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Revista Brasileira de Terapia Intensiva

AMIB - Associação de Medicina Intensiva Brasileira


ISSN: 0103-507X
Online ISSN: 1982-4335

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Oliveira-Abreu M, Almeida ML. Manuseio da ventilação mecânica no trauma cranioencefálico: hiperventilação e pressão positiva expiratória final. Rev Bras Ter Intensiva. 2009;21(1):72-79



Review Article

Management of mechanical ventilation in brain injury: hyperventilation and positive end-expiratory pressure

Manuseio da ventilação mecânica no trauma cranioencefálico: hiperventilação e pressão positiva expiratória final

Matheus Oliveira-AbreuI, Mônica Lajana de AlmeidaII

ISpecialist in Cardiorespiratory Physiotherapy by the Instituto do Coração (InCor) of the Hospital das Clínicas of the Faculdade de Medicina, Universidade de São Paulo - USP - São Paulo (SP), Brazil
IIProfessor of the Faculdade Social and of the União Metropolitana de Educação e Cultura - UNIME - Salvador (BA), Brazil

Submitted on June 8, 2008
Accepted on March 9, 2009

Corresponding author:

Matheus Oliveira Abreu
Rua Florentino Silva, 243 - Itaigara
CEP: 41815-400 - Salvador (BA), Brazil
Phone: (11) 8539-4667
E-mail: [email protected]



The study intended to make a critical review on use of pulmonary hyperventilation maneuvers and the different positive end-expiratory pressures applied to traumatic brain injury patients. As a reference were used publications in English, Spanish and Portuguese, contained in the following databases: MedLine, SciELO and LILACS, from 2000 to 2007, we included all studies about the use of pulmonary hyperventilation maneuvers and the different positive end-expiratory levels used for adult patients with brain injury at acute or chronic stage. Thirty one trials were selected, 13 about pulmonary hyperventilation, as prophylaxis, prolonged or optimized and 9 shows the levels of positive end-expiratory pressures used, ranging from 0 to 15 cmH2O. The prophylactic hyperventilation maneuver in the first 24 hours can lead to an increase of cerebral ischemia; the prolonged hyperventilation must be avoided if intracranial pressure did not increase; however optimized hyperventilation seems to be the most promising technique for control of the intracranial pressure and cerebral perfusion pressure; the rise of the positive end-expiratory pressure, up to 15cmH2O, can be applied in a conscientious form aiming to increase arterial oxygen saturation in lung injury.

Keywords: Brain trauma; Intracranial hypertension; Intracranial pressure; Positive-pressure respiration; Hyperventilation




Traumatic brain injury (TBI) is worldwide the main cause of morbidity mortality in individuals less than 45 years old with higher prevalence in the male gender. It takes place in about 40% of victims of trauma, and 20% of them die on the spot or in the first day of admission and 80% in the first seven days after the event.(1-3)

TBI is a non-degenerative or congenital injury caused by an aggression or started by a process of high energy acceleration or deceleration of the brain inside the cranium which generates an anatomical damage or functional impairment of the scalp, cranium, meninges and encephalus.(4,5) It can be caused by traffic accident, falls, aggressions, cold steel or firearm perforation, major catastrophes and sport activities.(6) When appropriate, drugs and alcohol in the organism must be examined.(7)

Two different mechanisms determine severity of trauma (1) first insult, which takes place at the time of impact; (2) second insult which represents a pathological process subsequent to the initial clinical changes of trauma.(1)

Lowering of the level of consciousness is the main risk factor for bronchoaspiration and later admission to the intensive care unit (ICU) for the purpose of detecting and treating complications of the primary injury and supply a better condition for brain function recovery.(8) Therefore patients with problems related to the central nervous system (CNS) often need ventilation support due to acute respiratory failure (ARF), not always caused by the neurological condition itself, such as decrease of the respiratory drive, but because of lung disease.(9)

Mechanical ventilation is an essential therapeutic device for patients with severe TBI, since it aims to protect the airway by endotracheal intubation and permits sedation, including curarization thus avoiding damages caused by hypoxemia and hyercapnia.(10)

Based on ventilation therapies adopted during the last years for patients with TBI, mainly for those presenting intracranial hypertension (ICH) this review intended to compare the different ventilation techniques used for management of patients with TBI and the impact on the parameters of neurological monitoring.



