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Hudson 2012
Hudson 2012
Hudson 2012
629
a relatively sudden onset (from hours to days) and a substantial change from
the patient’s baseline condition. Dysfunction of the respiratory system indi-
cates that the abnormal gas exchange may be caused by abnormalities in any
element of the respiratory system (e.g., a central nervous system abnormality
affecting the regulation of breathing or a musculoskeletal thoracic abnormal-
ity affecting ventilation; Chapter 83), in addition to abnormalities of the lung
itself. The term respiration refers, in a broad sense, to the delivery of oxygen
(O2) to metabolically active tissues for energy usage and the removal of
carbon dioxide (CO2) from these tissues (Table 104-1). Respiratory failure
is a failure of the process of delivering O2 to the tissues and/or removing CO2
from the tissues. Abnormalities in the periphery (e.g., cyanide poisoning,
pathologic distribution of organ blood flow in sepsis) can also lead to tissue
104
PEEP Positive end-expiratory pressure (used when positive pressure during
exhalation is applied with mechanical ventilation)
P/F PaO2/FIO2 ratio
hypoxia; although these conditions represent forms of respiratory failure in increases markedly. The value of the partial pressure of O2 in the arterial
the broadest terms, this chapter focuses on respiratory failure resulting from blood (Pao2) that demarcates this vulnerable zone is the point of the oxyhe-
dysfunction of the lungs, chest wall, and control of respiration. moglobin dissociation relationship at which any further decrease in the Pao2
results in sharp decreases in the amount of hemoglobin saturated with O2
PATHOBIOLOGY (Sao2) and in the arterial blood O2 content (Cao2). Although arbitrary, acute
Abnormal gas exchange is the physiologic hallmark of acute respiratory respiratory failure is often defined in practice as occurring when the Pao2 is
failure, which can be classified in several ways (Table 104-2). Although gas less than 55 mm Hg (Fig. 104-1). In general, the locus on the curve that
exchange can be abnormal for either oxygenation or CO2 removal, significant indicates the partial pressure at which O2 is being unloaded to the tissues is
hypoxemia is nearly always present when patients with acute respiratory the most important determinant of how much O2 is available for the cells and
failure breathe ambient air. If CO2 is retained at a potentially life-threatening their mitochondria. Usually, the ability to unload O2 at the tissue level more
level, this is usually accompanied by significant hypoxemia (see later). The than compensates for small decreases in the amount of O2 picked up in the
life-threatening aspect of the condition places the degree of abnormal gas lungs when the oxyhemoglobin dissociation curve is shifted rightward. With
exchange in a clinical context and calls for urgent treatment. a leftward shift in the curve, O2 is bound more tightly to hemoglobin, so less
The diagnosis of acute respiratory failure requires a significant change in O2 is available for tissue delivery.
blood gases from baseline. Many patients with chronic respiratory problems These clinical considerations imply that any definition of acute respiratory
can function with blood gas tensions that would be alarming in a physiologi- failure based on an absolute level of Pao2 is arbitrary. A healthy, young, con-
cally normal individual. Over time, these patients with so-called chronic ditioned individual climbing at high altitude may have a Pao2 of less than
respiratory failure or chronic respiratory insufficiency develop mechanisms 50 mm Hg because of the reduction in inspired O2 pressure. This individual
to compensate for inadequate gas exchange. Conversely, this chronic condi- is not in acute respiratory failure, even though the Pao2 may be in the low
tion makes patients vulnerable to insults that could be easily tolerated by a 40s. A patient who has chronic obstructive pulmonary disease (COPD) and
previously healthy individual. whose usual range of Pao2 is 50 to 55 mm Hg would not be considered to be
In acute respiratory failure, the O2 content in the blood (available for tissue in acute respiratory failure if the Pao2 was 50 mm Hg. However, if a patient’s
use) is reduced to a level at which the possibility of end-organ dysfunction usual Pao2 was 60 to 70 mm Hg, a Pao2 of 50 mm Hg would be associated
CHAPTER 104 ACUTE RESPIRATORY FAILURE
631
CaO2 diseases such as Guillain-Barré syndrome, or chest wall disease such as flail
SaO2 chest; Chapter 86). In contrast, V Q mismatch and shunting are associated
100 Dissolved with an elevated P(A-a)o2, which may or may not coexist with hypoventila-
20
tion. The normal value for P(A-a)o2 varies as a function of the fraction of
inspired O2 (Fio2), increasing as Fio2 increases.
80 When V Q mismatch or shunting is the cause of hypoxemia, some alveo-
15 lar regions have increased PAco2 and reduced PAo2; the blood in the vessels
CaO2 (mL/dL)
perfusing these alveoli reflects these abnormal gas tensions. The increased
SaO2 (%)
Normal arterial
Mixed venous
10
response to enhanced O2 administration. Hypoxemia caused by V Q mis-
40
match can be corrected to a nearly complete O2 saturation of the hemoglobin
in most patients by a relatively small increase in Fio2, such as from 0.24 to
5 0.28 by face mask or 1 to 2 L/minute O2 by nasal prongs, in patients with
20 acute exacerbations of COPD. If the airways to poorly ventilated alveoli
remain open and the enriched O2 mixture is administered for an adequate
length of time (ranging from a few minutes to 20 minutes, depending on the
0 0 degree of V Q inequality), the increased Pio2 is reflected by an increased
0 20 40 60 80 100 600 PAo2 and an increased Pao2. When a shunt is present (no ventilation but
continued perfusion), a relatively small increase in the Fio2 has little or no
PaO2 (mm Hg)
effect on the Pao2, and even large increases in Fio2 up to 1.0 result in only
FIGURE 104-1. Oxyhemoglobin association-dissociation curve. The axis for oxygen modest increases in Pao2 (Fig. 104-2).
