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

Abstracts

O objetivo desse artigo foi realizar uma revisão de literatura sobre a utilização de manobras de hiperventilação pulmonar e os níveis de pressão positiva expiratória final empregados em pacientes com trauma cranioencefálico. Foram utilizados como referências publicações em inglês, espanhol e português, contidas nas bases de dados: MedLine, SciELO e LILACS, de 2000 até 2007, tendo como critérios de inclusão: manobra de hiperventilação pulmonar e o nível de pressão positiva expiratória final aplicado ao paciente adulto com trauma cranioencefálico, agudo ou crônico. Foram selecionados 31 estudos, sendo 13 sobre a utilização da hiperventilação pulmonar, como profilática, prolongada ou otimizada e 9 abordavam o emprego da pressão positiva expiratória final, em níveis que variaram de 0 a 15 cmH2O. A hiperventilação profilática nas primeiras 24 horas pode levar a um aumento da isquemia cerebral; a hiperventilação prolongada deve ser evitada na ausência de elevada pressão intracraniana; já a hiperventilação otimizada parece ser a técnica mais promissora no controle da pressão intracraniana e da pressão de perfusão cerebral. A elevação da pressão positiva expiratória final até 15 cmH2O pode ser aplicada, de forma consciente, com o objetivo na elevação da saturação arterial de oxigênio em presença de injúria pulmonar.

Traumatismos craniocerebrais; Hipertensão intracraniana; Pressão intracraniana; Respiração com pressão positiva; Hiperventilação

REVIEW ARTICLE

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

Matheus Oliveira-Abreu^I; Mônica Lajana de Almeida^II

^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

Author for correspondence

ABSTRACT

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

INTRODUCTION

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.

METHODS

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).

PHYSIOPATHOLOGY OF TRAUMATIC BRAIN INJURY

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⁾

LITERATURE REVIEW

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.

CONCLUSION

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.

