When to use hyperventilation to lower intracranial pressure

GUIDELINES

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Effects of Hyperventilation and Rebreathing on Nasal Airflow

The partial pressure of carbon dioxide in arterial blood is the major factor that influences ventilation mediated by peripheral and central chemoreceptors. The pressure of carbon dioxide can be lowered by hyperventilation and increased by breath holding or asphyxia. These changes in the partial pressure of carbon dioxide are accompanied by changes in the drive to breathe and by changes in nasal airway resistance.

Tatum65 studied anesthetized dogs and rabbits and demonstrated that partial asphyxia caused a nasal vasoconstrictor response, whereas hyperventilation caused nasal vasodilation. The nasal vasoconstrictor response to partial asphyxia was abolished on section of the cervical sympathetic nerves, whereas the vasodilator response to hyperventilation was unaffected. Rebreathing from a bag or prolonged breath holding in humans decreased nasal airway resistance, whereas hyperventilation increased nasal airway resistance.66

The nasal vasoconstrictor response to an elevation in blood carbon dioxide can be explained by a reflex increase in sympathetic nervous activity mediated by peripheral and central chemoreceptors. The reduction in nasal airway resistance associated with asphyxia and rebreathing has some functional significance, because the increase in nasal patency facilitates ventilation. The nasal vasodilator response to a decrease in blood carbon dioxide is more difficult to explain, because it is unaffected by section of the sympathetic nerves65 and may be mediated by parasympathetic pathways.67

Medical history questionnaire

Hyperventilation can be prevented most effectively through the recognition and management of anxiety. An anxiety questionnaire (see Chapter 2) may be included as part of the medical history the patient completes before the doctor begins treatment. Treatment can then be modified to accommodate the patient’s fears. The stress reduction protocol is an invaluable asset in this quest. Though there are no specific questions on the long- or short-form medical histories that relate to hyperventilation, question 5 (Have you had problems with prior dental treatment?) offers a patient the opportunity to mention prior bad dental office experiences or dental fears.

Hyperoxia–Hyperventilation Test

The hyperoxia test aids in differentiating between primary lung disease and congenital heart disease with right-to-left shunting. The test is performed by placing the infant in 100% oxygen for 5-10 minutes followed by monitoring oxygenation by arterial blood gas or noninvasive measures (seeChapter 64). In patients with primary lung disease, oxygen should diffuse into the poorly ventilated areas and improve oxygenation by 5-10 minutes of oxygen exposure. Persistent hypoxemia after this time period would suggest the presence of right-to-left shunting.

A modification of the hyperoxia test combining hyperoxia with hyperventilation can be used to distinguish between structural congenital heart disease and primary (or persistent) pulmonary hypertension of the newborn (PPHN), both of which have right-to-left shunting. Inhalation of 100% oxygen improves oxygenation in some patients with PPHN. In response to hyperventilation with 100% oxygen (Paco2 25-30 mm Hg), more infants with PPHN achieve Pao2 levels higher than 100 mm Hg. In contrast, patients with anatomically fixed right-to-left shunting rarely generate a Pao2 well above 40-50 mm Hg, even with inhalation of 100% oxygen and hyperventilation.

Hyperventilation

Hyperventilation reduces ICP via a reduction of CBV. Unfortunately, hyperventilation also causes a reduction in CBF and, therefore, the main concern when patients are hyperventilated is the possibility of inducing cerebral ischemia. Prophylactic hyperventilation of TBI patients to a Paco2 of 3.4 kPa (26 mmHg) has been shown to be detrimental to outcome and aggressive hyperventilation to below a Paco2 of 3.5 kPa is therefore not recommended. There is an ongoing controversy about the risk of moderate hyperventilation (Paco2 4.5–3.5 kPa; 34–26 mmHg) to cause ischemia in brain injury. Nevertheless, it is recommended to monitor cerebral oxygenation if moderate hyperventilation is used. Our means of monitoring critical reductions of CBF during hyperventilation are very limited. Sjvo2 or Pbtio2 monitors are frequently used to avoid overaggressive hyperventilation (Bratton et al., 2007e). There is growing awareness that hyperventilation should be used sparingly, primarily to treat ICP plateau waves and herniation. For TBI patients, the Brain Trauma Foundation guidelines recommend moderate hyperventilation as a short-term measure only, except when other forms of medical ICP treatment have failed (Bratton et al., 2007f).

Hyperventilation

Under normal conditions, Paco2 is the most powerful determinant of CBF and, between a range of 20 and 80 mm Hg, CBF is linearly responsive to PaCO2. Formerly, so-called therapeutic hyperventilation was recommended as a method to reduce ICP. Unfortunately, however, this reduction in ICP is accomplished by reducing CBF, which is important in meeting the brain's metabolic demands. A low Paco2, therefore, and the resulting low CBF, may result in cerebral ischemia, whereas high Paco2 levels can result in cerebral hyperemia and high ICP. Normal ventilation is currently the goal for severe TBI patients in the absence of cerebral herniation, and Paco2 is maintained in the normal range, from 35 to 45 mm Hg.10 In the case of life-threatening cerebral herniation or significant ICP elevation, therapeutic hyperventilation is appropriate only as a short-term intervention, bridging to more definitive therapy (eg, craniectomy). Therefore, hyperventilation is recommended only as a temporizing measure for the reduction of elevated ICP and should not be used for routine management or prophylaxis. Hyperventilation should be avoided during the first 24 hours after injury when CBF is often critically reduced. If hyperventilation is used, jugular venous oxygen saturation (Sjo2) or brain tissue O2 partial pressure (Btpo2) measurements are recommended to monitor oxygen delivery.10,64 The neurologic effects of hypocapnia are illustrated inFig. 34.15.

