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312 PART IV Noncoronary Diseases: Diagnosis and Management
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hypotension may be the primary findings on examination.
Cardiogenic pulmonary edema superimposed on abnormal lung
parenchyma, such as in emphysema, will often give bilateral
patchy radiographic infiltrates and not necessarily the classic
central batwing distribution. In such cases, a history of underlying
heart disease and compatible physical examination may aid in
arriving at the presumptive diagnosis of congestive heart failure.
In recent years, an increase in the use of brain natriuretic peptide
(BNP) levels have been used to support the diagnosis of heart
failure. A review by Korenstein et al. pooled over 3,000 patients
and determined that BNP of less than 100 pg/mL essentially
rules out the diagnosis of heart failure, whereas a BNP greater
than 400 pg/mL has a sensitivity and specificity of 81% and
90%, respectively.6 Elevated levels do not distinguish between
right and left ventricular failure and may be seen in patients
having pulmonary emboli and cor pulmonale. BNP levels have
also been noted to be elevated in patients with septic shock
without evidence of clinical heart failure.
The most helpful feature in separating these disorders is the
radiographic response to therapy. Radiographically, pneumonia
resolves over 3 to 12 weeks, whereas cardiogenic pulmonary
edema may clear over days. In the absence of supportive clinical
evidence for left ventricular failure, diffuse infiltrates may represent noncardiogenic pulmonary edema, pulmonary hemorrhage,
or interstitial pneumonitis. Noncardiogenic pulmonary edema
(presenting in ARDS) most often occurs in hospitalized patients.
If a patient presents to the hospital with ARDS, a diagnosis of
severe bilateral pneumonia should strongly be considered. Most
patients with ARDS have one of the common precipitating factors
leading to this disorder. The common predisposing events include
sepsis, hypotension, massive aspiration, severe pneumonia, and
massive trauma or transfusions. Less common precipitating events
include pancreatitis, drug overdose, and recent cardiopulmonary
bypass. The diagnostic criteria for ARDS were updated in 2012
(see Table 30.1) and replaced with the Berlin Definition.3 Major
changes from the prior consensus definition include elimination
of the term “acute lung injury,” removal of the pulmonary capillary
wedge pressure criterion, and addition of minimal ventilator
settings.3 Mechanical ventilation strategies with low tidal volumes
of 6 to 8 mL/kg of ideal body weight and plateau pressures less
than 30 to 32 cm H2O have been shown to significantly reduce
mortality in patients with ARDS.7 Comprehensive reviews of
ARDS have been published8 and therapeutic trials and protocols
are maintained on the ARDSNet website (www.ARDSNet.org).
In a patient with a history of joint complaints, an undiagnosed
rash or unexplained renal insufficiency, a diagnosis of vasculitis
or collagen vascular disease should be considered. In the presence
of an acute drop in hematocrit, pulmonary hemorrhage syndrome
may be entertained, in which case a definitive diagnosis may
require bronchoscopy to allow proper treatment and management.
In some cases, pulmonary hemorrhage is not accompanied by
hemoptysis.
The Infectious Diseases Society of America (IDSA) in conjunction with the American Thoracic Society (ATS) has published
consensus guidelines on the management of community-acquired
pneumonia in adults. The antibiotic regimen chosen by the IDSA/
ATS mainly relies on macrolides (with or without a β-lactam)
or respiratory fluoroquinolones (e.g., levofloxacin or moxifloxacin) for outpatient therapy. Respiratory fluoroquinolones or
cephalosporins plus macrolides are recommended for hospitalized
patients. The IDSA and ATS also published guidelines in 2016
to distinguish between hospital-acquired pneumonia (HAP) and
ventilator-associated pneumonia (VAP). A prior category of
health care–associated pneumonia (HCAP) was removed from
the guidelines due to increasing evidence that many of these
patients are not at risk for multidrug-resistant pathogens and
treating them as such may have implications for antibiotic
stewardship.9 Management of severe pneumonia emphasizes
early, appropriate antibiotics in adequate doses. Initial broadspectrum therapy is narrowed based on microbiologic cultures
and clinical response.9 If patients receive an initially appropriate
antibiotic regimen, efforts should be made to shorten the duration
of therapy from the traditional 14 to 21 days to periods as short
as 7 days if the patient has a good clinical response with resolution
of clinical features of infection and the etiologic pathogen is not
Pseudomonas aeruginosa.
10
Pneumonia may be difficult to distinguish from atelectasis
presenting as a localized infiltrate. Atelectasis can be seen with
pulmonary embolism (PE), diaphragmatic dysfunction with
volume loss, splinting from rib fracture or pleuritis, and in
mechanically ventilated patients. The presenting signs and
symptoms including dyspnea, chest pain, and fever, and leukocytosis may overlap in many instances. High clinical suspicion
is needed to prevent missing the diagnosis of PE. Mortality of
untreated PE has been reported to be about 30% compared to
8% with appropriate treatment.11 High-probability V/Q scans
carry a positive predictive value for PE of 88%.12 With the addition
of strong clinical suspicion, the positive predictive value is as
high as 96%. About 12% of patients with low-probability V/Q
scan may have angiographically proven PE. Therefore, if PE is
clinically suspected, further evaluation after a low-probability
scan is needed. Evaluation of the lower extremities for deep
venous thrombosis (DVT) with Doppler ultrasonography is
noninvasive and, if positive, obviates the necessity to perform
pulmonary angiography. If the patient does not have a high
pretest probability of PE, some advocate repeating Doppler
ultrasonography after 72 hours. If both Doppler studies are
negative, there is a very low probability of significant PE. Pulmonary angiography has been shown to be safe in the 755 patients
enrolled in the Prospective Investigation of Pulmonary Embolism
Diagnosis (PIOPED) study. The diagnostic utility of V/Q scans
for acute PE persists even in the presence of preexisting cardiac
or pulmonary disease.
13,14
In recent years, there has been an
increased use of D-dimer testing in patients presenting to the
emergency department. D-dimer is formed from the degradation
products of cross-linked fibrin by plasmin. It is very sensitive
but nonspecific (elevated in almost all patients with carcinoma
and most seriously ill hospitalized patients) for either DVT or
PE. A negative D-dimer using enzyme-linked immunosorbent
assays (ELISA) has a negative predictive value of 95%.
15
Righini and colleagues16 showed that a diagnostic strategy
that included clinical probability, D-dimer, Doppler ultrasonography, and helical chest CT was highly cost-effective. A negative
D-dimer in the setting of a negative Doppler ultrasound may
CHAPTER 30 Acute Respiratory Failure 313
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obviate the need for further testing. Helical chest CT with a PE
protocol has virtually replaced pulmonary angiography. The great
benefit of chest CT is in providing additional diagnoses to explain
the patient’s symptoms; sensitivity and specificity ranges from
78% to 100%. Its accuracy drops in the areas of atelectasis and
segmental or subsegmental vessels. Multidetector scanning
increases the sensitivity to 89% and can visualize thrombi up to
the sixth pulmonary artery branch. The Prospective Investigative
Study of Acute Pulmonary Embolism Diagnosis (PISAPED)
investigators published diagnostic algorithms based on their 40
years of experience that relies heavily on ventilation/perfusion
lung scanning and used multidetector scanning in only 16% of
the cases when there was discordance between pretest probability
and lung scanning. This option may be very useful in patients
who cannot tolerate intravenous iodinated contrast dye owing
to renal insufficiency.