saturation in the arterial blood (SaO2) is on the left, and the axis for arterial content of oxygen
(CaO2) is on the right. CaO2 is the sum of the oxygen dissolved in plasma (denoted as “Dis-
solved” in the figure) plus the oxygen bound to hemoglobin. At a normal hemoglobin, most
CLINICAL MANIFESTATIONS
of the oxygen is carried in combination with hemoglobin, with only a relatively small The hallmark of acute respiratory failure is the inability to maintain adequate
amount of oxygen dissolved in plasma. When the value of the arterial partial pressure of oxygenation or the inability to maintain an appropriate Paco2. Patients are
oxygen (PaO2) is on the “flat” portion of the curve (PaO2 ≥60 to 65 mm Hg, normal partial typically dyspneic and tachypneic, unless progressive respiratory failure
pressure of carbon dioxide [PCO2], and normal pH), raising the PaO2 further has relatively
little effect on total oxygen content. Increases in temperature, PCO2, hydrogen ion concen-
causes fatigue—sometimes leading to respiratory arrest—or a drug overdose
tration, or 2,3-diphosphoglycerate cause a rightward shift in the oxyhemoglobin associa- or neuromuscular condition prevents an appropriate respiratory response to
tion-dissociation curve. hypoxia and/or the hypercapnic acidosis. Neurologic function may deterio-
rate, and myocardial ischemia or even infarction may be precipitated by the
hypoxemia. In addition, each cause has its own specific manifestations (see
later).
with a substantial risk for a further life-threatening reduction in oxygenation;
this patient should be considered to have acute respiratory failure. DIAGNOSIS
Traditionally, the level of arterial CO2 partial pressure (Paco2) that defines As part of the diagnosis of acute respiratory failure, the physician has three
acute respiratory failure has been 50 mm Hg or greater, if accompanied by objectives: (1) confirm the clinical suspicion that acute respiratory failure is
arterial acidosis with a pH of 7.30 or less. The Paco2 is linked to pH because present, (2) classify the type of acute respiratory failure (e.g., hypoxemia
it is generally thought that acidosis leads to tissue dysfunction and symptoms. caused by hypoventilation vs. hypoxemia caused by V Q mismatch or
Patients with severe COPD may have chronic CO2 retention, but renal com- shunting), and (3) determine the specific cause (e.g., acute lung injury sec-
pensation for the respiratory acidosis protects them against abnormalities ondary to sepsis or decompensated COPD because of acute bronchitis).
related to the elevation in CO2. A further acute rise in Paco2 can precipitate Defining the type of acute respiratory failure and determining the specific
symptoms and other organ dysfunction; however, even severe respiratory cause are prerequisites to optimal management.
acidosis (pH 7.1) seems to be better tolerated than metabolic acidosis of the The initial approach to diagnosis consists of considering information from
same pH in most previously healthy individuals if arterial and tissue oxygen- four sources: (1) clinical history and physical examination; (2) physiologic
ation is adequate. abnormalities, particularly arterial blood gas derangements, which help
establish the pathophysiologic mechanisms of hypoxemia; (3) chest radio-
Pathophysiology graphic findings; and (4) other tests aimed at elucidating specific causes. In
Five mechanisms can lead to a reduction in Pao2: (1) decreased inspired many cases, the clinical picture from the history is so clear that the presump-
partial pressure of O2 (Pio2) (e.g., at high altitude or when breathing a tive type of acute respiratory failure (and sometimes the cause) is obvious,
reduced percentage O2 mixture); (2) hypoventilation; (3) ventilation- so treatment can be started while confirmatory laboratory studies are ordered.
perfusion ( V Q ) mismatch; (4) shunting of blood from the pulmonary to In other cases, a clinician may be asked to see a patient because of an abnor-
systemic circulation, bypassing the alveoli anatomically or functionally; and mal chest radiograph or abnormal arterial blood gases ordered by someone
(5) abnormal diffusion of O2 from the alveoli into the capillary blood. In else and may elicit the pertinent history based on these clues. When the
essence, a shunt is an extreme V Q mismatch in which blood perfuses degree of hypoxemia is life-threatening, therapeutic decisions must be made
alveoli with no ventilation; it is differentiated clinically from other V Q quickly, even if data are limited. The clinician must obtain updated informa-
mismatching by the response to breathing supplemental O2 (see later). tion continually and should view most therapeutic decisions as therapeutic
For clinical purposes, diffusion abnormalities are not an important cause trials, with careful monitoring to assess desired benefits and possible detri-
of hypoxemia at sea level because there is sufficient time for adequate diffu- mental effects.
