Page 668 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 54: Acute-on-Chronic Respiratory Failure 487

respiratory failure due to muscle weakness. Cellular and molecular adap- the work of each breath remains constant, an increase in respiratory
.
tations of the respiratory musculature differ between the diaphragm and rate increases the load. Increased minute ventilation (Ve) requirements
the intercostal muscles. The diaphragmatic myocytes adopt an “aerobic” can be divided into those due to excess carbon dioxide production
fatigue-resistant Type I phenotype with prolonged loading (Table 54-1). (V ˙ CO 2 ) and those from worsened dead space. The first category includes
By contrast the intercostal muscles undergo relatively greater glycolytic excessive caloric intake, fever, agitation, muscular exertion (including
adaptation to chronic loading. 81 shivering and respiratory distress) and hypermetabolism due to injury
Although accessory muscle fatigue is likely to contribute to the precipi- or infection. New dead space may be caused by pulmonary embolism,
tation of an ACRF event, systematic evaluation has failed to demonstrate hypovolemia, PEEP (including PEEPi), or shallower breathing (which
that low-frequency fatigue contributes to prolonged mechanical ventila- raises the dead space fraction, V /V ). Partitioning of the lung mechanics
d
t
tion and failure to liberate. For example, none of 17 “weaning-failure” into resistive and static components in the intubated COPD patient may
patients developed objective fatigue (transdiaphragmatic pressure changes be inaccurate if the end-inspiratory pause maneuver is too short and if
with phrenic nerve stimulation), despite three-quarters of patients having there is rapid spontaneous respiratory effort. 86
a diaphragmatic tension-time index (TTdi) greater than 0.15—a level
associated with diaphragmatic fatigue by several other investigators. 49 MULTIFACTORIAL RESPIRATORY FAILURE
In order to analyze respiratory failure in a way that facilitates manage-
ADDITIONAL CAUSES OF INCREASED LOAD ment, it is important to dissect the very complex real-life patient into
(SEE FIG. 54-2) simple components of deranged neuromuscular competence and load.
■ INCREASED RESISTIVE LOAD However, the patient with ACRF due to isolated rib fracture or hypo-
kalemia is uncommon. More often, numerous contributors to both
In patients with COPD, the respiratory system load is chronically elevated decreased strength and increased load are implicated. For example, a
owing to abnormal airway resistance and increased elastance. The increase patient admitted with pneumonia and worsening bronchospasm may
in airway resistance is caused by bronchospasm, airway inflammation, also have hypophosphatemia, heart failure, and malnutrition. Further,
and physical obstruction by mucus and scarring. One common cause of patients with COPD are significantly more likely to suffer from
increased flow resistance, and the one most amenable to pharmacologic comorbid cardiovascular and cerebrovascular disease and diabetes
87
intervention, is bronchospasm. The disease course in most patients mellitus, all of which can contribute to and compound acute ACRF
with COPD includes an asthmatic component, and bronchial hyper- in COPD. Aspiration at the time of intubation, abdominal disten-
reactivity to provocation may be as common in COPD as in asthma. tion related to attempts to feed enterally, and overzealous parenteral
82
Exacerbations of bronchospasm increase resistive workload, precipitating nutrition complete the picture of multifactorial ACRF. Although the
ACRF. Superimposed heart failure may also cause increased airway resis- situation in such a patient may seem overwhelmingly complex, we
tance, mimicking asthma (“cardiac asthma”). Upper airway obstruction is caution against a “shotgun” approach to evaluation and management
much less common, but since these patients frequently have a history of of patients with multifactorial respiratory failure. Despite the tempta-
prior intubation, tracheal stenosis should be considered. Finally, sleep dis- tion to provide all possible interventions for these very ill patients, a
ordered breathing, which commonly coexists with COPD, may need to be systematic approach to each component of respiratory failure leads
excluded. Especially once the patient is intubated, clues to this underlying logically to a plan for treatment.
cause of dynamic upper airway obstruction (eg, snoring) may be impos- ■
sible to discern. In the proper setting (an obese, hypersomnolent patient), APPROACH TO THE PATIENT
this possibility should be vigorously pursued. The endotracheal tube (ETT) Failure to aggressively treat mild to moderate acute exacerbations of
itself presents a significant resistive workload, especially when a small size COPD prior to the development of ACRF and other organ failure is
83
(<7.5 mm internal diameter) is chosen. The angulation and length of the associated with an increased risk of emergency hospitalization and
tube and the presence of secretions also affect flow resistance. Additionally, delayed recovery. We generally urge caution in extrapolating clinical
88
ventilator circuit heat and moisture exchangers (“HME filters”) impose data from studies of respiratory failure complicating acute status asth-
significantly greater dead space and tube resistance than heated humidi- maticus to ACRF from COPD; the time course, biological mechanisms
84
fiers in ventilated ACRF patients. Automatic tube compensation (ATC) of bronchospasm and airway inflammation as well as propensity for
algorithms available on some modern ventilators are designed to maintain reversibility differ between these conditions. However, it is important
airway pressure by continuously calculating pressure drop across the ETT to appreciate that up to a third of patients with ACRF have underlying
during inspiration and to decrease airway pressure during expiration to reversible airway obstruction consistent with the diagnosis of asthma
82
maintain constant alveolar pressure. However, ATC may be insufficient and that a tailored approach is required for those patients. The unequiv-
to compensate fully for the imposed resistive load of the ETT. 85 ocal role of noninvasive positive pressure mechanical ventilation (NIV)
■ INCREASED LUNG ELASTIC LOAD justifies its position as the cornerstone in the therapeutic approach to
critically ill patients with ACRF (see Chap. 44). We consider NIV to be
Contributors to lung stiffness include pulmonary edema (cardiogenic the “bookends” in the therapeutic library of therapy for ACRF, providing
and noncardiogenic), pneumonia, interstitial fibrosis or inflammation, firm support on either end of an exacerbation of ACRF. This approach
tumor, and atelectasis. As noted above, bronchospasm not only causes is discussed below but incorporates early initiation of NIV to avoid
increased flow resistance but simultaneously worsens the elastic load by MV and improve survival and later use of this tool for early liberation
augmenting PEEPi. from MV. We describe below three phases of management of the ACRF
■ INCREASED CHEST WALL ELASTIC LOAD patient: early ACRF, late ACRF requiring intubation for MV, and libera-
tion from the ventilator.
The chest wall includes the thorax, diaphragm, and abdomen. Therefore, Phase 1: Early ACRF: The goals of management in the patient not yet
obesity, rib fracture, pneumothorax, pleural effusion, ascites, chest wall intubated are to avoid mechanical ventilation when that is possible and
abnormalities, and abdominal distention (see Chap. 58) contribute to to recognize progressive respiratory failure when it is not. The proven
the work of breathing. These factors are particularly relevant in the efficacy of NIV to decrease mortality, avert the need for intubation,
postoperative setting. reduce complications—specifically hospital-acquired pneumonias—and
■ MINUTE VENTILATION LOADS shorten duration of hospital stay with a favorable health economic
impact makes this therapy one of the most important developments in
Dividing the work of breathing into resistive and static components is the management of these patients, because it buys time for the physician
a useful way of analyzing the effort of each breath. However, even if to treat precipitants of ACRF and for the patient to improve.

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