17
Exacerbation of underlying obstructive lung disease is the
most common cause of hypoxemic respiratory failure in patients
who do not have infiltrates on chest radiography. The most
important precipitants of ARF in patients with COPD are airway
infection, congestive heart failure, anatomic interference with
chest wall function (e.g., pleural effusion, pneumothorax, or rib
fracture), and medication noncompliance.18 Additionally, PE and
oversedation can precipitate respiratory distress. The most
common bacteria isolated from the airway and lungs of patients
with COPD are Haemophilus influenzae, Streptococcus pneumoniae,
and Moraxella catarrhalis.19 Antibiotics have been shown to be
beneficial in patients having at least two of the following: dyspnea,
increased sputum production, and sputum purulence.20 Therefore,
a β-lactam antibiotic (e.g., amoxicillin, oral cephalosporin) or
trimethoprim-sulfamethoxazole is frequently given during
exacerbations of COPD. Studies have documented the benefit
of oral corticosteroids in acute exacerbations of COPD. A large
randomized, controlled study of 271 patients with COPD
exacerbation who were randomly assigned to receive either
systemic corticosteroids or placebo for up to 2 weeks demonstrated
that systemic corticosteroids reduced the 30-day treatment failure
rate (23% vs. 33%), 90-day treatment failure rate (37% vs. 48%),
and hospital stay (8 vs. 10 days) while improving lung function.
A dose of 40 mg of prednisone per day for 5 days is recommended
by the most recent Global Initiative for Chronic Obstructive
Lung Disease (GOLD) guidelines, which are available online at
www.goldcopd.org.
21
Another cause of respiratory failure with a normal chest
radiograph is a right-to-left shunt. The presence of a significant
shunt can be suspected when arterial hypoxemia is resistant to
improvements with higher FIO2. An acute rise in right-sided
cardiac pressures from PE or from right ventricular myocardial
infarction (MI) may cause a right-to-left shunt through a patent
foramen ovale. An echocardiogram with a bubble study may be
used to detect a cardiac shunt. Finding radio-macroaggregated
albumin in the brain or kidney after a lung perfusion scan is a
sensitive and specific way of identifying the presence of a pulmonary or cardiac right-to-left shunt.
Microatelectasis is another cause of respiratory failure with
a normal chest radiograph. This disorder almost always occurs
in the setting of inadequate ventilation and is frequently seen
in postoperative patients or in the setting of splinting secondary
to chest wall pain. Diffuse alveolar collapse leads to bronchial
breath sounds at the base of the lung without the infiltrate that
is seen with obstructive atelectasis. The use of analgesics for
pain, incentive spirometry, and the addition of positive pressure
to the airway leads to resolution of this process. In hospitalized
patients, inspiratory positive pressure breathing devices with
nebulized therapy is often beneficial, especially in postoperative
patients.
Hypercapnia may develop in patients with either a “black”
(normal) chest radiograph or “white” (infiltrative) chest radiograph. Hypercapnic respiratory failure results usually from alveolar
hypoventilation, severe V/Q mismatching, or a combination of
the two. In patients with normal lungs, it generally occurs in
the setting of reduction in central nervous system respiratory
drive or acute neuromuscular weakness. In both cases, alveolar
hypoventilation is the predominant mechanism. In patients with
preexisting lung disease, hypercapneic respiratory failure usually
occurs in the setting of severe lung disease and V/Q mismatching.
Whatever the triggering event may be, the patient is generally
incapable of increasing the minute ventilation needed to compensate for the increased ventilatory workload requirements.
Reduction in central nervous system respiratory drive may
be caused by sedative-hypnotic medications or depressed mental
status from organic and metabolic or hypoxic encephalopathy.
Although patients with stroke or brain hematoma rarely have
clinically significant depression of respiratory drive, hypercapnia
may still occur if the breaths are shallow with small tidal volumes,
increasing dead space ventilation and resulting in alveolar
hypoventilation. Acute hypoxemia that results in global brain
hypoxia may then lead to depression of mental status and alveolar
hypoventilation.
Neuromuscular weakness is a less common cause of clinically
significant alveolar hypoventilation. Typically, the tidal volume
is reduced secondary to shallow breathing, with an increased
respiratory rate in an attempt to restore minute ventilation. This
type of shallow and rapid breathing increases dead space ventilation and, given the same minute ventilation, alveolar ventilation
will be reduced. Amyotrophic lateral sclerosis, high cervical spinal
cord injury, Guillain-Barré syndrome, myasthenia gravis, phrenic
nerve paralysis, and muscular dystrophy may result in both
hypercapneic and hypoxemic respiratory failure. Hypercapnia
may also result from respiratory muscle fatigue after a period
of sustained rapid breathing as seen in the later stages of acute
exacerbations of asthma or COPD.
Hypercapnic respiratory failure that occurs in the absence
of respiratory drive depression or neuromuscular weakness is
usually caused by severe V/Q mismatching and often associated
with conditions that increase CO
production. For example, fever
2
increases VCO2 by 13% for each degree Celsius.22 Patients with
severe preexisting V/Q abnormality, in particular those with large
low V/Q areas, may not be able to compensate for the increased
workload. Therefore, when compensatory efforts fail in a COPD
patient with pneumonia and fever, hypercapnia ensues. Patients
with severe lung disease, baseline hypoxemia, and hypercapnia are
also at risk of worsening hypercapnia when they receive oxygen
supplementation. When these patients require oxygen therapy
314 PART IV Noncoronary Diseases: Diagnosis and Management
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for hypoxemic exacerbation, extreme caution must be exercised
to prevent providing too much oxygen. Low-flow oxygen (1 to
2 L/min nasal cannula or 24% to 28% FIO2 by mask) should
be started and titrated up until the saturation is approximately
90%. If acute severe hypercapnia occurs, assisted ventilation is
the treatment of choice. The pathophysiology of this process
is still being debated and may involve three mechanisms.
23–25
Worsening of V/Q mismatching is believed by many to be the
major mechanism. Additionally, displacement of CO2 molecules
from hemoglobin (the Haldane effect) has been proposed
but probably plays only a small role. Finally, suppression of
hypoxic ventilatory drive has long been debated and remains
controversial.
MANAGEMENT
The initial approach to managing patients in acute respiratory
failure is supportive. The essential first steps remain assessment
of airway patency, presence of breathing, and adequacy of circulatory function. Once this is ensured, specific treatments must be
directed at the underlying disease that initiated respiratory failure.
