Chapter 4

Liberation and Weaning from Mechanical Ventilation and Extubation

Critical care clinicians routinely “liberate” their patients from mechanical ventilation to allow them to resume breathing on their own. Although the transition from assisted to spontaneous ventilation traditionally has been referred to as “weaning,” the process does not have to be gradual or time-consuming. Patients can be classified into simple, difficult, and prolonged weaning categories based on the time they require to wean. Successful weaning is reported over a relatively short period for ~55% of patients (i.e., the simple weaning group), with a minority of patients requiring weeks or more to wean. This chapter addresses two basic questions: (1) When should mechanical ventilation be stopped and the patient extubated? (2) What strategy should be used to liberate a patient from mechanical ventilation?

Ideally, mechanical ventilation should be stopped as soon as the patient can breathe spontaneously and protect his or her airway. To determine this point, several critical tasks should be performed:

1. Ascertain the patient’s baseline health and respiratory status, i.e., before the development of acute respiratory failure, by obtaining a thorough medical history from the patient or the patient’s family.

2. Determine why mechanical ventilation was first initiated, appreciating both the mechanism and pathophysiology of the patient’s respiratory failure (see Chapter 1).

3. Determine the progress the patient has made toward recovery.

4. Assess the patient’s ability to maintain adequate oxygenation, ventilation, and airway protection.

The best strategy for successful discontinuation of mechanical ventilation should be the safest and fastest available approach, considering patient-specific factors. The pros and cons of the methods used to discontinue mechanical ventilation, as well as their relative safety and efficacies—based on experience and controlled clinical trials—are discussed here.

When to Stop Mechanical Ventilation: The “First Fix What’s Broken” Approach

In this approach, one starts with the underlying assumption that patients cannot be successfully removed from mechanical ventilation unless the problems causing their respiratory failure in the first place are treated and reversed. To accomplish this, one should begin by identifying how the patient’s respiratory failure developed (see Chapter 1). Failure of nonrespiratory organ systems that contributed to the need for mechanical ventilation (e.g., cardiac arrest resulting from a primary cardiac arrhythmia) also need to be addressed appropriately before mechanical ventilation is stopped.

Using a systematic approach (identify both the initial and ongoing disease processes that contribute to a patient’s need for mechanical ventilation) can provide clarity in complex patients. For example, a patient being mechanically ventilated immediately after undergoing heart surgery may have a depressed central nervous system (CNS) drive to breathe because of the effects of intraoperative opioids. Moreover, the function of the patient’s chest bellows may be compromised by restriction from the operative incision and associated pain as well as by pleural effusions, or by phrenic nerve dysfunction secondary to cold cardioplegia or direct nerve injury. Furthermore, both the mechanics and gas exchange could additionally be affected by the presence of an underlying baseline lung disease—such as chronic obstructive pulmonary disease (COPD)—as well as by acute processes, including atelectasis and pulmonary edema. Finally, the same patient may also have increased CO₂ production because of shivering as a result of hypothermia after cardiac bypass surgery. Collectively, these factors may increase the respiratory effort and, in turn, the work of breathing (WOB) that is required to maintain adequate oxygenation and ventilation.

In the aforementioned example, the workload required by the patient’s respiratory pump (also referred to as the ventilatory demand) is increased by the presence of (1) an increased ratio of dead space to tidal volume (V_D/V_T), (2) airflow obstruction, (3) pulmonary edema, (4) atelectasis, and (5) increased CO₂ production (from shivering) (Table 4.1). At the same time, the ventilatory pump capacity may be limited by the surgical incision and pain, loss of lung volumes from multiple causes, respiratory muscle dysfunction caused by phrenic nerve injury, poor diaphragmatic perfusion, electrolyte disorders, and residual effects of neuromuscular blockers (Table 4.2).

TABLE 4.1

Factors and Causes Increasing Ventilatory Demand

Factors	Causes
Increased V_D/V_T	Acute respiratory distress syndrome, asthma, emphysema, pulmonary emboli
Increased oxygen consumption	Fever, increased work of breathing, morbid obesity, sepsis, shivering, trauma
Increased respiratory quotient (increased CO₂ production relative to O₂ consumption)	Excessive carbohydrate feeding
Decreased set point for PaCO₂	Anxiety, central neurogenic hyperventilation, hepatic failure, hypoxemia, metabolic acidosis, renal failure, sepsis

V_D/V_T, dead space-to-tidal volume ratio.

