Chapter 14: Initial Settings for Mechanical Ventilation

Ventilatory support should be instituted when a patient's ability to maintain gas exchange has failed to the level that death is imminent if support is not provided. Respiratory failure is categorized as hypercapnic or hypoxemic. Once the decision is made to initiate mechanical ventilation, selection of the initial ventilator settings is based on the patient's physiologic status and the best available evidence. Whenever mechanical ventilation is considered, the ethical consequences of the decision must also be addressed.

Hypoxemic respiratory failure is characterized by a failure to oxygenate. Hypercapnic respiratory failure is a failure of the ventilatory pump (ventilatory muscles). Frequently, respiratory failure is a result of both hypoxemic and hypercapnic failure, and can be classified as compensated or uncompensated.

Hypercapnic Respiratory Failure

The ventilatory pump comprises the diaphragm and chest wall muscles, as well as the neural control of them. This is responsible for ensuring adequate alveolar ventilation. Four aspects of the ventilatory pump, either alone or in combination, can result in pump failure: weak muscles, excessive load, impaired neuromuscular transmission, motor neuron disease, or decreased respiratory drive (Table 14-1). Hypercapnic respiratory failure results in an elevated Paco₂.

Weak respiratory muscles may occur as a result of inherited myopathies and muscular dystrophies malnutrition, electrolyte imbalance, inadequate peripheral nerve function, or compromised substrate delivery. Long term use of corticosteroids and aminoglycoside antibiotics or calcium channel blockers can impair neuromuscular transmission. Chronic pulmonary disease and neuromuscular disease may precipitate pump failure because of a decrease in the force-velocity relationship of the muscle, decreasing maximal muscular contraction. Ventilatory muscle force may also be decreased by the mechanical disadvantage caused by a flattening of the diaphragm as in severe chronic obstructive pulmonary disease or a deformed thoracic cage as in kyphoscoliosis. Patients in the ICU who are mechanically ventilated, especially those paralyzed and receiving steroids, may develop critical illness myopathies. In addition, chronic pulmonary disease or neuromuscular disease may lead to detraining, atrophy, or fatigue of ventilatory muscles, all leading to a reduced efficiency of ventilation and carbon dioxide retention.

Excessive load may cause hypercapnic failure, but it is usually associated with other factors that compromise pump function. For patients with chronic pulmonary or neuromuscular disease, the increased load resulting from secretion accumulation, mucosal edema, or bronchospasm may precipitate failure. For patients with thoracic deformities, increased ventilatory load is a chronic problem. Any factor that elevates minute ventilation requirements increasing ventilatory load may precipitate failure when associated with reduced neuromuscular capability.

Depressed respiratory drive may be caused by drugs, hypothyroidism, or diseases affecting the respiratory center. Increased respiratory drive may also precipitate acute respiratory failure, especially when coupled with compromised pump function and increased ventilatory load. For example, metabolic acidosis, increased carbon dioxide production, and dyspnea-related anxiety may result in an intolerable increase in ventilatory drive.

Hypoxemic Respiratory Failure

Failure of the lungs to maintain arterial oxygenation is hypoxemic respiratory failure (Table 14-2). Hypoxemic respiratory failure usually does not result in carbon dioxide retention unless acute or chronic pump failure is also present. Hypoxemic respiratory failure can usually be treated with oxygen, but mechanical ventilation may be necessary in severe cases of acute respiratory distress syndrome (ARDS), heart failure, or pneumonia.

From a physiologic perspective, indications for mechanical ventilation are listed in Table 14-3. Acute respiratory failure requires mechanical ventilation when the Paco₂ is elevated sufficiently to cause an acute acidosis (pH < 7.30), although the precise limits on pH and Paco₂ must be individually evaluated in each patient.

Impending ventilatory failure is an indication for mechanical ventilation when the patient's clinical course indicates deterioration despite maximum treatment. Examples include the patient with neuromuscular disease, or the patient with asthma who demonstrates increasingly compromised respiratory function in the presence of maximum therapy.