Specific therapy for each of these disorders is beyond the scope
of this chapter but has been reviewed.
In most cases, administration of supplemental oxygen is
required. The ultimate goal of oxygen therapy is to provide
adequate oxygen to the tissues to preserve tissue and organ
function. Because there is no clinically useful measure of cellular
oxygen tension, tissue hypoxia can only be indirectly predicted
from overall organ function and oxygen transport. The critical
level of hypoxemia that compromises organ function varies
depending on the organ system and local factors. Clinical studies
in patients without adaptive mechanisms suggest that short-term
memory is adversely affected at PaO2 less than 55 mm Hg.27
Generally, PaO2 of about 60 mm Hg, usually corresponding to
SaO2 of about 90%, is considered to be an adequate target. Further
increase in PaO2 offers little additional benefit because of the
shape of the oxygen–hemoglobin dissociation curve and may
potentially increase the risk of hypercapnia in some patients.
Therefore, hypoxemic patients with severe lung disease, especially
those with baseline hypercapnia, must be monitored closely with
serial blood gases for correction of hypoxemia and prevention
of worsening hypercapnia. The use of pulse oximetry to follow
the adequacy of oxygenation may be appropriate if the pulse
oximetry saturation (SpO
) has been properly calibrated to
2
accurately reflect co-oximetry saturation (SaO2) of the patient
when hypercapnia is not a concern.
Once the decision for oxygen supplementation has been made,
the next step is to choose the method of delivery. In patients who
are intubated, delivery of oxygen can be accomplished through a
ventilator or through a T-piece, the latter if mechanical breaths
are not needed. For patients who are not intubated, there are
several choices of oxygen delivery systems. A nasal cannula is the
most commonly used low-flow system. It delivers pure (100%)
oxygen at various rates up to 5 to 6 L/min and is able to achieve an
FIO2 reported as high as 48%. High-flow nasal cannula (HFNC)
devices deliver oxygen at rates up to 60 L/min in adults, or 8 L/
min in infants. At these rates, HFNC can provide an FIO2 up to
26
100% with constant delivery due to dead space washout creating
an oxygen reservoir. In adults with acute hypoxemic respiratory failure without hypercapnia, high-flow oxygen therapy is a
reasonable alternative to standard oxygen therapy or noninvasive
positive pressure ventilation.28 These systems are simple to use
and comfortable, allowing the patient to speak, eat, and drink
without much interference. However, as is true with all low-flow
systems, the FIO2 is not accurate, depending on several factors,
including total minute ventilation.
29,30
A simple face mask also delivers low-flow oxygen with a
somewhat higher FIO2 than a simple nasal cannula because of
the presence of 100 to 200 mL of reservoir space between the
mask and the patient’s face. It must be removed transiently when
the patient eats or drinks. Face masks with reservoir bags come
in two varieties. A partial rebreather mask has a reservoir that
is filled with pure oxygen mixed with a small amount of early
exhaled gas that mainly comes from high oxygen tension dead
space. This mask is able to achieve FIO2 of 0.6 to 0.8. A nonrebreather mask has a reservoir containing pure oxygen and is
not mixed with exhaled gas. In addition, there are one-way
exhalation valves allowing exhaled gas to leave the mask without
inhaling air. This mask allows the achievement of FIO2 close to
0.9, but not quite 1.0, because of the presence of small amounts
of exhaled gas in the space between the mask and the face.
Venturi masks are low-flow masks that use the Bernoulli
principle to entrain room air when pure oxygen is delivered
through a small orifice, resulting in a large total flow at predictable
FIO2. The size of the orifice determines the FIO2. This oxygen
delivery system is useful in patients with ARF who require
oxygen supplementation, but in whom there is substantial risk
for development of or worsening hypercapnia because the FIO2
does not fluctuate significantly even with considerable changes
in the patient’s minute ventilation. Venturi masks or a Venturi
device in a humidifier-mixer is accurate only to 40% to 50%
FIO2; above this range, many patients overbreathe the system.
When a higher FIO2 is required, a high-flow mask (e.g., Misty-Ox
[Medline]) and a high-flow regulator (that can go up to 30 L/
min) are recommended. With all these masks, there is significant
deterioration of oxygen delivery as the respiratory rate increases,
as when the patient is in respiratory distress. At 30 breaths/min,
the FIO2 delivered by a 15-L oxygen mask can drop from 95%
to 60% owing to entrainment of ambient air and dilution of the
inspired oxygen concentration. In a study by Wagstaff and Soni,29
high levels of inspired oxygen concentration were achieved by
a 15-L nasal cannula using a Vapotherm system (Equipro) that
humidifies and warms the oxygen–air mix and makes it more
tolerable to the patient. An alternative is to use a non-rebreather
mask in which a reservoir bag with a one-way flap is connected
to the mask and fills during the patient’s expiration.
Aside from the risk of hypercapnia, there are other risks
associated with oxygen therapy. High FIO2 decreases the amount
of inert nitrogen that fills and stabilizes peripheral airways and
alveoli while oxygen is being rapidly removed from the alveoli,
resulting in atelectasis. Absorption atelectasis causes a decrease
in vital capacity and an increase in right-to-left shunt, which
leads to worsening of hypoxemia. This is more frequently seen
at FIO2 above 0.7. High FIO2 can also lead to tracheobronchitis
CHAPTER 30 Acute Respiratory Failure 315
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and acute lung injury with capillary leak syndrome.31 When this
happens, it is often difficult to distinguish from worsening of
the underlying condition that initially precipitated ARF. In general,
FIO2 of 1.0 can be used for 24 hours and FIO2 of 0.9 can be
used for 72 hours without significant sequelae. FIO2 of 0.6 or
less is usually well tolerated without significant long-term histologic and physiologic changes. If a patient requires very high
FIO2 with the above methods, ventilatory-assist devices should
be considered to allow the FIO2 to be lowered, thereby decreasing
the risks of atelectasis and oxygen toxicity. These include noninvasive ventilation using continuous positive airway pressure
(CPAP) through nasal or face mask and invasive mechanical
ventilation through an endotracheal tube.
Over the past few years, there has been a renewed interest in
the use of noninvasive ventilation in the management of ARF.
Several pilot studies have shown useful applications of these
techniques in avoiding intubation in some patients with ARF.
Larger clinical trials are needed to further define the role of
noninvasive mechanical ventilation in ARF, especially in those
patients with advance directives for no intubation and with
potentially reversible processes causing ARF.
Although positive airway pressure can be applied to nonintubated patients, these techniques may lead to gastric distention
and vomiting. CPAP is best tolerated at low levels (10 cm H2O)
and for brief periods. Bilevel positive airway pressure allows for
the inspiratory pressure to be set at a higher level (e.g., 10 to
20 cm H2O) than the expiratory pressure (e.g., 0 to 10 cm H2O).