From Lanken PN: Respiratory failure: an overview. In Carlson RW, Geheb MA (eds): Principles and Practice of Medical Intensive Care. Philadelphia: WB Saunders, 1993, pp 754-763.

TABLE 4.2

Factors and Examples Reducing Ventilatory Capacity

Adapted from Lanken PN: Respiratory failure: an overview. In Carlson RW, Geheb MA (eds): Principles and Practice of Medical Intensive Care. Philadelphia: WB Saunders, 1993, pp 754-763.

Categories of Problems to Consider and Fix

Neurologic Impairment and Central Nervous System Drive Problems

Three categories of neurologic impairment may prevent or delay discontinuation of mechanical ventilation and successful extubation:

1. Loss of upper airway protective reflexes

2. Decreased level of consciousness

3. Effects on the central respiratory drive by hypoventilation syndromes or metabolic acid-base disturbances

Loss of Upper Airway Protection

After extubation, some patients may be at risk of clinically significant aspiration or failure to clear their respiratory secretions. Both can prevent patients from being able to safely maintain spontaneous, independent breathing. Before extubation, patients should be assessed for the presence of adequate cough and gag reflexes and their ability to cough well enough to clear their secretions (Table 4.3). Although unsettled, there are data that some patients without a gag reflex can still be successfully extubated. If patients lack a good cough, however, and are unable to clear secretions by themselves, weaning can continue but extubation should be delayed. If, with repeated testing over several days, the patient cannot adequately protect the airway or clear tracheal secretions, the patient should get an elective tracheostomy. This allows a secure access to the airways for suctioning secretions and is more comfortable than continuation of an endotracheal (ET) tube. A tracheostomy is also useful for monitoring aspiration of oral fluids during assessment of swallowing function and usually enhances the patient’s ability to communicate (Chapter 22).

TABLE 4.3

Criteria for Adequate Protection of Upper Airway ^∗

^∗Criteria 1 through 3 must be met before extubation. If only criterion 4 is not fulfilled, the patient can be extubated except if there is a high risk of massive aspiration, such as with partial small bowel obstruction. In all cases, swallowing function after extubation must be carefully tested before any oral intake (see Chapter 22).

The presence of swallowing dysfunction should be assessed in all recently extubated patients before oral intake. This is especially important in patients with poor or absent gag reflexes, patients with tracheostomies, or those with a history of suspected aspiration events (Chapter 22).

Decreased Mental Status

Intensive care unit (ICU) patients commonly have a decreased level of consciousness, often because they are sedated with medications. Level of consciousness influences attempts at weaning and extubation in two ways. First, a depressed mental status may result in loss of upper airway protection, as discussed earlier. Second, patients with decreased mental status may also have a decreased respiratory drive. As long as respiratory drive is considerably impaired, assisted ventilation is necessary. However, when the lack of respiratory drive is due to the absence of chemical stimuli to breathe (i.e., a low PaCO₂ with high pH), a tapering of assistance in breathing is reasonable and often effective. For example, well-oxygenated patients who are alkalemic because of iatrogenic hyperventilation while on mechanical ventilation may not breathe until their PaCO₂ levels are allowed to return to normal.

Several pivotal trials have demonstrated that strategies that minimize sedation can positively influence key patient outcomes, including ventilator weaning. Daily interruption of sedation—with sedatives held in mechanically ventilated patients until they are wakeful—has been found to reduce the average number of days patients spend requiring assisted ventilation. Additional approaches to minimize sedation, including the use of shorter-acting agents or administration of sedative medications in bolus form, especially if done according to a goal directed sedation protocol (carried out by the ICU nursing staff) as opposed to continuous intravenous (IV) infusions, have also been shown beneficial in weaning (Chapter 5). Furthermore, combining the practice of daily sedation interruptions with spontaneous breathing trials (SBTs) resulted in a greater number of ventilator-free days in mechanically ventilated medical patients in a multicenter trial in the United States. Interruption of sedation, however, may increase the risk of self-extubation, and patients should be closely monitored as they resume consciousness.

