As shown in Figure 20-2, increases in Paco2 and decreases in Pao2 result in increases in ICP. Thus, normal oxygenation and acid-base balance are goals of ventilation in patients with an increased ICP. Increases in alveolar pressure may result in an increase in ICP due to a decrease in venous return and a decrease in cardiac output.
The effects of Paco2, Pao2, and cerebral perfusion pressure on cerebral blood flow. Note that hypercarbia and hypoxemia increase cerebral blood flow, and thus intracranial pressure. Normally, cerebral blood flow remains relatively constant over a wide range of cerebral perfusion pressures (autoregulation), but this relationship is lost with acute head injury (loss of autoregulation).
Indications for mechanical ventilation in patients with head injury are listed in Table 20-2. The most common reason to ventilate these patients is central respiratory depression due to the primary injury. In such patients, lung function may be near normal and mechanical ventilation is straightforward. In patients with traumatic injury, associated injuries to the spine, chest, and abdomen may also require the initiation of mechanical ventilation. Positive pressure ventilation may be necessary due to neurogenic pulmonary edema. Finally, some therapies for acute head injury (eg, barbiturates, sedation, and paralysis) result in central respiratory depression, necessitating mechanical ventilation.
Table 20-2Indications for Mechanical Ventilation in Patients With Acute Head Injury ||Download (.pdf) Table 20-2 Indications for Mechanical Ventilation in Patients With Acute Head Injury
• Depression due to primary neurologic injury
• Associated injuries to the spine, chest, and abdomen
• Neurogenic pulmonary edema
• Treatment with respiratory suppressant medications (barbiturates, sedatives, paralytics)
Recommendations for initial ventilator settings for patients with head injury are listed in Table 20-3 and Figure 20-3. Full ventilator support is almost always initially required for these patients, and can be provided by continuous mandatory ventilation (A/C). Because of the depressed neurologic status of these patients and the need to control Paco2, pressure support ventilation as the initial mode in these patients is usually not appropriate. As respiratory status improves and spontaneous breathing becomes acceptable, pressure support ventilation can be used.
Table 20-3Initial Mechanical Ventilator Settings With Head Injury ||Download (.pdf) Table 20-3 Initial Mechanical Ventilator Settings With Head Injury
|Setting ||Recommendation |
|Mode ||CMV (A/C) |
|Rate ||15-25 breaths/min |
|Volume/pressure control ||Volume or pressure |
|Tidal volume ||6-8 mL/kg IBW provided that plateau pressure ≤ 30 cm H2O |
|Inspiratory time ||1 s |
|PEEP ||5 cm H2O provided that PEEP does not increase ICP |
| ||1.0 |
An algorithm for mechanical ventilation of the patient with head injury.
Because patients with head injury often have relatively normal lung function, oxygenation is usually not a problem. With these patients, 100% oxygen is initially administered and can be rapidly weaned using pulse oximetry. A Pao2 more than 80 mm Hg is often used because this minimizes the potential for periodic episodes of hypoxemia and associated rises in ICP. An initial PEEP level of 5 cm H2O is usually appropriate and adequate. Although there is concern related to the effects of PEEP on ICP, PEEP usually does not adversely affect ICP at levels less than or equal to 10 cm H2O. With neurogenic pulmonary edema, the management of oxygenation is similar to that with other causes of ARDS, although care must be taken to avoid the effects of high MAP on ICP. In patients requiring high levels of PEEP, the head of the bed should be raised to minimize the effect of the increased intrathoracic pressure and ICP should be carefully monitored.
The choice of volume-controlled or pressure-controlled ventilation is based on clinician's bias. A tidal volume in the range of 6 to 8 mL/kg ideal body weight can be used provided that plateau pressure is kept below 30 cm H2O. This is usually not a problem, because these patients typically have a nearly normal lung and chest wall compliance. The ventilatory goal is to maintain the Pco2 35 to 45 mm Hg and pH 7.35 to 7.45. If the patient has concomitant acute or chronic respiratory disease, a lower tidal volume is selected. A respiratory rate appropriate to achieve normal acid-base balance should be chosen. This can often be achieved at a rate of 15 to 25 breaths/min. An inspiratory time of 1 second is usually adequate.
Monitoring of mechanically ventilated head-injured patients is similar to that of any mechanically ventilated patient (Table 20-4). If minute ventilation is increased to produce iatrogenic hyperventilation for a short period of time, the presence of auto-PEEP must be evaluated. Capnography may be useful to monitor the level of ventilation in these patients, who often have normal lung function and do not tolerate well an increase in Paco2.
Table 20-4Monitoring of the Mechanically Ventilated Patient With Head Injury ||Download (.pdf) Table 20-4 Monitoring of the Mechanically Ventilated Patient With Head Injury
• Peak alveolar pressure, mean airway pressure, auto-PEEP
• and end-tidal
• Intracranial pressure, jugular venous oxygen saturation
• Pulse oximetry
• Heart rate and systemic blood pressure
Close observation of ICP should be used when ventilator settings are manipulated. If an ICP monitor is not present, clinical signs of an increased ICP (eg, pupillary response, posturing, changes in level of consciousness) should be evaluated when ventilator changes occur. Although airway clearance is important in these patients, care must be taken to avoid deleterious increases in ICP during suctioning. Nutritional support is necessary to facilitate healing and weaning from mechanical ventilation. Pulmonary embolism can occur in patients with prolonged immobility, and pulmonary infection is also common in these patients.
Jugular venous bulb oxygen saturation (Sjvo2) and brain Po2 (Pbo2) from a probe placed into the brain may be used as an index of the adequacy of cerebral oxygenation. The use of these monitors is controversial. If used, Sjvo2 less than 50% or Pbo2 less than 15 mm Hg are treatment thresholds.
Liberation should not be considered until respiratory depressant therapy is no longer required. Ventilator discontinuation can often be initiated before the patient's neurologic function is maximally restored if the ventilatory drive is intact. For some patients, maintenance of a stable airway is required for a longer time than ventilatory support (ie, tracheostomy). However, extubation should not be delayed solely on the basis of depressed neurologic status. Due to central neurologic dysfunction, ventilator liberation, extubation, and decannulation of some of these patients can be prolonged and difficult. Weaning approaches should incorporate spontaneous breathing trials and appropriate rest following a failed trial of spontaneous breathing.
An apnea test is commonly conducted as part of the diagnosis of brain death. Before conducting the apnea test, the following prerequisites should be met: core temperature more than or equal to 36.5°C, systolic blood pressure more than or equal to 90 mm Hg, euvolemia, normoxemia (or Pao2 > 200 mm Hg breathing 100% oxygen), and eucapnia (or Paco2 > 40 mm Hg in the patient with chronic hypercapnia). The following procedure is used:
Disconnect the ventilator.
Administer 6 L/min O2, either by T-piece or by a catheter passed into the trachea.
Observe the patient closely for signs of respiratory movements. If respiratory movements occur, the apnea test is negative (ie, does not support the clinical diagnosis of brain death), and mechanical ventilation is resumed.
If respiratory movements do not occur, measure arterial blood gases after 8 minutes and reconnect the ventilator.
If respiratory movements are absent and Paco2 is more than 60 mm Hg (or 20 mm Hg greater than baseline), the apnea test result is positive and consistent with the clinical diagnosis of brain death.
If hypotension or desaturation occurs during the apnea test, the ventilator is reconnected and the test is resumed at a later time.
If no respiratory movements are observed, Paco2 is less than 60 mm Hg, and no adverse effects occur, the test may be repeated with 10 minutes of apnea.