There have been multiple meta-analyses on noninvasive positive
pressure ventilation (NPPV), which range from bilevel positive
airway pressure machines applied via a full face mask all the way
to a conventional ventilator connected to a mask device that
covers the whole face. Its success varies according to the purpose
and the diagnosis for which it is used. The best survival data
and earliest applications were in exacerbations of COPD and
acute cardiogenic pulmonary edema. In COPD, the application
of NPPV decreased both mortality and length of hospital stay
with a number needed to treat of five. Intubation risk was reduced
by 28% in a meta-analysis by Keenan and colleagues.
31a
In
cardiogenic pulmonary edema, mortality was reduced by 45%.32
Other trials proved its effectiveness in acute respiratory failure
following lung resection, acute asthma, solid organ transplantation, and in immunocompromised patients. NPPV has also been
used in weaning patients from mechanical ventilation; the
application of NPPV in one study of 443 patients shortened
33
mechanical ventilation by approximately 10.5 days.
Other studies,
however, have shown increased mortality when NPPV is used
in patients requiring vasopressors, lack of improvement of
respiratory acidosis, refractory hypoxemia, fatigue, and inability
to clear secretions. These clinical parameters should be evaluated
1 hour after initiation of NPPV, when the first arterial blood gas
is obtained. Confalonieri developed a chart predicting the success
of NPPV that included Acute Physiology and Chronic Health
Evaluation II (APACHE II) score, acidosis, level of consciousness,
and respiratory rate.34 As can be imagined, patients with a
depressed level of consciousness, a pH less than 7.25, and a
respiratory rate greater than 35 are more likely to fail and would
probably benefit from urgent intubation without a trial of NPPV.
All studies evaluating NPPV published exclusion criteria that
may very well be deemed as contraindications: cardiac or respiratory arrest; hemodynamic instability; the uncooperative patient;
and patients with facial trauma, copious secretions, or significant
risk of aspiration. Those patients should undergo intubation
and conventional mechanical ventilation. Intubation facilitates
the delivery of higher tidal volumes and the application of positive
end-expiratory pressure needed to avert oxygen toxicity.
Mechanical Ventilation
Mechanical ventilation is a method of supporting intubated
patients during illness when spontaneous ventilation is inadequate
to sustain life or to achieve a therapeutic target. The clinical
objectives are (1) to correct hypoxemia, (2) to correct acute
respiratory acidosis, (3) to relieve respiratory distress, (4) to
prevent or reverse atelectasis, (5) to rest respiratory muscles or
prevent fatigue, (6) to allow sedation and neuromuscular blockade,
(7) to decrease systemic or myocardial oxygen consumption, (8)
to reduce intracranial pressure through controlled hyperventilation, and (9) to stabilize the chest wall.
In general, mechanical ventilators can be divided into two
categories: negative pressure ventilators and positive pressure
ventilators. The iron lung is the prototype of negative pressure
ventilators that gained popularity during the polio epidemics.
Today, newer generations of negative pressure ventilators are
still available under different names, such as cuirass, body suit,
Porta-Lung, pneumobelt, pneumowrap, pneumosuit, and other
more portable devices. They function by creating a negative
pressure outside the chest wall, causing chest wall expansion
and subsequent inspiration that simulates physiologic breathing.
On release of the negative pressure, exhalation is passively
accomplished. In the hospital setting, positive pressure ventilators
are the mainstay of mechanical ventilation owing to various
features and adjunctive modes that allow for more sophisticated
delivery of conditioned gas and assistance in ventilation.
Positive pressure inflation of the lung can be achieved with
machines that terminate inspiration according to volume, pressure,
or time. The latest generation of positive pressure ventilation
allows the physician to select among these options and allows
for pressure support (a flow-cycled mode of ventilation) and
reverse inspiratory to expiratory (I/E) ratio ventilation.
Volume-cycled ventilators deliver preset inspiratory flow to
achieve a target volume, regardless of the pressure required. This
system guarantees the tidal volume unless the peak pressure
during inspiration exceeds the high-pressure limit, in which case
the resulting volume is less than the preset volume. High pressure
delivered to diseased, noncompliant lungs may predispose to
barotrauma. Pressure-cycled ventilators deliver preset positive
pressure throughout inspiration; however, the resulting tidal
volume is variable depending on the compliance of the lungs.
A true time-cycled ventilator does not depend on the patient’s
lung characteristics or even whether the ventilator is attached
to the patient to end inspiration; therefore, it is important to
recognize that a complete ventilatory cycle may occur without
generating a tidal volume. Pressure support ventilation can be
used either as a ventilatory mode or as an adjunctive mode. As
a ventilatory mode, the pressure is set to produce a desired level
35
316 PART IV Noncoronary Diseases: Diagnosis and Management
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of tidal volume similar to a pressure-cycled system. In an adjunctive mode, the pressure is set just high enough to overcome the
tubing and circuit resistance during inspiration such that the
level of pressure support does not increase the spontaneous tidal
volume of the patient. A pressure support of 5 to 10 cm H2O is
usually adequate for the adjunctive mode.
Volume-cycled ventilators are most commonly used in the
intensive care unit. In an assist-control (AC) mode, each patient
breath that is recognized by the ventilator is assisted with a preset
volume and flow rate in addition to a number of mandatory
breaths per minute. In an intermittent mandatory ventilation
(IMV) mode, the patient can take spontaneous unassisted
breaths between the mandatory breaths. A synchronized IMV
(SIMV) mode synchronizes the machine mandatory breaths to
the patient’s spontaneous breaths to avoid breath stacking. A
pressure support system can be used to augment the spontaneous
breaths of patients in the SIMV mode while at the same time
guaranteeing a minimum number of mandatory breaths.
AC mode allows the patient to rest because each recognized
spontaneous breath is assisted. Patients with respiratory muscle
fatigue should be allowed to rest on this mode. Patients with sepsis
and hypotension benefit from this mode by decreasing respiratory
muscle work, which accounts for a significant portion of oxygen
consumption during hypoperfusion syndromes. Similarly, in
patients with cardiogenic pulmonary edema, decreased work
of breathing translates to decreased myocardial oxygen demand.
However, in patients with abnormal homeostatic mechanisms,
such as hepatic encephalopathy, increased central respiratory
drive may result in respiratory alkalosis. The SIMV mode is
more homeostatic because the patient can determine the tidal
volume needed; however, the work of breathing is higher and
proportional to the amount of spontaneous ventilation relative
to the assisted ventilation. The SIMV mode is primarily used in
patients with severe air flow obstruction who tend to air trap
when each breath is a relatively large, positive pressure breath.
