube. If breath sounds and chest wall
movement are absent on the left side, the tube may be in the right mainstem
bronchus. The person intubating the client should be able to reposition the tube without repeating the
entire intubation procedure.
The nurse auscultates over the stomach to rule
out esophageal
intubation. If the tube is in the stomach, louder breath sounds are heard over the stomach than over the
chest and abdominal
distention may be present. Chest wall movement and breath sounds are continuously monitored
until tube placement is verified by chest x-ray
examination.
STABILIZING THE TUBE. The nurse, respiratory therapist, or anesthesia personnel stabilize the ET tube at the mouth or nose. The tube is marked at the level at which it touches the
incisor tooth or naris. Two persons working together use a head halter
technique to secure the tube.
An oral airway may also need to be inserted to
keep the client from biting an oral tube. One person stabilizes the tube at the
correct position and prevents head movement while a second person applies the
tape. After the procedure is completed, the nurse verifies the presence of
bilateral and equal breath sounds and the level of the
tube.
NURSING CARE. The nurse assesses tube placement, cuff
pressure, breath sounds, and chest wall movement regularly. The nurse prevents
pulling or tugging on the tube by the client
to prevent dislodgment or "slipping" of the tube and checks the pilot
balloon to ensure that the cuff is inflated.
Suctioning, coughing, and speaking attempts place extra stress on the
tube and also can cause dislodgment. Neck flexion moves the tube away from the carina; neck extension moves the
tube closer to the
carina. Rotation of the head also causes the tube to move. Mouth secretions and
tongue movement can loosen the
tape and allow malposition of the tube. When other measures fail, the nurse applies soft wrist
restraints, as ordered, for the
client who is voluntarily or involuntarily pulling on the tube. This intervention is a last
resort to prevent accidental extubation. Adequate
sedation (chemical restraint) may be
necessary to decrease agitation or prevent extubation. The nurse obtains
permission for restraints from the client or
family after explaining the rationale.
Complications of an ET or nasotracheal tube can occur
at each stage of the process: during placement, while in place, during
extubation, or after extubation (either early or late). Trauma and complications can occur to the face; eye; nasal and paranasal areas; oral, pharyngeal, bronchial,
tracheal, and pulmonary areas; esophageal and gastric areas; and cardiovascular, musculoskeletal, and neurologic
systems.
MECHANICAL VENTILATION. Mechanical ventilation to support and maintain
respiratory function is widely used on medical-surgical units, in nursing homes, and in the
home setting, as well as in
critical care units. The nurse plays a pivotal role in the coordination of care
and the prevention of complications.
The goals of mechanical ventilation are to improve oxygenation and ventilation and decrease the
amount of oxygen and work needed
to accomplish an effective breathing pattern. Mechanical ventilation is used to support the client
until lung function is adequate or until the acute episode has passed. A ventilator does not cure diseased lungs; it provides
ventilation until the lungs are
able to resume the process of breathing. Therefore the nurse must remember why the client is
using the ventilator so that aggressive attempts to correct the underlying cause of the respiratory failure are always at
the forefront of the management
plan. If normal oxygenation, ventilation, and respiratory muscle strength are achieved, mechanical
ventilation can be discontinued.
TYPES OF VENTILATORS. A wide variety of ventilators are available. The ventilator selected depends on the severity of the
disease process and the length of time that ventilator support is required. Two major types of ventilators
are negative-pressure and
positive-pressure ventilators.
Negative-Pressure Ventilators. The negative-pressure ventilator
is noninvasive. The iron lung, widely used during the poliomyelitis epidemic in the 1940s, is the prototype for the negative-pressure ventilator. The client is placed in an airtight apparatus that surrounds
either the chest area or the
entire body and leaves the head exposed. During inspiration,
with the expansion of the chest wall, negative pressure is generated in the chest cavity. Because of the pressure
gradient, air rushes from the atmosphere (high pressure) into the thoracic
cavity (low pressure). At a preset time, negative pressure ceases and expiration occurs. Thus negative-pressure ventilators create pressure gradients
that mimic normal physiologic
ventilation.
Newer negative-pressure ventilators include the
cuirass, poncho, and body
wrap. These ventilators are used for clients with
neuromuscular disease, central nervous system disorders, spinal cord injuries, and chronic obstructive pulmonary disease (COPD). Clients may use negative-pressure
ventilation for home nighttime
ventilatory support so that their muscles
can rest. Advantages are that an artificial airway is not required and the newer models are lightweight and
easy to use. The enclosing
ventilator makes some direct nursing care more difficult. The client must be able to clear oral secretions and must have compliant (elastic) lungs to benefit
from this mode of ventilation,
Positive-Pressure Ventilators. The positive-pressure ventilator
is the most widely used type of ventilator in the acute
care setting. During inspiration, pressure is generated that pushes air into the lungs and expands the chest. In most instances an endotracheal (ET) tube or
tracheostomy is needed.
Positive-pressure ventilators are classified according to the mechanism that
ends inspiration and starts expiration. Inspiration is terminated or cycled in three major ways: pressure cycled, time cycled, or volume cycled.