In addition to medication-induced alterations in consciousness, it is important to assess for hypoventilation resulting from central sleep apnea (CSA), as this may also compromise weaning. CSA occurs as a result of impaired sensitivity to PaCO₂ or Pao₂ levels and can manifest in several ways, including as obesity hypoventilation syndrome (see Chapter 80) or periodic breathing (Cheyne-Stokes breathing). This is particularly problematic for patients ventilated with weaning modes that require them to initiate breaths. Patients with CSA may not respond to increasing hypercapnia with the expected elevation in respiratory rate or tidal volume. Moreover, these patients may appear comfortable during a weaning trial, despite an increased PaCO₂ level, which is only detected by measuring arterial or central venous blood gases. Not considering hypoventilation syndromes in the differential for difficult weaning may make patients seem unweanable when, in fact, they only require scheduled ventilatory support at night and with naps (Chapter 25).

In contrast to patients with hypoventilatory syndromes who do not breathe enough, some patients breathe too much. This includes some patients with brain stem strokes who present with marked tachypnea as a result of central neurogenic hyperventilation. This is challenging because, in general, adults cannot sustain persistent respiratory rates of more than 36 to 40 breaths per minute for too long before they develop respiratory muscle fatigue. Suppression of respiratory drive by high-dose opioids may be successful in such patients, allowing them to be weaned.

Metabolic Acid-Base Disorders

In addition to alterations in ventilation secondary to sedation or CSA, the CNS control of respiratory drive is also affected by both metabolic acidoses and alkaloses. Normally, patients compensate for a metabolic acidosis (serum HCO₃⁻ <18 to 20 mEq/L) by “blowing down” (compensating) their PaCO₂ to maintain their arterial pH in or near the normal range. This respiratory compensation is achieved by hyperventilating, which increases alveolar and minute ventilation (see Chapter 83), but ultimately it may exceed a person’s ventilatory capacity and lead to respiratory muscle fatigue. Thus, in addition to correcting the underlying cause of the metabolic acidosis, patients may require bicarbonate supplementation in order for them to wean.

Alternatively, patients with a severe metabolic alkalosis (serum HCO₃^– >45 to 55 mEq/L) may have an elevated arterial pH, which results in a decreased stimulus to breathe, even when their PaCO₂ levels increase (Chapter 83). This can promote development of hypercapnia, as respiratory compensation for the metabolic alkalosis. Hypercapnia, in these situations, may be mistakenly attributed to respiratory muscle fatigue, an assumption that can delay weaning.

Chest Bellows and Peripheral Nervous System Problems

In some patients, respiratory muscle weakness occurs as a primary event (e.g., in some neuromuscular disorders; see Chapter 67). In other patients, decreased respiratory muscle strength may occur secondary to the effects of critical illness or respiratory failure (see Chapter 48 and Table 4.2), such as when fatigued respiratory muscles need additional time to recover (which may take up to 1 day). Moreover, with muscle disuse—as occurs with modes of mechanical support that do not require significant engagement of the patient’s respiratory muscles—or protein malnutrition, the muscles atrophy. Indeed, evidence of histologic myofiber atrophy has been demonstrated in the diaphragm of humans mechanically ventilated for less than 1 day, possibly because of altered proteolysis. In response to concerns regarding ICU-acquired weakness, several clinical trials were found that, compared to usual care, daily physical and occupational therapy coupled with sedative interruptions resulted in earlier weaning, as evidenced by a greater number of ventilator-free days and a larger number of patients who regained their baseline functional independence (Chapters 5 and 21) .

Decreased muscle function may also be exacerbated by metabolic disorders such as hypophosphatemia and hypokalemia. Furthermore, severe hyperinflation—from airflow obstruction and auto–positive end-expiratory pressure (auto-PEEP)—compromises the efficiency of the length-tension relationship of the normally situated diaphragm and exacerbates the effects of muscle weakness.

Changes in Chest Bellows Function

Various factors can limit lung or chest expansion. In postoperative states, both the architecture of the incisions as well as the degree of pain may limit expansion. Prior to modern pain management strategies (see Chapter 87), on the first postoperative day, a patient’s vital capacity often decreased to only ~25% of preoperative values after thoracotomy as well as after upper abdominal surgeries (e.g., open cholecystectomy). Other common factors that can alter expansion include the presence of a flail chest (resulting from trauma or closed chest cardiac resuscitation), pleural effusions, major atelectasis as well as abdominal distention (from air, ascites, dialysate, or edema). Similarly, intra-abdominal hypertension and abdominal compartment syndrome (Chapters 90 and 97)—often a result of extensive fluid resuscitation—can limit diaphragmatic excursion, thereby decreasing forced vital capacity (FVC) and increasing dead space ventilation.