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ICU Alert: Worsening respiratory function can signal ARDS
Author: Ruth Kleinpell, RN-CS, PhD, ACNP,CRN, FAAN

Course Objectives

The purpose of this article is to increase nurses’ understanding of acute respiratory distress syndrome,
including the risk factors, pathophysiology, signs and symptoms, and treatment. After you study the
information presented here, you will be able to —

• Discuss the pathophysiology of acute respiratory distress syndrome.

• Identify treatment goals for acute respiratory distress syndrome.
• Discuss the role of the nurse in identifying and managing patients with acute respiratory distress
syndrome.

Despite progress in managing acute care disease, acute respiratory distress syndrome (ARDS)
continues to pose challenges for critical care clinicians. In fact, the respiratory failure that characterizes
ARDS is a common cause of morbidity and mortality, with mortality rates of 40% to 50%.1 In the U.S.,
an estimated 150,000 people are affected with ARDS each year.1,2

However, the seasoned critical care nurse knows that astute assessment can offset these bleak statistics.
For example, prompt recognition of the distinct signs and symptoms of acute lung injury, often a
harbinger of ARDS, can set a targeted treatment plan in motion. Likewise, early recognition of the
progressively worsening respiratory function seen in ARDS can alert the team that the patient will need
special types of mechanical ventilation to preserve and improve oxygenation.

A variety of conditions that predispose the lungs to injury can cause ARDS. Both direct and indirect
injuries can lead to ARDS. Direct injuries are those that cause inflammation and injury to the lung
directly, such as pneumonia, aspiration, and contusion injuries. Indirect injuries are those that affect the
lung indirectly through conditions such as infections such as sepsis or through acute illness states such
as shock and pancreatitis. While many factors influence the development of ARDS, patients with
multiple trauma, higher severity of illness, and underlying comorbid conditions are at increased risk.3

Acute lung injury

ARDS is generally preceded by acute lung injury. Acute lung injury (ALI) is a less severe form of
respiratory failure that occurs when there is injury to the alveoli, the functional units of the lungs where
gas exchange occurs. It can be clinically difficult to differentiate ALI from ARDS because both involve
inflammation and injury to the lung. But recognizing signs of worsening respiratory status is important
because as lung injury progresses, ALI results in ARDS.

An American-European consensus conference in 1994 established criteria for differentiating ALI and
ARDS.4 In patients with ALI or ARDS, alveolar damage results in altered gas exchange. The criteria
state that both ALI and ARDS are associated with an acute onset, bilateral infiltrates on chest X-ray,
and low pulmonary artery wedge pressure, an indirect measure of the pressure in the left atrium of the
heart and/or the absence of left atrial hypertension. This latter clinical feature indicates that the cause of
the pulmonary edema is not cardiac-related.

The one feature that distinguishes ARDS from ALI is a worsened state of oxygenation. This is seen in
the PaO2/FIO2 ratio, which reflects the status of oxygenation. The PaO2/FIO2 ratio can be calculated
from knowing the amount of oxygen a patient is breathing (FIO2) and the PaO2 value from an arterial
blood gas. A normal PaO2/FIO2 ratio is near 500 mm Hg. In ALI, the PaO2/FIO2 ratio is less than 300
mm Hg. In ARDS, the PaO2/FIO2 ratio is less than 200 mm Hg.4 The need for increasing oxygen
requirements with persistently low levels of oxygen saturation and arterial oxygen content on an
arterial blood gas is a sign that ALI is progressing to ARDS. This is also known as "refractory
hypoxemia," meaning that although increasing amounts of oxygen are provided, the level of hypoxemia
continues or even worsens due in part to the lung injury that occurs in ALI/ARDS.

ARDS is diagnosed based on signs and symptoms indicating progressively worsening respiratory
functioning. All patients with ARDS have ALI, yet, as mentioned, differentiating when ALI has
progressed to ARDS is often a challenge. The clinical parameters of the definitions of ALI and ARDS,
i.e., the PaO2/FIO2 ratio, can help clinicians to determine whether a patient has ALI or ARDS and to
distinguish when ALI has progressed to ARDS.

Clinical features

The clinical features of ALI and ARDS include shortness of breath, increased respiratory rate, and
hypoxemia that is resistant to oxygen therapy: No matter how much oxygen patients are receiving, they
continue to exhibit low oxygenation levels. Other signs and symptoms of ARDS and ALI include
decreased lung compliance, respiratory alkalosis due to an increasing respiratory rate and
hyperventilation, diffuse crackles or rales heard on chest auscultation, and bilateral diffuse infiltrates
seen on chest X-ray due to developing pulmonary edema.4,5