Hyperventilation

Hyperventilation has been used in the treatment of severe TBI for the past 20 years. Recent pathophysiological understanding of TBI and the mechanism of ICP lowering of hyperventilation have put it under recent scrutiny. Hyperventilation decreases ICP by decreasing CO2 leading to cerebral vasoconstriction. This in turn leads to decreased cerebral blood flow (CBF). Aggressive sustained hyperventilation may lead to cerebral ischemia and stroke, especially in the severe TBI patient who may already have alterations in CBF and autoregulation.

Hyperventilation does have utility in the deteriorating TBI patient as a temporizing measure until more definitive treatment of elevated ICP may be implemented.

Current BTF recommendations show level II evidence against the routine use of prophylactic hyperventilation to Paco2 less than 25 mm Hg.9 Level III evidence exists that hyperventilation may be used as a temporizing measure in the acutely deteriorating patient.9 Hyperventilation should be avoided in the first 24 hours after TBI when CBF may be critically reduced. If hyperventilation is used, there is level III evidence for jugular venous oxygen monitoring or brain tissue oxygen tension monitoring.9

Hyperventilation

Hyperventilation has been used in the treatment of severe TBI since the late 1990s. A pathophysiologic understanding of TBI and the mechanism of ICP lowering of hyperventilation have put it under scrutiny. Hyperventilation decreases ICP by decreasing CO2 leading to cerebral vasoconstriction. This in turn leads to decreased cerebral blood flow (CBF). Aggressive sustained hyperventilation may lead to cerebral ischemia and stroke, especially in the severe TBI patient who may already have alterations in CBF and autoregulation.

Current BTF recommendations show level II evidence against the routine use of prophylactic hyperventilation to Paco2 less than 25 mm Hg.8 Hyperventilation should be avoided in the first 24 hours after TBI when CBF may be critically reduced. Prior recommendations for the use of hyperventilation as a temporizing measure in critically ill patients were not supported by further evidence in the most recent update.8,13

Hyperventilation

Hyperventilation should not be used routinely in these patients because of the risk of further compromising cerebral perfusion. Hyperventilation can be used for brief periods when there is acute neurologic deterioration or if intracranial hypertension is refractory to other treatment interventions. Under these circumstances, intraparenchymal brain-tissue oxygen monitoring is utilized to titrate the degree of hyperventilation and to avoid cerebral ischemia (Table 5). The use of prophylactic hyperventilation (PaCO2 = 35 mmHg) therapy during the first 24 h after severe TBI should be avoided because it can compromise cerebral perfusion during a time period when CBF is already decreased.

Hyperventilation (HV)

HV is a standard procedure during routine EEG recording. It is thought that the usefulness of HV depends on vasoconstriction secondary to resultant decreased CO2 concentration, thus inducing relative cerebral ischemia and decreased glucose utilization. Subjects may complain of lightheadedness or tingling in the extremities. Even tetany secondary to hypocalcemia may occur with particularly vigorous HV. The procedure is most effective in the young; in the elderly it has little effect.

The standard response is moderate to high-voltage, often rhythmic, delta and theta slowing with bifrontal preponderance (Figure 2-7). In the young, nearly continuous delta may be evoked. HV may bring out epileptiform discharges and focal slowing (Figure 2-8). In unmedicated children with absence epilepsy, it will provoke an absence seizure. As a rule, HV is carried out for 3 minutes with vigorous exhalation at an increased but not particularly rapid rate. Rapid HV moves little air and has correspondingly little effect. After the conclusion of HV the record should return to baseline levels in about 1 minute. If return to baseline occurs after a protracted period, it may represent an abnormality. The classic cause of a long return to baseline is hypoglycemia.

HV is often omitted in subjects over the age of 65 years due to its low yield. An elderly person's vascular system, probably due to disease, is less responsive to the metabolic changes precipitated by HV. In cases of suspected epilepsy, however, HV may be useful despite these limitations. Note that there are few contraindications for performing HV. In general, it is not performed in patients with pulmonary and cardiac disease. HV may be performed in patients with brain tumors, although if the resting record reveals clear focal slowing, the procedure probably offers little additional information.

Hyperventilation

HV is performed by asking the patient to breathe deeply at a rate of 18–24 breaths per minute for 2–3 min. Patients with severe cardiac or pulmonary disease, uncontrolled hypertension, sickle cell anemia, active asthma, or a recent ischemic event (such as myocardial infarction, stroke, transient ischemic attack, or subarachnoid hemorrhage) should not undergo HV (Holmes et al., 2004). In these situations, HV-induced hypocapnia and alkalosis may result in decreased cerebral perfusion or vasospasm that could further compromise circulation. A normal HV response is characterized by diffuse high-amplitude theta or delta background slowing (buildup) and is exaggerated during fasting (relative hypoglycemia). The EEG usually returns to baseline within 2 min after HV ends. Focal changes on the EEG during HV that do not resolve afterward are considered pathological.

HV is very effective in activating generalized 3-Hz spike-and-wave abnormalities (Fig. 7.6). Patients demonstrating hesitation or interruption of speech, memory, or activity during prolonged bursts of 3-Hz spike-and-wave discharges are likely undergoing an electroclinical absence seizure (Holmes et al., 2004). Generalized slow spike-and-wave at 1.5–2.5 Hz and focal interictal spikes and sharp waves can also infrequently be activated by HV. HV can also accentuate focal slowing caused by an underlying structural lesion or focal area of cortical dysfunction.