sion of O2 during the transit of a red blood cell through the pulmonary capil-
lary bed, even in the presence of severe lung disease. Even when diffusion Clinical Evaluation
abnormalities are present and contribute to hypoxemia, V Q mismatch and The presentation often reflects one of three clinical scenarios: (1) the effects
shunting nearly always coexist and are quantitatively more important causes of hypoxemia and/or respiratory acidosis, (2) the effects of primary (e.g.,
of hypoxemia. Except at high altitude or when a subject is breathing a gas pneumonia) or secondary (e.g., heart failure) diseases involving the lungs,
mixture low in O2, hypoventilation, V Q mismatch, and shunting are the and (3) the nonpulmonary effects of the underlying disease process. The
dominant causes of acute respiratory failure. clinical effects of hypoxemia and/or respiratory acidosis manifest mainly in
If only hypoventilation is present, the resulting hypoxemia is associated the central nervous system (e.g., irritability, agitation, changes in personality,
with a normal difference between the calculated alveolar and the measured depressed level of consciousness, coma) and the cardiovascular system (e.g.,
arterial oxygenation levels (P(A-a)o2). In this setting, an elevated Paco2 sug- arrhythmias, hypotension, hypertension) (Table 104-3). In patients with
gests disease processes that affect nonpulmonary respiratory function (e.g., underlying COPD (Chapter 88) with a gradual onset of acute respiratory
central respiratory depression resulting from drug overdose, neuromuscular failure, central nervous system abnormalities may be the major presenting
632 CHAPTER 104 ACUTE RESPIRATORY FAILURE
• •
Valv=6.1 Valv=5.6
Cv O 2=11.9 Cv O 2=11.9
Pv O 2=32 Pv O 2=31
Pv CO 2=46 Pv CO 2=46
FIGURE 104-2. Arterial oxygenation. Comparison of the
C cO 2=14.8 C cO 2=20.1 C cO 2=11.9 C cO 2=19.9 effect on arterial oxygenation of increasing the fraction of
P cO 2=41 P cO 2=117 P cO 2=32 P cO 2=105 inspired oxygen (FIO2) from breathing ambient air (FIO2 = 0.21) (A)
P cCO 2=46 P cCO 2=32 P cCO 2=46 P cCO 2=37 and breathing 100% oxygen (FIO2 = 1.0) (B) with a low ventilation-
(left) and a shunt (right), using a two-
to-perfusion ratio ( V Q)
compartment lung model. Shunting and decreased V Q can lead
Ca O 2=16.9 Ca O 2=16.9 to identical arterial blood gases (partial pressure of oxygen in
Pa O 2=50 PaO2=50 arterial blood [PaO2] = 50 mm Hg; partial pressure of carbon
FI O2=0.21 PaCO 2=40 PaCO 2=40 dioxide in arterial blood [PaCO2] = 40 mm Hg). The response to
supplemental oxygen administration is markedly different.
A Hypoxemia is only partially corrected by breathing 100% oxygen
• •
Valv=5.8 when a shunt is present because arterial oxygenation represents
Valv=6.3
an average of the end-capillary oxygen content (CCO2) from
PaO2=665 PaO2=682 PaO2=677 various parts of the lung, not an average of the partial pressures
of oxygen (partial pressure of carbon dioxide in the end-capillary
PaCO 2=48 PaCO 2=31 PaCO 2=36
blood [PcCO2]). When the CCO2 values are mixed, the PaO2 is deter-
mined from the resultant content of oxygen in the arterial blood
(CaO2) by the oxyhemoglobin association-dissociation relation-
(as is often the case in patients
ship (see Fig. 104-1). With low V Q
Cv O 2=17.0 Cv O 2=14.1 with chronic obstructive pulmonary disease), an increase in FIO2
Pv O 2=53 Pv O 2=38 increases the alveolar partial pressure of oxygen (PO2) of the low
Pv CO 2=48 Pv CO 2=46 V Q unit and leads to a marked increase in arterial PO . The values
2
in this figure were generated from modeling to result in the same
C cO 2=22 C cO 2=22 C cO 2=14.1 C cO 2=22 PaCO2 (40 mm Hg) for all four situations shown; this is the reason
alv) for some of the
for slight changes in alveolar ventilation ( V Q
P cO 2=665 P cO 2=682 P cO 2=38 P cO 2=667
conditions. Several assumptions are made: (1) no diffusion limita-
P cCO 2=48 P cCO 2=31 P cCO 2=46 P cCO 2=36
tion is present; (2) oxygen consumption = 300 mL/minute, and
CO2 production = 240 mL/minute; (3) cardiac output = 6.0 L/
Ca O 2=22 Ca O 2=19.1 minute; (4) the low V Q regions in the left panels represent 60%
of the cardiac output perfusing alveoli with a V Q 25% of normal;
PaO2=672 PaO2=76
PaCO 2=40 PaCO 2=40 and (5) the shunts in the right panels represent a 37% shunt
FI O2=1.0
(i.e., 37% of the cardiac output is perfusing alveoli with no
B ventilation).
TREATMENT
General Measures
The management of acute respiratory failure depends on its cause, its clini-
cal manifestations, and the patient’s underlying status. Certain goals apply to
all patients: (1) improvement of the hypoxemia to eliminate or markedly
B reduce the acute threat to life, (2) improvement of the acidosis if it is consid-
ered life-threatening, (3) maintenance of cardiac output or improvement if
cardiac output is compromised, (4) treatment of the underlying disease
process, and (5) avoidance of predictable complications.
