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CHAPTER 60: Liberation From Mechanical Ventilation 537

In order to minimize the duration of ventilator dependence, the clini- in Chaps. 29 and 48. By discerning the causes of respiratory failure, the
cian must: clinician can initiate appropriate treatments early and understand which
parameters best reflect disease resolution.
1. Identify the pathogenesis of respiratory failure in each patient, and
institute appropriate treatment. ■ STEP TWO: PREVENT IATROGENIC COMPLICATIONS
2. Prevent iatrogenic complications. Although not emphasized in most discussions of “weaning” from
3. Detect when the patient is ready to breathe. mechanical ventilation, strategies that avoid further injury during
■ STEP ONE: TREAT THE CAUSES OF RESPIRATORY FAILURE mechanical support are extremely important to ultimately returning the
patient to spontaneous breathing. Such injuries can be characterized as
Although it may seem intuitive that an organized, systematic approach those wrought directly by the ventilator, and those associated with being
in the ICU. Ventilator-induced lung injury (VILI) (see Chap. 51) refers to
aimed at remedying the pathogenesis of disease should expedite lib- a number of mechanisms by which lung injury is amplified in ARDS but
eration from mechanical ventilation, this has been examined rarely. A can be produced in otherwise healthy lungs as well. 11,12 Ventilator-induced
10
protocol that combined identifying and repairing causes of failure with diaphragm dysfunction (VIDD) describes the loss of respiratory muscle
recognizing readiness to breathe, reduced ventilator days and costs. function related to mechanical ventilation and acute illness, and is dis-
From this study it is not possible to determine the relative importance of cussed more fully in Chap. 49. Patients with severe airflow obstruction
13
disease reversal and readiness assessment, but both are likely important. are at risk for dynamic hyperinflation and adverse consequences such as
Accordingly, from the very first day a patient requires intubation it is hypotension and diminished venous return (see Chap. 54). 14
worthwhile defining the mechanisms causing the need for mechanical Indirect complications of mechanical ventilation include aspiration,
ventilation (Fig. 60-1). which should be prevented by maintaining the head of the bed of all
Hypotheses regarding pathogenesis can be confirmed shortly after ventilated patients at 30° unless contraindicated. Ventilated patients
15
intubation by evaluating the chest radiograph, arterial blood gases, lung are often sedentary for a substantial portion of each day and therefore
ultrasound, and ventilator pressure and flow waveforms as described at risk of deep venous thrombosis, justifying universal prophylaxis with
pharmacologic therapies (preferred) or pneumatic compression devices
(if anticoagulants are contraindicated). Gastric mucosal protection
16
should be provided for ventilated patients. Protein pump inhibitors,
17
H -receptor blockers, sucralfate, and antacids have been used to prevent
2
Narcotics gastric injury. Whether continuous feeding of the gut, which usually
Sedatives neutralizes pH, obviates the need for prophylaxis remains unclear.
Hypothyroidism Arguably, one of the most important advances in care of critically
ill, ventilated patients is realization that medications administered in
the past to facilitate comfort can be harmful. Accumulating evidence
suggests that sedatives and opiates promote a variety of neurocognitive
Amyotrophic lateral sclerosis complications. Most importantly, deep sedation prevents mobilization
Polio and there is now strong evidence that disuse atrophy and prolonged
disability result when critically ill patients remain at bedrest and deeply
sedated. Minimal use of such medications coupled with early physi-
Phrenic nerve injury 18,19
=
Guillain-Barré syndrome cal therapy improves outcomes of mechanically ventilated patients,
including fewer days of ventilation. Sedatives and opiates have been
Strength + Drive
Myasthenia gravis associated with other serious complications of critical illness including
Aminoglycoside toxicity delirium, 20-21 depression, posttraumatic stress disorder, and persistent
Botulism cognitive deficits. 22-25 When these medications are used, they should be
Neuromuscular competence
used on a “PRN” basis 26,27 titrated to the minimal amount to maintain
Chronic overloading/fatique
Electrolyte deficiencies a comfortable, arousable patient (Chap. 22). Continuous infusions of
Sepsis sedatives and opiates should be avoided whenever possible, as both
Shock classes of medications are fat soluble and may accumulate causing pro-
Malnutrition longed sedation. If continuously infused medications are used, a period
of daily awakening improves outcomes. 18,28 Sedative guidelines have
been updated to reflect these new findings. 27
Status asthmaticus One method of reducing the amount of sedative is to adjust ventilator
COPD settings in accord with patient comfort before resorting to large doses
Kyphoscoliosis of sedatives and narcotics. Of course, this may not be possible, or may
Obesity lead to settings that risk VILI or dynamic hyperinflation. Since patients’
Edema respiratory status changes often, daily examination for comfortable ven-
Pneumonia Load tilator settings may be useful as described in Chaps. 48 and 49.
Resistance Interstitial fibrosis Another complication of critical illness is fluid overload. 29,30 It is not
uncommon for survivors of critical illness to accumulate 10 or even 20 L
Elastance Fever of fluid prior to beginning the recovery process. When positive pres-
Sepsis sure is removed from the chest during spontaneous breathing, blood is
Minute volume Pulmonary embolism
Hypovolemia centralized, so it is not unexpected that congestive heart failure is among
the most common reasons for weaning failure. An accumulating body of
FIGURE 60-1. The neuromuscular circuit. This diagram summarizes the components of evidence suggests that cumulative fluid balance is a determinant of the
neuromuscular competence and respiratory muscle load and illustrates processes which can duration of ventilator dependence. 29-31 Early initiation of fluid restriction
affect the strength-load balance leading to ventilatory failure. (Reproduced with permission targeting a central venous pressure of 4 cm H O enhances outcomes of
2
from Manthous CA, Siegel M. Ventilatory failure. In: Matthay et al, eds. Pulmonary and Critical patients with ARDS. Much hypervolemia can be prevented by avoiding
30
Care Yearbook, vol 3. St. Louis, Mosby; 1996, Chap. 2.) maintenance fluid infusions, accounting daily for the net fluid balance,

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