Dr. Aidah Abu Elsoud AlkaissiAn-Najah National University

Faculty of Nursing

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Based on the content in this chapter, the student should be able to:

■ Compare and contrast the causes, definition, assessment findings,and outcomes between acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).

■ Relate the assessment and diagnostic findings of ARDS to the

pathophysiological processes.■ Describe mechanical ventilation strategies used to

prevent ventilator-associated lung injury (VALI).■ Explain the management of patients with ARDS and

rationalesfor the interventions.■ Discuss potential complications of ARDS and the relatedinterventions.

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Acute respiratory distress syndrome (ARDS) represents a complex clinical syndrome (rather than a single disease process) and carries a high risk of mortality.

The severity of the clinical course, the uncertainty of the outcome, and the reliance on the full spectrum of critical care resources for treatment means that the entire health care team is challenged.

For nearly 30 years, researchers and clinicians have investigated the nature of the pathological process and explored treatment options with the goal of improving outcome.

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Through this application of research to practice we know that some previous strategies have been ineffective, and new innovations in mechanical ventilation, sedation, nutrition, and pharmacological intervention are now important research initiatives.

A key role for the critical care nurse is early detection and prevention of ARDS.

Therefore, with respect to ARDS, it is essential for critical care nurses to be knowledgeable of risk factors, assessment tools and protocols, and preventive strategies.

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ARDS was first described in 1967 and was termed adult (rather than acute) respiratory distress syndrome because of a misconception (A mistaken thought, idea, or notion; a misunderstanding) that the syndrome occurred only in adults.

Recognition of the prevalence of this syndrome in younger patients led to the current terminology.

Diagnostic criteria for ARDS have been hard to define because ARDS is at the extreme end of a continuum of acute, hypoxic lung injury resulting in acute respiratory failure.

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In 1994, the American-European Consensus Conference members proposed diagnostic criteria for acute lung injury (ALI) and ARDS, with ALI as the less severe form of this syndrome manifested by hypoxia and noncardiogenic lung edema1 (Table 27-1).

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table 27-1 ■ Comparison of Acute Lung Injury (ALI)

and Acute Respiratory Distress Syndrome (ARDS)

Criterion ALI ARDS

PaO2:FIO2 ratio, regardles of PEEP level

(ALI) Less than 300

Less than 200

Chest x-ray

(ALI) Bilateral infiltrates

(ARDS) Bilateral infiltrates

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Pulmonary artery wedg pressure

(ALI) Less than 18 mm Hg or no indication

of left atrial hypertension

(ARDS) Less than 18 mm Hg or no indication of left atrial hypertension

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The causes of ARDS are many and diverse.

The syndrome may be precipitated by either direct or indirect pulmonary injury, possibly in previously healthy people who are exposed to an insult (Box 27-1).

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box 27-1 Risk Factors for Acute Respiratory Distress Syndrome (ARDS)

Indirect Pulmonary Injury■ Shock of any etiology■ Sepsis■ Hypothermia■ Hyperthermia■ Drug overdose■ Disseminated intravascular coagulation (DIC)■ Multiple transfusions■ Cardiopulmonary bypass■ Eclampsia■ Burns■ Pancreatitis■ Severe nonthoracic trauma

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Direct Pulmonary Injury■ Pulmonary infections■ Toxic inhalation■ Aspiration (gastric fluids, near-drowning)■ Pneumonitis Systemic Inflammatory Response Syndrome (SIRS) Criteria SIRS is manifested by two or more of the following:■ Temperature greater than 100.4F (38C) or less than 96.8F (36C)■ Heart rate greater than 90 beats/minute■ Respiratory rate greater than 20 breaths/minute or an

arterial carbon dioxide tension (PaCO2) less than 32 mm Hg

■ White blood cell count greater than 12,000 cells/mm3 or less than 4,000 cells/mm3 OR more than 10% immature (band) forms

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Symptoms may not manifest for up to 72 hours after the initial insult, making association with the cause sometimes difficult.

For example, direct injury occurs through aspiration, pulmonary infection (bacterial, fungal, viral, or mycobacterial), neardrowning, thoracic trauma, and toxic inhalation.

Indirect injury that results in ARDS includes sepsis syndrome, burns, trauma, multiple blood transfusions, cardiopul monary bypass, pancreatitis, and fat emboli.

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The question of whether these causes result in the same pathological changes in the lung is under investigation, but the clinical presentation and treatment are similar.

Most patients with ARDS require a period of mechanical ventilation support.

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Current research findings indicate that the incidence of ARDS has been difficult to determine because of the variation in diagnostic criteria.

It is estimated that 150,000 cases per year occur in the United States with an associated mortality rate of 30% to 70%.

This statistic represents a decrease from the 90% mortality rate over the last decades.

The patients most at risk for development of ARDS are elderly (older than 65 years), with a severe acute illness on presentation to critical care (e.g., sepsis) or with additional risk factors such as a preexisting chronic disorder.

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any individual with one of the potential precipitating causes of ARDS is susceptible, and nurses need to be vigilant for early warning signs—even, for example, in a young trauma patient.

ARDS has developed in approximately one third of patients with sepsis (regardless of the bacterial source) or severe trauma.

Critical care techniques to provide life support for individuals with ARDS have reached a point where death results from complications such as ventilator-acquired pneumonia, sepsis, or multiorgan dysfunction, rather than from respiratory failure

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In 1967, Ashbaugh and others described ARDS in case reports of 12 patients presenting with acute tachypnea, decreased lung compliance, diffuse pulmonary infiltrates on chest x-ray, and hypoxemia.