When the mandatory rate is set beyond the patient’s spontaneous
rate, or if the patient is completely paralyzed, the two modes are
practically indistinguishable and the patient will receive only the
mandatory breaths. Newer modes of ventilation include airway
pressure release ventilation (APRV) and bilevel modes. The first
one allows for CPAP with an intermittent pressure release phase. A
(high pressure) and P
P
high
(low pressure) are set and the patient
low
is allowed spontaneous breathing independent of the ventilator
cycle. Rather than continuously distending and deflating the
alveoli, the P
cycle and only briefly releases to P
maintains inflation during the entire respiratory
high
, thus aiding in ventilation
low
and CO2 removal. Oxygenation is improved in this mode through
alveolar recruitment by increasing the mean airway pressure
(P
) or by increasing the time at P
high
improved by changing the pressure gradient between P
P
or by increasing release frequency. APRV mode may result
low
high
(T
). Ventilation is
high
high
and
in lower peak airway pressures and less sedation for the patient
but has not been shown to impact mortality.
36
In addition to ventilator modes, prone positioning has been
extensively studied. Most research shows an improvement in
oxygenation and PaO2/FIO2 ratios. Additionally, Guerin et al.
showed significant improvement in 28- and 90-day mortality
when prone positioning was applied early for patients with
severe ARDS.
37
After the mode of ventilation is decided, the tidal volume,
respiratory rate, FIO2, and inspiratory flow rate must be set on
the ventilator. The range of tidal volumes used in mechanical
ventilation is between 5 and 15 mL/kg of ideal body weight.
When low tidal volumes (6 to 8 mL/kg ideal body weight) are
used, positive end-expiratory pressure (PEEP) or sighs (generally
each sigh volume is 2 to 3 times tidal volume) should be given
at set intervals to prevent microatelectasis. As a general rule,
with severe airway obstruction or ARDS, 6 mL/kg up to 8 mL/
kg tidal volume is reasonable (refer to the ARDSnet.org ventilator
chart). Postoperative patients with normal lungs are frequently
started on 8 to 12 mL/kg whereas patients with neuromuscular
disease receive 10 to 15 mL/kg. It is generally safe to select a
tidal volume that generates a peak alveolar pressure of 35 cm
H2O or less (with plateau pressures <30 to 32 cm H2O). The
rate should be chosen in conjunction with the tidal volume to
provide minute ventilation that maintains a normal pH. A rate
of 12 to 18 breaths/min is usually adequate. Once the patient is
stable, the ventilator rate is often adjusted 2 to 4 breaths/min
below the total respiratory rate. This prevents excessive work of
breathing in the SIMV mode and provides an adequate backup
rate in the AC mode.
In emergent situations, the FIO2 should be set at 0.9 or 1.0
with later adjustments guided by arterial blood gases. The FIO2
can be titrated down to achieve an SaO2 of more than 90%
(usually a PaO2 of 60 mm Hg). More than 24 hours with an FIO2
of 0.9 or greater or prolonged use of an FIO2 of 0.6 or greater
requires the addition of PEEP for prevention of oxygen toxicity.
In general, this can be achieved with a PEEP of 5 to 15 cm H2O.
The inspiratory flow rate is usually set by the respiratory therapist
at a level of 40 to 55 L/min. It is mandatory for the peak flow
setting (inspiratory flow rate) of the ventilator to be greater than
the patient’s inspiratory flow demand. Otherwise, the patient
breathes against the resistance of the ventilator circuitry, which
results in the patient “fighting the ventilator.” The flow setting
should be 3.5 to 4 times the minute ventilation to achieve an I/E
ratio of 1 : 1.2 to 1 : 1.5. In patients with severe obstructive lung
disease, I/E ratios of 1 : 4 to 1 : 6 may be necessary.
Complications may arise during the course of mechanical
ventilatory support. A deliberate and stepwise approach should
be followed in the management process. Patient distress may
arise from general discomfort, from inadequate ventilation or
from the feeling of dyspnea. If hypoventilation is part of the
overall strategy, the patient needs to be sedated. Accidental
hypoventilation may result from kinking of the endotracheal
tube, mucus plugging, accidental main stem intubation, pneumothorax, ventilator circuit leak, or ventilator disconnection. If
the ventilator alarms have been set properly, they are frequently
the first indicator of the acute problem, especially in a comatose,
sedated, or paralyzed patient. A high-pressure alarm is usually
caused by obstruction of the airway or acute change in lung
compliance, whereas a low-volume alarm suggests decreased
respiratory drive, a leak within the system, or a disconnected
ventilator. During a high-pressure alarm distress, the patient
should be disconnected from the ventilator and hand ventilated
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with a bag valve mask at an FIO2 of 1.0 while a systematic search
for the cause is being done. Unequal breath sounds may suggest
a pneumothorax or slippage of the endotracheal tube into a
main stem bronchus. Acute changes in hemodynamics are more
suggestive of the former. Difficulty in hand ventilation should
suggest kinking of the tube or mucous plugs; therefore, a suction
catheter should be passed for diagnostic and therapeutic purposes.
Chest radiography may aid the diagnosis and demonstrate lobar
or complete collapse of the lung. If aggressive chest physiotherapy
and inhaled mucolytics (e.g., Pulmozyme) are not effective,
bronchoscopy may be required. If tension pneumothorax is
strongly suspected, placement of a 14-gauge needle (angiocatheter)
into the second intercostal space along the midclavicular line
can relieve the tension immediately. Once this is done, a chest
tube should always be placed whether a tension pneumothorax
was present or not since the patient is receiving positive pressure
ventilation and the catheter may have punctured the visceral
pleura.
When a leak in the circuit is suspected, the ventilator tubing
can be changed. If the leak is from the endotracheal tube, it can
happen anywhere from the valve of the pillow to the cuff. A
three-way stopcock inserted into the valve may correct the
problem if the leak comes from the valve, obviating the need to
change the endotracheal tube. If it does not stop the leak, the
site of the leak may be in the pillow, the pilot line, or the cuff
itself and may necessitate replacement of the endotracheal tube
over a flexible stylet.
Pneumonia occurs in approximately 30% of patients receiving
ventilator support. The risk increases with the duration of ventilator support at a rate of about 1% per day.
3
Pneumonia may be
difficult to diagnose in patients with a “white” chest radiograph
and may require either empirical therapy with a presumptive
diagnosis or the use of bronchoscopy with a sterile brush with
greater than or equal to 103 CFU/mL on quantitative culture
considered a significant finding (or 104 on bronchoalveolar lavage
or 105 on endotracheal aspirate).
Physiologic measurements—such as maximum inspiratory
pressure (PI
= −20 cm H2O), vital capacity (VC = 10 mL/kg)
max
and minute ventilation (MV = 15 L/min) are used to determine
when a weaning trial should be done. Recently, the ratio of
respiratory frequency (f) to tidal volume (Vt) during 1 minute
of spontaneous breathing was found to be more accurate.39 If
f/Vt is less than 100 breaths/min per liter, a weaning trial is likely
to be successful. The usual method of weaning includes trials
of increased spontaneous breathing through a T tube or on
pressure support ventilation (PSV, up to 10 cm H2O). When
patients can breathe spontaneously for more than 30 minutes
to 2 hours without a significant change in their hemodynamics,
respiratory rate, or minute ventilation, they can usually be successfully extubated.
