Sedatives and narcotics should be discontinued several hours before a breathing trial to reduce the likelihood of inadequate drive to breathe. Indeed, while several studies have indicated that protocol-driven approaches to weaning have identified patients earlier for extubation than routine care by clinicians on a day-to-day basis, other investigations protocolizing a daily interruption of sedatives have been associated with a decreased time of mechanical ventilation and diminished time in the ICU.25 It is likely that these are two tightly linked ICU activities—sedation and mechanical ventilatory support—and that clinicians are not extremely adept at identifying prospectively when patients do not need one or the other. A simple approach to this problem is to discontinue sedatives frequently and, in those patients awakening in a stable condition, to perform an SBT.
Ventilator Mode and Duration of the SBT
Pressure support, continuous positive airway pressure (CPAP), and T-piece trials are the most common methods used to test readiness for liberation from mechanical ventilation. The choice of whether to use pressure support or to allow the patient to breathe without inspiratory assistance through the endotracheal tube remains a point of physician style. Some data suggest that the endotracheal tube can increase resistive load significantly,48 which theoretically could contribute to failure. Consequently, many investigators have suggested that a pressure support of 5 to 8 cm H2O can be used to counter this tube-related load. Recent studies have suggested, however, that pressure support intended to overcome tube resistance unloads the respiratory muscles compared with extubated breathing. These data suggest that T-piece breathing most closely approximates the work of unassisted breathing after extubation.49,50 Nonetheless, one study suggested that the rate of extubation failure following successful trials of pressure support equal to 8 cm H2O was not greater than following successful T-piece trials.51 Another study found similar rates of successful extubation following trials of pressure support of 7 cm H2O versus T piece.52
The first SBT need be only 30 minutes53 because extending the trial longer does not enhance the clinician's ability to assess the patient's readiness for extubation. The proper duration of subsequent SBTs in those who fail has not been studied (30 to 120 minutes generally are used). Thus the available data suggest that patients should be considered for a trial of extubation after a successful trial (30 to 120 minutes) of either T piece, CPAP, or pressure support of 5 to 8 cm H2O.
The Patient Who Fails Initial SBTs
Failure of an SBT is most often a clinical diagnosis. The clinical signs of failure include rapid-shallow breathing, tachycardia (>110 beats per minute), hypertension (increment of more than 20 mm Hg), mental status changes, and subjective distress. These signs result from (1) decrements in gas exchange, (2) cardiovascular events, and/or (3) other (noncardiopulmonary) issues. When a patient fails an SBT, clinicians frequently focus on specific ventilator regimes aimed at improving respiratory muscle function. Although some studies in animal models have suggested that respiratory muscle exercise may be helpful,54 to date no study has suggested that the ventilator can be used to expedite the recovery from respiratory failure. If “exercise” is attempted, all attempts should be made to avoid exhausting the patient (generally accomplished if respiratory rates stay below 30/min). However, instead of concentrating on the ventilator, the clinician should turn attention to treatable factors underlying the patient's respiratory failure (Table 44-3). Some traditional weaning parameters are helpful in making this determination. For example, a markedly reduced maximum negative inspired pressure suggests respiratory muscle weakness. An elevated rapid-shallow breathing index (the respiratory rate per minute divided by the tidal volume in liters) suggests imbalance of respiratory muscle load and capacity. Reasons for abnormalities then can be examined by systematic diagnostic and therapeutic interventions.
Table 44–3. Reversible Factors Contributing to Ventilatory Failure—Daily Correction of Reversible Contributors to Ventilatory Failure Expedites Patient Recovery ||Download (.pdf)
Table 44–3. Reversible Factors Contributing to Ventilatory Failure—Daily Correction of Reversible Contributors to Ventilatory Failure Expedites Patient Recovery
|Reduce Respiratory Load||Improve Respiratory Strength|
|Resistance||Replace K+, Mg2+, PO42− to normal|
|Inhaled bronchodilators||Treat sepsis|
|Corticosteroids||Nutritional support without overfeeding (aim to achieve a normal prealbumin)|
|Removal of excess airway secretions||Consider stopping aminoglycosides|
|Treatment of upper airway obstructions||Rule out:|
|Elastance||Neurologic disease/occult seizures|
|Treat pulmonary edema||Oversedation|
|Reduce dynamic hyperinflation||Critical illness myopathy/polyneuropathy|
|Drain large pleural effusions|
|Detect intrinsic PEEP|
|Therapy for pulmonary embolism|
|Maintain least PEEP possible|
|Correct metabolic acidoses|
Analyzing Failure of an SBT
Acute hypercapnia during weaning frequently results from an imbalance between respiratory pump capacity and load. Normal individuals who are subjected to resistance loading exhibit rapid-shallow breathing as a sign of impending respiratory failure.55,56 When the patient is clearly failing an SBT, it should be discontinued (even before a blood gas analysis demonstrates gas exchange abnormalities) because patients who are “weaned” to exhaustion frequently take several days to recover adequately to resume trials.