Later researchers used histological examination of lungs of patients with ARDS to show lung fibrosis that was unlike other diseases.

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This led to new understanding that the pathological process was not limited to the lung endothelium, but was a result of alterations of lung epithelium and vascular tissue, and the development of hyaline membranes edema, and impaired gas exchange are hallmarks of the pathophysiology.

The pathological pulmonary alterations of ARDS are directly related to a cascade of events resulting from release of cellular and biochemical mediators.

The activation, interactions, and multisystem actions of biological mediators are extremely complex.

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Systemic inflammatory response syndrome (SIRS) describes the inflammatory response occurring throughout the body as a result of some systemic insult (bodily injury, irritation, or trauma).

Most patients with ARDS manifest the symptoms that define SIRS (see Box 27-1), and the respiratory system may be the earliest and most common organ system to be involved in the systemic response.

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Thus, an understanding of the pathophysiology of SIRS and knowledge of the interventions used for SIRS are important in relation to ARDS.

Often, patients with SIRS develop multisystem organ dysfunction (MODS), primarily in the liver and kidney.

As endothelial damage progresses and tissue hypoxia ensues (To follow as a consequence or result) from the severely impaired gas exchange, the inflammatory response is perpetuated (To prolong the existence of) and the SIRS cascade intensifies (upregulates) with the release of more mediators.

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Adequate pulmonary gas exchange depends on open, air-filled alveoli; intact alveolar–capillary membranes; and normal blood flow through the pulmonary vasculature.

In ARDS, diffuse alveolar–capillary membrane damage occurs and increases membrane permeability.

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Alterations in alveolar–capillary membrane integrity allow fluids to move from the vascular space into the interstitial and alveolar space.

The resultant interstitial and alveolar edema and eventual alveolar collapse impair both oxygenation and ventilation.

The pathogenesis of ARDS is illustrated in Figure 27-1. Inflammatory mediators cause the pulmonary vascular bed to vasoconstrict.

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Pulmonary hypertension and reduced blood flow to portions of the lung results Because of the reduction in blood flow an decreased hemoglobin in capillaries, there is a decrease in oxygen available for diffusion and transport, further impairin oxygenation.

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The pathological changes affect pulmonary blood vessels, gas exchange, and lung and bronchial mechanics.

The overall picture of ARDS is one of impaired diffusion of oxygen and elimination of carbon dioxide into pulmonary capillary blood.

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Ventilation is impaired because of a decrease in lung compliance and an increase in airway resistance.

Increased membrane permeability, fluid-filled and collapsed alveoli, and dysfunctional surfactant, a substance that normally decreases the surface tension of alveoli and prevents their collapse, cause decreased lung compliance.

Mediator-induced bronchoconstriction causes airway narrowing and increased airway resistance, restricting the flow of air into the lungs.

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There is progression in the pathological changes associated with ARDS, starting with increasing pulmonary edema in the early stages and progressing to inflammation, fibrosis, and impaired healing in the later stages.

Recognizing the dynamic nature of the morphological changes involved with ARDS enables the nurse to understand the changes in physical assessment, mechanical ventilation strategies, treatment, and management that occur throughout the patient’s critical care stay.

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There are distinct stages in the progression of ARDS(Table 27-3). In stage 1, diagnosis is difficult because the signs of

impending (To threaten to happen) ARDS are subtle (difficult to detect).

Clinically, the patient exhibits increased dyspnea and tachypnea, but there are few radiographic changes.

At this point, neutrophils are sequestering (To remove or set apart); however, there is no evidence of cellular damage.

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Within 24 hours (a critical time for early treatment), the symptoms of respiratory distress increase in severity, with cyanosis, coarse bilateral crackles (the sharp sound of snapping noises) on auscultation, and radiographic changes consistent with patchy infiltrates.

It is at this point (stage 2) that the mediator-induced disruption of the vascular bed results in increased interstitial and alveolar edema.

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The endothelial and epithelial beds are increasingly permeable to proteins.

The hypoxia is resistant to supplemental oxygen administration, and mechanical ventilation will most likely be commenced (To enter upon or have a beginning) in response to a worsening ratio of arterial oxygen to inspired oxygen (PaO2/FIO2 ratio).

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From the 2nd to the 10th day after injury (stage 3), evidence of SIRS is present, with hemodynamic instability, generalized edema, the possible onset of nosocomial infections, increasing hypoxemia, and lung involvement.

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Air bronchograms may be evident on chest radiography as well as decreased lung volumes and diffuse interstitial markings.

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Stage 4, which develops after 10 days, is typified by few additional radiographic changes.

There is increasing multiorgan involvement, SIRS, and increases in the arterial carbon dioxide tension (PaCO2) as progressive lung fibrosis and emphysematous (An abnormal distention of body tissues caused by retention of air) changes result in increased dead space.

Fibrotic lung changes result in ventilation management difficulties, with increased airway pressure and development of pneumothorace

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Throughout the stages of ARDS, the reliance on diagnostic tests is important.

In the early stages, the need to establish cause may require specific tests, such as blood cultures, bronchoalveolar lavage cultures, and computed tomography (CT) examinations for abscess (e.g., abdominal abscesses).

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In later stages, further vigilance is required to intervene for early management of any nosocomial infections.