40
Extracorporeal Membrane Oxygenation
Extracorporeal membrane oxygenation (ECMO) is a method
for providing prolonged cardiopulmonary support to patients
with severe acute respiratory failure. There are two types of
ECMO: venoarterial (VA), which provides respiratory and
hemodynamic support, and venovenous (VV), which provides
respiratory support only. The Conventional ventilatory support
versus Extracorporeal membrane oxygenation for Severe Acute
Respiratory failure (CESAR) trial demonstrated significantly
increased survival without disability at 6 months in patients
who were randomly assigned to care in an ECMO center in a
single United Kingdom center compared to conventional management in non-ECMO centers (63% vs. 47%). This study has several
limitations, including the fact that 25% of patients referred for
ECMO did not receive this therapy (16 recovered with conventional care and 5 died before transfer). However, several other
trials have also demonstrated a survival benefit associated with
ECMO for neonates, children, and adults with respiratory failure.
Therefore referral to an ECMO center should be considered for
adults with severe ARDS who are not improving with conventional
management or who may need a bridge to lung transplantation.
Guidelines for the use of ECMO are maintained by the Extracorporeal Life Support Organization and available on their website
at www.elso.org.
41
CONCLUSION
Acute respiratory failure implies an inability to maintain adequate
oxygenation for tissues or adequate removal of carbon dioxide
from tissues. The differential diagnosis should be informed by
the radiographic appearance of the chest radiograph and by the
patient’s history and physical examination. A specific diagnosis
should be pursued, which frequently requires ancillary studies
such as blood or sputum cultures, bedside spirometry, perfusion
lung scan, or a CT angiogram using multidetector scanners. This
allows the physician to initiate specific therapy for the underlying
cause of acute respiratory failure. These patients often require
supportive therapy.
The full reference list for this chapter is available at
ExpertConsult.com.
CHAPTER 30 Acute Respiratory Failure 317.e1
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2. Murray JF. Gas exchange and oxygen transport. In: Normal Lung:
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3. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, et al.
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4. Wagner PD, West JB. Ventilation-perfusion relationships. In:
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5. Venkatesan P, Gladman J, Macfarlane JT, et al. A hospital study
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7. Petrucci N, Iacovelli W. Lung protective ventilation strategy for
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8. Marini JJ. Advances in the understanding of acute respiratory
distress syndrome: summarizing a decade of progress [Review].
Curr Opin Crit Care. 2004;10(4):265–271.
9. Kalil AC, Metersky ML, Klompas M, et al. Management of adults
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Society of America and the American Thoracic Society. Clin
Infect Dis. 2016;63(5):e61.
10. Mandell LA, Wunderink RG, Anzueto A, et al. Infectious diseases
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11. Dalen JE, Alpert JS. Natural history of pulmonary embolism.
Prog Cardiovasc Dis. 1975;17:259–270.
12. The PIOPED Investigators. Value of the ventilation/perfusion
scan in acute pulmonary embolism. JAMA. 1990;263:2753–2759.
13. Stein PD, Coleman E, Gottshalk A, et al. Diagnostic utility of
ventilation/perfusion lung scans in acute pulmonary embolism is
not diminished by pre-existing cardiac or pulmonary disease.
Chest. 1991;100:604–606.
14. Lesser BA, Leeper KV, Stein PD, et al. The diagnosis of acute
pulmonary embolism in patients with chronic obstructive
pulmonary disease. Chest. 1992;102:17–22.
15. Stein PD, Hull RD, Patel KC, et al. D-dimer for the exclusion of
acute venous thrombosis and pulmonary embolism: a systematic
review. Ann Intern Med. 2004;140(8):589–602.
16. Righini M, Nendaz M, Patel KC, et al. Influence of age on the
cost effectiveness of diagnostic strategies for suspected
pulmonary embolism. J Thromb Haemost. June 26, 2007;
[Epub].
17. Palla A, Bardi G, Ribas C. Diagnosis of pulmonary embolism.
Semin Thromb Hemost. 2006;32:822–830.
18. Curtis JR, Hudson LD. Emergent assessment and management of
acute respiratory failure in COPD. Clin Chest Med.
1994;15:481–500.
19. Fagon J, Chastre J, Trouillet J, et al. Characterization of distal
bronchial microflora during acute exacerbation of chronic
bronchitis. Am Rev Respir Dis. 1990;142:1004–1008.
20. Anthonisen NR, Manfreda J, Warren CPW, et al. Antibiotic
therapy in exacerbations of chronic obstructive pulmonary
disease. Ann Intern Med. 1987;106:196–204.
21. The Global Strategy for Diagnosis, Management and Prevention
of COPD; updated 2016. Available at: www.goldcopd.org.
22. Irwin RS, et al. A physiologic approach to managing respiratory
failure. In: Rippe JM, Irwin RS, Alpert JS, eds. Intensive Care
Medicine. 2nd ed. Boston: Little, Brown & Co; 1991:449–454.
23. Aubier M, Murciano D, Fournier M, et al. Central respiratory
drive in acute respiratory failure of patients with chronic
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191–199.
24. Aubier M, Murciano D, Milic-Emili J, et al. Effects of the
administration of O2 on ventilation and blood gases in patients
with chronic obstructive pulmonary disease during acute
respiratory failure. Am Rev Respir Dis. 1980;122:747–754.
25. Stradling JR. Hypercapnia during oxygen therapy in airways
obstruction: a reappraisal [Editorial]. Thorax. 1986;41:897–902.
26. George RB, Light RW, Matthay MA, eds. Chest Medicine:
Essentials of Pulmonary and Critical Care Medicine. 3rd ed.
Baltimore: Williams & Wilkins; 1995.
27. Snider GL, Fairley HB, Fulmer JD, et al. Scientific basis of oxygen
therapy: national conference on oxygen therapy. Chest. 1984;86:
236–239.
28. Lee JH, Rehder KJ, Willifor L, Cheifetz IM, Turner DA. Use of
high flow nasal cannula in critically ill infants, children, and
adults: a critical review of the literature. Intensive Care Med.
2013;39(2):247–257.
29. Wagstaff TAJ, Soni N. Performance of six types of oxygen
delivery devices at varying respiratory rates. Anaesthesia.
2007;62:492–503.
30. Deleted in review.
31. Jenkinson SG. Oxygen toxicity. J Intensive Care Med. 1988;3:
137–152.
31a. Keenan SP, Sinuff T, Cook DJ, Hill NS. Which patients with
acute exacerbation of chronic obstructive pulmonary disease
benefit from non-invasive positive pressure ventilation? A
systematic review of the literature. Ann Intern Med.
2003;138(11):861–870.
32. Hess DR, Fessler HE. Should noninvasive positive-pressure
ventilation be used in all forms of acute respiratory failure?
Respir Care. 2007;52:568–581.
33. Ferrer M, Esquinas A, et al. Noninvasive ventilation during
persistent weaning failure: a randomized-controlled trial. Am J
Respir Crit Care Med. 2003;168:70–76.