Pressure-Cycled
Ventilators. Pressure-cycled ventilators (which are
infrequently used) push air into the lungs until a preset airway pressure is reached. Tidal volumes and
inspiratory time are
variable. Pressure-cycled ventilators may be used for short periods, such as in the postanesthesia
care unit and for respiratory
therapy.
Time-Cycled
Ventilators. Time-cycled ventilators push air into the lungs until a preset time has elapsed. Tidal volume and pressure are variable, depending on the
characteristics of the client and
the ventilator. The time-cycled ventilator is used primarily in
pediatric and neonatal populations.
Volume-Cycled Ventilators. Volume-cycled ventilators push
gas into the lungs until a preset volume is delivered. A constant tidal volume
is delivered regardless of the pressure needed to deliver the tidal volume.
However, a pressure limit is
set to prevent excessive pressure from being exerted on the lungs. The
advantage of the volume-cycled ventilator is that a constant tidal volume is
delivered regardless of the changing compliance of the lungs and chest wall or the airway resistance found
in the client or ventilator.
Microprocessor Ventilators. Microprocessor ventilators are the most sophisticated of the positive-pressure ventilators. A computer or microprocessor is built into the
ventilator to allow ongoing
monitoring of ventilatory functions, alarms, and client parameters. The ventilator often has components
of volume-, time-, and pressure-cycled ventilators. The microprocessor
ventilator is more responsive to clients who have severe
lung disease, who require prolonged weaning trials, and who may not be able to be ventilated on older, volume-cycled ventilators. Examples include the Bear IV
and V, Puritan-Bennett 7200, Erisa, and Siemens Servo Ń and Servo D.
MODES OF VENTILATION. The mode of ventilation describes the way in which the client receives breaths
from the ventilator.
Controlled
Ventilation. Controlled ventilation is the least-used mode. The client receives a set
tidal volume at a set rate.
This mode may be used for clients who cannot initiate respiratory effort (e.g., those with polio or
Guillain-Barre syndrome). It may also be used for
clients who are "paralyzed" as
part of their medical management, such as those in status epilepticus or those
with severely elevated intracranial pressure. With controlled ventilation, if the client attempts to initiate a breath, the efforts are blocked by the
ventilator. This maneuver may result in the client's "fighting" the
ventilator.
Assist-Control Ventilation. Assist-control
(AC) ventilation is the most
commonly used mode. It is used mainly as a resting mode. The ventilator takes over the work of
breathing for the client. The
tidal volume and ventilatory rate are preset on the ventilator. If the client does not trigger
spontaneous breaths, a minimal
ventilatory pattern is established. The ventilator is also programmed to respond to the client's
inspiratory effort if he or she does initiate a breath. In this case, the ventilator delivers the preset tidal volume
while allowing the client to control the rate of
breathing.
One disadvantage of the AC mode is that if the
client's spontaneous ventilatory rate increases, the ventilator continues to deliver a preset tidal volume with each breath. He or she may then hyperventilate, and respiratory
alkalosis occurs. Causes of
hyperventilation, such as pain, anxiety, or acid-base imbalances, must be corrected.
Synchronized
Intermittent Mandatory Ventilation. Synchronized
intermittent mandatory ventilation (SIMV) is similar to AC ventilation in that tidal volume and
ventilatory rate are preset on the ventilator.
Therefore if the client does not breathe, a
minimal ventilatory pattern is established. In contrast to the AC mode,
SIMV allows breathing spontaneously at the
client's own rate and tidal volume between the ventilator breaths. SIMV can be used as a primary ventilatory mode or as a weaning modality. When SIMV is used
as a weaning mode, the number of mechanical breaths (SIMV breaths) is gradually
decreased (e.g., from 12 to 2), and the client gradually resumes spontaneous breathing. The
mandatory ventilator breaths are delivered when
the client is ready to inspire, promoting synchrony between the ventilator and the client.
Other Modes of Ventilation. Newer modes of ventilation,
such as pressure support and continuous flow (flow-by), are available only in
microprocessor ventilators. Both modalities decrease the work of breathing and are often
used for weaning clients from
mechanical ventilation. Other modes are maximum mandatory ventilation (MMV), inverse inspiration-expiration (I/E) ratio, permissive
hypercapnia, airway pressure release ventilation, proportional assist
ventilation, high-frequency
ventilation, jet ventilation, and high-frequency oscillation. Many of these modes need
specialized ventilators, tubing, or airways.
VENTILATOR CONTROLS AND SETTINGS. The volume-cycled ventilator is the most widely used
ventilator in the acute care
setting. Regardless of the type of volume-cycled ventilator used, the controls
and types of settings are universal. The physician prescribes the ventilator settings, and usually the ventilator is readied or
set up by the respiratory
department. The nurse assists in connecting the client to
the ventilator. Monitoring of the ventilator settings is part of the nursing care.
Tidal Volume. Tidal volume (Vt) is the
volume of air that the client
receives with each breath; it can be measured on either inspiration or expiration. The average prescribed
Vt ranges between 7 and 10 mL/kg
of body weight (see the Evidence-Based
Practice for Nursing box above). Adding a zero to the weight of clients in kilograms gives an estimate
of tidal volume.
Rate, or Breaths per Minute. Rate, or breaths per minute, is the number of ventilator breaths delivered
per minute. The rate is
usually set between 10 and 14 breaths per minute.