Ongoing monitoring of routine blood chemistry and hematology is done to ensure stability in metabolic parameters and optimization of existing function.

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Recent research has focused on the use of plasma and bronchoalveolar lavage samples for detection of mediators, particularly elevated amounts of interleukin-1 (IL-1) and tumor necrosis factor-α(TNF-α), as early markers for diagnosis of ARDS.

Of particular interest and importance are th following tests in the management of ARDS.

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BLOOD GAS ANALYSIS Deterioration of arterial blood gases (ABGs),

despite interventions, is a hallmark of ARDS.

Initially, hypoxemia (an arterial oxygen tension, or PaO2, of <60 mm Hg) may improve with supplemental oxygen; however, refractory hypoxemia (no improvement of PaO2 with supplemental oxygen) and a persistently low SaO2 eventually develop.

Early in acute respiratory failure, dyspnea and tachypnea are associated with a decreased PaCO2.

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Hypercarbia (the physical condition of having the presence of an abnormally high level of carbon dioxide in the circulating blood) develops as gas exchange and ventilation become increasingly impaired.

Arterial pH in the early phase may be high (>7.45), a finding that is consistent with respiratory alkalosis secondary to rapid respirations and a low PaCO2.

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The arterial pH measurements in ARDS are typically lower because of respiratory and ventilatory failure and tissue hypoxia, anaerobic metabolism, and subsequent metabolic acidosis.

Base excess and deficit follow a similar trend, depending on the degree of tissue and organ hypoxia.

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Measurement of arterial lactate is commonly ordered as an indication of tissue hypoxia and anaerobic metabolism.

An elevated blood lactate concentration is common in early ARDS and resolves as oxygenation improves.

Lactate measurement is not done routinely once adequate, although perhaps not optimal, oxygenation has been achieved.

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RADIOGRAPHIC STUDIES In the early phase of ARDS, the chest

radiographic changes are usually negligible.

Within a few days, the chest x-ray findings show patchy bilateral alveolar infiltrates, usually in the dependent lung fields.

This may be mistaken for cardiogenic pulmonary edema.

Over time, these patchy infiltrates progress to diffuse infiltrates, consolidation, and air bronchograms.

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CT of the chest also shows areas of infiltrates and consolidation of lung tissue (A condition in which lung tissue becomes firm and solid rather than elastic and air-filled because it has accumulated fluids and tissue debris).

Daily chest x-rays are important in the continuing evaluation of the progression and resolution of ARDS and for ongoing assessment of potential complications, especially pneumothoraces.

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INTRAPULMONARY SHUNT MEASUREMENT An intrapulmonary shunt is a type of

ventilation–perfusion mismatch.

It may be defined as the percentage of cardiac output that is not oxygenated owing to pulmonary blood flowing past collapsed or fluid-filled and nonventilated alveoli (a physiological shunt), absence of blood flow to ventilated alveoli (alveolar dead space), or a combination of both of these conditions

Normally, an intrapulmonary shunt of 3% to 5% is present in all people.

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Advanced respiratory failure and ARDS are associated with a shunt of 15% or more because of the pathological changes in blood flow, endothelial disruption, and alveolar collapse.

As the intrapulmonary shunt increases to 15% and greater, more aggressive interventions, including mechanical ventilation, are required because this level of shunt is associated with profound hypoxemia and may be life-threatening.

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The intrapulmonary shunt fraction may be estimated using a simple calculation, the ratio of arterial oxygen to inspired oxygen (i.e., the PaO2/FIO2 ratio).

In general, a PaO2/FIO2 ratio greater than 300 is normal, a value of 200 is associated with an intrapulmonary shunt of 15% to 20%, and a value of 100 is associated with an intrapulmonary shunt of more than 20%.

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LUNG COMPLIANCE, AIRWAY RESISTANCE, AND PRESSURES

Lung mechanics are altered in ARDS, resulting in reduced alveolar ventilation and pulmonary gas exchange.

Lung compliance, or distensibility, is decreased as the alveoli become fluid-filled or collapsed.

More effort and greater pressure are required to move air into the lungs as they become increasingly “stiff.”

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In addition, the resistance to airflow into and out of the lungs increases with the accumulation of secretions and mediator-induced bronchoconstriction.

Because the patient with ARDS requires mechanical ventilation to support oxygenation and ventilation, lung compliance and airway resistance can be evaluated by assessing ventilator pressures and tidal volume changes.

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Precise measurement of airway resistance involves measurement of airflow velocity and airway diameter; however, airway resistance may be estimated by comparing the ventilator peak inspiratory pressure to the plateau (static) pressure at end inspiration.

A difference between these two pressures of 10 cm H2O or less would suggest a normal airway resistance, whereas a difference greater than 10 cm H2O would suggest increased resistance.

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Although evaluating the airway resistance by calculating the difference between the peak inspiratory pressure and the plateau pressure does not provide an exact measurement, this method is useful for trending changes and evaluating the effectiveness of interventions that are directed toward reducing airway resistance.

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Lung compliance likewise may be estimated and trended.

The static lung compliance calculation uses the plateau pressure and requires use of a specific constant associated with different types of mechanical ventilators.

Dynamic lung compliance is less precise because its calculation uses the peak inspiratory pressure, which does not eliminate resistance factors; however, it is simpler and may be useful to trend through the course of ARDS.

Cdyn VT (PIP −PEEP)

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where Cdyn dynamic lung compliance; VT tidal volume;

PIP peak inspiratory pressure; and PEEP positive end-expiratory pressure.