Pathophysiology

In ARDS, clinical lung injury occurs in the lining of the alveoli, also called the alveolar epithelial
membrane. Simultaneously, injury occurs to the lining of the capillary, or endothelium, which
participates in gas exchange with the alveoli. Normally, the endothelial-epithelial barrier allows the
exchange of oxygen and carbon dioxide. Substances in the blood such as proteins and fluid do not cross
the barrier into the lungs. Damage to the endothelial-epithelial membranes results in movement of
protein-rich fluid into the alveoli, causing fluid filling of the alveoli that impairs gas exchange.
Increased permeability pulmonary edema is a recognized hallmark of ARDS.6 The lung damage that
occurs in ARDS includes alveolar-capillary membrane injury, inflammation, and increased
permeability pulmonary edema.6

Four distinct phases of injury occur in ARDS.3 The first phase starts at the time of acute injury. The
second phase, also known as the latent period, can last hours or days. Often, few clinical signs and
symptoms are seen in these beginning phases of lung injury.

During the third phase, the acute respiratory failure phase, patients exhibit progressive dyspnea,
tachypnea, hypoxemia, and decreasing lung compliance. This is due to the progressive lung injury
occurring within the lungs, specifically to the cells lining the alveoli. This acute phase, often termed the
early phase of ARDS, is characterized by injury to the endothelial-epithelial barrier, which leads to
pulmonary edema and injury to the cells of the lungs. Excessive inflammation occurs, and mediators
released from white blood cells, particularly neutrophils and macrophages, release protein-based
substances called cytokines. Cytokines - including tumor necrosis factor alpha, interleukins, platelet-
activating factor, and complement - worsen lung injury by increasing endothelial permeability,
increasing inflammation, and causing dysfunction of endothelial cells. Neutrophils are activated and
recruited to the lungs, where they degranulate and release proteolytic enzymes - enzymes that cause the
splitting of proteins - as well as stimulate the production of oxygen-free radicals, both of which
potentiate lung injury. The life span of neutrophils can be lengthened in ARDS, and the accumulation
of these white blood cells within the airspace further contributes to lung injury and impaired
oxygenation.

There are two types of pneumocytes (cells that line the alveoli in the lungs), Type 1 and Type 2. These
cells make up the alveolar epithelial membrane. Type 2 cells produce surfactant, which normally
functions to decrease the surface tension in the alveoli and keeps the alveoli distended or open for gas
exchange. Type 2 cells also are responsible for maintaining normal ion transport.3 Injury to the
pneumocytes leads to loss of epithelium integrity, decreased surfactant production, and altered ion
transport, resulting in edema accumulation within the alveoli.3,5,7 Because of the damage to the
epithelium, hyaline membranes - a collection of damaged cells that result in thickening of the
epithelium - form, and progressive fibrosis occurs.7,8 This part of the third phase is often called the late
phase of ARDS. Continued endothelial damage leads to altered permeability and movement of protein-
rich fluid into the alveolar airspace, further impairing alveolar gas exchange.6 As a result, diffuse lung
injury occurs and acute respiratory failure results.

In the fourth phase of ARDS, called the clinical phase, severe physiologic abnormalities are seen such
as refractory hypoxemia and pulmonary shunting (decreased blood flow to the lungs), impairing
oxygenation.6,8

Recovery from ALI/ARDS depends on the resolution of the injury to the lungs. The resolution of
pulmonary edema and lung inflammation determines recovery from acute lung injury. Persistence and
progression of lung injury can lead to pulmonary fibrosis, pulmonary vascular destruction, and multiple
organ failure, which can be associated with a poor prognosis.6 Patients often require mechanical
ventilation for up to several weeks to help support respiratory functioning while the lungs heal.
Functional resolution occurs when there is return of the alveolar epithelial barrier and resolution of the
alveolar edema.8 The recovery process is variable and depends on the severity of the patient's illness,
disease state, and comorbidities. Full recovery of the lungs can take six to 12 months.3,8 Residual
impairment, such as altered gas exchange with exercise, may persist. Patients who require prolonged
mechanical ventilation are at the highest risk for developing impaired respiratory functioning.3

Management

The management of ARDS requires treatment of the underlying cause as well as aggressive supportive
care for respiratory failure. Patients with ARDS often experience severe shortness of breath and
difficulty breathing. The mainstay treatment is supplemental oxygenation. Mechanical ventilation
therapy is often required because of respiratory failure. The goals of treatment are to increase
oxygenation, minimize pulmonary edema, and improve functioning of the lungs. A variety of
alternative modes of ventilation continue to be tested, including noninvasive positive pressure
ventilation.5 Mechanical ventilation using high pressure or volumes can promote barotrauma to the
lungs. The use of low-volume targeted ventilation is the suggested ventilatory strategy for protecting
the lungs of patients with ARDS.9 Lung-protective ventilation strategies, such as low tidal volume
ventilation and low FIO2 and pressure settings, are recommended as the goal is to provide oxygen
while minimizing further lung injury.3

The most appropriate method of mechanical ventilation for the treatment of ARDS has been debated
over the years. In 1994, the ARDS Network, a National Institutes of Health-sponsored network of more
than 20 hospitals, was organized to research treatment strategies. As part of its research, a large study
was conducted to assess the impact of low tidal volume ventilation (6 ml/kg of body weight) compared
to higher tidal volume ventilation (12 ml/kg of body weight). Patients receiving lower tidal volume
ventilation were found to have decreased mortality rates.9 The study results have since been critiqued;
however, lower tidal volume ventilation strategies (5 to 7 ml/kg of body weight) continue to be
recommended for the treatment of ARDS.