Fraction of Inspired Oxygen. The fraction of inspired oxygen (Fio2) is the oxygen concentration delivered to the client. The prescribed Fio2 is
determined by the arterial blood gas
(ABG) value and the condition. Ventilators can provide 21% to 100% oxygen,
depending on need.
The oxygen delivered to the client is warmed to
body temperature (98.6° F [37° C]) and humidified to 100%. Humidification and warming are necessary because upper air passages of the respiratory tree, which normally
warm, humidify, and filter air, are
bypassed by the endotracheal (ET) tube or tracheostomy tube. Humidification and warming prevent mucosal
damage and facilitate clearance of secretions.
Sighs. Sighs are volumes of air that are 1.5 to 2 times the set tidal volume, delivered 6 to 10 times
per hour. These may be used to prevent atelectasis in special circumstances.
Sighs are rarely used,
however, because they can cause barotrauma (lung
damage from excessive pressure) and have not been shown to be useful.
Peak Airway (Inspiratory) Pressure. Peak airway (inspiratory) pressure (PIP) indicates the pressure
needed by the ventilator to
deliver a set tidal volume at a given dynamic compliance.
The PIP measurement appears on the digital readout
or display on the front or top of the ventilator. Peak pressure is the highest
pressure indicated during inspiration. Monitoring trends in PIP reflect changes
in resistance of the lungs and
resistance in the ventilator. An increased PIP reading means increased
airway resistance (bronchospasm, or pinched tubing), increased amount of
secretions, pulmonary edema, or decreased
pulmonary compliance (the lungs or chest
wall are "stiffer" or harder to inflate). An upper pressure limit is
set on the ventilator to prevent barotrauma. When the limit is reached, the high-pressure alarm sounds,
and the remaining volume is not given.
Continuous Positive
Airway Pressure.
Continuous positive airway pressure (CPAP) is the
application of positive airway
pressure throughout the entire respiratory cycle for spontaneously breathing clients. Sedating medications
should be given cautiously
or not at all when receiving CPAP so that respiratory effort is not suppressed. CPAP keeps the
alveoli open during
inspiration and prevents alveolar collapse during expiration. This process
results in increased functional residual capacity (FRC), improved gas exchange, and improved oxygenation.
CPAP is used primarily to help in the weaning process.
During CPAP, no ventilator breaths are delivered; the
ventilator delivers oxygen and provides monitoring and an alarm system. The
respiratory pattern is determined by the client's efforts. Normal levels of CPAP are 5 to 15 cm H2O, adjusted to promote adequate oxygenation. If no pressure
is set on the ventilator, the client receives no positive pressure. The client is essentially using the
ventilator as a T-piece with
alarms.
Newer modifications of CPAP include nasal CPAP and bi-level positive airway pressure (BiPAP). The
physician uses these modifications for select indications.
Positive End-Expiratory Pressure. Positive end-expiratory pressure (PEEP) is positive pressure exerted
during the expiratory phase of
ventilation. PEEP improves oxygenation by enhancing gas exchange and preventing atelectasis.
It is indicated for the treatment of persistent hypoxemia that does not improve with an acceptable oxygen
concentration. PEEP is often
added when the partial pressure of arterial oxygen (Pao2) value remains low with an Fio2 of 50% to 70% or
greater.
The need for PEEP indicates a severe gas exchange
disturbance. It is important to lower the Fio2 delivered whenever possible. Prolonged use of a high Fio2
can result in lung damage
from the toxic effects of oxygen. PEEP prevents alveoli from collapsing; the
lungs are kept partially inflated so that alveolar-capillary gas exchange is
facilitated throughout the ventilatory
cycle. The effect should be an increase in arterial blood oxygenation so that the Fio2 can be
decreased.
PEEP is "dialed in" with the PEEP dial on
the control panel. The amount of
PEEP is often 5 to 15 cm H2O and is read (monitored) on the
peak airway pressure dial, the same dial used to read the PIP. When PEEP is added, the dial does not return to zero at the end of exhalation;
rather, it returns to a
baseline that has been increased from zero by the amount of PEEP applied.
Flow. Flow
is how fast the ventilator delivers each breath. It is usually set at 40 L/min.
If a client is agitated, is restless, has a widely fluctuating pressure reading on inspiration, or has other signs of air hunger, the flow may be
set too low. Increasing the
flow should be tried before using chemical restraints.
Other Settings. Other settings may be used, depending on the type of ventilator and mode of ventilation.
Examples of additional settings
include inspiratory and expiratory cycle, waveform, expiratory resistance, and
plateau.
NURSING MANAGEMENT. The institution of mechanical ventilation
involves a complex decision-making process for
both the client/family and the health care professionals. Both physical and psychologic concerns of the
client and family must be addressed.
The mechanical ventilator frequently causes anxiety for the client and family.
Therefore the nurse carefully explains the purpose of the ventilator and notes
that the client might feel some
different sensations. The client and family are encouraged to express
their concerns. The nurse acts as the coach who both physically and
psychologically helps and supports the
client and family through this experience. In emergencies these explanations
may not be accomplished until the emergency has been controlled. Clients undergoing mechanical ventilation in intensive care
units (ICUs) often experience delirium, or "ICU psychosis." These
persons require frequent, repetitive
explanations and reassurance.