The normal dynamic lung compliance is approximately 100 mL/cm H2O.

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Close monitoring of airway pressures, including the mean airway pressure, the peak inspiratory pressure, and the plateau pressure, is an important component of patient assessment in ARDS.

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Increases in these pressures as tidal volumes are maintained to achieve a normal PaCO2 indicate reduced compliance and increased resistance to airflow.

As airway pressures rise, the lung epithelium is traumatized, resulting in further lung tissue damage

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Volutrauma (lung epithelial damage) or barotrauma from persistently elevated airway pressures thus has additional deleterious (Having a harmful effect; injurious) effects on ventilation and oxygenation.

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Therapeutic modalities for the treatment of ARDS have remained elusive (difficult to describe).

Treatment is supportive; that is, while contributing factors are corrected or reversed and the lungs heal, care is taken that treatment does no further damage.

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Oxygenation and Ventilation OXYGEN DELIVERY One of the hallmarks of ARDS is refractory

hypoxemia; therefore, attention to improving oxygen delivery is paramount (having superior power and influence).

Strategies include optimizing normal oxygen delivery parameters, including hemoglobin, cardiac output, and oxygen saturation.

Oxygen delivery is the amount of oxygen delivered to the tissues and organs every minute and depends on the flow of oxygenated blood through the tissue beds.

Oxygen delivery is determined by hemoglobin, arterial oxygenation, and cardiac output:

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DaO2 CO (Hgb SaO2 1.38) (PaO2 0.0031)

where DaO2 oxygen delivery; CO cardiac output;

Hgb hemoglobin; SaO2 arterial oxygen saturation;

and PaO2 arterial oxygen tension.

Adequate oxygen delivery, defined as a DaO2 of greater than 800 mL O2/minute, is essential to meet tissue requirements

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for oxygen, thereby preventing anaerobic metabolism and hypoxia, which can trigger and perpetuate (cause to continue ) SIRS.

Critically ill patients with ARDS have high demands for oxygen to maintain organ function.

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Hemoglobin combines with oxygen to form oxyhemoglobin; therefore, sufficient amounts of hemoglobin are necessary to carry oxygen to the cells.

There is little research to support the intuitive (spontaneously derived from or prompted by a natural tendency) concept that normal or increased hemoglobin is required to promote oxygen delivery in patients with SIRS or ARDS.

Recent studies on transfusion requirements indicate that values of approximately 8.0 g/dL are sufficient for critically ill patients, except for those with cardiac disease.

Therefore, transfusion to maintain normal hemoglobin is no longer accepted therapy and should be discouraged.

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Cardiac output is typically altered in ARDS because of the SIRS response, the effect of hypoxemia on the myocardium, and the decrease in venous return induced by mechanical ventilation.

Evaluation of the cardiac output is important to assess oxygen delivery and initiate appropriate interventions.

Therapies to optimize cardiac output are directed toward enhancing preload and contractility and normalizing afterload.

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Use of a thermodilution pulmonary artery catheter to assess oxygen delivery and consumption is routine for patients with ARDS to ensure that the appropriate interventions are instituted.

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Fick's equation: SvO2 = SaO2 -VO2 / 13.9 x Q x [Hb]

Continuous SVO2 monitoring allows the minute-to-minute assessment of total tissue oxygen balance (i.e., the relationship between oxygen delivery and oxygen consumption).

SVO2 varies directly with cardiac output, Hb, and SaO2, and inversely عكسيا with VO2 (oxygen consumption.)

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The normal SVO2 is 75%, which indicates that under normal conditions, tissues extract 25% of the oxygen delivered.

An increase in VO2 or a decrease in arterial oxygen content (SaO2 x Hb) is compensated by increasing CO or tissue oxygen extraction.

When the SVO2 is less than 30%, tissue oxygen balance is compromised, and anaerobic metabolism ensues.

A normal SVO2 does not ensure a normal metabolic state but suggests that oxygen kinetics are either normal or compensated.

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Diagram of Pulmonary artery catheter

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Preload can be defined as the initial stretching of the cardiac myocytes prior to contraction.

other indices of preload are used such as ventricular end-diastolic volume or pressure. For example, when venous return is increased, the end-diastolic pressure and volume of the ventricle are increased,

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Afterload can also be described as the pressure that the chamber of the heart has to generate in order to eject blood out of the chamber, and thus is a consequence of the aortic pressure, since the pressure in the ventricle must be greater than the systemic pressure in order to open the aortic valve. Everything else held equal, as afterload increases, cardiac output decreases.

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Fluid administration to ensure adequate intravascular volume and optimize preload is important before other interventions are initiated.

Controversy exists regarding the administration of crystalloids or colloids in patients with ARDS because of the increased permeability of capillaries and the risks of worsening pulmonary function.

In general, the pulmonary artery wedge pressure (PAWP) should be maintained at greater than 12 mm Hg and breath sounds and ABGs closely monitored during fluid administration.

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◦ as measured by a pulmonary artery catheter, is the pressure measured in a pulmonary artery distal to an occlusion of that artery.

◦ It is important to measure PCWP to diagnose the severity of left ventricular failure

◦ When these pressures are above 20 mmHg, pulmonary edema is likely to be present, which is a life-threatening condition.

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Positive inotropic agents, such as dopamine or dobutamine, are used to enhance contractility and increase cardiac output.