34. Confalonieri M, Garuti G, et al. A chart of failure risk for
noninvasive ventilation in patients with COPD exacerbation. Eur
Respir J. 2005;25:348–355.
35. Slutsky AS. Mechanical ventilation. Chest. 1993;104:1833–1859.
36. Habashi NM. Other approaches to open-lung ventilation: airway
pressure release ventilation. Crit Care Med. 2005;33:s228–s240.
37. Guerin C, Reigmer J, Richard JC, et al. Prone positioning in
severe acute respiratory distress syndrome. NEJM. 2013;368(23):
2159–2168.
38. Deleted in review.
39. Yang KL, Tobin MJ. A prospective study of indexes predicting
the outcome of trials of weaning from mechanical ventilation. N
Engl J Med. 1991;324:145–150.
40. Esteban A, Alia I, Tobin MJ, et al. Effect of spontaneous
breathing trial duration on outcome of attempts to discontinue
mechanical ventilation. Am J Respir Crit Care Med. 1999;159:
512–518.
41. Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and economic
assessment of conventional ventilator support versus
extracorporeal membrane oxygenation for severe adult
respiratory failure (CESAR): a multicenter randomized
controlled trial. Lancet. 2009;374(9698):1351.
31
https://t.me/medicina_free
Massive Acute Pulmonary Embolism
Narain Moorjani, Susanna Price
OUTLINE
Pathophysiology, 319
Clinical Presentation, 319
Diagnosis and Risk Stratification, 319
Investigations for Risk Stratification, 320
High Clinical Probability, 320
Low or Intermediate Clinical Probability, 320
Management, 321
Anticoagulation, 321
Fibrinolysis, 322
Pulmonary Embolectomy, 323
Catheter-Directed Thrombectomy, 324
ICU Management, 324
Optimization of Right Ventricular Preload, 324
Maximizing Right Ventricular Contractility, 325
Right Ventricular Afterload, 325
Coronary Perfusion Pressure, 325
Device Support, 325
Inferior Vena Cava Filter, 326
Long-Term Anticoagulation, 326
Outcomes, 326
Conclusion, 326
Acute pulmonary embolism (PE) represents the sudden obstruction of part or all of the pulmonary arterial vasculature, usually
caused by embolization of thrombus from the deep veins within
the lower limbs and pelvis. It may also be caused by embolism
of air, fat, or amniotic fluid. PE is the third most common cause
of cardiovascular death (after coronary artery disease and stroke);
more than 600,000 cases are thought to occur in the United
States annually.1 PE has been found in 18% of autopsies and in
the majority (70%) of these was considered to be the main or
a contributory cause of death.2 The incidence increases exponentially with age, with the mean age at presentation of 62 years
men and women are affected equally.
Although no predisposing factors are identified in approximately 20% of patients (idiopathic or unprovoked PE),5 the
majority have either patient-related or setting-related attributable
risk factors (secondary or provoked PE). Patient-related factors
include advanced age, previous venous thromboembolism, active
cancer, underlying coagulopathy (including Factor V Leiden and
prothrombin mutations), smoking, hormone replacement therapy,
and oral contraceptives.
an increased risk of PE include heart failure, stroke, respiratory
failure, sepsis, and inflammatory bowel disease.8 Setting-related
risk factors include protracted immobility secondary to major
general/orthopedic surgery, major fracture, travel, pregnancy,
chemotherapy, or the presence of a central venous line.9 Commonly, more than one risk factor is present.
Historically, PE was classified according to the anatomic burden
of the thrombus in the pulmonary vasculature.10 Patient outcome
is, however, more dependent on the associated hemodynamic
6,7
Medical conditions associated with
4
2,3
compromise, such as the presence of circulatory arrest, hypotension, or right ventricular dysfunction.
reclassified into three different prognostic categories
1. High-risk (massive) PE (20% of cases), which is a lifethreatening condition and defined as PE in the presence of:
a. Arterial hypotension (systolic blood pressure <90 mm Hg
or a drop of >40 mm Hg) for more than 15 minutes or
requiring inotropic support, which is not caused by a new
arrhythmia
b. Cardiogenic shock (oliguria, lactic acidosis, cool extremities,
;
or altered level of consciousness)
c. Circulatory collapse in patients with syncope or undergoing
cardiopulmonary resuscitation (CPR)
2. Intermediate-risk (submassive) PE (32% of cases), which is
defined as PE with a systolic blood pressure greater than 90 mm
Hg but echocardiographic evidence of right ventricular (RV)
dysfunction or pulmonary hypertension, or the presence of
elevated markers of myocardial injury (such as troponin)
3. Low-risk (nonmassive) PE (48% of cases), which is defined
as PE with a systolic blood pressure greater than 90 mm Hg
and no evidence of RV dysfunction, pulmonary hypertension,
or elevated markers of myocardial injury.
Data from the International Cooperative Pulmonary Embo-
lism Registry (ICOPER) demonstrated 90-day mortality for
patients with massive PE of 52% compared to 15% for those
with submassive and nonmassive PE.5 Similarly, data from the
Management Strategy and Prognosis of Pulmonary Embolism
Registry (MAPPET) demonstrated a 65% in-hospital mortality for
patients with acute PE requiring CPR compared to 25% for those
5
PE has therefore been
11,12
:
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CHAPTER 31 Massive Acute Pulmonary Embolism 319
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presenting with cardiogenic shock and 8% for hemodynamically
stable patients.13 The presence of RV dysfunction is associated
with a 2-fold increase in 90-day mortality.
14
PATHOPHYSIOLOGY
Obstruction of flow through the main pulmonary arteries results
in increased afterload on the RV. In addition, release of vasoactive
mediators, including thromboxane A2 and serotonin, results in
pulmonary vasoconstriction and increased pulmonary vascular
resistance.15 The resultant increase in RV wall tension results in
displacement of the interventricular septum to the left and
impaired left ventricular (LV) filling.16 If untreated, the RV outflow
obstruction also results in reduced preload in the LV, reduced
cardiac output, and, eventually, circulatory collapse and shock.17
Younger patients with otherwise normal underlying cardiac
function may tolerate the hemodynamic stress placed by a large
PE without developing RV dysfunction or shock. In patients
with compromised cardiac function, however, the onset of RV
failure and circulatory collapse may be more rapid. In addition,
hypoxia may result from the low cardiac output entering the
pulmonary circulation, ventilation–perfusion mismatch, and the
presence of a right-to-left shunt (through a patent foramen ovale,
opened by increased right-sided pressure).
18
CLINICAL PRESENTATION
The clinical presentation of PE varies widely. Massive PE may
present with severe dyspnea at rest, syncope, or even cardiac
arrest, whereas nonmassive PE may be asymptomatic or have
limited symptoms. Past medical history may include some risk
factors for venous thromboembolism. Physical signs include
tachycardia, tachypnea, systemic hypotension, and cyanosis.
Clinical evidence of RV dysfunction includes distended neck
veins, parasternal heave, accentuated pulmonary component of
the second heart sound, and a systolic murmur consistent with
tricuspid regurgitation. An RV gallop rhythm may also be heard.