When caring for a ventilated client, the nurse
is concerned with the client first and the ventilator
second. It is vital that the nurse
understand why the mechanical ventilation is required. Causes such as
excessive amounts of secretions, sepsis, and trauma require different
interventions to facilitate ventilator independence. In addition, an
appreciation of the client's chronic
health problems, particularly chronic obstructive pulmonary disease (COPD), left-sided heart failure, anemia, and
malnutrition, is essential. These problems may impede weaning from mechanical ventilation and
therefore warrant close monitoring
and intervention.
Three nursing goals in caring for the client with
mechanical ventilation are to monitor and evaluate the response to the ventilator, manage the ventilator system
safely, and prevent complications.
Monitoring the Client's Response. A major nursing responsibility
is to monitor and evaluate the client's response to the
ventilator. The nurse assesses vital signs and listens to breath sounds every 30 to 60 minutes
initially, monitors non-invasive respiratory parameters (e.g., capnography and
pulse oximetry), and checks arterial blood gas (ABG) values. Vital signs change
during episodes of hypercapnia and hypoxemia. The nurse notes any precipitating causes and corrects
them promptly.
The nurse assesses the breathing pattern in
relation to the ventilatory
cycle to determine whether the client is fighting or tolerating
the ventilator. Breath sounds are assessed and recorded, including bilateral
equal breath sounds to ensure proper
endotracheal (ET) tube placement. To determine the frequency of suctioning needed, the nurse observes
secretions for type, color, and
amount.
The
area around the ET tube or tracheostomy site is assessed at least every 4 hours for color, tenderness, skin irritation, and drainage. Continuous noninvasive
monitoring provides
information to guide the client's activities, such as weaning, physical or
occupational therapy, and self-care. These activities can be paced so that oxygenation and ventilation are
adequate. The nurse interprets ABG values to evaluate ventilation and suggests ventilator settings that
help the client.
Because the nurse spends the most time with the
client, he or she is most likely to be the first person to recognize slight
changes in vital signs or ABG values and fatigue or distress. The nurse promptly confers with the physician and implements the appropriate interventions.
While
monitoring and evaluating the client's clinical status, the nurse also serves as a resource for addressing the psychologic needs of the client and family. Anxiety
can play a major role in the tolerance of mechanical ventilation. Therefore
skilled and sensitive nursing care promotes psychologic well-being and
facilitates synchrony with the ventilator. Because the client cannot speak, communication can be frustrating
and anxiety producing. The client and family may panic because they believe
that the voice has been lost. They must be reassured that although the ET tube
prevents speech, it is temporary.
Alternative, creative methods of communication
must be individualized to meet the client's needs. Magic Slates, writing paper, computers, and tracheostomy tubes that permit talking are potential means of facilitating
communication. Finding a successful means for communication is important because the client often feels isolated as a
result of the inability to speak. Anticipation of the client's needs; easy
access to frequently used
belongings; visits from family, friends, and pets; and a nursing call
light within reach are effective ways of
giving a sense of control over the environment. In addition, the client
can participate in self-care.
Managing the Ventilator System. Ventilator settings are
ordered by the physician and include tidal volume, respiratory rate, fraction
of inspired oxygen (Fio2), mode of ventilation (assist-control [AC]
ventilation, synchronized intermittent
mandatory ventilation [SIMV]), and any adjunctive modes, such as positive end-expiratory pressure
(PEEP), pressure support, or
continuous flow.
The nurse performs and documents ventilator checks according
to the standards of the unit or facility and responds promptly to emergencies
as indicated by alarms. During a ventilator
check, the ventilator settings ordered by the physician are compared with the
actual settings. The level of water in the humidifier and the temperature of the
humidification system are
checked to ensure that they are within normal limits. Extremes in temperature cause damage to the mucosa of the airways. Any condensation in the ventilator
tubing is removed by draining water
into drainage collection receptacles, which should be emptied frequently. For
prevention of bacterial contamination, moisture and water from the
tubing are never allowed to enter the
humidifier.
Mechanical ventilators have alarm systems that warn
the nurse of a problem
with either the client or the ventilator. Alarm systems must be activated and functional at all
times. The nurse must
recognize an emergency and intervene promptly so that complications are prevented. If the cause of the alarm cannot be determined, the nurse
ventilates the client manually
with a resuscitation bag until the problem is corrected by a second nurse, the respiratory therapist,
or a physician. The two major
alarms on a ventilator indicate either a high pressure or a low exhaled volume.
Ensuring proper functioning of the ventilator also includes care of the ET or tracheostomy tube. A patent
airway is maintained through
suctioning only as needed. The following are indications for suctioning in the
ventilated client:
•
Presence of secretions
•
Increased peak airway (inspiratory) pressure (PIP)
•
Presence of rhonchi (wheezes)
•
Decreased breath sounds
Careful maintenance of the ET or tracheostomy tube
also ensures a patent airway. The nurse
frequently assesses the tube's position,
especially for the client whose airway is attached to heavy ventilator tubing that may pull on the tracheostomy or
ET tube. The ventilator tubing is positioned in such a way that the client can move without pulling on the ET or tracheostomy tube. The ET tube can move and
slip into the right mainstem
bronchus. To detect minimal changes in the tube's position, the level at which the tube touches the client's teeth or nose is marked. The nurse gives mouth
care frequently to promote adequate
oral hygiene and to prevent loosening of the tape that holds the tube.