Vasoconstrictors, such as norepinephrine, may be added to the therapies to counteract the Systemic inflammatory response syndrome

(SIRS) induced vasodilation.

Vasoconstricting agents, however, must be administered cautiously because many vascular beds, especially in the lungs, are constricted, also as a result of SIRS mediators and hypoxia.

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Patients receiving inotropic or vasoactive drugs require regular evaluation of cardiac output, systemic vascular resistance, and PAWP, in addition to continuous arterial blood pressure monitoring.

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The plateau pressure is the pressure applied (in positive pressure ventilation) to the small airways and alveoli. It is believed that control of the plateau pressure is important, as excessive stretch of alveoli has been implicated as the cause of ventilator induced lung injury.

The peak pressure is the pressure measured by the ventilator in the major airways, and it strongly reflects airways resistance.

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involves filling the lungs with a fluid. This fluid is perfluorocarbon, also called Liquivent

or Perflubron. The liquid has some unique properties. It has a

very low surface tension, similar to surfactant, a substance that is produced in lungs and prevents the alveoli from collapsing and sticking together during exhalation.

It also has a high density, oxygen readily diffuses through it, and it may have some anti-inflammatory properties.

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In PLV, the lungs are filled with the liquid, the patient is then ventilated with a conventional ventilator using a protective lung ventilation strategy.

This is called partial liquid ventilation. The hope is that the liquid will help the transport

of oxygen to parts of the lung that are flooded and filled with debris, help remove this debris and open up more alveoli improving lung function.

The study of PLV involves comparison to protocolized ventilator strategy designed to minimize lung damage.

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High frequency ventilation incorporates techniques using ventilation frequencies of greater than 60 breath per minute and tidal volumes between 1 and 5 ml/kg resulting in lower airway pressures and reduced barotrauma.

Arapidly oscillating gas flow is created by a device that acts like a woofer on aloudspeaker, producing a high frequency rapid change in direction of gas flow

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Deleterious effects of HFOV include increased trapping of air in the alveoli (auto-PEEP) and increased mean airway pressures to high levels in some patients.

Research is ongoing as to the possible effectiveness of this mode of ventilation.

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Kinetic therapy (systematic mechanical rotation of patients with 40[degrees] turns) improve pulmonary function more than the improvement in function achieved via the standard of care (turning patients every 2 hours)

helps prevent ventilator-associated pneumonia and lobar atelectasis in critically ill patients

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Kinetic bed therapy and prone positioning have been implicated in improvements in oxygenation in patients with ARDS, but there remains no conclusive evidence that mortality is decreased.

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Improved gas exchange More uniform alveolar ventilation Recruitment of atelectasis in dorsal regions Improved postural drainage Redistribution of perfusion away from edematous,

dependent regions

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MECHANICAL VENTILATION The goal of therapy is to improve tissue oxygenation

and ventilation.

Methods to deliver appropriate levels of oxygen and allow for removal of carbon dioxide include types of mechanical ventilation and positioning.

Techniques to limit ventilator-associated (or induced) lung injury (VALI), including the use of low tidal volumes (<6 mL/kg predicted body weight), the use of adequate PEEP (to reduce the risk of using a high fraction of inspired oxygen and precipitating oxygen toxicity), and limiting plateau pressures to 30 cm H2O or less are under study, as are novel therapies such as extracorporeal lung-assist technology, partial liquid ventilation, and high-frequency oscillation ventilation

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Multiple modes of mechanical ventilation are available to support the patient with respiratory failure.

In general, the principle of “do no harm” includes use of the lowest fraction of inspired oxygen (FIO2) to achieve adequate oxygenation and use of small tidal volumes (<6 mL/kg) to minimize airway pressures, thus preventing or reducing lung damage (barotrauma and volutrauma) while maintaining the PaCO2 within a relatively normal range.

PEEP prevents collapse and opens alveolar sacs, allowing diffusion of gases across the alveolar–capillary membrane.

Recommended values for PEEP are 10 to 15 cm H2O, but values in excess of 20 cm H2O are acceptable to reduce inspired oxygen requirements or maintain adequate oxygenation.

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Pressure-controlled ventilation limits the peak inspiratory pressure to a set level (as opposed to volume-controlled ventilation, which delivers a set tidal volume despite the pressure required to move the set volume into the lungs).

Pressure-controlled ventilation also uses a decelerating inspiratory airflow pattern to minimize the peak pressure while delivering the necessary tidal volume.

Patients on pressure-controlled ventilation mode typically require significant amounts of sedation and pharmacological paralysis to prevent attempts at breathing and dyssynchrony with the ventilator.

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Airway pressure release ventilation is similar to pressure-controlled ventilation but with the advantage of allowing the patient to initiate breaths; therefore, these patients do not require the same level of sedation or paralysis to achieve pressure limited ventilation.

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Inverse ratio ventilation is another strategy thought to improve alveolar recruitment.

Reversal of the normal inspiratory:expiratory ratio (I:E ratio) to 2:1 or 3:1 prolongs inspiration time, preventing complete exhalation.

An inverse I:E ratio is achieved through manipulation of the mechanical ventilator.

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This increased end-expiratory volume creates auto-PEEP (intrinsic PEEP) that is added to the applied extrinsic PEEP.

The theoretical advantages include reduced alveolar pressures and overall PEEP levels. This therapy requires patients to be sedated or given paralytics to improve tolerance.

