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Review
. 2017 Jul 17:8:250.
doi: 10.3389/fneur.2017.00250. eCollection 2017.

Hyperventilation Therapy for Control of Posttraumatic Intracranial Hypertension

Affiliations
Review

Hyperventilation Therapy for Control of Posttraumatic Intracranial Hypertension

Daniel Agustín Godoy et al. Front Neurol. .

Abstract

During traumatic brain injury, intracranial hypertension (ICH) can become a life-threatening condition if it is not managed quickly and adequately. Physicians use therapeutic hyperventilation to reduce elevated intracranial pressure (ICP) by manipulating autoregulatory functions connected to cerebrovascular CO2 reactivity. Inducing hypocapnia via hyperventilation reduces the partial pressure of arterial carbon dioxide (PaCO2), which incites vasoconstriction in the cerebral resistance arterioles. This constriction decrease cerebral blood flow, which reduces cerebral blood volume and, ultimately, decreases the patient's ICP. The effects of therapeutic hyperventilation (HV) are transient, but the risks accompanying these changes in cerebral and systemic physiology must be carefully considered before the treatment can be deemed advisable. The most prominent criticism of this approach is the cited possibility of developing cerebral ischemia and tissue hypoxia. While it is true that certain measures, such as cerebral oxygenation monitoring, are needed to mitigate these dangerous conditions, using available evidence of potential poor outcomes associated with HV as justification to dismiss the implementation of therapeutic HV is debatable and remains a controversial subject among physicians. This review highlights various issues surrounding the use of HV as a means of controlling posttraumatic ICH, including indications for treatment, potential risks, and benefits, and a discussion of what techniques can be implemented to avoid adverse complications.

Keywords: cerebral hypoxia; cerebral ischemia; hyperventilation; hypocapnia; intracranial hypertension; intracranial pressure; severe traumatic brain injury.

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Figures

Figure 1
Figure 1
The CO2 physiology from cells to alveoli.
Figure 2
Figure 2
The effects of arterial CO2 on cerebral blood flow.
Figure 3
Figure 3
The cerebral effects of hypocapnia.
Figure 4
Figure 4
The Xenon CT imaging that showed cerebral blood flow (CBF) decrease and O2 extraction fraction (OEF) increase after hyperventilation.
Figure 5
Figure 5
Six DO NOT rules.
Figure 6
Figure 6
The practical algorithm to perform HV safety. Hyperemia definition: increase in mean velocity (mv) of mean cerebral artery in TCD (TRANSCRANIAL DOPPLER) of more than 2 standard deviations.

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