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1999, Número 2

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Med Crit 1999; 13 (2)


Hiperventilación en trauma severo de cráneo y el monitoreo de la presión tisular de oxígeno cerebral

Carmona SJA, Maas A

Idioma: Español
Referencias bibliográficas: 43
Paginas: 49-58
Archivo PDF: 172.32 Kb.


RESUMEN

Objetivo. Describir los efectos de la hiperventilación sobre la oxigenación tisular cerebral (ptO2C).
Diseño. Estudio prospectivo y observacional.
Sitio. Unidad de cuidados intensivos neurológicos. Pacientes. Noventa pacientes con traumatismo severo de cráneo (Escala de Coma de Glasgow ≤ 8).
Intervenciones. Monitoreo de PIC, PPC y PtO2c por catéter tipo Clark y gases arteriales antes y después de la hiperventilación.
Mediciones. Diariamente, durante 15 minutos se incrementó el 20% del volumen minuto basal del ventilador en los 5 días posteriores al trauma. La PaCO2 disminuyó 3.3 ± 1.8 mm Hg (p ‹ 0.001) y la DPtO2c 2.8 ± 3.7 mm Hg (p ‹ 0.001). La D PtO2c incrementó de 0.8 ± 2.3 mm Hg en el 1er día hasta 6.1 ± 2.3 en el 5o día. En los 2 primeros días, no hubo diferencias significativas en la reactividad PaCO2/PtO2c entre ambos grupos pronósticos (pronóstico bueno y malo). Sin embargo, a partir del 3er día, la pérdida de oxígeno fue mayor en el grupo con peor pronóstico, llegando a ser significativa en el 5o día (p ‹ 0.05).
Conclusiones. La hiperventilación disminuyó la ptO2c, posible riesgo para el desarrollo de isquemia cerebral. El incremento de la reactividad a la PACO2 entre el 2o y 5o día afecta la oxigenación cerebral.


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