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Permissive (not strict) hypercapnia is a strategy that allows the PaCO2 to rise slowly above normal through reduction of tidal volume, therefore limiting the plateau and peak airway pressures.

A PaCO2 between 55 and 60 mm Hg and a pH of 7.25 to 7.35 are tolerated when achieved in a gradual fashion.

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Regardless of the recent interest in ventilation strategies, no method has been shown to be superior in the treatment of ARDS, and ventilation management and choice remains a complex decision based on the application of multiple methods for individual cases

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The process involves the machine taking the blood without oxygen, the "blue" blood from the right side of the heart, and pumping it through the artificial lung, the oxygenator. Once the blood is oxygenated, or "red," it is warmed before returning to the patient

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Extracorporeal lung-assist technology involves the use of large vascular cannulas to remove blood from the patient.

A pumping device and circuit circulate the blood, and one or two “artificial lungs” remove carbon dioxide and oxygenate the blood.

Extracorporeal membrane oxygenation (ECMO) and extracorporeal carbon dioxide removal (ECCO2R) may potentially be effective in the management of ARDS, but at present their use is controversial.

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These highly invasive, high-risk technologies allow the lungs to “rest” because near-apneic ventilation or ventilation with small tidal volumes and slow respiratory rates greatly reduces airway pressures while gas exchange takes place in the artificial membrane lungs.

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The need for intensive resources and personnel with a high degree of expertise, coupled with the potential for devastating complications (particularly intracranial hemorrhage) and a lack of conclusive benefits for patients with ARDS, make extracorporeal lung-assist technology of limited use.

In the pediatric population, the use of ECMO has demonstrated benefit with improved survival rates.

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Frequent position change is well established as a means to prevent and reverse atelectasis and facilitate removal of secretions from the airways.

Although not a treatment for ARDS, turning a patient side to side, having the patient sit upright, and using the Trendelenburg position for postural drainage are necessary interventions to prevent worsening of respiratory failure due to atelectasis and pneumonia.

Continuous lateral rotation using a kinetic therapy bed turns patients slowly 60 degrees to each side over 11 minutes and is useful to enhance secretion removal

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Prone positioning, in the patient’s bed or using a Stryker frame, improves pulmonary gas exchange, facilitates pulmonary drainage in the dorsal lung regions, and aids resolution

of consolidated dependent alveoli (in the supine position), particularly in the dorsal lung regions.

The evidence for the effectiveness of prone positioning, now a common intervention with ARDS, is variable.

Randomized, controlled trials are under way and these results will be necessary before support for prone positioning becomes clear

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There are alternative explanations for the improved oxygenation associated with prone positioning, and the question of whether the improvement in oxygenation persists beyond 4 hours remains controversial.

The risks associated with this technique include loss of airway control through accidental extubation, loss of vascular access, facial edema and development of pressure areas, and difficulties with cardiopulmonary resuscitation (CPR).

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Pharmacological Therapy. TREATMENT Most of the pharmacological agents used in

the ARDS population are supportive.

Many agents have been developed as treatments directed toward specific mediators to disrupt or interfere with the development of SIRS.

Most of these promising pharmacological interventions have ultimately proven to be ineffective in humans, notably anti- (Tumor Necrosis Factor (TNF) drugs, most anti-inflammatory mediators, and inhaled gases such as nitric oxide.

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Of the treatments now available, the most promising are surfactant, corticosteroids (used in late-stage ARDS), and ketoconazole (Ketoconazole is a synthetic antifungal drug used to prevent and treat skin and fungal infections, especially in immunocompromised patients ) (used for prevention and in the very early stages).

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Antibiotic therapy is appropriate in the presence of a known microorganism but should not be used prophylactically.

The signs of SIRS are similar to those of infection (i.e., tachycardia, fever, increased white blood cell count), thus creating the temptation to treat the patient with SIRS with antimicrobial therapy.

It is essential to identify a source of infection (isolation of specific bacteria through blood, wound, pulmonary, and other cultures) before initiation of antibiotics

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Prophylactic antibiotic therapy has not been shown to improve outcome.

Emphasis is on prevention of infection, especially nosocomial infection related to the use of invasive vascular catheters and ventilators (e.g., ventilator-associated pneumonia [VAP]).

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Bronchodilators and mucolytics are useful in ARDS to assist in maintaining airway patency and reducing the inflammatory reaction and accumulation of secretions in the airways.

The response to therapy is evaluated by monitoring airway resistance and pressures and lung compliance.

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Exogenous surfactant replacement therapy has been used for several years in neonates with hyaline membrane disease to decrease alveolar surface tension and facilitate the maintenance of open alveolie

Administration of surfactant to adults with ARDS has shown some usefulness, but requires further investigation.

A phase II trial is underway using synthetic surfactant with novel inhalation techniques to improve drug delivery.

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The use of corticosteroids to decrease the inflammatory response in late stages of ARDS is regaining popularity with recent case studies and one randomized, controlled trial supporting low doses in the 7- to 10-day range of ARDS.

Further research is underway to determine whether these results remain consistent in larger studies.

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Newer pharmacological agents directed toward blocking mediators and the SIRS inflammatory cascade are under investigation, but none has proven effective in treating ARDS.

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Nitric oxide is an inhaled gas that causes selective pulmonary vasodilation and therefore reduces the deleterious effects of pulmonary hypertension.