REFERENCES

• 1. Werner C, Engelhard K. Pathophysiology of traumatic brain injury. Br J Anaesth. 2007;99(1):4-9. Review.
• 2. Ferrari D. Trauma: questão de saúde pública. RE Rev Emergê Clín . 2006;5:12-4.
• 3. Gottesman RF, Komotar R, Hillis AE. Neurologic aspects of traumatic brain injury. Int Rev Psychiatry. 2003;15(4):302-9.
• 4. Dutton RP, McCunn M. Traumatic brain injury. Curr Opin Crit Care. 2003; 9(6):503-9. Review.
• 5. Ribas GC. Traumatismo cranioencefálico. In: Nitrini R, Bacheschi LA. A neurologia que todo médico deve saber. 2a. ed. São Paulo: Atheneu; 2003. p. 189-203.
• 6. Paranhos JLR, Moura AD. Traumatismo cranioencefálico. In: David CM, editor. Medicina intensiva. Rio de Janeiro: Revinter; 2004. p. 770.
• 7. Braunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL, editors. Harrison medicina interna. 16a. ed. Rio de Janeiro: McGraw-Hill; 2006. v. 2.
• 8. Zink BJ. Traumatic brain injury outcome: concepts for emergency care. Ann Emerg Med. 2001;37(3):318-32.
• 9. André C, Freitas GR, organizadores. Terapia intensiva em neurologia e neurocirurgia. Rio de Janeiro: Revinter; 2002.
• 10. Belda FJ, Aguilar G, Soro M, Maruenda A. Manejo ventilatório del paciente con traumatismo craneoencefálico grave. Rev Esp Anestesiol Reanim. 2004;51(3):143-50.
• 11. Tavares MP. Tratamento clínico do traumatismo crânioencefálico [ Internet]. Disponível em: <http://www.medstudents.com.br/neuroc/neuroc1.htm > Acesso em: 27 jul. 2006.
• 12. Giugno KM, Maia TR, Kunrath CL, Bizzi JJ. Tratamento da hipertensão intracraniana. J Pediatr (Rio J). 2003;79(4):287-96.
• 13. Stocchetti N, Maas AI, Chieregato A, van der Plas AA. Hyperventilation in head injury: a review. Chest. 2005;127(5):1812-27.
• 14. Deem S. Management of acute brain injury and associated respiratory issues. Respir Care. 2006;51(4):357-67.
• 15. Vincent JL, Berré J. Primer on medical management of severe brain injury. Crit Care Med. 2005;33(6):1392-9. Erratum in: Crit Care Med. 2005;33(9):2157. Comment in: Crit Care Med. 2005;33(11):2723; author reply 2723.
• 16. Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS, Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT, Nemecek A, Newell DW, Rosenthal G, Schouten J, Shutter L, Timmons SD, Ullman JS, Videtta W, Wilberger JE, Wright DW. Guidelines for the management of severe traumatic brain injury. XIV. Hyperventilation. J Neurotrauma. 2007;24 Suppl 1:S87-90. Erratum in: J Neurotrauma. 2008;25(3):276-8. multiple author names added.
• 17. Ghajar J. Traumatic brain injury. Lancet. 2000;356(9233):923-9. Review.
• 18. Caricato A, Conti G, Della Corte F, Mancino A, Santilli F, Sandroni C, et al. Effects of PEEP on the intracranial system of patients with head injury and subarachnoid hemorrhage: the role of respiratory system compliance. J Trauma. 2005;58(3):571-6.
• 19. Andrade FC, Andrade Júnior FC. Usos e abusos da hiperventilação nos traumatismos crânio-encefálicos graves. Arq Neuropsiquiatr. 2000;58(3A)648-55.
• 20. Falcão ALE, Araujo S, Dragosavac D, Terzi RGG, Thiesen R AS, Cintra EA, et al. Hemometabolismo cerebral: variações na fase aguda do coma traumático. Arq Neuropsiquiat. 2000; 58(3B):877-82.
• 21. Marik PE, Varon J, Trask T. Management of head trauma. Chest. 2002;122(2):699-711.
• 22. Valadka AB, Robertson CS. Surgery of cerebral trauma and associated critical care. Neurosurgery. 2007;61(1 Suppl): 203-20; discussion 220-1.
• 23. Vender JR. Hyperventilation in severe brain injury revisited. Crit Care Med. 2000;28(9):3361-2.
• 24. Brain Trauma Foundation. Management and prognosis of severe traumatic traumatic brain injury. New York (NY): The Brain Trauma Foundation, 2000.
• 25. Helmy A, Vizcaychipi M, Gupta AK. Traumaticbraininjury: intensive care management. Br J Anaesth. 2007;99(1):32-42. Review.
• 26. Gamberoni C, Colombo G, Aspesi M, Mascheroni C, Severgnini P, Minora G, et al. Respiratory mechanics in brain injured patients. Minerva Anestesiol. 2002;68(4):291-6.
• 27. Georgiadis D, Schwarz S, Baumgartner RW, Veltkamp R, Schwab S. Influence of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure in patients with acute stroke. Stroke. 2001;32(9):2088-92.
• 28. Videtta W, Villarejo F, Cohen M, Domeniconi G, Santa Cruz R, Pinillos O, et al. Effects of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure. Acta Neurochir Suppl. 2002;81:93-7.
• 29. Huynh T, Messer M, Sing RF, Miles W, Jacobs DG, Thomason MH. Positive end-expiratory pressure alters intracranial and cerebral perfusion pressure in severe traumatic brain injury. J Trauma. 2002;53(3):488-92; discussion 492-3.
• 30. Mascia L, Majorano M. Mechanical ventilation for patients with acute brain injury. Curr Opin Crit Care. 2000;6(1):52-6.
• 31. Koizumi MS, Lebrão ML, Mello-Jorge MHP, Primerano V. Morbimortalidade por traumatismo crânio-encefálico no município de São Paulo, 1997. Arq Neuropsiquiatr. 2000;58(1):81-9.

Publication Dates

• Publication in this collection
  04 May 2009
• Date of issue
  Mar 2009

History

• Received
  08 June 2008
• Accepted
  09 Mar 2000