The precise methods for improving hypoxemia depend on the cause of the
acute respiratory failure. An increase in the inspired O2 concentration is a
cornerstone of treatment for nearly all patients, however.
The level of acidosis that requires treatment other than for the underlying
C disease process is not clear. Although normalization of the arterial pH was
suggested in the past, respiratory acidosis is apparently well tolerated in many
FIGURE 104-3. Chest radiographs (left) and computed tomography (CT) scans (right)
of the three most common findings in diseases causing acute respiratory failure. A, Rela- patients with severe ARDS, so a patient with a pH of 7.15 or greater may not
tively clear chest, consistent with an acute exacerbation of airway disease (e.g., asthma, require bicarbonate therapy. If the acidemia coexists with clinical complica-
chronic obstructive pulmonary disease) or a central nervous system or neuromuscular tions, such as cardiac arrhythmias or a decreased level of consciousness, that
disease as the cause of acute respiratory failure. B, Localized alveolar filling opacity, most have no other obvious cause, treatments to increase pH should be considered.
commonly seen with acute pneumonia. C, Diffuse bilateral alveolar filling opacities The therapeutic goal is alleviation or reduction of the accompanying compli-
consistent with acute lung injury and acute respiratory distress syndrome. The CT scan in cations by improving the level of acidosis; it usually is not necessary to normal-
C shows a small left pneumothorax and cavities or cysts that are not apparent on the ize the pH (Chapter 120).
anteroposterior chest radiograph. The maintenance of cardiac output is crucial for O2 delivery in acute respira-
tory failure, especially because mechanical ventilation and positive end-expi-
ratory pressure (PEEP) may compromise cardiac output. Placement of a
thromboembolism. If shunting is the major explanation for the hypox- pulmonary artery catheter allows measurement of cardiac output and filling
emia, processes that fill the air spaces (e.g., cardiogenic pulmonary edema, pressures, but patients who have these catheters do no better than similar
noncardiogenic pulmonary edema in acute lung injury or ARDS, or puru- patients managed without them. 1
Many therapeutic interventions that improve short-term physiologic vari-
lent pulmonary secretions in acute pneumonia) or, less commonly, an ables may worsen long-term, clinically important outcomes. Transfusing all
intracardiac or anatomic intrapulmonary shunt is the likely cause. Condi- patients to maintain a hemoglobin greater than 10 g/dL increases mortality in
tions that fill air spaces should be confirmed by an abnormal chest radio- critically ill patients who have not had an acute myocardial infarction and do
graph; if the radiograph is normal, an intracardiac shunt should be not have unstable angina, even though the O2 carrying capacity of the blood
considered and confirmed by echocardiography. is acutely increased. Use of a relatively large tidal volume (e.g., 12 mL/kg pre-
dicted body weight, which is equivalent to approximately 10 to 10.5 mL/kg
Chest Radiography measured body weight in patients who are somewhat overweight) increases
mortality in patients with ARDS when compared with a lower tidal volume
The chest radiograph in acute respiratory failure is likely to show one of three
(6 mg/kg predicted body weight), even though it raises PaO2 more in the
patterns (Fig. 104-3): (1) normal (or relatively normal), (2) localized alveo- short term than does a lower tidal volume. Conservative use of fluids improves
lar filling opacities, or (3) diffuse alveolar filling opacities. Diffuse interstitial lung function and shortens the duration of mechanical ventilation and inten-
opacities are also possible, but diseases that cause this pattern usually have a sive care. 2
more gradual onset and are associated with chronic respiratory failure. If the Improvements in oxygenation, acid-base status, and cardiac output are of
chest radiograph is normal (i.e., it is clear or relatively clear), airway diseases, no more than temporary benefit unless the underlying disease processes are
such as COPD and asthma, or pulmonary vascular diseases, such as throm- diagnosed and treated properly. In patients with acute lung injury, sepsis may
boembolism, are more likely. If a localized alveolar filling abnormality is worsen injury to the lung and other organs despite optimal supportive care.
Similarly, if the precipitating cause of acute respiratory failure in a patient with
present, pneumonia is the major consideration, but pulmonary embolism COPD is not identified and treated, supportive care is likely to be futile. Com-
and infarction should also be considered. When diffuse (bilateral) alveolar plications may arise from the physiologic effects of the gas exchange abnor-
filling abnormalities are present, cardiogenic pulmonary edema, acute lung mality, from the disease processes causing the acute respiratory failure, from
injury (e.g., as seen in sepsis, trauma, or aspiration of gastric contents), and being critically ill and its associated incursions on homeostasis (e.g., sleep
diffuse pneumonia are the major considerations. The combination of the deprivation), or from iatrogenic complications of therapy.
chest radiograph and the arterial blood gas interpretation can be helpful. The
finding of a significant shunt may suggest acute lung injury in a patient in Mechanical Therapy to Improve Oxygenation
A PaO2 greater than 60 mm Hg is usually adequate to produce an SaO2 in
whom this diagnosis was not clinically obvious; the chest radiograph should the low to middle 90s. The PaO2 can be increased by the administration of
help to confirm that possibility. supplemental O2, by pharmacologic manipulations, by continuous positive
airway pressure (CPAP), by mechanical ventilation with or without maneuvers
Other Evaluations such as PEEP, and by the prone position. PEEP, pharmacologic manipulations,
All patients with acute respiratory failure should have a complete blood and positioning are used primarily in patients with acute lung injury (see later).