In spite of widespread use, to date, nitric oxide has not been shown to improve mortality or oxygenation beyond the first 24 hours of therapy, although there is some evidence of effectiveness for children and neonates

Other agents that have demonstrated no positive effects on the outcomes of ARDS are:

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■ Antioxidants, such as N-acetylcysteine (Inhaled acetylcysteine is indicated for mucolytic ("mucus dissolving") therapy as an adjuvant in respiratory conditions with excessive and/or thick mucus production)

N-acetylcysteine, a glutathione analog, replenishes glutathione, a natural antioxidant, possibly decreasing endothelial damage caused by oxygen radicals and reducing the ventilatory time in patients with mild to moderate ALI, but not ARDS.

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Antilipid mediators, such as prostacyclin (prostaglandin I2 [PGI2]), and nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or indomethacin.

These agents theoretically interact with the arachidonic acid cascade metabolites, which produce lung endothelial injury and inflammation.

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■ Monoclonal antibodies. These agents were developed to interfere with specific mediators that increase white blood cell (neutrophil) adhesion and activation, contribute to the inflammatory response, and cause endothelial injury.

■ Pentoxifylline. This drug was thought to be an effective anticytokine agent.

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SEDATION Effective use of sedation to promote

comfort and reduce respiratory effort, thus decreasing oxygen demand, is an important consideration for nurses dealing with patients with ARDS.

Neuromuscular blocking agents and general anesthetics such as propofol are all used to decrease the work of breathing and facilitate ventilation for patients with ARDS.

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These have long- and short-term side effects.

The risks include polyneuropathy of critical illness, overfeeding with lipids, and prolongation of days requiring ventilation.

Recent studies have focused on distinguishing between pain, anxiety, and delirium, all possible reasons for patients in critical care to require pharmacological interventions.

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It is vital for all people administering these agents to realize why each is being given, what the goals of therapy are, and what the long-term implications of overuse can be.

These considerations are balanced with the need to decrease oxygen demand and provide comfort for patients requiring intensive ventilation management and undergoing potentially uncomfortable procedures.

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Nutritional Support Early initiation of nutritional support is

essential for patients with ARDS because we now realize that nutrition plays an active therapeutic role in recovery from critical illness.

There are two major theoretical reasons to use early enteral feeding as a therapeutic intervention in SIRS and ARDS.

Mediators (TNF-αand IL-1 in particular) stimulate release of proteolytic enzymes that stimulate protein catabolism from skeletal muscle.

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Persistent protein loss is compounded by interstitial loss through capillary leak and downregulation of messenger RNA (mRNA) production of intravascular proteins such as albumin.

Reference was made to changes in circulatory patterns due to hypoxic sympathetic nervous system reactions.

In this way, there is decreased perfusion to the gut.

After resuscitation, increases in neutrophil release further damage the injured, reperfused colon through increased vascular endothelial permeability, thus releasing normal gut bacteria into the systemic circulation and leading to increases in the incidence of peritonitis, pneumonia, and sepsis.

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The mechanism through which enteral feeding improves outcome remains unproven, but the reduction in mortality in the critically ill who are enterally fed indicates that this practice is of general benefit.

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A balanced caloric, protein, carbohydrate, and fat intake is calculated based on metabolic needs, with particular attention paid to specific amino acids, lipid, and carbohydrate intake.

Patients with SIRS or ARDS usually require 35 to 45 kcal/kg/day.

High-carbohydrate solutions are avoided to prevent excess carbon dioxide production.

Intralipids are judiciously (Having or exhibiting sound judgment) administered to prevent further upregulation of the lipid mediators of SIRS, which contribute to inflammation and lung injury.

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The problem that faces the practitioner is the ability to deliver enteral nutrition in the face of decreased gut motility.

Insertion of small bowel feeding tubes may be considered.

The role of total parenteral nutrition is controversial and some clinicians rarely use it, either alone or in combination with enteral nutrition.

The risk of aspiration associated with enteral feeding needs to be appreciated, and careful monitoring of absorption and gut function is essential.

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PREVENTION OF COMPLICATIONS Complications of ARDS are primarily related

to SIRS, VALI, and immobility imposed by critical illness.

The most serious of these is the development of MODS due to hypoxemia, hypoxia, and the persistent inflammatory response.

The mortality rate of ARDS continues to be more than 60% when associated with MODS.

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Mechanical ventilation with high levels of PEEP, high tidal volumes, and volume-controlled modes predisposes the patient with ARDS to volutrauma and barotrauma, as previously described.

Barotrauma may present as a pneumothorax, pneumomediastinum, or subcutaneous or interstitial emphysema.

Prompt chest tube insertion is required for the presence of a pneumothorax.

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Prevention of volutrauma and barotrauma by maintaining the lowest possible airway pressures, PEEP, and tidal volumes may be achieved through the use of pressure-limiting modes of mechanical ventilation.

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As discussed, frequent repositioning and prone positioning accompanied by chest physiotherapy help to reduce stasis of secretions and facilitate removal.

Endotracheal suctioning using the endotracheal tube to remove secretions is necessary but poses risks related to disconnecting the ventilator and introducing microorganisms.

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The use of in-line suction catheters reduces incidence of nosocomial pneumonia related to suctioning.

Suctioning only when indicated (to avoid inducing a reduction in the SaO2), using sterile technique, and avoiding use of saline instillation reduce the transmission of bacteria into the lungs.

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Deep venous thrombosis (DVT) and subsequent pulmonary embolus may be life-threatening complications of immobility. Initiation of DVT prophylaxis within 48 hours of admission minimizes the risk for development of DVT.