The presence of a pleural rub, in association with pleuritic chest
pain, may be secondary to pleural irritation caused by pulmonary
infarction. These clinical features may also be used for risk
stratification.
19,20
DIAGNOSIS AND RISK STRATIFICATION
Clinical features and predisposing risk factors have been incorporated into clinical scoring systems that are used to predict the
likelihood of PE and determining subsequent investigations.
These include the Wells Score, Simplified Geneva Score, and
Pulmonary Embolism Severity Index (PESI; Table 31.1).
19–21
The
TABLE 31.1 Clinical Scoring Systems Used to Determine Risk Following Acute PE
Variable Points
Wells Score
Predisposing factors
Previous DVT or PE 1.5
Recent surgery or immobilization 1.5
Cancer 1
Symptoms
Hemoptysis 1
Clinical signs
Heart rate >100 beats/min 1.5
Clinical signs of DVT 3
Clinical judgment
Alternative diagnosis less likely than PE 3
Clinical probability (3 levels) Total
Low 0–1
Intermediate 2–6
High ≥7
Clinical probability (2 levels)
PE unlikely 0–4
PE likely >4
Simplified Geneva Score
Predisposing factors
Age >65 years 1
Previous DVT or PE 1
Surgery or fracture within 1 month 1
Active malignancy 1
Symptoms
Unilateral lower limb pain 1
Hemoptysis 1
19
20
Variable Points
Clinical signs
Pain on deep palpation of lower limb and unilateral edema 1
Heart rate 75–94 beats/min 1
Heart rate > 94 beats/min 2
Clinical probability Total
PE unlikely 0–2
PE likely >2
Pulmonary Embolism Severity Index
Age 1 per year
Male gender 10
Cancer: active or past history 30
Heart failure 10
Chronic lung disease 10
Heart rate >110 beats/min 20
Systolic blood pressure <
Respiratory rate >30 beats/min 20
Temperature <36
Altered mental status (disorientation, lethargy, stupor, or coma) 60
Oxygen saturation <90% on room air 20
Clinical interpretation (mortality at 30 days)
Class 1: very low mortality risk (0%–1.6%) <66
Class 2: low mortality risk (1.7%–3.5%) <86
Class 3: moderate mortality risk (3.2%–7.1%) <106
Class 4: high mortality risk (4.0%–11.4%) <126
Class 5: very high mortality risk (10.0%–24.5%) >126
100 mm Hg 30
o
C 20
21
DVT, Deep venous thrombosis; PE, pulmonary embolism.
320 PART IV Noncoronary Diseases: Diagnosis and Management
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most extensively validated and widely used clinical scoring system
is the Wells score.
22
INVESTIGATIONS FOR RISK STRATIFICATION
The chest radiograph (CXR) is usually abnormal in patients
with acute PE.
other features such as atelectasis or pleural effusion can be used
to exclude other causes of dyspnea or chest pain. Arterial blood
gas (ABG) analysis usually demonstrates hypoxemia (partial
pressure of oxygen [PaO2] <80 mm Hg), with hypocapnia and
respiratory alkalosis.25 In up to 20% of patients, a normal PaO2
and alveolar-arterial gradient may be found. Alternatively,
hypercapnia with respiratory and metabolic acidosis may be
seen in patients with massive PE requiring cardiopulmonary
resuscitation (CPR). Following assessment of the clinical and
hemodynamic status of the patient using a clinical scoring system,
the patients are subdivided into different probabilities of PE.
23,24
Although mainly nonspecific, the absence of
HIGH CLINICAL PROBABILITY
If the patient has a high clinical probability of PE as determined
by the clinical scoring systems, then multidetector computed
tomography pulmonary angiography (CTPA) is required to
determine the presence of thrombus within the pulmonary arterial
vasculature.11 CTPA has become the imaging of choice in patients
with suspected PE because of its speed of scanning, widespread
availability, and high sensitivity and specificity (>90%).26 It
provides excellent visualization of the pulmonary arterial vasculature, including the main, lobar, and segmental pulmonary
arteries along with characterization of extravascular structures
(Fig. 31.1).
An alternative imaging modality, such as VQ scintigraphy,
may also be required in patients with a contraindication to CTPA,
such as those with renal failure or contrast allergy.27 In hemodynamically unstable patients who cannot be transferred for
CTPA, echocardiography may be required.
LOW OR INTERMEDIATE
CLINICAL PROBABILITY
If the patient has been classified as having a low or intermediate
clinical probability of PE, a D-dimer enzyme-linked immunoabsorbent assay (ELISA) should be performed as the first-line
investigation (sensitivity 96% and specificity 39%).28 Serum
D-dimer is a degradation product of cross-linked fibrin and acts
as an indirect marker for thrombosis and subsequent fibrinolysis.
As the D-dimer ELISA has a high negative predictive value (NPV),
its absence effectively rules out acute PE and an alternative
diagnosis should be sought.29 The positive predictive value (PPV)
of elevated serum D-dimer levels, however, is low, as although
D-dimer is very specific for fibrin, fibrin can be produced in a
wide variety of conditions, including aortic dissection, cancer,
inflammation, and infection.
should undergo a CTPA.
Once the diagnosis of acute PE has been made, the patients
are stratified into low-risk (nonmassive), intermediate-risk
(submassive), and high-risk (massive) groups, according to the
presence of hypotension, shock and/or RV dysfunction. The
clinical status of the patient will differentiate the high-risk
(massive) PE from non-high-risk PE patients. Echocardiography
can then be used to further delineate non-high-risk PE patients
into intermediate-risk PE (with evidence of RV dysfunction) or
low-risk PE (with no RV dysfunction) groups.32 Surrogate markers
of RV dysfunction include RV dilatation (RV end-diastolic
dimension >30 mm), interventricular septal flattening with
paradoxical motion, increased RV/LV ratio (>0.9), RV hypokinesis,
pulmonary hypertension (pulmonary artery systolic pressure
>30 mm Hg), and increased tricuspid regurgitation jet velocity
(>2.6 m/s), which are found in approximately 25% of patients
with acute PE (Fig. 31.2).
Echocardiography can also be used to exclude other important
causes of acute circulatory collapse, including acute myocardial
infarction (MI), pericardial tamponade, or type A aortic dissection.
Normal RV size and function on echocardiography in a patient
30,31
Hence, if positive, the patient
11
33,34
A
Fig. 31.1 Contrast-enhanced computed tomography pulmonary angiography (CTPA) axial images
showing (A) a large saddle embolus at the pulmonary artery bifurcation (arrow) with extension
into both the left and right pulmonary arteries, and (B) evidence of right heart strain shown by
enlarged right heart chambers, a right ventricle (RV)/left ventricle (LV) ratio greater than 1.5, and
displacement of the interventricular septum. (Courtesy Dr. Deepa Gopalan, Cambridge, UK.)
B
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