Many factors may reduce respiratory muscle strength or increase respiratory muscle loads in critically ill patients. In patients who fail due to strength-load imbalance, we quantify neuromuscular function and the three elements of respiratory muscle load (resistance, elastance, and minute volume; see above) each day so as to define/treat reversible elements. Critical illness frequently is associated with a catabolic state, malnutrition, and electrolyte deficiencies that can contribute to respiratory muscle weakness. Some patients recovering from severe illness develop a polyneuropathy57–60 that has been hypothesized to contribute to reduced respiratory pump function and prolonged need for mechanical ventilation.58,59 Sepsis occurs frequently in critically ill patients and is a relatively common reason for weaning failure. Numerous studies suggest that sepsis has a negative impact on respiratory muscle function,61–65 and this effect is mediated by cytokines.63,64 In addition, treatments that are used commonly in critically ill patients, such as administration of corticosteroids66–68 and neuromuscular blockers,69–71 also negatively affect respiratory muscle function. Mechanical ventilation itself may contribute to disuse atrophy of the respiratory muscles, thus contributing to the pathogenesis of prolonged ventilator dependence.54,72 Bronchospasm and increased airway secretions frequently contribute to resistive loading of the respiratory muscles. Elevated airway resistance greater than 15 cm H2O/L per second frequently can be reversed by removing excessive airway secretions73 or treating with aerosolized bronchodilators.74 If resistance remains greater than 15 cm H2O/L per second despite bronchodilators in a patient who repeatedly fails to wean, a therapeutic trial of corticosteroids may be helpful.
Finally, numerous factors contribute to increased respiratory system elastance, ranging from acute lung injury to abdominal distention. Pulmonary edema and pneumonia are common reversible causes of increased lung elastance. Occult PEEP also increases elastic load75 and can contribute to respiratory muscle fatigue by increasing the work of assisted76 and unassisted breathing. Increased minute volumes associated with lung injury, hypermetabolic states of critical illness (e.g., sepsis), pulmonary embolism, and overfeeding could contribute to dynamic hyperinflation during the recovery process, thus increasing mechanical loads on the recovering respiratory muscles.
Acute hypercapnia does not necessarily connote weaning failure. In three relatively common situations, hypercapnia during an SBT trial is not accompanied by physiologic decompensation and does not signal ventilatory failure. First, occasional patients with chronic hypercapnia are hyperventilated iatrogenically to a normal PCO2, and over the course of days in the ICU, the bicarbonate concentration also decreases to normal. When these patients resume spontaneous breathing, their PCO2 rises to their baseline level, leading to an acute respiratory acidosis. The clinician must decipher whether the acute acidosis is arising from strength-load imbalance, in which case the patient usually shows other signs of failure, or from preceding iatrogenic hyperventilation. Similarly, when some patients with chronic hypercapnic respiratory failure are given a high fraction of inspired oxygen, they acutely retain CO2 in the absence of strength-load imbalance.77–79 Reduction in the supplemental oxygen to yield a saturation of 90% to 92% may reverse this iatrogenic cause of hypercapnia. Finally, some patients who have primary metabolic alkalosis will have compensatory hypoventilation and hypercapnia.