count, including a platelet count; routine blood chemistry tests; prothrombin The initial choice of the concentration and amount of supplemental O2 is
based on the severity of the hypoxemia, the clinical diagnosis, the likely mech-
time; and urinalysis to screen for possible underlying causes and comorbid anism causing the hypoxemia, and the O2 delivery systems available. For the
conditions. Other blood tests should be guided by the clinical picture. Exam- tracheal FIO2 to be the same as the delivered FIO2, the O2 delivery system must
ples include a serum amylase level if pancreatitis is a possible cause of ARDS deliver a flow that matches the patient’s peak inspiratory flow rate with gas of
and thyroid indices if severe hypothyroidism is a possible cause of hypoven- a known FIO2. High-flow O2 blenders can achieve this goal by delivering gas at
tilation. Blood cultures are recommended whenever sepsis is suspected. 80 L/minute or greater to a nonintubated patient. These systems require a
Any abnormal fluid collections, especially pleural effusion (Chapter 99), large flow of O2 (from a wall unit or tank), however, and are not universally
should be aspirated for diagnostic purposes. Sputum Gram stain and culture available. Other systems for nonintubated patients (including nasal prongs,
simple face masks, and non-rebreather and partial rebreather masks) use a
are indicated when pneumonia is suspected.
634 CHAPTER 104 ACUTE RESPIRATORY FAILURE
simple regulator that mixes room air with O2 at 12 L/minute from a wall unit found a higher incidence of significant bleeding in patients receiving sucral-
or tank, with resulting flows that are frequently unable to match the patient’s fate than in those receiving ranitidine. Evidence also indicates that proton
peak inspiratory flow rate. The patient entrains more air from the environment, pump inhibitors may be useful in the acute care setting. There is little firm
and the resulting tracheal FIO2 or partial pressure of oxygen in inspired gas evidence to guide nutritional management in patients with acute respiratory
(PIO2) is unknown. The amount of air entrained depends on the patient’s inspi- failure (Chapters 221 and 224).
ratory pattern and minute ventilation. Although the resulting FIO2 is unknown, Current evidence supports maintaining the head of the bed at a 45-degree
these systems are satisfactory if the delivery is constant and if they result in angle to reduce aspiration in critically ill patients. Attempts should be made
adequate arterial O2 saturation, as monitored by arterial blood gases or oxim- to ensure a normal day-night sleep pattern, including minimizing activity and
etry. Nasal prongs can deliver a tracheal FIO2 of approximately 0.50, and non- reducing direct lighting at night. The patient should change position fre-
rebreather masks can deliver 50 to 100% O2; in both cases, this depends on quently, including sitting in a chair and walking short distances if possible,
the inspiratory pattern and flow rate. If only hypoventilation or V Q mismatch even while receiving mechanical ventilatory support. Mobilization can
is present, only a small increment in FIO2 (e.g., an FIO2 of 0.24 or 0.28 delivered enhance the removal of secretions, help maintain musculoskeletal function,
by a Venturi principle face mask or by mechanical ventilation; or 1 to 2 L/ reduce the risk of deep vein thrombosis, and provide psychological benefits.
minute O2 delivered by nasal prongs) is likely to be required. By comparison,
if marked shunting or many lung units with low but not zero V Q are the cause
of hypoxemia, a considerably higher FIO2 (e.g., >0.7) may be required, and even
this high FIO2 may not reverse the hypoxemia. A common practice when a
SPECIFIC ACUTE RESPIRATORY FAILURE
significant shunt is suspected is to give an FIO2 of 1.0, then adjust the FIO2 SYNDROMES
downward as guided by the resulting PaO2 or SaO2. Chronic Obstructive Pulmonary Disease
The O2 concentration that is toxic to the lungs in critically ill patients is not
known, but prior injury may provide tolerance to O2 toxicity, whereas other EPIDEMIOLOGY AND PATHOBIOLOGY
conditioning agents, such as bleomycin, may enhance oxidative injury. An FIO2 The epidemiology and pathobiology of COPD are discussed in Chapter 88.
of 0.7 or higher is generally considered injurious to the normal human lung.
Because it is unknown what lower concentration is safe, however, patients
should be given the lowest FIO2 that provides an adequate SaO2 (≥90%). If an
CLINICAL MANIFESTATIONS
FIO2 equal to or greater than 0.5 to 0.7 is required for adequate oxygenation, When COPD causes acute respiratory failure, patients commonly have a
other measures, especially PEEP or CPAP, should be considered. Even a lower history of increasing dyspnea and sputum production. Acute respiratory
FIO2 of about 0.5 may be associated with impaired ciliary action in the airways failure may manifest in more cryptic ways, however, such as changes in
and impaired bacterial killing by alveolar macrophages, but the clinical impor- mental status, arrhythmias, or other cardiovascular abnormalities. Acute
tance of these effects is not known. respiratory failure must be considered whenever patients with COPD have
A low concentration of supplemental O2 can be administered by nasal significant nonspecific clinical changes.
prongs or nasal cannula, which most patients find comfortable and allows
them to cough, speak, eat, and drink while receiving O2. When the nasal pas-
sages are open, the PIO2 does not depend too much on whether the patient DIAGNOSIS
breathes through the nose or the mouth because O2 is entrained from the The diagnosis can be confirmed or excluded by arterial blood gas analysis.
