Discontinuation of Mechanical Ventilation

I. INTRODUCTION: The safe discontinuation of mechanical ventilation is the primary goal for physicians caring for patients with respiratory failure. Advancements in the understanding of sedation, delirium, and volume status management over the past 15 years, as well as modifications to ventilator strategies, have led to shorter time on mechanical ventilation and better hospital outcomes. A detailed understanding of the factors leading to respiratory failure and ways in which successful ventilator discontinuation can be achieved are paramount to the care of the intubated patient.

II. DEFINITIONS

A. SAT: Spontaneous awakening trial. The cessation of all sedatives, or decreasing doses of sedative infusions in order to allow a patient to reliably interact and follow commands

B. SBT: Spontaneous breathing trial. A decrease in the amount of support provided by a mechanical ventilator to test the patient’s ability to breathe without support

C. Weaning: Decreasing ventilator settings in a stepwise approach in order to determine the patient’s minimal ventilator needs

D. Ventilator Dependence: The inability to wean a patient from mechanical ventilation despite repeated attempts

E. Extubation: Removal of the endotracheal tube

F. Decannulation: Removal of the tracheostomy tube

III. VENTILATOR DEPENDENCE—can be due to a variety of reasons related to any component of the respiratory system. A thorough investigation into each of the etiologies described below is central to the care of ventilated patients.

A. Nervous System

1. Primary brain injury—can lead to damage to centers in the brain involved in the control and initiation of respiration. Examples include stroke, hemorrhage, mass effect, cerebral edema, seizures, and central apnea.

2. Sedating medications—can decrease the respiratory drive

3. Spinal cord and peripheral nerves—Damage to these structures can impair the function of the diaphragm and intercostal muscles.

4. Critical illness myopathy/polyneuropathy (CIM/CIP)—Each is multifactorial, related to length of immobility, degree of critical illness, use of systemic steroids, and paralytic agents. The presence of CIM or CIP can lead to impaired function of the diaphragm and accessory muscles of inhalation, resulting in respiratory failure.

5. Psychological: Untreated/undertreated anxiety or other psychiatric diseases may lead to unnecessary anxiety surrounding the removal of ventilator support. Reassurance or low-dose anxiolytics may be necessary, depending on the clinical scenario.

B. Respiratory Muscles

1. Electrolyte imbalances—Phosphate and magnesium are each central to muscular function. Severe depletions in each are associated with muscle weakness and may lead to difficulty with ventilator weaning.

2. Nutritional factors—Inadequate nutrition can lead to muscle catabolism, which may result in respiratory muscle weakness and prolonged reliance on mechanical ventilation. Conversely, overfeeding can result in excess CO2 production and resultant increases in minute ventilation.

3. Endocrine imbalances—Cortisol, insulin, and glucagon have been implicated in normal respiratory muscle function, and deficiencies in each have been hypothesized to lead to compromised function. Hypothyroidism may result in diaphragmatic weakness.

C. Pulmonary Mechanics—Increased resistance and decreased compliance each increase the amount of work required during respiration. The degree to which resistance and compliance are abnormal determines the degree to which a patient will be reliant on the ventilator.

1. Resistance—the opposition to airflow in the respiratory system

a. Increased airways resistance can be due to bronchospasm, increased respiratory secretions, airway inflammation, endotracheal or tracheostomy tube obstruction, or small diameter of endotracheal tube.

2. Compliance—the ability of the thorax and lungs to expand their volume as transmural pressure increases. Measured at end-inhalation during a breath hold; the reciprocal of elastic recoil.

a. The compliance of the chest wall may be impaired due to morbid obesity, chest wall bony abnormalities, or intra-abdominal processes that interfere with diaphragm function.

b. Lung compliance can be decreased as a result of consolidation, fibrosis, or pulmonary edema.

3. Auto-PEEP—increased end-expiratory intra-alveolar pressure caused by incomplete exhalation. Can be caused by increased resistance, rapid respirations, or by ventilator dyssynchrony. Of specific concern in patients with severe obstructive lung disease, which may make the patient dyssynchronous and complicate ventilator weaning

4. Minute ventilation—required to maintain normal acid–base status. Increased minute ventilation requirement may indicate increased CO2 production or increased dead space. High minute ventilation requirements (particularly >10 L/min) may not be tolerated by the newly extubated patient and should suggest to the clinician that a search for undiagnosed underlying causes be undertaken.

D. Inadequate Gas Exchange—High levels of FIO2 and PEEP may be required due to the compromise of the alveolar-arterial interface (i.e., significant pneumonia, ARDS, pulmonary edema, fibrosis).

E. Cardiovascular Disease—Patients for whom cardiac dysfunction is present may not tolerate the additional stress to the cardiovascular system that the removal of mechanical ventilation can cause. Underlying coronary artery disease may manifest as chest pressure or pain during an SBT or following extubation that is related to stress-induced cardiac ischemia. Patients with congestive heart failure may develop acute pulmonary edema due to the removal of all positive pressure and the subsequent increase in venous return.

IV. STANDARDIZED CARE OF THE INTUBATED PATIENT

A. The “ABCDE” bundle. Applied to all intubated patients on a daily basis

1. “AB”: Daily SAT (“A”) and SBT (“B”) to assess for extubation readiness

2. “C”: Choice of sedative

3. “D”: Delirium monitoring and management

4. “E”: Early mobilization of intubated patients

5. www.icudelirium.org—useful reference for clinicians

B. Addition of the SAT to the usual care of intubated patients (as opposed to sedation management at the discretion of the clinician) lead to fewer days on mechanical ventilation and in the ICU, with no difference in complications such as self-extubation.

C. Early Mobilization—Physical therapy that begins while intubated, during periods of lightened sedation, has been shown to be safe and leads to decreased mortality, more functional independence after hospital discharge, less delirium, and more ventilator-free days.

V. SEDATION MANAGEMENT: This will be addressed in more detail in Chapter 7. Below is a brief overview of an approach to sedation in the intubated patient.

A. Consider an “analgesia-first” strategy to treat pain symptoms, adding a sedative only if the patient remains uncomfortable after pain control is achieved.

B. Short-acting agents are preferred to long-acting agents, due to both quicker onset of action and shorter duration of effect once discontinued. Frequent renal and liver dysfunction in medical ICU patients affect timely clearance of medications.

C. Use lowest necessary continuous infusion rates. When possible, use intermittent IV bolus dosing rather than continuous infusion.

D. Use a validated scale to set sedation targets, such as the RASS (Richmond Agitation Sedation Scale).

1. Scale by which sedation is titrated, assessed by nursing frequently

2. –5 (unarousable) to +4 (combative)

3. Target: 0 (alert and calm) to – 1 (drowsy)

E. Sedative Choices

1. Propofol: GABA potentiation

a. Side effects: Hypotension, propofol infusion syndrome (rare), hypertriglyceridemia

2. Midazolam (Versed): GABA potentiation

a. Hepatic metabolites are also active GABA potentiators.

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