Additional mechanical ventilation strategies include keeping intrapulmonary pressure low and using
positive end-expiratory pressure (PEEP) - pressure delivered by the mechanical ventilator to help re-
expand collapsed alveoli. Because of altered surfactant production and pulmonary edema, the alveoli
are prone to collapse in ARDS. PEEP helps keep the alveoli open at the end of expiration to facilitate
gas exchange.

Other treatments used in ARDS include corticosteroids and anti-inflammatory agents, inhaled nitric
oxide (to reverse pulmonary vasoconstriction), and antioxidant therapy (to combat oxygen free radical
damage).3 While altered surfactant production is a known detrimental effect in ARDS, surfactant
therapy has not been shown to be beneficial.3,10 Based on ongoing research, future treatment strategies
may include the use of stem cells to enhance repair of injured lung tissue. Gene therapy also may play a
role because there is growing evidence that genetic variations exist in inflammatory responses, which
may be a predisposing factor to the development of ARDS.11

Nursing considerations

Nursing care of patients with ARDS involves close assessment and monitoring for changes in
respiratory status. Early detection and treatment of ALI and ARDS can promote better outcomes for
patients; therefore, monitoring and reporting respiratory status changes are an essential aspect of
nursing care. Changes include increased respiratory rate; adventitious lung sounds (e.g., rales,
wheezing); decreased oxygenation saturation; and shortness of breath.

Because a majority of patients will progress from needing supplemental oxygen to being intubated and
mechanically ventilated, anticipating the need for intubation when a patient's respiratory status is
declining is another important part of the nursing care of patients with ALI/ARDS. Mechanical
ventilation is a mainstay of treatment for the patient with ARDS, and low volume targeted ventilation
promotes the best delivery of oxygenation while also protecting the lungs.12,13 Nursing care of the
mechanically ventilated patient involves ensuring patency of the airway, ensuring patient safety and
comfort, monitoring oxygenation and airway pressure levels, and optimizing gas exchange. Infiltrates
in the lung are not uniformly distributed in ARDS, so changes in position can improve oxygenation.
Therefore, turning and patient repositioning are components of nursing care.

Prone positioning - positioning patients on their stomach - allows expansion of the lungs and improves
outcomes in patients with ARDS.14,15 Pronation therapy, however, can become complicated when
patients are acutely ill and intubated, and have various monitoring devices and intravenous lines.15
Pressure ulcers are also a concern when proning patients, so specific proning protocols should be
followed to minimize complications.16,17 Other complications that can occur with pronation therapy
include peripheral nerve injuries and corneal ulcerations. Therefore, nursing assessment and care of
patients receiving pronation therapy includes ensuring correct positioning as well as monitoring for
complications.17

Pain relief and sedation promote patient comfort and optimal oxygenation. Monitoring patients for
restlessness or anxiety and providing medication to promote relaxation can help patients breathe easier.

ARDS is a critical illness state; thus, patients can develop organ system dysfunction as a result of
altered oxygenation and decreased tissue perfusion. The development of multiple organ system
dysfunction can compound the effects of ARDS. This often results in higher mortality rates for patients
with ARDS. It is estimated that the majority of deaths in ALI/ARDS are from multiple organ
dysfunction rather than a direct respiratory cause.3 Therefore, astute nursing assessment related to
organ system dysfunction in addition to respiratory failure is an important part of care.

ARDS is an acute life-threatening illness with a possibly extended rehabilitation; providing information
and support to patients and families helps them understand the disease process. A variety of Web-based
references offer information, chat rooms, and stories from patients and families who have experienced
ARDS. (See, for example, www.ards.org and www.ardsfoundationil.com.)

Nurses caring for patients with ARDS must be knowledgeable about its risk factors, clinical
presentation, pathophysiology, and treatment. Several aspects of treatment for ARDS directly relate to
nursing care, including patient positioning and mechanical ventilation care, and can promote patients'
recovery.

Ruth Kleinpell, RN-CS, PhD, ACNP,CRN, FAAN, is an associate professor at Rush University College
of Nursing in Chicago, where she teaches in the critical care graduate and acute care NP program.
She also maintains active practice as an NP at Our Lady of the Resurrection Medical Center in
Chicago.

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