A review of literature on TBI was made using as reference publications in English, Spanish and Portuguese whose keywords were traumatic brain injury, intracranial hypertension, intracranial pressure, positive end-expiratory pressure (PEEP) and hyperventilation found in the MedLine, SciELO and LILACS databases, published from 2000 to 2007. Studies that approached different levels of PEEP and use of pulmonary hyperventilation maneuvers in the adult patient with acute or chronic TBI as well as impacts on the neurological parameters were selected.

Criteria were defined to assess the studies, guarantee the works quality, such as: (a) identification of the study for type of treatment and how the technique is performed; (b) methodological characteristic of clinical trials or of review articles. When evaluating qualitative attributes, were considered decrease or increase of the intracranial pressure (ICP) as well as normalization of the cerebral perfusion pressure (CPP) and mean arterial pressure (MAP).



Mechanism of TBI causes disruption of the hematoencephalic barrier permitting plasma components to easily cross this barrier towards the neural tissue (vasogennic edema). Hypoxia (secondary insult) affects the sodium-potassium ATPase of the cell membrane, promoting intracellular accumulation of sodium and subsequent water flow to the cell by osmotic gradient. As such, a cytotoxic edema occurs, however, at the sub acute and/or chronic stage. Therefore, the vasogenic edema, accrued by eventual localized areas of hemorrhage with mass effect, is primarily responsible for appearance of intracranial hypertension. Such mechanisms reach their peak in about three to five days.(11,12)

Changes in the brain flow, inflammation and edema are components of the pathogenesis of brain tissue alterations. The brain is contained in a rigid, not compliant structure in which a relatively low level of swollen tissue can increase the ICP. It also has a special self-regulatory system of the cerebral blood flow (CBF) maintained in normal conditions, even with MAP ranging from 50 to 140 mmHg. Self-regulation of the CBF is achieved by the rapid constriction and relaxation of the cerebral arterioles and venules in response to chemical and endothelial factors and to release of neurotransmitters from adjacent neurons.(8)

CBF relies on the difference of arterial pressure and cerebral venous pressure, being inversely proportional to the cerebral vascular resistance. CPP is calculated by the difference between MAP and the ICP. A CPP of 60 mmHg is commonly accepted as the minimal value needed for adequate cerebral perfusion.(11-13) ICP is determined by pressure of the cerebral parenchyma, cerebral blood volume and fluid volume.(3) Increase of ICP is common after TBI when intracranial compliance is unable to accommodate volume increase. The normal value of ICP in adults is 10 mmHg, values over 20 mmHg require therapeutic intervention. Values from 10 to 20 are considered slightly increased and between 20 and 40 mmHg moderately high. Over 40 mmHg are the severe cases of intracranial hypertension, when herniations of nervous tissue may occur.(8,14)

Hyperventilation may reduce ICP by hypocapnia that induces cerebral vasoconstriction with subsequent reduction of CBF. Routine induction of vasoconstriction by hypocapnia may cause an accidental decrease of the CBF, which would exacerbate perfusion deficit leading later to brain ischemia.(9.15-17)

PEEP increases functional residual capacity (FRC) and may reduce incidence of mechanical ventilation induced injury. However, it may have deleterious effects on the brain compartment by increase of in-trathoracic pressure that will increase central venous pressure (CVP) influencing return flow of blood to the heart. Finally, the cardiac output (CO) is reduced, with subsequent decrease of MAP and CPP.(18)



In this study 31 publications were selected from the year 2000 to 2007, 11 articles on utilization of pulmonary hyperventilation,(10,13,15-17,19-24) 7 on utilization of PEEP(4,18,26-30), two encompassing both subjects(14,25) and 11 general articles on TBI.(1-3,5-9,11,12,31) Only one article about pulmonary hyperventilation was clinical(20) while five were found about PEEP level.(18,26-29)

Pulmonary hyperventilation

Regarding pulmonary hyperventilation all nine articles mentioned prophylactic hyperventilation and agreed that it is not recommended in the first 24 hours, since CBF is reduced at this time after trauma(10,13,16,19,21-25). Six articles conclude that prolonged pulmonary hyperventilation must be avoided in the absence of high ICP as sustained vasoconstriction reduces CBF to deleterious levels and could generate brain ischemia.(10,14,19,21,23,24) There is a consensus about optimized hyperventilation for a short time with high ICP and the causal factor for increase of ICP must be sought and efforts be made to treat it. There is also a consensus about the cerebral vasoconstrictor effect of hypocapnia, generated by hyperventilation, which reduces CBF and ICP (Chart 1).

