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CHAPTER 52: Acute Lung Injury and the Acute Respiratory Distress Syndrome 449

CHAPTER Acute Lung Injury and the 7.45; if the pH is between 7.15 and 7.29, if the pH remains <7.15
52 Acute Respiratory Distress with RR of 35/min and NaHCO is considered or given, one can
3
increase the tidal volume in 1-mL/kg PBW increments until pH
Syndrome
exceeds 7.15 (ie, the Pplat target may be exceeded).
Mark E. Mikkelsen • The use of a recruitment maneuver (eg, 30 cm H O for 30 seconds
2
or 40 cm H O for 40 seconds), coupled with an increase in posi-
Paul N. Lanken tive end-expiratory pressure (PEEP) to maintain the recruitment
2
Jason D. Christie achieved, should be considered in patients with refractory hypox-
emia; however, clinicians should be vigilant for the development of
barotrauma or hypotension as a consequence of the maneuver, and
KEY POINTS
the trial should be ceased if either complication develops.
• Acute lung injury (ALI) and its more severe form, the acute respiratory • During assisted ventilation, one should use analgesia and/or
distress syndrome (ARDS), are common causes of acute hypoxemic sedation at the lowest doses required to synchronize the patient’s
respiratory failure (AHRF). The 2012 Berlin Definition eliminated respiratory efforts with the ventilator and to decrease oxygen
the term ALI; however, this term remains common to older literature. consumption (V ˙ ); one may also need to induce muscle paralysis
O 2
• Both ALI and ARDS are characterized by hypoxemia that is resistant by use of neuromuscular blocking agents (NMBA) and recent
to oxygen therapy; this is due to widespread alveolar filling or collapse. evidence suggests that early NMBA use in severe ARDS may be
• Initial therapy for all patients with ALI and ARDS should be associated with improved outcomes.
supplemental oxygen; failure to achieve 95% arterial saturation or • The use of a “dry” fluid management strategy should be consid-
greater confirms the presence of a large right-to-left shunt. ered given evidence that this approach improves lung function
• Most patients with ALI and ARDS require ventilatory support and shortens duration of mechanical ventilation and intensive care
because their AHRF is typically severe and may be prolonged. unit stays without increased nonpulmonary organ dysfunction in
the short term; however, this approach generally lowers cardiac
• If a patient with severe hypoxemia as indicated by arterial blood output and the question has been raised if its use may be associ-
gas analysis has a clear chest radiograph, consider a possible error ated with long-term cognitive impairment.
] or arterial oxygen
(eg, incorrect fractional inspired oxygen [Fi O 2 • If one uses a “dry” fluid management strategy, one should be
]); in such situations, also consider the possibility
tension [Pa O 2 guided by daily and cumulative net intake and output volumes
of other types of right-to-left shunts (eg, intracardiac shunts or
pulmonary arteriovenous malformations) or the continued perfu- and laboratory indices of hypovolemia (blood urea nitrogen
sion of an unventilated or poorly ventilated lung (eg, due to acute [BUN]:creatinine ratio and serum total bicarbonate) while moni-
mucous plugging of one main bronchus). toring for adequate urine output (>0.5 mL/kg PBW/h), effective
circulation (by physical signs), or invasive measurements (ie,
• The acute phase of ALI and ARDS is characterized by an exuda- mixed [or superior vena caval] venous cooximetry), adequate per-
tive alveolar flooding due to pulmonary capillary leak and by fusing pressure (ie, mean arterial pressure [MAP] ≥60 mm Hg),
extensive alveolar collapse due to loss of normal surfactant activ- and electrolyte abnormalities (serum sodium and potassium).
ity; while interventions directed at modulating inflammatory or • The use of a pulmonary artery catheter (PAC) to guide therapy,
other pathways of lung injury, optimizing alveolar fluid clearance, compared to a central venous catheter (CVC), is associated with
or restoring surfactant function hold theoretical promise, at pres- more complications and increased costs without a demonstrable
ent no specific pharmacologic therapy has been shown to improve benefit in outcomes; the PAC is not recommended for routine use
outcomes; currently one should provide lung-protective mechani- in the management of patients with ALI and ARDS.
cal ventilation and other supportive care while identifying and
treating the precipitating causes of ALI or ARDS. • Late-phase or fibroproliferative-phase ARDS (corresponding to
• Lung-protective ventilation of patients with ALI and ARDS should persistent ARDS of 1-week duration or more) is characterized by
subacute inflammation, proliferation of alveolar lining cells and
use a strategy with low tidal volumes and limits to end-inspiratory interstitial cells, and varying degrees of fibrosis.
pressure (ie, plateau pressures [Pplat]), to reduce the risk of ventilator-
induced lung injury (VILI); such a strategy gives higher priority to • In severe late-phase ARDS, a prolonged course of high-dose methyl-
the goal of decreasing the risk of VILI by limiting end-inspiratory prednisolone sodium succinate (MPSS) can improve gas exchange and
lung volume and pressure than the traditional goal of keeping arterial mechanics in some patients; however, use of MPSS increases the risk of
) and pH in the normal range. diffuse weakness that may be prolonged; results from one RCT found
carbon dioxide tension (P CO 2 that MPSS administration when added to a low-tidal-volume ventila-
between 55 and 80 mm Hg
• The target for oxygenation should be a Pa O 2 tion strategy that limited Pplat as described above did not significantly
and
(88%-95% saturation); one should achieve this by adjusting Fi O 2 improve mortality at 60 days (or ICU or hospital lengths of stay).
positive end-expiratory pressure (PEEP) with the goal of decreasing
to 0.5 to 0.6 (or less), concentrations that are less concerning for • In refractory ARDS, the use of extracorporeal life support at experi-
Fi O 2 enced centers, as a means to temporarily support cardiopulmonary
pulmonary oxygen toxicity. However, despite this recommendation,
it should be noted that the safety of a permissive hypoxemia approach function and minimize VILI and oxygen toxicity, may improve survival.
on nonpulmonary organ function has not been demonstrated.
• In general, the ventilatory strategy should start with a tidal volume Severe arterial hypoxemia that is resistant to supplemental oxygen is
of 6 mL/kg of predicted body weight (PBW) and with a Pplat target a common reason for admission to the ICU. This form of respiratory
that does not exceed 30 cm H O; if Pplat exceeds 30 cm H O with a failure, termed acute hypoxemic respiratory failure (AHRF), arises from
2
2
6 mL/kg PBW tidal volume, the latter should be decreased to 5 mL/ widespread flooding or collapse of alveoli. As a result, a substantial frac-
kg PBW; if Pplat still exceeds 30 cm H O, tidal volume should be tion of mixed venous blood traverses nonventilated alveoli (ie, alveoli
2
further decreased to 4 mL/kg PBW. with ventilation-perfusion ratio of 0). This in turn results in a large
• When changing to low-tidal-volume ventilation, one should right-to-left intrapulmonary shunt (Fig. 52-1). In addition to its adverse
increase the respiratory rate (RR) up to 35/min to maintain min- effects on oxygenation, fluid that accumulates in alveoli and interstitial
ute ventilation; the target for ventilation should be a pH of 7.30 to tissues increases lung stiffness, which decreases lung compliance. This
imposes a larger mechanical load on the patient’s respiratory system,

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