Hypoxemia (PaO2 <60 mm Hg or saturation less than 90% on 50% inspired oxygen) can occur during weaning for several reasons. Old age, obesity, and recumbency predispose to a lower functional residual capacity (FRC), which can contribute to atelectasis and subsequent hypoxemia during the transition to unassisted breathing. Thus patients should be sitting at greater than a 30-degree angle during spontaneous breathing. Respiratory muscle weakness and sedatives or narcotics may lead to shallow breathing and atelectasis. Lung injury, a common complication of critical illness, is associated with surfactant depletion and an increased propensity for atelectasis during the withdrawal of positive-pressure ventilation. Thus many pulmonary factors can contribute to hypoxemia during SBTs. Hypoxemia also can result from cardiovascular changes during weaning.
The transition to unassisted breathing is associated with centralization of blood and increased left heart afterload, which may predispose patients with baseline left ventricular dysfunction to develop cardiogenic pulmonary edema.6–15 SBTs also may increase the level of circulating catechols,80 which could induce increases in heart rate, blood pressure, and arrhythmias. Tachycardia during weaning frequently is a sign of inadequate cardiopulmonary reserve and subsequent weaning failure. Moreover, in patients with coronary artery disease, if mechanical loads and catechol-induced changes are sufficient, weaning can trigger cardiac ischemia that could contribute to the clinical signs of weaning failure81–84 (see Fig. 44-2). In a study of 93 medical patients being weaned from mechanical ventilation, ST-segment changes were noted in 6% of all patients and in 10% of those with a preceding history of coronary artery disease. Moreover, weaning-related ischemia tended to increase the risk of weaning failure.84
In patients who are clinically hypervolemic or who have left ventricular dysfunction, pre-emptive diuresis and nitrate therapy can be helpful in attenuating acute increases in preload during SBTs. Continuous monitoring of ST segments and treatment with additional nitrates also may be helpful in patients who experience ischemia during weaning.84
Other Reasons for SBT Failure
Even though most weaning failures are of cardiopulmonary etiology, other exogenous factors also may contribute to failure.
Ventilator and Circuit Elements
The ventilator and its circuitry can contribute to weaning failure by two mechanisms: (1) by increasing respiratory loads enough during an SBT to fatigue the respiratory muscles and (2) by imposing significant respiratory muscle work during “rest” periods. The resistance of the endotracheal tube increases with time, and this increase occasionally can be of sufficient magnitude to impede weaning. The ventilator circuit provides increased dead space and in some modes (for older ventilators) can require excessive work to trigger a “sticky” demand valve. Some studies suggest that flow triggering may reduce the ventilator-imposed work of breathing compared with pressure-triggered modalities.85,86 Thus the ventilator circuit can load87,88 and covertly fatigue the respiratory muscles when patients are presumed to be “resting,” as well as when they are weaning. Patient-ventilator synchrony during “rest” periods reduces the likelihood that the ventilator is contributing to weaning failure.87,89,90 Irregular pressure-volume curves or frequent, large esophageal or intravascular pressure fluctuations during assisted ventilation may help to identify patients who are working hard on the ventilator.91 Empirical manipulation of inspiratory flow rates, waveforms, and triggering mechanisms may aid in improving patient-ventilator synchrony.86 Finally, in patients with obstructive lung disease, intrinsic PEEP may increase significantly the work required to trigger ventilator-supported breaths (so-called trigger asynchrony). In selected patients, addition of applied PEEP to nearly match intrinsic PEEP can reduce this ventilator-induced load.76
Psychological and Housekeeping Issues
Subjective distress, including anxious appearance and sweating, are nonspecific signs of weaning failure. Anxiety during breathing trials may manifest as rapid-shallow breathing, tachycardia, and hypertension that are interpreted as weaning failure by caregivers. Bedside personnel should explain the weaning process; so-called verbal anesthesia is effective in some patients. The use of sedatives to treat anxiety must be undertaken with caution because most of these drugs also depress respiratory function. Haloperidol or very low doses of benzodiazepines can be used to facilitate comfort in these exceptional patients. However, subjective distress most frequently signals that the cardiopulmonary system requires additional repair before resuming unassisted breathing.
The effect of re-establishing patient day-night cycles remains to be well studied.92–94 In patients who fail initial trials of breathing, we are careful to ensure sleep at night and wakefulness, if not exercise, during the day.