posterior nasal pharynx during a breath taken through the mouth. The level The pH is helpful in assessing whether the hypoventilation is partly or exclu-
of O2 can be adjusted by the flow rate to the nasal prongs. In patients with sively acute: The pH drops by approximately 0.08 for each 10 mm Hg rise in
COPD, flows as low as 0.5 to 2 L/minute are usually adequate unless an intra- the Paco2 in acute respiratory acidosis without renal compensation. By com-
pulmonary shunt is contributing to the hypoxemia, as usually occurs in acute parison, in chronic respiratory acidosis with normal renal compensation, the
pneumonia. At flows greater than approximately 6 L/minute, only a small
pH drops only about 0.03 for each 10 mm Hg rise in the Paco2.
further augmentation in the PIO2 can be achieved. Because gas flow through
the nose has a drying and irritating effect, a face mask should be considered
at high flow rates. O2 face masks using the Venturi principle allow the regula- TREATMENT
tion of FIO2 and can be particularly useful when COPD is suspected, and it is
important to avoid the CO2 retention that can be associated with the unregu- General Care
lated administration of O2. A higher FIO2 of 0.5 to nearly 1.0 can be adminis- As soon as acute respiratory failure is confirmed in a patient with COPD,
tered through a non-rebreathing face mask with an O2 reservoir. If an FIO2 attention must focus on detecting any precipitating events (Table 104-4),
equal to or greater than 0.70 is required for more than several hours, particu- including decreased ventilatory drive, commonly because of oversedation;
larly in an unstable patient, endotracheal intubation should be considered so decreased muscle strength or function, often related to electrolyte abnormali-
O2 can be administered by a closed system with reliable maintenance of the ties, including hypophosphatemia and hypomagnesemia; decreased chest
patient’s SaO2. Indications for placing an artificial airway in a patient with acute wall elasticity, possibly related to rib fracture, pleural effusion, ileus, or ascites;
respiratory failure include airway protection against massive aspiration of atelectasis, pneumonia, or pulmonary edema; increased airway resistance,
gastric contents, delivery of an increased FIO2, facilitation of prolonged caused by bronchospasm or increased secretions; or increased metabolic O2
mechanical ventilation, and to aid in the control of respiratory secretions requirements, such as with systemic infection. Many of these abnormalities
(Chapter 105). can impair the cough mechanism, diminish the clearance of airway secretions,
Ventilatory maneuvers that may increase arterial oxygenation include and precipitate acute respiratory failure.
mechanical ventilation itself and the administration of PEEP or CPAP, all of
which allow ventilation of areas of the lung that were previously poorly ven- Infection
tilated or unventilated. Although large tidal volumes with mechanical ventila- The most common specific precipitating event is airway infection, espe-
tion may open areas of atelectasis and may improve oxygenation initially, cially acute bronchitis. The role played by viral agents, Mycoplasma pneu-
these higher tidal volumes can cause lung injury, particularly if the lung is moniae, chronic contaminants of the lower airway such as Haemophilus
already injured (Chapter 105). influenzae and Streptococcus pneumoniae, and other acute pathogens is diffi-
CPAP refers to the maintenance of positive pressure during the respiratory cult to determine on a clinical or even microbiologic basis. Acute exacerba-
cycle while breathing spontaneously. PEEP refers to the maintenance of posi- tions of COPD commonly result from new infections rather than re-emergence
tive pressure throughout the expiratory cycle when it is applied together with of an infection from preexisting colonization. Antibiotics modestly shorten the
mechanical ventilation (Chapter 105). CPAP and PEEP can result in recruitment duration of the exacerbation, with no significant increase in toxicity, compared
of microatelectatic regions of the lung that are perfused but were not previ- with placebo; the impact of antibiotics on the subsequent emergence of resis-
ously ventilated, thus contributing substantially to hypoxemia. CPAP and PEEP tant organisms is not known. It is standard practice to use antibiotics to treat
have the theoretical advantage of keeping some of these regions open during a patient with COPD who has an exacerbation severe enough to cause acute
exhalation, thus preventing cyclic closure and reopening of lung units, which respiratory failure and who has evidence consistent with acute tracheobron-
can result in alveolar wall stress and injury. chitis (Chapters 88 and 96). Pneumonia may account for 20% of cases of acute
respiratory failure in patients with COPD. Compared with the physiologically
Supportive Measures normal population, patients with COPD who have community-acquired pneu-
Every patient with acute respiratory failure is at risk for deep vein thrombo- monia are more likely to have gram-negative enteric bacteria or Legionella
sis, pulmonary thromboembolism, and gastric stress ulceration. Prophylactic infections and are more likely to have antibiotic-resistant organisms.
anticoagulation is recommended in patients who are not at high risk for bleed-
ing complications; sequential leg compression therapy may be preferred for Other Precipitating Causes
high-risk patients (Chapter 81). Other common precipitating causes of acute respiratory failure include
The best means of preventing stress ulceration is not known, but current heart failure and worsening of the underlying COPD, often related to noncom-
evidence indicates that the use of an H2-blocker is superior to the gastric pliance with medications. Less common and often difficult to diagnose in this
administration of sucralfate, based on a large randomized, controlled trial that setting is pulmonary thromboembolism.