Preventing
Complications.
Most complications are
due to the positive
pressure from the ventilator. Nearly every body system is affected.
Cardiac Complications. Cardiac complications of mechanical ventilation include hypotension and fluid
retention. Hypotension is caused by the application of positive pressure,
which increases intrathoracic pressure and inhibits blood return to the heart. The decreased venous return
to the right side of the heart decreases cardiac output and is clinically
reflected as hypotension.
Hypotension is most frequently seen in the client who is dehydrated or requires
a high PIP to be ventilated. The nurse instructs the client to avoid a
Valsalva maneuver and plans
care to prevent constipation, which could result in a Valsalva maneuver.
Fluid is retained because of decreased cardiac output.
The kidneys receive less
blood flow and stimulate the renin-angiotensin-aldosterone system to retain
fluid. In addition, humidified air
via the ventilator system can contribute to fluid retention. If humidification is not adequate, the
airways become dehydrated and
the secretions solidify. The nurse monitors the client's fluid intake and output, weight,
hydration, and signs of
hypovolemia.
Lung Complications. The lungs experience barotrauma (damage to the lungs by positive pressure), volutrauma
(damage to the lung
by excess volume delivered to one lung over the other), and acid-base
abnormalities. Barotrauma includes pneumothorax, subcutaneous emphysema, and
pneumomediastinum.
Clients at risk for barotrauma have diseases of chronic airflow limitation (CAL), have blebs, are
on PEEP, have dynamic
hyperinflation, or require high pressures to ventilate the lungs (because of decreased compliance
or "stiff lungs, as seen in acute respiratory
distress syndrome [ARDS]). Blood gas
abnormalities, another pulmonary complication
of mechanical ventilation, can be corrected by appropriate ventilator changes and adjustment of
fluid and electrolyte imbalances.
Gastrointestinal and
Nutritional Complications. Gastrointestinal (GI) alterations result from the
stress of mechanical ventilation.
Stress ulcers occur in approximately 25%
of clients receiving mechanical ventilation. Prophylactic
antacids, sucralfate (Carafate,
Sulcrate4*1), and the histamine blockers cimetidine (Tagamet) and ranitidine (Zantac)
are often instituted as soon as the client is intubated. Changes in the pressure relationship between the thoracic and abdominal cavities can
also produce or induce a paralytic ileus. This problem may affect absorption of nutrients through the GI system,
requiring short-term parenteral nutritional support.
Malnutrition is a prevalent problem in clients
receiving mechanical ventilation. Because many other acute or life-threatening
events are occurring simultaneously, nutrition is often neglected. Malnutrition is an extreme problem
for these clients and is a
major reason why they cannot be weaned from the ventilator. In malnourished clients the
respiratory muscles lose their mass
and strength. The diaphragm, which is the major muscle of inspiration, is affected early in this
process. When the diaphragm
and other muscles of respiration are weakened, an ineffective breathing pattern
emerges, fatigue occurs, and the client cannot be
weaned from the ventilator.
A balanced diet via the parenteral or enteral route is
essential whenever a ventilator is used. Furthermore, nutrition for the client with chronic obstructive pulmonary disease (COPD) requires that special attention be given
to the percentage of carbohydrates
in the diet. During metabolism, carbohydrates
are broken down to glucose to produce energy (adenosine triphosphate), carbon
dioxide, and water. Excessive carbohydrate loads increase carbon dioxide
production, which the client with chronic obstructive pulmonary disease (COPD)
may be unable to exhale. Hypercapnic respiratory failure
results. Enteral and parenteral formulas with a higher fat content (e.g., Pulmocare, NutriVent,
intralipids) can be an alternative source of calories to combat this
problem.
Another important aspect of nutritional support
is electrolyte replacement.
Electrolytes also have a major impact on the efficiency of respiratory muscle
function. Specifically, the nurse
and physician closely monitor potassium, calcium, magnesium, and phosphate
levels, and the nurse replenishes deficiencies as ordered. All four electrolytes are important in
respiratory muscle contraction and function and can easily be added to the nutritional regimen.
Infection. Infections are always a potential threat for the client requiring a ventilator. The ET or
tracheostomy tube bypasses the body's normal process of filtering and warming
air and provides
bacteria with direct access to the lower parts of the
respiratory system. Within 48 hours,
the artificial airway is usually colonized
with bacteria, and an environment is established in which pneumonia can develop. In addition, aspiration of colonized fluid from the mouth or the
stomach can occur and be a source of
pathogens. Pneumonia is associated with prolonged hospitalization and
increased morbidity. Therefore the focus must
be on prevention of infections through
strict adherence to infection control, especially hand-washing, during
suctioning and care of the tracheostomy or ET
tube. To prevent pneumonia, the nurse implements ongoing oral care and
pulmonary hygiene, including chest physiotherapy, postural drainage, and turning and positioning.