In the first hours after TBI, absolute values of CBF match those of an ischemic event and in this case the hyperventilation maneuver does not always reduce ICP to improve CPP. The ideal value for PaCO2 is the one that keeps ICP < 20 mmHg and cerebral extraction of oxygen (CEO2) between 24% and 42% to avoid brain ischemia.(20) PaCO2 must be kept at 35mmHg and 40 mmHg while hyperventilation is reserved for cases with cerebral herniation.(15,21)

Prophylactic and prolonged hyperventilation maneuvers are not recommended during the first 24 hours,(10,13,14,16,17,19,22-24) or out of the intensive care unit.(25) Hyperventilation is recommended whenever there is monitoring of ICP(16) being indicated for a short time in episodes of its elevation. In prolonged hyperventilation, jugular venous oxygen saturation (SjO2) and partial oxygen pressure in the brain tissue (PbrO2) must be monitored.(14)

Clinical data showed worse prognosis in severe TBI, routinely treated with hyperventilation. Hyperventilation becomes appropriate in two situations: (1) treatment of difficult to control ICH; (2) CBF at normal level or high at onset of ICH. Also when brain deterioration with suspicion of intracranial mass lesion has occurred.(22)

Hyperventilation may be needed at times of acute brain deterioration or in long periods of ICH refractory to sedation, paralysis, drainage of cerebrospinal fluid and osmotic diuretics.(24)

In an aggressive form hyperventilation may produce sites of brain ischemia. If, after fluid drainage, ICP remained between 20 to 25 mmHg, hyperventilation must be used in an effort to maintain PaCO2 between 30 to 35 mmHg. In presence of ICH refractory to drugs and surgical procedures, PaCO2 < 30 mmHg must be maintained with monitoring of SjO2 and CBF.(17)

Utilization of positive end-expiratory pressure

Among the articles on PEEP, five include levels ranging from 0 to 15 cmH2O and suggest that PEEP may be used, whenever statistically significant increases of ICP have not occurred.(4,14,27,29,30) Videtta et al. observed a significant increase of ICP in PEEP of 10 to 15 cmH2O without significant changes of CPP.(28) Gamberoni et al. disclosed changes in respiratory mechanics due to TBI(26) and three articles showed that, in patients with poor pulmonary compliance, use of PEEP up to 12 cmH2O, caused insignificant increase of ICP (Chart 2).(14,18,25)

Moderate levels of PEEP, as 15 mmH2O or even higher, can be safely used in patients with cerebral lesions, mainly in those with low pulmonary compliance.(26) It was observed and suggested that PEEP levels up to 12 cmH2O resulted in a non-significant rise in ICP.(27)

Application of PEEP at 10 and 15 cmH2O levels significantly increased ICP, without significant change in CPP, in patients with acute lung injury (ALI).(28) Increased in levels of PEEP from 0 to 12 cmH2O generated a decrease of MAP in patients wit normal compliance and these same values in patients with poor compliance did not bring about significant variations. Therefore, normal respiratory compliance is one of the factors assisting transmission of harmful effects of PEEP to the intracranial system.(18)

Careful control of plateau pressure, up to 30 cmH2O must be a rational practice with due surveillance of ICP and CPP when there is elevation of PaCO2.(14) To use or not low levels of PEEP to avoid elevation of ICP is inadequate as it does not correct hypoxemia, which could reduce ICP by better cerebral oxygenation.(4,25) Effect of PEEP on brain circulation relies on intracranial compliance an on the absolute value of ICP. ICP will not be affected while it remains above CVP generated by PEEP.(30)

Because of methodological problems there are few epidemiological studies on TBI and this is a hindrance also found in more developed countries.(31) Ventilation management based upon scientific knowledge is needed for these patients and may interfere in their prognosis.



Based upon scientific studies, as well as on better understanding of the physiopathology of TBI and its aftermaths, prophylactic hyperventilation in the first 24 hours to achieve a decrease of ICP by cerebral vasoconstriction may lead to an increase of the injured cerebral area due to tissue hypoperfusion. Prolonged hyperventilation must be avoided if ICP is not high. However, optimized hyperventilation in short periods seems to be the most promising technique for control of ICP and CPP.

Elevation of PEEP, limited to 15 cmH2O, may be applied in an responsible way to improve alveolar oxygenation and increase of SaO2 in lung injury, ensure an improvement of lung compliance.



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Received from the União Metropolitana de Educação e Cultura - UNIME - Salvador (BA), Brazil.



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