Low-dose heparin, graded elastic stockings, external pneumatic compression devices, frequent mobilization, and ambulation have shown utility in reducing DVT formation.

The physiological aging process compounds the severity of the metabolic insults and complications of ARDS

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Signs of pneumothorax include extreme dyspnea, hypoxia (indicated by a decrease in SaO2), and an abrupt increase in PIP.

Breath sounds may be decreased or absent on the affected side; however, this sign may not be reliable in the patient on positive-pressure ventilation.

Observation of the patient may reveal a tracheal deviation (to the opposite side) or the sudden development of subcutaneous emphysema.

The most ominous signs of tension pneumothorax are hypotension and bradycardia that can deteriorate into a cardiac arrest without timely medical intervention.

The physician or other qualified health care professional may decompress the chest by inserting a needle to evacuate the trapped air until a chest tube can be inserted

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Ventilator-associated pneumonia (VAP) is the second most common hospital-acquired infection and the leading cause of death from nosocomial infections.

Intubated patients have a 10-fold increase in the incidence of nosocomial pneumonia, and the critically ill patient who is mechanically ventilated is especially at risk for development of VAP.

Factors that lead to nosocomial pneumonia are oropharyngeal colonization, gastric colonization, aspiration, and compromised lung defenses.

Mechanical ventilation, reintubation, self-extubation, presence of a nasogastric tube, and supine position are a few of the associated risk factors for VAP.

Maintenance of the natural gastric acid barrier in the stomach plays a major role in decreasing incidence and mortality from nosocomial pneumonia.

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The widespread use of antacids or histamine type 2 receptor (H2) blockers can predispose the patient to nosocomial infections because they decrease gastric acidity (increase alkalinity).

Used to guard against stress bleeding, these medications may increase colonization of the upper gastrointestinal tract by bacteria that thrive in a more alkaline environment.

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VAP is defined as nosocomial pneumonia in a patient who has been mechanically ventilated (by endotracheal tube or tracheostomy) for at least 48 hours at the time of diagnosis.

A patient should be suspected of having a diagnosis of VAP if the chest x-ray shows new or progressive and persistent infiltrates.

Other signs and symptoms can include

fever higher than 100.4°F (38°C), leukocytosis, new-onset purulent sputum or cough, and worsening gas exchange.

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There are numerous strategies for the prevention of VAP.

The first step in preventing VAP is to prevent colonization by pathogens of the oropharynx and gastrointestinal tract.

Basic nursing care principles, such as meticulous handwashing and the use of gloves when suctioning patients orally or through the endotracheal tube, are essential.

Gloves should also be worn when suctioning through closed-suction devices.

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In addition, critically ill patients have an increased risk for colonization by the microorganisms contributed by poor oral hygiene.

Oral care for a mechanically ventilated patient involves brushing the patient’s teeth (approximately every 2 to 4 hours), using antiseptic solutions and alcohol-free mouthwash to cleanse the mouth, applying a water-based mouth moisturizer to maintain the integrity of the oral mucosa, and thoroughly suctioning oral secretions.

Additional nursing studies evaluating the effectiveness of various methods of oral care in the prevention of VAP are needed in the mechanically ventilated population to establish oral care guidelines.

No evidence-based protocols on oral care and prevention of VAP exist.

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In patients receiving enteral feedings, the head of the bed should be elevated 30 to 45 degrees (unless contraindicated) to decrease the risk of aspiration.

Long-term (i.e., longer than 3 days) endotracheal tubes and gastric tubes should be placed orally (unless contraindicated or not tolerated by the patient).

This intervention reduces the risk of the patient contracting infectious maxillary sinusitis, which is associated with the development of VAP.

Last, the use of an endotracheal tube that provides a port for the continuous aspiration of subglottic secretions (CASS) appears to prevent the development of VAP in the first week of intubation, and may decrease the overall incidence of VAP.

The use of the CASS endotracheal tube is typically reserved for those patients who can be identified as potentially requiring long-term ventilation.

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These bacteria are referred to as multidrug resistant (MDR). Pseudomonas aeruginosa is the most common MDR

Gram-negative bacterium causing VAP. Pseudomonas has natural resistance to many antibiotics and has been known to acquire resistance to every antibiotic except for polymyxin B.

Klebsiella pneumoniae has natural resistance to some beta-lactam antibiotics such as ampicillin. Resistance to cephalosporins and aztreonam

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Enterobacter

Citrobacter

Stenotrophomonas maltophilia often colonizes people who have endotracheal tubes or tracheostomies but can also cause pneumonia. It is often resistant to a wide array of antibiotics but is usually sensitive to co-trimoxazole

Acinetobacter are becoming more common and may be resistant to carbapenems such as imipenem and meropenem

Burkholderia cepacia is an important organism in people with cystic fibrosis and is often resistant to multiple antibiotics

Methicillin-resistant Staphylococcus aureus is an increasing cause of VAP. As many as fifty percent of Staphylococcus aureus isolates in the intensive care setting are resistant to methicillin.

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combinations include (but are not limited to): vancomycin/linezolid and ciprofloxacin, cefepime and

gentamicin/amikacin/tobramycin vancomycin/linezolid and ceftazidime Ureidopenicillin plus β-lactamase inhibitor

such as piperacillin/tazobactam or ticarcillin/clavulanate

a carbapenem (e.g., imipenem or meropenem)

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