Muscular
Complications. Overall muscle deconditioning can occur because of immobility. Getting out of
bed, ambulating with
assistance, and performing exercises with the nurse, physical therapist, and occupational therapist
not only improve muscle tone
and strength but also boost morale, facilitate gas exchange, and promote
oxygen delivery to all muscles.
Ventilator Dependence. The final complication of mechanical ventilation is ventilator dependence, or inability to wean.
Ventilator dependence can be psychologic or physiologic but more often has a physiologic basis. The
longer a client uses a ventilator, the more difficult is the weaning process because the respiratory muscles fatigue
and cannot assume breathing. The health care team attempts to optimize all major body systems and to exhaust every
method of weaning before a client is declared
unweanable.
The physician and nurse, often with a social worker or
psychologist and a member of the clergy, discuss with
the family and the client, as able, the
client's quality of life, goals, and values. In accordance with this
discussion, arrangements are
made for home ventilation, nursing home placement, or withdrawal of life support (in terminal cases). Special
units and facilities are available to
maximize the rehabilitation and weaning
of ventilator-dependent clients.
WEANING. Weaning is the process of going from ventilatory dependence to spontaneous breathing. The
weaning process can be
prolonged if complications develop. Many of these complications can be avoided
by skillful nursing care. For example, turning and positioning the client not
only promote comfort and prevent skin breakdown but also facilitate gas
exchange and prevent pulmonary complications, such as pneumonia and
atelectasis.
EXTUBATION. Removal of the endotracheal (ET) tube is termed extubation. The tube is removed
when the indication for intubation has been resolved. Before removal, the nurse explains the procedure. The nurse or respiratory therapist sets
up the prescribed oxygen delivery system at the bedside and brings in the
equipment for emergency reintubation. The
client is hyperoxygenated and the ET tube thoroughly suctioned, as is the oral cavity. The cuff of the ET tube is then rapidly deflated, and the tube is
removed at peak inspiration. The
nurse instructs the client to take deep breaths and to cough. It is
normal for large amounts of oral secretions
to have accumulated in the back of the throat. Oxygen is administered by
face mask or nasal cannula. The fraction of
inspired oxygen (Fio2) is usually ordered at 10% higher than the level
that was maintained while the ET tube was in place.
Monitoring after extubation is essential. The nurse monitors the vital
signs every hour initially, assesses the ventilatory pattern, and assesses for
any signs or symptoms of respiratory distress. It is common to experience
hoarseness and a sore throat for a few days
after extubation. The client is instructed to sit in a semi-Fowler's
position, take deep breaths every V2
hour, use an incentive spirometer every 2 hours, and limit speaking in the immediate period after extubation. These measures facilitate gas exchange
and decrease laryngeal edema and vocal cord irritation. The client is observed
closely for signs or symptoms of upper airway obstruction. Early signs are mild dyspnea, coughing, and the inability to expectorate
secretions. With the onset of these signs,
the nurse notifies the physician, who
evaluates the need for reintubation. The nurse is especially concerned if the client develops stridor, a late
sign of a narrowed airway. Stridor is a high-pitched, crowing noise
during inspiration caused by laryngospasm or edema
above or below the glottis. Racemic epinephrine, a topical aerosol vasoconstrictor, is given, and
reintubation may be performed.
CHEST TRAUMA
Chest injuries are directly responsible for
approximately 25% of all civilian traumatic deaths; 50% of
the injured succumb before
arriving at health care facilities. Only 5% to 15% of
all chest injuries require thoracotomy. The
remainder can be treated with basic
resuscitation, intubation, or chest tube placement.
The emergency initial approach to all chest injuries is ABC (airway, breathing, circulation) followed by rapid assessment and treatment of potentially
life-threatening conditions.
Pulmonary Contusion
OVERVIEW
Pulmonary contusion, a potentially lethal injury, is
the most common chest injury
seen in the United States.
After a contusion, respiratory failure can develop over time rather than instantaneously. This condition most frequently
follows injuries caused by
rapid deceleration during vehicular accidents. Interstitial hemorrhage, which
is almost invariably associated with
intra-alveolar hemorrhage, accompanies pulmonary contusion.
The resultant interstitial edema causes a decrease in pulmonary compliance and a decreased area for gas exchange. The client usually becomes hypoxemic and
dyspneic. The bronchial mucosa
becomes irritated, and the client has increased bronchial secretions.
COLLABORATIVE MANAGEMENT
Assessment
Clients with pulmonary contusion who may initially be
asymptomatic can develop respiratory failure. These clients present with
hemoptysis, decreased breath sounds, crackles, and wheezes. The chest x-ray film of the client with
pulmonary contusion
may show a hazy opacity in the lobes or parenchyma. If there is no disruption of the
parenchyma, re-sorption of the lesion often occurs
without treatment.
Interventions
Treatment includes maintenance of ventilation and
oxygenation. Central
venous pressure (CVP) is monitored closely, and fluid
intake is restricted accordingly. The client in obvious respiratory distress may require mechanical ventilation with positive
end-expiratory pressure (PEEP) to inflate the lungs and provide
positive-pressure ventilation.