CHAPTER 104 ACUTE RESPIRATORY FAILURE
635
TABLE 104-4 KEY PRINCIPLES IN THE MANAGEMENT OF TABLE 104-5 DISORDERS ASSOCIATED WITH ACUTE LUNG
CHRONIC OBSTRUCTIVE PULMONARY INJURY AND ACUTE RESPIRATORY DISTRESS
DISEASE PATIENTS WITH ACUTE RESPIRATORY SYNDROME
FAILURE COMMON
1. Monitor and treat life-threatening hypoxemia (these measures should be Sepsis (gram-positive or gram-negative bacterial, viral, fungal, or parasitic infection)
performed virtually simultaneously). Diffuse pneumonia (bacterial, viral, or fungal)
a. Assess the patient clinically, and measure oxygenation by arterial blood gases Aspiration of gastric contents
and/or oximetry. Trauma (usually severe)
(1) If the patient is hypoxemic, initiate supplemental oxygen therapy with
nasal prongs (low flows [0.5-2. L/min] are usually sufficient) or by LESS COMMON
Venturi face mask (24 or 28% oxygen delivered). Near-drowning (fresh or salt water)
(2) If the patient needs ventilatory support, consider noninvasive ventilation. Drug overdose
(3) Determine whether the patient needs to be intubated; this is almost Acetylsalicylic acid
always a clinical decision. Immediate action is required if the patient is Heroin and other narcotic drugs
comatose or severely obtunded. Massive blood transfusion (likely a marker of severe trauma, but also seen with
b. A reasonable goal in most patients is PaO2 of 55-60 mm Hg or SaO2 of 88-90%. severe gastrointestinal bleeding, especially in patients with severe liver disease)
c. After changes in FIO2, check blood gases and check regularly for signs of Leukoagglutination reactions
carbon dioxide retention. Inhalation of smoke or corrosive gases (usually requires high concentrations)
2. Start to correct life-threatening acidosis. Pancreatitis
a. The most effective approach is to correct the underlying cause of ARF (e.g., Fat embolism
bronchospasm, infection, heart failure).
b. Consider ventilatory support, based largely on clinical considerations. UNCOMMON
c. With severe acidosis, the use of bicarbonate can be considered, but it is often Miliary tuberculosis
ineffective, and there is little evidence of a clinical benefit. Paraquat poisoning
3. If ventilatory support is required, consider noninvasive mechanical ventilation. Central nervous system injury or anoxia (neurogenic pulmonary edema)
a. The patient must have intact upper airway reflexes and be alert, cooperative, Cardiopulmonary bypass
and hemodynamically stable.
b. Careful monitoring is required; if the patient does not tolerate the mask,
becomes hemodynamically unstable, or has a deteriorating mental status,
consider intubation.
4. Treat airway obstruction and the underlying disease process that triggered the PROGNOSIS
episode of ARF. Acute respiratory failure in patients with severe COPD is associated with an
a. Treat airway obstruction with pharmacologic agents: systemic corticosteroids in-hospital mortality of 6 to 20%. The severity of the underlying disease and
and bronchodilators (ipratropium and/or β-adrenergic agents). the severity of the acute precipitating illness are important determinants of
b. Improve secretion clearance: encourage the patient to cough, administer chest hospital survival. Hospital mortality is higher if the respiratory failure is asso-
physical therapy if cough is impaired and a trial appears effective. ciated with a pH less than 7.25. The pH, the Paco2, and other clinical char-
c. Treat the underlying disease process (e.g., antibiotics, diuretics).
5. Prevent complications of the disease process and minimize iatrogenic acteristics are not very reliable in predicting a particular patient’s chances of
complications. survival.
a. Pulmonary thromboembolism prophylaxis: use subcutaneous heparin if no
contraindications exist. Acute Lung Injury/Acute Respiratory
b. Gastrointestinal complications: administer prophylaxis for gastrointestinal
bleeding.
Distress Syndrome
c. Hemodynamics: if the patient is ventilated, monitor and minimize auto-PEEP. DEFINITION
(1) Treat the underlying obstruction.
(2) Minimize minute ventilation; use controlled hypoventilation. ARDS was first described in 1967 as the abrupt onset of diffuse lung injury
(3) Use small tidal volumes; increase the inspiratory flow rate to decrease the characterized by severe hypoxemia (shunting) and generalized pulmonary
inspiratory time and lengthen the expiratory time. infiltrates on the chest radiograph in the absence of overt cardiac failure. In
d. Cardiac arrhythmias: maintain oxygenation and normalize electrolytes. the early 1990s the term acute lung injury was officially introduced to include
ARF = acute respiratory failure; Fio2 = fraction of inspired oxygen; Pao2 = partial pressure of traditional ARDS and less severe forms of lung injury. Both acute lung injury
oxygen in arterial blood; PEEP = positive end-expiratory pressure; Sao2 = oxygen saturation. and ARDS, by definition, require bilateral pulmonary infiltrates compatible
with pulmonary edema in the absence of clinical heart failure (usually deter-
mined by the lack of elevated left atrial pressures). The two are differentiated
by the degree of abnormal oxygenation: Patients are defined as having acute
lung injury if the Pao2 divided by the Fio2 (Pao2/Fio2, also called the P/F
ratio) is less than or equal to 300. When the Pao2/Fio2 is less than or equal
Site of Care to 200, the patient meets the criteria for ARDS.