Many intensivists have reasoned that by reducing ventilatory support gradually, the respiratory muscles exercise at subfatiguing loads, leading to gradual improvement in function. Some studies have suggested that respiratory exercises (repetitions of low-load resistive breathing) can lead to successful extubation in patients who have failed previously.95 However, there are as yet no studies proving that respiratory muscle training, through the use of graded withdrawal of ventilatory support, hastens the recovery to unassisted breathing.
Two recent studies have assessed the role of “weaning” strategies in expediting liberation of the subset of those who fail initial SBTs. Brochard and colleagues51 studied 456 medical-surgical patients being considered for weaning, of whom 347 (76%) were extubated successfully on the first day of weaning. One hundred and nine patients who failed an initial SBT were randomized to be weaned by one of three strategies: (1) T-piece trials of increasing length until 2 hours could be tolerated, (2) intermittent mandatory ventilation with attempted reductions of 2 to 4 breaths per minute twice a day until 4 breaths per minute could be tolerated, and (3) pressure-support ventilation (PSV) with attempted reductions of 2 to 4 cm H2O twice a day until 8 cm H2O could be tolerated. Patients randomized to the three strategies were similar with regard to disease severity and duration of ventilation before weaning. Patients assigned to T-piece were placed on assist control overnight, whereas synchronized intermittent mandatory ventilation (SIMV) patients remained on an unspecified SIMV rate, and PSV patients remained at an unspecified level of pressure support. There was no difference in the duration of weaning between the T-piece and SIMV groups, but PSV led to significantly shorter weaning compared with the combined T-piece and SIMV cohorts. Interestingly, PSV and T-piece were not compared directly. These authors concluded that “the outcome of weaning from mechanical ventilation was influenced by the ventilatory strategy chosen, and the use of PSV resulted in significant improvement compared with other strictly defined weaning protocols using T-piece or SIMV.”
Esteban and colleagues96 performed a similar study of 546 medical-surgical patients, 416 (76%) of whom were extubated successfully on their first day of weaning. The 130 patients who failed were randomized to undergo weaning by (1) once-a-day T-piece trial, (2) two or more T-piece or CPAP trials each day as tolerated, (3) PSV with attempts at reduction of 2 to 4 cm H2O at least twice a day, and (4) SIMV with attempts at reducing 2 to 4 breaths per minute at least twice a day. Patients assigned to the four groups were similar with regard to demographic characteristics, acuity of illness, and a number of cardiopulmonary variables. Duration of ventilation before weaning was shorter in the SIMV group than in other groups. The mode of ventilation at night was not specified. The weaning success rate was significantly better with once-daily T-piece trials than for PSV and SIMV. Twice-daily T-piece trials were not significantly better, and PSV was not superior to SIMV. The median duration of weaning was 5 days for SIMV, 4 days for PSV, and 3 days for the T-piece regimens. These authors concluded that “a once-daily trial of spontaneous breathing led to extubation about three times more quickly than intermittent mandatory ventilation and about twice as quickly as pressure-support ventilation.”
The statistical methods used in these studies warrant some comment. The first study51 asserts the superiority of pressure-support weaning to T-piece but does not compare these directly. The second study96 presents “adjusted” rates of successful weaning—the nature of the adjustments and their impact on the results are unclear because raw data were not presented. However, several important conclusions can be drawn from these relatively large studies. First, and most important, most patients can be extubated successfully on the first day that physicians recognize readiness after a brief trial (30 to 120 minutes) of breathing through a T-piece. Weaning is not necessary for most patients. Second, both studies suggest that in patients who have failed an initial T-piece trial, SIMV weaning prolongs the duration of mechanical ventilation. These conclusions depend on the precise algorithms used in the studies—it is possible that if a more “aggressive” SIMV algorithm were used, no difference would be noted. However, if one considers the results of these studies together, choices of ventilator mode do not appear to have a major impact in speeding the recovery to unassisted breathing. Clinicians frequently use SIMV or PSV as the initial approach before attempting a T-piece trial. Since most patients are extubated successfully after a brief T-piece trial, such an approach is likely to prolong mechanical ventilation for many patients. PSV weaning may be equivalent to T-piece weaning in carefully controlled protocols. However, in our experience, in busy ICUs, respiratory therapists and nurses frequently are unable to “keep up” with the demands of such protocols—so pressure-support withdrawal protocols have the risk of prolonging ventilation unless followed strictly.