A vicious circle occurs in which more muscle
effort is required for
ventilation, and the client becomes progressively hypoxemic. Attempting to compensate causes the client to tire easily, become less efficient in
breathing, and become more fatigued and hypoxemic.
Flail chest may also be associated with a
pulmonary contusion accompanied by parenchymal damage. The sequela to this
situation is the probable development
of acute respiratory distress syndrome
(ARDS).
Rib Fracture
OVERVIEW
After chest wall contusion, rib fractures are the next
most common injury to
the chest wall. Rib fractures most frequently result from direct blunt trauma to the chest,
usually with involvement of
the fifth through ninth ribs. Direct force applied to the ribs tends to fracture them and drive
the bone ends into the
thorax. Thus there is a potential for intrathoracic injury, such as
pneumothorax or pulmonary contusion. Pneumothorax is almost invariably present
if ribs one through four are fractured.
COLLABORATIVE MANAGEMENT
The
client usually experiences pain with movement and splints the chest defensively. Thoracic splinting
results in impaired ventilation
and inadequate clearance of tracheo-bronchial secretions. If the client has pre-existing pulmonary disease,
the likelihood of atelectasis and pneumonia related to the
rib fracture is increased. Clients with injuries to the first or second ribs, flail
chest, seven or more fractured ribs, or expired volumes less than 15 mL/kg
have a poor prognosis; intrathoracic injury
occurs in 50% of
these cases.
Treatment for uncomplicated rib fractures is
nonspecific because the fractured ribs unite
spontaneously. The chest is usually not
splinted by tape or other materials. The primary consideration for the
client is to decrease pain so that adequate
ventilatory status is maintained. An intercostal nerve block may be used if pain is severe. Potent
analgesia that causes respiratory
depression is avoided.
Flail Chest
OVERVIEW
Flail
chest (paradoxical respiration) is the inward movement of the thorax during inspiration, with outward
movement during expiration. It
usually involves one hemithorax (one side of the chest) and results from multiple rib fractures
caused by blunt chest trauma. Flail chest is frequently associated with
high-speed vehicular accidents. It is more common in older clients. It is associated with a high mortality
rate (40%) and is one of the most
critical chest injuries.
Flail chest occurs when a loose segment of chest
wall is left because of a
fracture of two or more adjacent ribs. The movement of this segment becomes
paradoxic to the expansion and contraction of
the rest of the chest wall. Flail chest can
also occur from bilateral fracture of multiple costochondral junctions (without rib fracture) anteriorly,
such as might occur during cardiopulmonary resuscitation on an older adult. There
may be associated injury to the lung tissue under the flail segment. Gas exchange is significantly impaired, as is the ability to cough and clear secretions. Defensive
splinting because of the rib fracture further reduces the client's ability to
exert the extra effort required for breathing, which may contribute later to
failure to wean.
COLLABORATIVE MANAGEMENT
Assessment
The nurse assesses the client with a flail chest for
paradoxic chest movement, dyspnea, cyanosis, tachycardia, and hypotension. Anxiety is often associated with pain
and dyspnea.
Interventions
Interventions for flail chest include administration
of humidified oxygen, pain management, promotion of
lung expansion through deep
breathing and positioning, and secretion clearance by coughing and tracheal
aspiration.
The client with a flail chest may be treated
conservatively with vigilant
respiratory care. The physician may prescribe mechanical ventilation if such
complications as respiratory failure or shock ensue. The physician and the
nurse monitor arterial blood gas (ABG) values closely, along with vital capacity.
With severe hypoxemia and hypercapnia, the client is intubated and mechanically
ventilated with PEEP. With pulmonary contusion or an underlying pulmonary
disease, the potential for respiratory failure increases. Flail chest is best stabilized by positive-pressure
ventilation rather than surgical intervention. Operative stabilization is reserved for extreme cases of
flail chest.
The nurse monitors the client's vital signs and fluid and electrolyte balance closely so that hypovolemia
or shock can be treated immediately. If the client has a pulmonary contusion,
the nurse monitors central venous pressure (CVP) and administers fluids as ordered. The nurse assesses
for pain and intervenes to relieve the pain. The physician may order analgesic medication by the IV, epidural, or nerve
block route.
The
nurse gives psychosocial support to the extremely anxious client by explaining
all procedures, talking slowly, and
allowing time to verbalize feelings and concerns.
Pneumothorax
OVERVIEW
Any thoracic injury that allows accumulation of
atmospheric air in the pleural
space results in a rise in intrathoracic pressure and a reduction in vital capacity, depending on
the amount of
pulmonary collapse produced. Pneumothorax is often caused by blunt chest trauma and is associated
with some degree of hemothorax. The pneumothorax can be open (when the pleural cavity has become exposed to the
outside air, as through an open wound in the chest
wall) or closed.
COLLABORATIVE MANAGEMENT
Assessment findings commonly include the
following:
•
Diminished
breath sounds on auscultation
•
Hyperresonance
on percussion
•
Prominence of the involved side of the chest, which moves poorly with respirations
•
Deviation of the trachea away from (closed) or toward (open) the affected side
In addition, the client may have pleuritic pain,
tachypnea, and subcutaneous
emphysema (air under the skin in the subcutaneous tissues).