Many patients with COPD and acute respiratory failure can be managed on
a general medical hospital floor rather than in an intensive care unit if the
precipitating cause of acute respiratory failure has been diagnosed and is EPIDEMIOLOGY
potentially responsive to appropriate therapy, if any blood gas abnormalities Acute lung injury and ARDS are major public health problems and major
respond to O2 therapy and are not life-threatening, if the patient can cooperate causes of death. The annual incidence of acute lung injury is about 80 cases
with the treatment, and if appropriate nursing and respiratory care can be per 100,000 adult population. Case-fatality rates are 30 to 50% and are highly
provided (Chapter 88). An unstable patient who requires closer observation dependent on disease severity and the underlying predisposing condition.
and monitoring should be admitted to an intensive care unit.
Yes No
Adjust FIO2 to yield SaO2 88-95% Intubate: volume cycled ventilation: VT 6 mL/kg
Consider NIPPV to relieve dyspnea PBW; FIO2 1.0; PEEP 5 cm H2O assist
control mode; conscious sedation and
maintain comfort
Code status discussed; NPO; H2 blocker; DVT
SaO2<88%
prophylaxis; semi-recumbent (45°) position
SaO2>95%
Increase PEEP in 3-5 cm H2O increments
(or consider ARDSNet PEEP/FIO2 ladder)
Reduce FIO2 until
FIO2<0.6
SaO2<96%
Monitor ABG, blood pressure, urine output,
capillary refill time, and (if available)
cardiac index FIO2£0.6
Inadequate perfusion Adequate perfusion
Repeat ABG
Decrease FIO2 by 0.1 decrements to 0.4 Maintain ventilator settings Increase PEEP by 3-5 cm H2O increments
and/or decrease PEEP by 3-5 cm H2O to Continue pulse oximetry; to maximum of 25 cm H2O and/or
8 cm H2O (or consider ARDSNet repeat ABG in 4-8 h or increase FIO2 by 0.1 increments to 1.0
PEEP/FIO2 ladder) as clinically indicated
Repeat assessment of plateau pressure
Wean from ventilator as tolerated
and ABG
SaO2 remains<88%
PaO2 remains<55 mm Hg
FIGURE 104-4. Algorithm for the initial management of acute respiratory distress syndrome. ABG = arterial blood gas analysis; CO2 = carbon dioxide; DVT = deep vein thrombosis;
FIO2 = inspired oxygen concentration; MSOF = multisystem organ failure; NIPPV = noninvasive intermittent positive-pressure ventilation; O2 = oxygen; PaCO2 = arterial partial pressure
of carbon dioxide; PaO2 = arterial partial pressure of oxygen; PBW = predicted body weight; PEEP = positive end-expiratory pressure; Pplat = plateau pressure; RR = respiratory rate;
SaO2 = arterial oxygen saturation; VT = tidal volume.
TABLE 104-7 ARDSNet VENTILATORY MANAGEMENT
PROTOCOL FOR TIDAL VOLUME AND PLATEAU
PRESSURE
Calculate PBW:
Male PBW: 50 + 2.3 (height in inches − 60) or 50 + 0.91 (height in centimeters
− 152.4)
Female PBW: 45.5 + 2.3 (height in inches − 60) or 45.5 + 0.91 (height in
centimeters − 152.4)
Select assist control mode
Set initial VT at 8 mL/kg PBW
Reduce VT by 1 mL/kg at intervals < 2 hr until VT = 6 mL/kg PBW
Set initial RR to approximate baseline minute ventilation (maximum RR = 35/min)
Set inspiratory flow rate higher than patient’s demand (usually > 80 L/min)
Adjust VT and RR further to achieve Pplat and pH goals
If Pplat > 30 cm H2O: decrease VT by 1 mL/kg PBW (minimum = 4 mL/kg PBW)
If pH ≤ 7.30, increase RR (maximum = 35)
If pH < 7.15, increase RR to 35; consider sodium bicarbonate administration or
increase VT
PBW = predicted body weight; Pplat = plateau pressure (airway pressure at the end of delivery of a
tidal volume breath during a condition of no airflow); RR = respiratory rate; Vt = tidal volume.
See the ARDSNet website (http://www.ardsnet.org) for further details about the protocol, including
the approach for setting positive end-expiratory pressure and fraction of inspired oxygen.
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Respiratory Distress Syndrome (ARDS) Clinical Trials Network: pulmonary-artery versus central
venous catheter to guide treatment of acute lung injury. N Engl J Med. 2006;354:2213-2224.
2. The National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clini-
cal Trials Network. Comparison of two fluid-management strategies in acute lung injury. N Engl J
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3. Ram FS, Lightowler JV, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of
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acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis.
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SUGGESTED READINGS
Del Sorbo L, Slutsky AS. Acute respiratory distress syndrome and multiple organ failure. Curr Opin Crit
Care. 2011;17:1-6. Review.
Esan A, Hess DR, Raoof S, et al. Severe hypoxemic respiratory failure: part 1—ventilatory strategies.
Chest. 2010;137:1203-1216. Review.
Raoof S, Goulet K, Esan A, et al. Severe hypoxemic respiratory failure: part 2—nonventilatory strategies.
Chest. 2010;137:1437-1448. Review.