Oxygenation deficit is the least likely indication for mechanical ventilation. However, the severe hypoxemia caused by ARDS or pneumonia may require mechanical ventilation. When a high Fio₂ (> 0.80) is required, mechanical ventilation should be considered. Unloading the work of the ventilatory pump with mechanical support frequently improves oxygenation status because of the reduced oxygen cost of breathing, and also due to the higher mean airway pressure.

Hemodynamic compromise is common when mechanical ventilation is started. Mean intrathoracic pressure transitions from negative to positive when mechanical ventilation is begun. Adequate ventilation and oxygenation may result in decreased autonomic tone. Sedation is frequently provided at the initiation of mechanical ventilation, which can lead to hypotension. The hemodynamic compromise associated with the initiation of mechanical ventilation may need to be treated with fluid administration and vasoactive drugs.

Actual ventilator settings depend on the level of patient interaction with the ventilator, the underlying pathophysiology, and the respiratory mechanics. Patients of similar size and age, one presenting with a drug overdose and the other with severe asthma, should not be ventilated in the same manner.

Mode

There is much controversy over the best mode and little evidence to direct the choice of mode. More importantly, during the initial phases of mechanical ventilation, full support should usually be provided. This may be accomplished with continuous mandatory ventilation (assist/control) applied as either volume-controlled ventilation (VCV) or pressure-controlled ventilation (PCV). The key is to set the rate high enough to ensure little if any spontaneous effort is required by the patient.

Volume and Pressure Levels

Because of concern regarding ventilator-induced lung injury, plateau pressure should not exceed 30 cm H₂O unless chest wall compliance is reduced. The V_T should be 4 to 8 mL/kg ideal body weight (IBW). Patients with normal lungs (eg, overdose, postoperative) should have the V_T set at 6 to 8 mL/kg IBW and those with lung disease should receive a V_T of 4 to 8 mL/kg (Table 14-4). The IBW used to set the absolute tidal volume is calculated as:

Setting of pressure control is determined by the tidal volume (V_T) delivered. Pressure levels should be set to achieve a V_T similar that that with VCV. Regardless of approach used to deliver V_T, the actual volume delivered to a patient's lungs should be small (4-8 mL/kg) in patients with lung disease, and may be moderate (6-8 mL/kg IBW) in patients with normal lungs.

Flow Pattern, Peak Flow, and Inspiratory Time

With VCV, the peak flow and flow pattern are set on the ventilator. Although a descending ramp flow pattern may potentially improve V_T distribution, a rectangular flow pattern may be equally acceptable during the initiation of mechanical ventilation. Peak flow should be set initially to produce an inspiratory time less than or equal to 1 second. For patients triggering the ventilator, flow and inspiratory time should be set according to inspiratory demand. Inspiratory time should be set so that it is less than the expiratory time to avoid air trapping and hemodynamic compromise.

Rate

The rate chosen depends on tidal volume, pulmonary mechanics, and Paco₂ (Table 14-4). For patients with obstructive lung disease, lower rate in the range of 8 to 12/min, as well as lower minute ventilation, are set low to avoid the development of auto-positive end-expiratory pressure (auto-PEEP). For patients with acute lung injury, an initial rate of 20 to 25/min is generally adequate to produce an acceptable minute ventilation. Patients with normal lungs usually tolerate an initial rate set at 15 to 20/min. Adjustments to rate are made after monitoring the effect of mechanical ventilation.

Fio₂ and PEEP

At initiation of mechanical ventilation, Fio₂ of 1.0 is recommended and then titrated to 88% to 95% oxygen saturation measured with pulse oximetry, for a Pao₂ of 55 to 80 mm Hg. An initial PEEP of 5 cm H₂O is set to maintain functional residual capacity and prevent atelectasis. In the setting of acute lung injury, higher levels of PEEP are appropriate.

Before committing a patient to mechanical ventilatory support, consideration should be given to the reversibility of the disease process. If there is little likelihood of reversing the acute disease process, the potential for long-term ventilation must be weighed against the result of not providing ventilatory support. Noninvasive ventilation may be appropriate while discussions regarding the advisability of intubation and long-term support can be evaluated. In some patients, such as those with progressive neuromuscular disease, either full time noninvasive ventilation or tracheostomy with long-term ventilation initiated as per patient wishes.