A chest x-ray study is used for diagnosis. Chest tubes
may be indicated to
allow the air to escape and the lung segment to reinflate.
Tension Pneumothorax
OVERVIEW
Tension
pneumothorax, one of the most rapidly developing and life-threatening complications of blunt chest trauma,
results from an air leak in the lung or chest wall. Air forced into the thoracic cavity causes complete collapse of the
affected lung. Air that enters the pleural space during expiration does not
exit during inspiration. As a result, air progressively accumulates under
pressure, compresses the mediastinal vessels, and interferes with venous return. Because this process
leads to decreased diastolic
filling of the heart, cardiac output is compromised. If not promptly detected and treated, tension pneumothorax is quickly fatal. Typical causes of
tension pneumothorax are blunt
chest trauma, mechanical ventilation with positive end-expiratory pressure (PEEP), closed-chest
drainage (chest tubes), and
insertion of central venous access catheters.
COLLABORATIVE MANAGEMENT
Assessment
Assessment findings with tension pneumothorax include
the following:
•
Asymmetry of the thorax
•
Tracheal deviation to the unaffected side
•
Respiratory distress
•
Absence of breath
sounds on one side
•
Distended neck veins
•
Cyanosis
Hypertympanic sound on percussion over the
affected side Pneumothorax is
detectable on a chest x-ray film. ABG assays demonstrate hypoxia and respiratory alkalosis.
Interventions
The physician inserts a large-bore needle into the
second intercostal space in the midclavicular line of the affected side as initial treatment for tension pneumothorax. After
this lifesaving measure is
completed, the physician places a chest tube into the fourth intercostal space of the midaxillary line and
attaches the tube to a water seal
drainage system until the lung reinflates.
Hemothorax
OVERVIEW
Hemothorax is one of the most common problems encountered
after blunt chest trauma or penetrating injuries. A simple hemothorax
is a blood loss of less than 1500
mL into the thoracic cavity; a massive hemothorax is
a blood loss of more than
1500 mL.
Bleeding is frequently caused by injuries to
the lung parenchyma, such as pulmonary contusions or lacerations, which are often associated with rib and sternal
fractures. Massive intrathoracic bleeding in
blunt chest trauma generally stems from the
heart, great vessels, or major systemic arteries, such as the intercostal arteries.
COLLABORATIVE
MANAGEMENT
Assessment
Physical assessment findings vary with the size of the
hemothorax. If the
hemothorax is small, the client may be asymptomatic. If the hemothorax is
larger, the client experiences respiratory
distress. In addition, breath sounds are diminished on auscultation. The percussion note on the involved
side is dull. Blood in the
pleural space is visible on a chest x-ray film and confirmed by diagnostic thoracentesis.
Interventions
Interventions are aimed at evacuating the blood in the
pleural space to normalize pulmonary function and to prevent infection related
to blood accumulation. The physician inserts anterior and posterolateral chest tubes to evacuate the
pleural space and to reduce the rash of clotted blood. The physician and the
nurse carefully monitor the chest tube drainage, and chest x-ray films are
evaluated serially.
The physician considers open thoracotomy when
there is initial evacuation of 1500
to 2000 mL
of blood or persistent bleeding at the rate of 200 mL/hr
over 3 hours. The nurse monitors the vital signs, blood loss,
and overall intake and output; assesses the
client's response to the chest tubes; and administers IV fluids and blood as
ordered. Autotransfusion of the blood lost
through chest drainage should be considered.
Tracheobronchial
Trauma
overview
Most
tears of the tracheobronchial tree result from severe blunt trauma primarily involving the mainstem bronchi.
Injuries to the cervical trachea usually occur at the
junction of the trachea and cricoid
cartilage. These injuries are frequently caused by striking the anterior neck against the dashboard or steering
wheel during a vehicular accident. Clients with lacerations of the trachea
develop massive air leaks, which produce pneumomediastinum (air in the
mediastinum) and extensive subcutaneous emphysema. Upper airway obstruction may also occur and produce severe respiratory
distress and inspiratory stridor.
Major cervical tears are managed by cricothyroidotomy
or tracheostomy below the level of injury.
COLLABORATIVE MANAGEMENT
The
nurse assesses the client for hypoxemia by ABG assays. The nurse administers oxygen appropriately. Depending
on the degree of injury,
the client may require mechanical ventilation or surgical repair. Frequent assessment of vital signs
is essential because the client is
likely to be hypotensive and in shock. The nurse continues to assess for subcutaneous emphysema
and auscultates the lungs
to assess for further complications every 1 to 2 hours
initially. Decreased breath sounds or wheezing may indicate further obstruction, atelectasis, or
pneumothorax.
PE. Fat emboli from fracture of a long bone and oil
emboli from
lymphangiography do not impede blood flow; rather, they result in vascular injury and acute respiratory
distress syndrome (ARDS). Amniotic fluid
embolus is associated with a mortality rate of 80% to 90%; it occurs in 1 per
20,000 to 30,000 deliveries
and can be a complication of abortion or amniocentesis. Septic emboli commonly arise from a
pelvic abscess, an infected IV
catheter, and nonsterile injections of illegal drugs. The problem with septic emboli lies in the
toxic effects of the
infection more than in the vascular occlusion.
