Weaning from mechanical ventilation

The concept of liberation and extubation

Weaning from mechanical ventilation refers to the transition period from total ventilatory support to spontaneous breathing. Approximately 70% of intubated mechanically ventilated patients are extubated after the first spontaneous breathing trial (SBT), either by ventilator disconnection or after breathing at low levels of pressure support for short periods ranging from 30 to 120 minutes. ^, The remaining patients (about 30%) require progressive withdrawal from artificial ventilatory support. In half of these patients, mechanical ventilation can be withdrawn in less than 1 week; however, the other half of patients require more than 1 week of mechanical ventilation. Importantly, in this latter group, the prognosis is markedly worse. ^,

Early liberation from mechanical ventilation and removal of the endotracheal tube is clinically important. Unnecessary prolongation of mechanical ventilation increases the risk of complications, including infections (particularly of bronchopulmonary origin), barotrauma, cardiovascular compromise, tracheal injuries, and muscle deconditioning. To maximize patient outcomes, clinicians should attempt to hasten the process that ultimately leads to removal of the endotracheal tube. Every additional day that passes after the first weaning attempt increases the risk of death.

Liberation and extubation are different concepts. Liberation refers to weaning from mechanical ventilation, meaning that the patient no longer requires ventilatory support. When liberation has been achieved, the clinician must consider a different question: “Is the patient able to breathe spontaneously and protect the airway without the endotracheal tube?” Removal of the endotracheal tube is referred to as extubation. The extubation failure rate is variable, ranging from 5% to 20% of extubated patients. ^,

Mechanisms that explain liberation failure

Respiratory pump failure

The most common reason for weaning failure is respiratory pump insufficiency, which is caused by an imbalance between the patient’s endurance capabilities and respiratory demands. Jubran and Tobin investigated the progression of respiratory mechanics during SBT in patients with chronic obstructive pulmonary disease (COPD). At the very beginning of the trials, patients who subsequently failed had a slightly higher airway resistance, respiratory system elastance, and intrinsic positive end-expiratory pressure (PEEP) compared with those who succeeded. However, during the trials, respiratory mechanics progressively worsened in patients who failed to achieve ventilator liberation. Subjects who failed quickly developed rapid, shallow breathing, and most also developed (but more slowly) an increase in partial pressure of carbon dioxide (PaCO ₂ ). Together, these abnormalities of mechanics and chemical drive resulted in increased inspiratory muscle effort. Breathing exertion was likely close to the threshold of muscle fatigue in some patients.

Laghi and Tobin studied 19 intubated patients during weaning from mechanical ventilation; of these, 11 patients failed and 8 succeeded. Several physiologic indices were measured before and 30 minutes after SBT. Before the SBT, the transdiaphragmatic twitch pressure, elicited by magnetic bilateral phrenic stimulation, did not differ between the patients who failed or succeeded at ventilator liberation, and this variable did not decrease after the trial in either group. Patients failing the SBT were reconnected to the ventilator because of clinical signs of intolerance. It was concluded that weaning failure was not accompanied by low-frequency diaphragmatic fatigue. Weaning failure patients did, however, exhibit severe diaphragmatic weakness, because twitch pressures were always low.

Common disorders that alter the balance of capacity and load in critical illness

Reduced neuromuscular capacity and reserve

Traditionally, peripheral muscular dysfunction—known as critical illness polyneuropathy —was associated with difficult weaning. However, in recent years, respiratory muscle dysfunction (mainly the diaphragm)—known as critical illness–associated diaphragm weakness —is a condition whose existence has become recognized and its properties better characterized. We now know that respiratory muscle dysfunction is independent of peripheral polyneuropathy and twice as prevalent (present in up to 60% of ventilated patients), exerting a greater impact on weaning. Diaphragm weakness is mainly associated with muscle disuse or a low level of effort associated with controlled ventilation modalities, but it has also been associated with a high breathing effort because of insufficient respiratory assistance. The optimal balance between diaphragm overuse and underuse is difficult to determine. However, it stands to reason that the appropriate level of assisted ventilation could prevent diaphragm atrophy.

Increased muscle loads

The increased work of breathing results from increased mechanical loads (elastic and/or resistive). Increased elastic workloads occur when lung and chest wall compliance are reduced (e.g., pulmonary edema, extreme hyperinflation during an acute asthmatic attack, pulmonary fibrosis, abdominal distention, severe obesity, trauma, or thoracic deformities). The presence of intrinsic PEEP is another example of increased elastic workload, and this phenomenon is relatively common, especially in patients with COPD. ^, Resistive work of breathing during critical illness may increase as a result of bronchospasm, excessive secretions, endotracheal tube resistance (which increases with kinking and deposition of secretions), and ventilator valves/circuits and humidifiers, especially when conditioning of inspired gases is provided with heat and moisture exchangers. The latter also increase the dead space posed by the external apparatus.

Cardiovascular dysfunction

The presence of cardiovascular dysfunction can contribute to weaning failure by augmenting the loads on the respiratory system and reducing neuromuscular capacity. ^, Cardiovascular dysfunction can result from physiologic changes that occur during the resumption of unassisted spontaneous breathing. When spontaneous breathing resumes, the intrathoracic pressure during inspiration is negative, leading to increased left ventricular preload and afterload. Increased heart loads augment myocardial oxygen demand and may precipitate myocardial ischemia in patients with coronary artery disease. Pulmonary vascular congestion may also increase.

Jubran and colleagues examined hemodynamics and mixed venous saturation in patients during weaning trials. Successfully weaned patients demonstrated increases in the cardiac index and oxygen transport compared with values observed during mechanical ventilation. Patients who failed weaning did not increase oxygen delivery to the tissues because, in part, of elevated right and left ventricular afterloads. Consequently, these abnormalities have the potential to jeopardize respiratory muscle function.

In intensive care unit (ICU) patients, congestive heart failure in predisposed patients may occur as a consequence of an increase in venous return, volume overload, or catecholamine release induced by physiologic stresses, such as weaning. Impairment of cardiovascular function can be magnified in cases with a positive fluid balance.

Studies have shown that using a T-tube (instead of pressure support and PEEP) to perform an SBT in difficult-to-wean patients may elicit an adverse cardiovascular response; when support is added (in the form of pressure support and PEEP), respiratory and cardiovascular function both improve.

In the ICU setting, noninvasive tools are available (e.g., echocardiography and measurement of plasma B-type natriuretic peptide [BNP]) to help diagnose cardiovascular dysfunction. Up to 50% of patients who fail a weaning test exhibit cardiogenic pulmonary edema (based on BNP measurements and/or echocardiography), which is more common in patients with COPD and in patients with underlying cardiac dysfunction.

Mekontso-Dessap and colleagues showed that BNP-guided administration of diuretics can reduce weaning time, particularly in patients with left ventricular systolic dysfunction. That same group of authors has also shown that isolated diastolic dysfunction may be associated with a longer weaning time and increased filling pressures, with impaired left ventricular relaxation potentially being a key mechanism for failure of the weaning trial.

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